PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
2562424-1	1989	British antilewisite (2,3-dimercaptopropanol; BAL) has long been used as an arsenic antidote, but its therapeutic efficacy is limited by its inherent toxicity.	Arsenic	76-83	poly (ADP-ribose) polymerase family, member 9	Mus musculus	46-49
24202416-2	1989	Concentrations of As(III) in the muM range and approximately 10-fold higher concentrations of As(V) led to a reduction of cellular proliferation and viability with a concomitant increase of LDH release and stimulation of lactate production.	Arsenic	18-20	latexin	Homo sapiens	33-36
2562424-2	1989	We synthesized two less toxic derivatives of BAL and investigated their potential as antidotes to organic arsenic.	Arsenic	106-113	poly (ADP-ribose) polymerase family, member 9	Mus musculus	45-48
3384494-2	1988	Occupational and environmental exposure to inorganic arsenic is associated with the occurrence of Raynaud"s phenomenon and objectively registered abnormal finger systolic blood pressure at local cooling (FSP).	Arsenic	53-60	C-X-C motif chemokine ligand 1	Homo sapiens	204-207
2465836-7	1988	The ability to study the properties of antigenic epitopes which preferentially bind to the very variable binding site of different MHC molecules raises the possibility of revealing the antigenic structures which bind to B27 molecules in patients with AS.	Arsenic	251-253	melanocortin 2 receptor accessory protein	Homo sapiens	220-223
18964516-2	1988	After the extract has been washed with 10M hydrochloric acid-2% thiourea solution to remove co-extracted copper and residual iron, arsenic(III) in the extract is oxidized to arsenic(V) with bromine solution in carbon tetrachloride and stripped into water.	Arsenic	131-138	PTOV1 extended AT-hook containing adaptor protein	Homo sapiens	56-62
18964492-1	1988	Arsenic and antimony in digested biological samples can be extracted with pyrrolidinecarbodithioate at pH 1 into chloroform and stripped with nitric acid for neutron-activation analysis (NAA).	Arsenic	0-7	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	103-107
2549882-6	1989	A combination assay of NCC-ST 439, CEA and CA 19-9 produced a high positive rates as 43.3% in primary and 86.2% in recurrent cases.	Arsenic	14-16	CEA cell adhesion molecule 3	Homo sapiens	35-38
2810799-4	1989	The degree of hemoglobin increase after administration of recombinant erythropoietin appeared to correlate with the intensity of inhibitory activity of AS.	Arsenic	152-154	erythropoietin	Homo sapiens	70-84
3236342-1	1988	Acute arsenic (As) administration produced in rat liver a decrease in the heme saturation of tryptophan pyrrolase (TP), accompanied by dose-related increases in 5-aminolevulinate synthetase (ALAS) and heme oxygenase (HO) activities, along with a corresponding decrease in cytochrome P-450 (P-450) concentration.	Arsenic	6-13	tryptophan 2,3-dioxygenase	Rattus norvegicus	93-113
3236342-1	1988	Acute arsenic (As) administration produced in rat liver a decrease in the heme saturation of tryptophan pyrrolase (TP), accompanied by dose-related increases in 5-aminolevulinate synthetase (ALAS) and heme oxygenase (HO) activities, along with a corresponding decrease in cytochrome P-450 (P-450) concentration.	Arsenic	6-13	tryptophan 2,3-dioxygenase	Rattus norvegicus	115-117
3236342-1	1988	Acute arsenic (As) administration produced in rat liver a decrease in the heme saturation of tryptophan pyrrolase (TP), accompanied by dose-related increases in 5-aminolevulinate synthetase (ALAS) and heme oxygenase (HO) activities, along with a corresponding decrease in cytochrome P-450 (P-450) concentration.	Arsenic	6-13	5'-aminolevulinate synthase 1	Rattus norvegicus	161-189
3236342-1	1988	Acute arsenic (As) administration produced in rat liver a decrease in the heme saturation of tryptophan pyrrolase (TP), accompanied by dose-related increases in 5-aminolevulinate synthetase (ALAS) and heme oxygenase (HO) activities, along with a corresponding decrease in cytochrome P-450 (P-450) concentration.	Arsenic	6-13	5'-aminolevulinate synthase 1	Rattus norvegicus	191-195
3236342-1	1988	Acute arsenic (As) administration produced in rat liver a decrease in the heme saturation of tryptophan pyrrolase (TP), accompanied by dose-related increases in 5-aminolevulinate synthetase (ALAS) and heme oxygenase (HO) activities, along with a corresponding decrease in cytochrome P-450 (P-450) concentration.	Arsenic	6-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	272-288
3236342-1	1988	Acute arsenic (As) administration produced in rat liver a decrease in the heme saturation of tryptophan pyrrolase (TP), accompanied by dose-related increases in 5-aminolevulinate synthetase (ALAS) and heme oxygenase (HO) activities, along with a corresponding decrease in cytochrome P-450 (P-450) concentration.	Arsenic	15-17	tryptophan 2,3-dioxygenase	Rattus norvegicus	93-113
3236342-1	1988	Acute arsenic (As) administration produced in rat liver a decrease in the heme saturation of tryptophan pyrrolase (TP), accompanied by dose-related increases in 5-aminolevulinate synthetase (ALAS) and heme oxygenase (HO) activities, along with a corresponding decrease in cytochrome P-450 (P-450) concentration.	Arsenic	15-17	tryptophan 2,3-dioxygenase	Rattus norvegicus	115-117
3236342-1	1988	Acute arsenic (As) administration produced in rat liver a decrease in the heme saturation of tryptophan pyrrolase (TP), accompanied by dose-related increases in 5-aminolevulinate synthetase (ALAS) and heme oxygenase (HO) activities, along with a corresponding decrease in cytochrome P-450 (P-450) concentration.	Arsenic	15-17	5'-aminolevulinate synthase 1	Rattus norvegicus	161-189
3236342-1	1988	Acute arsenic (As) administration produced in rat liver a decrease in the heme saturation of tryptophan pyrrolase (TP), accompanied by dose-related increases in 5-aminolevulinate synthetase (ALAS) and heme oxygenase (HO) activities, along with a corresponding decrease in cytochrome P-450 (P-450) concentration.	Arsenic	15-17	5'-aminolevulinate synthase 1	Rattus norvegicus	191-195
3236342-1	1988	Acute arsenic (As) administration produced in rat liver a decrease in the heme saturation of tryptophan pyrrolase (TP), accompanied by dose-related increases in 5-aminolevulinate synthetase (ALAS) and heme oxygenase (HO) activities, along with a corresponding decrease in cytochrome P-450 (P-450) concentration.	Arsenic	15-17	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	272-288
3672518-15	1987	Long-term pretreatment of rats with CCl4 slightly reduces the amount of MMA and DMA excreted in urine following a challenge dose of inorganic arsenic.	Arsenic	142-149	C-C motif chemokine ligand 4	Rattus norvegicus	36-40
3115333-7	1987	Four micrograms per milliliter AS-vWF caused a 69% reduction in total platelet adherence compared with citrated whole blood (P less than .001), and 4 micrograms/mL AS,AG-vWF led to a 48% reduction (P less than .005).	Arsenic	31-33	von Willebrand factor	Homo sapiens	34-37
3022321-5	1986	The molecular sizes of opioid receptor complexes were estimated as 313,000 +/- 13,500 in the presence of [D-Ala2, D-Leu5] enkephalin, NaCl and Gpp (NH)p; as 165,000 +/- 8,500 in the presence of NaCl only, or of both NaCl and Gpp (NH)p; as 217,000 +/- 6,600 in the presence of Gpp (NH)p only; and as 286,000 +/- 60,900 in the presence of MgCl2 only.	Arsenic	64-66	proenkephalin	Rattus norvegicus	122-132
2416880-3	1986	In the presence of [3H]palmitic acid, CoA, ATP, and Mg2+, acylation of endogenous PLP occurred at a linear rate for at least 2 h. The radioactivity was associated with the protein via an ester linkage, mainly as palmitic acid.	Arsenic	121-123	proteolipid protein 1	Homo sapiens	82-85
3527085-1	1986	We have previously shown that antisera raised in rabbits to certain enteric cross reactive strains of bacteria are capable of specifically lysing the peripheral blood lymphocytes of HLA-B27 positive patients with ankylosing spondylitis (B27+ AS+).	Arsenic	242-245	major histocompatibility complex, class I, B	Homo sapiens	182-189
2865691-8	1985	The mean plasma GH value [11.20-13.00 h] in animals receiving AS and CRF was not significantly different from those in animals receiving saline (i.v.)	Arsenic	62-64	gonadotropin releasing hormone receptor	Rattus norvegicus	16-18
3878756-1	1985	The culture filtrate of some bacteria contains a modifying factor which specifically interacts with the cells of HLA-B27-positive normal individuals (BS+ AS-); this modification results in a serologically detectable change similar to that seen on the cells of patients with ankylosing spondylitis (B27+ AS+).	Arsenic	154-156	major histocompatibility complex, class I, B	Homo sapiens	113-120
3878756-1	1985	The culture filtrate of some bacteria contains a modifying factor which specifically interacts with the cells of HLA-B27-positive normal individuals (BS+ AS-); this modification results in a serologically detectable change similar to that seen on the cells of patients with ankylosing spondylitis (B27+ AS+).	Arsenic	303-306	major histocompatibility complex, class I, B	Homo sapiens	113-120
4076075-4	1985	Both As and Se appear to be mobilized from household plumbing into tap water by the corrosive action of soft, mildly acidic water, while surface water catchment systems in areas impacted by acidic deposition may contain elevated soluble As levels.	Arsenic	5-7	nuclear RNA export factor 1	Homo sapiens	67-70
2415158-1	1985	Myelin basic protein (MBP)--the major extrinsic membrane protein of central nervous system myelin--from several species contains a rarely encountered highly conserved triproline segment as residues 99-101 of its 170-residue sequence.	Arsenic	8-10	myelin basic protein	Bos taurus	22-25
2992562-4	1985	Falls of angiotensin II were as great with 20 mg as with 50 mg of HOE 498, although the effect was more prolonged with 50 mg.	Arsenic	29-31	angiotensinogen	Homo sapiens	9-23
7169216-3	1982	The frequency of Hb Bart"s was 4.46% in AA phenotype, 5.25% in AS, and 6.67% in AC.	Arsenic	63-65	ADP ribosylation factor like GTPase 2 binding protein	Homo sapiens	20-24
3971587-4	1985	Agglutination occurring within 1 min (result coded as + + + +) corresponded to 761 +/- 366 micrograms/l of myoglobin; between 1 and 2 min (+ + +), to 285 +/- 101 micrograms/l; between 2 and 3 min (+ +), to 85 +/- 47 micrograms/l; between 3 and 4 min (+), to 51 +/- 38 micrograms/l; and after more than 4 min (-), to 31 +/- 16 micrograms/l.	Arsenic	51-61	myoglobin	Homo sapiens	107-116
6610633-2	1984	These modified fibroblasts are serologically similar to the cells (lymphocytes and fibroblasts) of B27-positive patients with ankylosing spondylitis (B27+AS+).	Arsenic	154-157	melanocortin 2 receptor accessory protein	Homo sapiens	99-102
6719100-4	1984	Urinary As consists of 10% each of InAs, MMAA and DMAA, the remaining 70% consisting of other forms of organic As.	Arsenic	8-10	metabolism of cobalamin associated A	Homo sapiens	41-45
6528814-2	1984	It was established that some of the metals (Cu, Cd, Bi) inhibited MAO activity both in vivo and in vitro experiments, others like Ni, Zn, As and Sn inhibited it only in vivo while Hg exerted inhibitory action only in vitro.	Arsenic	138-140	monoamine oxidase A	Rattus norvegicus	66-69
6415871-0	1983	Arsenic metabolites in urine and feces of hamsters pretreated with PCB.	Arsenic	0-7	pyruvate carboxylase	Homo sapiens	67-70
6415871-5	1983	PCB influenced the metabolism of arsenic by significantly increasing the proportion of DMA excreted into the urine of female hamsters during the 5 days after the arsenic administration, but did not alter the total amount of arsenic metabolites in any group of male or female hamsters.	Arsenic	33-40	pyruvate carboxylase	Homo sapiens	0-3
6602220-4	1983	When compared with Pr65gag, gPr80gag contains 7,000 daltons of additional amino acids, presumably as, or as part of, a leader sequence at or very close to its N terminus.	Arsenic	98-100	oxoglutarate receptor 1	Homo sapiens	28-33
6415871-5	1983	PCB influenced the metabolism of arsenic by significantly increasing the proportion of DMA excreted into the urine of female hamsters during the 5 days after the arsenic administration, but did not alter the total amount of arsenic metabolites in any group of male or female hamsters.	Arsenic	162-169	pyruvate carboxylase	Homo sapiens	0-3
6415871-5	1983	PCB influenced the metabolism of arsenic by significantly increasing the proportion of DMA excreted into the urine of female hamsters during the 5 days after the arsenic administration, but did not alter the total amount of arsenic metabolites in any group of male or female hamsters.	Arsenic	162-169	pyruvate carboxylase	Homo sapiens	0-3
6415871-7	1983	These results suggest that the metabolism of arsenic may be regulated by certain sex-relating factors which are influenced by PCB.	Arsenic	45-52	pyruvate carboxylase	Homo sapiens	126-129
6358457-3	1983	To elucidate the mechanism of this antimutagenicity, modifying effect of the arsenics on UV-induced cytotoxicity for Hs30R and NG30 (recA-; Exc+Rec-) cells was examined.	Arsenic	77-85	dimethylarginine dimethylaminohydrolase 2	Homo sapiens	127-131
6358457-3	1983	To elucidate the mechanism of this antimutagenicity, modifying effect of the arsenics on UV-induced cytotoxicity for Hs30R and NG30 (recA-; Exc+Rec-) cells was examined.	Arsenic	77-85	RAD51 recombinase	Homo sapiens	133-137
6358457-4	1983	In a nutrient medium containing the arsenics, the survived cell fraction of NG30 after ultraviolet (UV) irradiation was markedly increased, whereas that of Hs30R was not altered.	Arsenic	36-44	dimethylarginine dimethylaminohydrolase 2	Homo sapiens	76-80
6358457-5	1983	When the UV-exposed NG30 cells were subjected to recovery incubation in a nutrient medium containing the arsenics, the survived cell fraction was remarkably increased before the cell proliferation in a similar manner as liquid-holding recovery observed in an arsenic-free and non-nutrient medium in which DNA replication was suppressed.	Arsenic	105-113	dimethylarginine dimethylaminohydrolase 2	Homo sapiens	20-24
6358457-5	1983	When the UV-exposed NG30 cells were subjected to recovery incubation in a nutrient medium containing the arsenics, the survived cell fraction was remarkably increased before the cell proliferation in a similar manner as liquid-holding recovery observed in an arsenic-free and non-nutrient medium in which DNA replication was suppressed.	Arsenic	105-112	dimethylarginine dimethylaminohydrolase 2	Homo sapiens	20-24
6358457-6	1983	The arsenics were found to cause a delay of DNA replication in UV-irradiated NG30 cells.	Arsenic	4-12	dimethylarginine dimethylaminohydrolase 2	Homo sapiens	77-81
18963324-2	1983	The arsenicals (after reduction of arsenic to the tervalent state) readily react with 2,3-dimercaptopropanol (BAL) to yield their BAL complexes.	Arsenic	4-11	poly(ADP-ribose) polymerase family member 9	Homo sapiens	110-113
18963324-2	1983	The arsenicals (after reduction of arsenic to the tervalent state) readily react with 2,3-dimercaptopropanol (BAL) to yield their BAL complexes.	Arsenic	4-11	poly(ADP-ribose) polymerase family member 9	Homo sapiens	130-133
7302564-6	1981	Based on measured absorption and retention of arsenic in man, it is estimated that an ingestion intake rate of arsenic in terrestrial foods of 1 mg y-1 contributes a concentration of arsenic in the body of 0.28 microgram kg-1.	Arsenic	111-118	RNA, Ro60-associated Y1	Homo sapiens	148-151
7302564-6	1981	Based on measured absorption and retention of arsenic in man, it is estimated that an ingestion intake rate of arsenic in terrestrial foods of 1 mg y-1 contributes a concentration of arsenic in the body of 0.28 microgram kg-1.	Arsenic	111-118	RNA, Ro60-associated Y1	Homo sapiens	148-151
7302564-7	1981	The relationship is 0.14 microgram kg-1 per mg y-1 intake of organic arsenic in seafood.	Arsenic	69-76	RNA, Ro60-associated Y1	Homo sapiens	47-50
6263598-7	1980	The responsiveness to ACTH was nearly normal in patients receiving alternate-day therapy with prednisolone in such large doses as 50 or 60 mg every other day, but was completely suppressed in patients receiving 1.0 mg betamethasone every other day.	Arsenic	28-30	proopiomelanocortin	Homo sapiens	22-26
6895259-1	1981	The administration of trivalent arsenic, either as sodium arsenite or as the trypanocidal drug melarsoprol, to rats produced a profound induction of microsomal heme oxygenase (EC 1.14.99.3) in both liver and kidney and a concomitant decrease in cytochrome P-450 content.	Arsenic	32-39	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	245-261
7242389-1	1981	A microorganism oxidizing As(III) to As(V) was isolated from the water of a gold-arsenic deposit; the process occurs under the autotrophic conditions.	Arsenic	81-88	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	37-42
6451176-5	1980	Predisposing factors to AS, such as insertion of intrauterine device, hysterosalpingography, and curettage within 4 weeks of admission, were more common in the C-AS group.	Arsenic	24-26	catenin delta 1	Homo sapiens	160-164
184294-3	1976	The activity of glucose-6-phosphatase was inhibited in all of these sites in sections containing arsenic.	Arsenic	97-104	glucose-6-phosphatase, catalytic	Mus musculus	16-37
7440438-10	1980	In the experiments with lactating dairy cows, significantly higher levels of arsenic in milk were observed for cows fed either 3.2 or 4.8 mg of arsenic per kilogram of body weight from arsanilic acid or 3-nitro.	Arsenic	144-151	Weaning weight-maternal milk	Bos taurus	88-92
7440438-12	1980	Milk arsenic from 3-nitro returned to pre-experiment levels within 5 days after arsenic was removed from the feed.	Arsenic	5-12	Weaning weight-maternal milk	Bos taurus	0-4
7440438-12	1980	Milk arsenic from 3-nitro returned to pre-experiment levels within 5 days after arsenic was removed from the feed.	Arsenic	80-87	Weaning weight-maternal milk	Bos taurus	0-4
7440438-13	1980	In the experiment conducted with arsanilic acid, arsenic feeding was stopped after 5 days and milk arsenic levels returned to pre-experiment levels within 7 days.	Arsenic	99-106	Weaning weight-maternal milk	Bos taurus	94-98
7416158-5	1980	The effects of arsenic on erythropoietin-induced erythroid differentation revealed a significant inhibitory effect on young, proliferating marrow nucleated erythroid precursor cells.	Arsenic	15-22	erythropoietin	Mus musculus	26-40
466981-5	1979	Urine arsenic levels in Ajo children correlated positively with amount of tap-water consumed (r = .32, p less than.	Arsenic	6-13	nuclear RNA export factor 1	Homo sapiens	74-77
466981-7	1979	Tap-water drinkers had significantly higher urine arsenic levels than bottled water drinkers (t = 4.21 p less than .001).	Arsenic	50-57	nuclear RNA export factor 1	Homo sapiens	0-3
716436-2	1978	Absorption of arsenic caused elevated urinary levels over 5 days BAL treatment was started within three hours after arsenic ingestion.	Arsenic	14-21	poly(ADP-ribose) polymerase family member 9	Homo sapiens	65-68
716436-2	1978	Absorption of arsenic caused elevated urinary levels over 5 days BAL treatment was started within three hours after arsenic ingestion.	Arsenic	116-123	poly(ADP-ribose) polymerase family member 9	Homo sapiens	65-68
912819-5	1977	The subcell (HS1) is orthorhombic with as = 10.3, bs = 7.5 and cs = 2.54 A.	Arsenic	39-41	eukaryotic translation elongation factor 1 alpha 2	Homo sapiens	13-16
908300-7	1977	These results support the hypothesis that chronic, low level, arsenic exposure results in selective inhibition of mitochondrial-bound heme biosynthetic pathway enzymes (ALA synthetase and heme synthetase) resulting in a substantial increase in urinary porphyrins, uniquely characterized by a greater increase in uroporphyrin than coproporphyrin levels.	Arsenic	62-69	ferrochelatase	Homo sapiens	188-203
328881-4	1977	Studies of 61 members of seven families with 18 cases of AS revealed a frequency of 38% LR-ANA, 30% AS and 55% HLA-B27, but no correlations were found among these parameters.	Arsenic	57-59	major histocompatibility complex, class I, B	Homo sapiens	111-118
7440438-10	1980	In the experiments with lactating dairy cows, significantly higher levels of arsenic in milk were observed for cows fed either 3.2 or 4.8 mg of arsenic per kilogram of body weight from arsanilic acid or 3-nitro.	Arsenic	77-84	Weaning weight-maternal milk	Bos taurus	88-92
6450798-7	1980	The found data seemed to suggest that the milk protein rich diet caused retardation of the increase of arsenic concentrations in blood, liver and kidneys that might lead at a lower exposure rate to a decrease in arsenic content in tissues of exposed animals.	Arsenic	103-110	casein alpha s2-like A	Mus musculus	42-54
6450798-7	1980	The found data seemed to suggest that the milk protein rich diet caused retardation of the increase of arsenic concentrations in blood, liver and kidneys that might lead at a lower exposure rate to a decrease in arsenic content in tissues of exposed animals.	Arsenic	212-219	casein alpha s2-like A	Mus musculus	42-54
4702736-0	1973	[Excretion of arsenic in human urine after treatment with BAL].	Arsenic	14-21	poly(ADP-ribose) polymerase family member 9	Homo sapiens	58-61
1236014-0	1975	[Study of serum ceruloplasmin activity in workers in contact with arsenic and lead].	Arsenic	66-73	ceruloplasmin	Homo sapiens	16-29
13151520-0	1953	[Effect of trivalent arsenic compounds on prothrombin].	Arsenic	21-28	coagulation factor II, thrombin	Homo sapiens	42-53
5814136-0	1969	Suitability of hairless mice for experimenal work and their sensitivity to arsenic.	Arsenic	75-82	lysine demethylase and nuclear receptor corepressor	Mus musculus	15-23
13174823-0	1954	Treatment of arsenic and gold encephalopathy with BAL.	Arsenic	13-20	poly(ADP-ribose) polymerase family member 9	Homo sapiens	50-53
13182588-7	1954	Consolidation treatment was given in none of the North American clinics; seldom in Asia; by about one-third of the participants in Central and South America; and, for secondary syphilis, in 59% of European schedules.This study shows that with intensive treatment with PAM the saving in drug cost to clinics over the classical courses of arsenic and bismuth may be as much as pound4 per case, but the overhead expenses are, of course, not reduced.	Arsenic	337-344	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	268-271
13000406-0	1952	Action of BAL on the tumor-damaging potency of certain trivalent arsenic compounds.	Arsenic	65-72	poly(ADP-ribose) polymerase family member 9	Homo sapiens	10-13
14895374-0	1950	[First applications of BAL in Montevideo in the treatment of arsenic and mercury poisoning].	Arsenic	61-68	poly(ADP-ribose) polymerase family member 9	Homo sapiens	23-26
12994024-0	1952	[Arsenic and BAL; research on the arsenic in urine in 24 hours after an injection of arsenobenzol; relation with the quantity eliminated after the administration of BAL.	Arsenic	34-41	poly(ADP-ribose) polymerase family member 9	Homo sapiens	165-168
15390530-0	1949	The use of BAL in the treatment of the injurious effects of arsenic, mercury and other metallic poisons.	Arsenic	60-67	poly(ADP-ribose) polymerase family member 9	Homo sapiens	11-14
14801577-0	1950	[Elimination of arsenic under the effects of penicillin, sodium thiomalate and BAL in chronic arsenic poisoning].	Arsenic	16-23	poly(ADP-ribose) polymerase family member 9	Homo sapiens	79-82
15420733-0	1950	[Effect of BAL on acute and chronic poisoning with arsenic and mercury].	Arsenic	51-58	poly(ADP-ribose) polymerase family member 9	Homo sapiens	11-14
21001621-0	1946	Clinical uses of 2,3-dimercaptropropanol (BAL); the effect of BAL on the excretion of arsenic in normal subjects and after minimal exposure to arsenical smoke.	Arsenic	86-93	poly(ADP-ribose) polymerase family member 9	Homo sapiens	62-65
18892437-0	1948	A case of arsenic encephalopathy successfully treated with BAL.	Arsenic	10-17	poly(ADP-ribose) polymerase family member 9	Homo sapiens	59-62
15419061-0	1950	[Encephalitis due to arsenic treated with BAL].	Arsenic	21-28	poly(ADP-ribose) polymerase family member 9	Homo sapiens	42-45
18908858-0	1948	BAL in the treatment of arsenic ingestion of children.	Arsenic	24-31	poly(ADP-ribose) polymerase family member 9	Homo sapiens	0-3
21064305-0	1946	2,3 Dithiolpropanol ("BAL") as a specific detoxifying agent for arsenic.	Arsenic	64-71	poly(ADP-ribose) polymerase family member 9	Homo sapiens	22-26
21001627-0	1946	Clinical uses of 2,3-dimercaptopropanol (BAL); the effect of BAL on the excretion of arsenic in arsenical intoxication.	Arsenic	85-92	poly(ADP-ribose) polymerase family member 9	Homo sapiens	61-64
33894237-1	2021	Methylation of arsenic compounds in the human body occurs following a series of biochemical reactions in the presence of methyl donor S-adenosylmethionine (SAM) and catalyzed by arsenite methyltransferase (AS3MT).	Arsenic	15-22	arsenite methyltransferase	Homo sapiens	206-211
33545600-4	2021	Under optimal conditions, linear dynamic ranges of 0.2-15 ng mL-1 and 0.2-20 ng mL-1 were observed in the determination of As(III) and total As respectively.	Arsenic	123-125	L1 cell adhesion molecule	Mus musculus	61-65
33545600-4	2021	Under optimal conditions, linear dynamic ranges of 0.2-15 ng mL-1 and 0.2-20 ng mL-1 were observed in the determination of As(III) and total As respectively.	Arsenic	123-125	L1 cell adhesion molecule	Mus musculus	80-84
33894237-11	2021	These along with epigenetic down-regulation of AS3MT may be responsible for higher susceptibility in arsenic exposed individuals.	Arsenic	101-108	arsenite methyltransferase	Homo sapiens	47-52
33957193-0	2021	Arsenic exposure in drinking water reduces Lgr5 and secretory cell marker gene expression in mouse intestines.	Arsenic	0-7	leucine rich repeat containing G protein coupled receptor 5	Mus musculus	43-47
33957193-6	2021	qPCR analysis revealed a 40% reduction in Lgr5 transcripts, an ISC marker, in the arsenic-exposed mice, although there were no changes in the protein expression of Olfm4.	Arsenic	82-89	leucine rich repeat containing G protein coupled receptor 5	Mus musculus	42-46
33957193-7	2021	Secretory cell-specific transcript markers of Paneth (Defa1), Goblet (Tff3), and secretory transit amplifying (Math1) cells were reduced by 51%, 44%, and 30% respectively, in the arsenic-exposed mice, indicating significant impacts on the Wnt-dependent differentiation pathway.	Arsenic	179-186	defensin, alpha 1	Mus musculus	54-59
33957193-7	2021	Secretory cell-specific transcript markers of Paneth (Defa1), Goblet (Tff3), and secretory transit amplifying (Math1) cells were reduced by 51%, 44%, and 30% respectively, in the arsenic-exposed mice, indicating significant impacts on the Wnt-dependent differentiation pathway.	Arsenic	179-186	trefoil factor 3, intestinal	Mus musculus	70-74
33610991-5	2021	Results revealed the two major fractions of As in aggregates were humic-bound and Fe and Mn oxides-bound [both around 30% under 800 mg kg-1 of As(V)].	Arsenic	44-46	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	143-148
33957193-7	2021	Secretory cell-specific transcript markers of Paneth (Defa1), Goblet (Tff3), and secretory transit amplifying (Math1) cells were reduced by 51%, 44%, and 30% respectively, in the arsenic-exposed mice, indicating significant impacts on the Wnt-dependent differentiation pathway.	Arsenic	179-186	atonal bHLH transcription factor 1	Mus musculus	111-116
33957193-8	2021	Further, protein levels of phosphorylated beta-catenin were reduced in the arsenic-exposed mice, which increased the expression of Wnt-dependent transcripts CD44 and c-myc.	Arsenic	75-82	catenin (cadherin associated protein), beta 1	Mus musculus	42-54
33957193-8	2021	Further, protein levels of phosphorylated beta-catenin were reduced in the arsenic-exposed mice, which increased the expression of Wnt-dependent transcripts CD44 and c-myc.	Arsenic	75-82	CD44 antigen	Mus musculus	157-161
20893421-0	1947	BAL: Its Use in Arsenic, Mercury, and Gold Poisoning.	Arsenic	16-23	poly(ADP-ribose) polymerase family member 9	Homo sapiens	0-3
33957193-10	2021	Similar comparisons between Math1 and Defa1 show that terminal differentiation into Paneth cells is also reduced in the arsenic-exposed mice.	Arsenic	120-127	atonal bHLH transcription factor 1	Mus musculus	28-33
33957193-10	2021	Similar comparisons between Math1 and Defa1 show that terminal differentiation into Paneth cells is also reduced in the arsenic-exposed mice.	Arsenic	120-127	defensin, alpha 1	Mus musculus	38-43
33865896-7	2021	In the 10 muM Cd group, m6A methylation levels at MT1JP-84, CDKN2B-AS-257, and CDKN2B-AS-329 were reduced.	Arsenic	67-69	cyclin-dependent kinase inhibitor 2B	Rattus norvegicus	60-66
33845054-7	2021	Arsenic exposure levels of the subjects showed significant positive associations with serum Th2-mediators- interleukin (IL)-4, IL-5, IL-13, and eotaxin without any significant changes in Th1 mediators- interferon-gamma and tumor necrosis factor-alpha.	Arsenic	0-7	interleukin 4	Homo sapiens	107-125
32772315-0	2021	GSTM1 and GSTT1 Null Genotype Polymorphisms and Susceptibility to Arsenic Poisoning: a Meta-analysis.	Arsenic	66-73	glutathione S-transferase mu 1	Homo sapiens	0-5
32772315-0	2021	GSTM1 and GSTT1 Null Genotype Polymorphisms and Susceptibility to Arsenic Poisoning: a Meta-analysis.	Arsenic	66-73	glutathione S-transferase theta 1	Homo sapiens	10-15
33739591-0	2021	Running head MBP-activated autoimmunity plays a role in arsenic-induced peripheral neuropathy and the potential protective effect of mecobalamin.	Arsenic	56-63	myelin basic protein	Rattus norvegicus	13-16
33739591-7	2021	These data implicated that MBP-activated autoimmunity and the related neuroinflammation probably contributed to As-induced mechanical hyperalgesia and MeCbl exerted a protective role probably via maintenance the integrity of BNB and inhibition of neuroinflammation.	Arsenic	112-114	myelin basic protein	Rattus norvegicus	27-30
33545467-0	2021	Groundwater development leads to decreasing arsenic concentrations in the San Joaquin Valley, California.	Arsenic	44-51	N-alpha-acetyltransferase 50, NatE catalytic subunit	Homo sapiens	74-77
33545467-1	2021	In the San Joaquin Valley (SJV), California, about 10% of drinking water wells since 2010 had arsenic concentrations above the US maximum contaminant level of 10 mug/L.	Arsenic	94-101	N-alpha-acetyltransferase 50, NatE catalytic subunit	Homo sapiens	7-10
33845054-8	2021	The ratios of Th2 to Th1 mediators were significantly increased with increasing exposure to As.	Arsenic	92-94	negative elongation factor complex member C/D	Homo sapiens	21-24
33845054-7	2021	Arsenic exposure levels of the subjects showed significant positive associations with serum Th2-mediators- interleukin (IL)-4, IL-5, IL-13, and eotaxin without any significant changes in Th1 mediators- interferon-gamma and tumor necrosis factor-alpha.	Arsenic	0-7	interleukin 5	Homo sapiens	127-131
33845054-7	2021	Arsenic exposure levels of the subjects showed significant positive associations with serum Th2-mediators- interleukin (IL)-4, IL-5, IL-13, and eotaxin without any significant changes in Th1 mediators- interferon-gamma and tumor necrosis factor-alpha.	Arsenic	0-7	interleukin 13	Homo sapiens	133-138
33845054-7	2021	Arsenic exposure levels of the subjects showed significant positive associations with serum Th2-mediators- interleukin (IL)-4, IL-5, IL-13, and eotaxin without any significant changes in Th1 mediators- interferon-gamma and tumor necrosis factor-alpha.	Arsenic	0-7	C-C motif chemokine ligand 11	Homo sapiens	144-151
33845054-7	2021	Arsenic exposure levels of the subjects showed significant positive associations with serum Th2-mediators- interleukin (IL)-4, IL-5, IL-13, and eotaxin without any significant changes in Th1 mediators- interferon-gamma and tumor necrosis factor-alpha.	Arsenic	0-7	interferon gamma	Homo sapiens	202-250
33978648-2	2021	The reaction of the two-electron reducing agent [AlCp*]4 (Cp* = C5Me5) with arsenic nanoparticles gave rise to a mixture of two unprecedented deca- and dodecanuclear Al-As clusters.	Arsenic	76-83	allantoicase	Homo sapiens	49-53
34048950-5	2021	Once arsenic is sequestered into the vacuole, PHR1 stability is restored, and PHT1;1 expression is recovered.	Arsenic	5-12	photolyase 1	Arabidopsis thaliana	46-50
34048950-5	2021	Once arsenic is sequestered into the vacuole, PHR1 stability is restored, and PHT1;1 expression is recovered.	Arsenic	5-12	phosphate transporter 1;1	Arabidopsis thaliana	78-84
34038756-0	2021	Arsenic induces autophagy-dependent apoptosis via Akt inactivation and AMPK activation signaling pathways leading to neuronal cell death.	Arsenic	0-7	thymoma viral proto-oncogene 1	Mus musculus	50-53
34000557-5	2021	Genes conferring tolerance to As (arsA), Hg (merA) or Cu (tcrB) were used as biomarkers of widespread metal tolerance operons.	Arsenic	30-32	arylsulfatase A	Homo sapiens	34-38
34050381-0	2021	Resveratrol attenuates arsenic-induced cognitive deficits via modulation of Estrogen-NMDAR-BDNF signalling pathway in female mouse hippocampus.	Arsenic	23-30	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	85-90
34050381-0	2021	Resveratrol attenuates arsenic-induced cognitive deficits via modulation of Estrogen-NMDAR-BDNF signalling pathway in female mouse hippocampus.	Arsenic	23-30	brain derived neurotrophic factor	Mus musculus	91-95
34047175-6	2021	Such PML induction drives P53 activation, favoring blasts response to chemotherapy or arsenic in vivo.	Arsenic	86-93	PML nuclear body scaffold	Homo sapiens	5-8
34047175-6	2021	Such PML induction drives P53 activation, favoring blasts response to chemotherapy or arsenic in vivo.	Arsenic	86-93	tumor protein p53	Homo sapiens	26-29
34028595-5	2021	In addition, an inhibitory effect of Cd, Pb, As, and Fe on SIRT3 has been demonstrated.	Arsenic	45-47	sirtuin 3	Homo sapiens	59-64
33736254-9	2021	Several differentially expressed genes (such as OXR1, OXSR1, INSR, and PPARA) and changed metabolites (such as pyruvate, acetate, and L-phenylalanine) were involved in the combined toxicity of As and PA.	Arsenic	193-195	oxidation resistance 1	Homo sapiens	48-52
33736254-9	2021	Several differentially expressed genes (such as OXR1, OXSR1, INSR, and PPARA) and changed metabolites (such as pyruvate, acetate, and L-phenylalanine) were involved in the combined toxicity of As and PA.	Arsenic	193-195	oxidative stress responsive kinase 1	Homo sapiens	54-59
33736254-9	2021	Several differentially expressed genes (such as OXR1, OXSR1, INSR, and PPARA) and changed metabolites (such as pyruvate, acetate, and L-phenylalanine) were involved in the combined toxicity of As and PA.	Arsenic	193-195	peroxisome proliferator activated receptor alpha	Homo sapiens	71-76
33978648-4	2021	Additionally, two different dialanes [AlCp*X]2 (X = Br, I) were employed as one-electron reducing agents, forming calix like coordination compounds upon reaction with nano arsenic.	Arsenic	172-179	allantoicase	Homo sapiens	38-42
33960401-0	2021	The SLIM1 transcription factor is required for arsenic resistance in Arabidopsis thaliana.	Arsenic	47-54	ETHYLENE-INSENSITIVE3-like 3	Arabidopsis thaliana	4-9
33960401-3	2021	Here, we report that mutant alleles in the SLIM1 transcription factor are substantially more sensitive to arsenic than cadmium.	Arsenic	106-113	ETHYLENE-INSENSITIVE3-like 3	Arabidopsis thaliana	43-48
33960401-4	2021	Arsenic treatment caused high levels of oxidative stress in the slim1 mutants, and slim1 alleles were impaired in both thiol and sulfate accumulation.	Arsenic	0-7	ETHYLENE-INSENSITIVE3-like 3	Arabidopsis thaliana	64-69
33960401-5	2021	We further found enhanced arsenic accumulation in roots of slim1 mutants.	Arsenic	26-33	ETHYLENE-INSENSITIVE3-like 3	Arabidopsis thaliana	59-64
33960401-6	2021	Transcriptome analyses indicate an important role for SLIM1 in arsenic-induced tolerance mechanisms.	Arsenic	63-70	ETHYLENE-INSENSITIVE3-like 3	Arabidopsis thaliana	54-59
33960401-7	2021	The present study identifies the SLIM1 transcription factor as an essential component in arsenic tolerance and arsenic-induced gene expression.	Arsenic	89-96	ETHYLENE-INSENSITIVE3-like 3	Arabidopsis thaliana	33-38
33960401-7	2021	The present study identifies the SLIM1 transcription factor as an essential component in arsenic tolerance and arsenic-induced gene expression.	Arsenic	111-118	ETHYLENE-INSENSITIVE3-like 3	Arabidopsis thaliana	33-38
33960401-8	2021	Our results suggest that the severe arsenic sensitivity of the slim1 mutants is caused by altered redox status.	Arsenic	36-43	ETHYLENE-INSENSITIVE3-like 3	Arabidopsis thaliana	63-68
33545379-0	2021	Neuroglobin Alleviates Arsenic-Induced Neuronal Damage.	Arsenic	23-30	neuroglobin	Rattus norvegicus	0-11
33956289-0	2021	Regulation of arsenic methylation: identification of the transcriptional region of the human AS3MT gene.	Arsenic	14-21	arsenite methyltransferase	Homo sapiens	93-98
33956289-1	2021	The human enzyme As(III) S-adenosylmethionine methyltransferase (AS3MT) catalyzes arsenic biotransformations and is considered to contribute to arsenic-related diseases.	Arsenic	82-89	arsenite methyltransferase	Homo sapiens	65-70
33956289-1	2021	The human enzyme As(III) S-adenosylmethionine methyltransferase (AS3MT) catalyzes arsenic biotransformations and is considered to contribute to arsenic-related diseases.	Arsenic	144-151	arsenite methyltransferase	Homo sapiens	65-70
34044194-5	2021	In addition, the as-synthesized GAAP-CDs showed excellent selectivity towards ClO- ions in the presence of various interfering chemicals.	Arsenic	17-19	transmembrane BAX inhibitor motif containing 4	Homo sapiens	32-36
34014776-0	2021	Sex-Specific Effects of Prenatal and Early Life Inorganic and Methylated Arsenic Exposure on Atherosclerotic Plaque Development and Composition in Adult ApoE-/- Mice.	Arsenic	73-80	apolipoprotein E	Mus musculus	153-157
34014776-2	2021	Different oxidation and methylation states of arsenic exist in the environment and are formed in vivo via the action of arsenic (+3 oxidation state) methyltransferase (As3MT).	Arsenic	46-53	arsenite methyltransferase	Mus musculus	120-166
34014776-2	2021	Different oxidation and methylation states of arsenic exist in the environment and are formed in vivo via the action of arsenic (+3 oxidation state) methyltransferase (As3MT).	Arsenic	46-53	arsenite methyltransferase	Mus musculus	168-173
33545379-4	2021	In this study, we aimed to study the effects of Ngb knockdown in arsenite-treated rat neurons on levels of apoptosis markers and reactive oxygen species and serum Ngb levels of subjects from arsenic-endemic regions in China.	Arsenic	191-198	neuroglobin	Rattus norvegicus	48-51
33545379-5	2021	We discovered that arsenic-induced apoptosis and reactive oxygen species production were enhanced in Ngb-knocked-down rat neurons.	Arsenic	19-26	neuroglobin	Rattus norvegicus	101-104
33848561-0	2021	Effect of Arsenic-containing Hydrocarbon on the Long-term Potentiation at Schaffer Collateral-CA1 Synapses from Infantile Male Rat.	Arsenic	10-17	carbonic anhydrase 1	Rattus norvegicus	94-97
33545379-6	2021	Silencing of Ngb aggravated the arsenic-induced decrease in the rate of Bcl-2/Bax and the levels of Bcl-2 protein following arsenite treatment.	Arsenic	32-39	neuroglobin	Rattus norvegicus	13-16
33545379-6	2021	Silencing of Ngb aggravated the arsenic-induced decrease in the rate of Bcl-2/Bax and the levels of Bcl-2 protein following arsenite treatment.	Arsenic	32-39	BCL2, apoptosis regulator	Rattus norvegicus	72-77
33545379-6	2021	Silencing of Ngb aggravated the arsenic-induced decrease in the rate of Bcl-2/Bax and the levels of Bcl-2 protein following arsenite treatment.	Arsenic	32-39	BCL2 associated X, apoptosis regulator	Rattus norvegicus	78-81
33545379-6	2021	Silencing of Ngb aggravated the arsenic-induced decrease in the rate of Bcl-2/Bax and the levels of Bcl-2 protein following arsenite treatment.	Arsenic	32-39	BCL2, apoptosis regulator	Rattus norvegicus	100-105
33545379-7	2021	The results also showed that serum Ngb levels were independently negatively correlated with arsenic concentration in drinking water.	Arsenic	92-99	neuroglobin	Rattus norvegicus	35-38
33545379-8	2021	Furthermore, the serum Ngb levels of four groups (245 individuals ) according to different degree exposure to arsenic were 815.18 +- 89.52, 1247.97 +- 117.18, 774.79 +- 91.55, and 482.72 +- 49.30 pg/mL, respectively.	Arsenic	110-117	neuroglobin	Rattus norvegicus	23-26
33545379-9	2021	Taken together, it can be deduced that Ngb has protective effects against arsenic-induced apoptosis by eliminating reactive oxygen species.	Arsenic	74-81	neuroglobin	Rattus norvegicus	39-42
33609750-0	2021	Long non-coding RNA DICER1-AS1-low expression in arsenic-treated A549 cells inhibits cell proliferation by regulating the cell cycle pathway.	Arsenic	49-56	dicer 1, ribonuclease III	Homo sapiens	20-26
33609750-0	2021	Long non-coding RNA DICER1-AS1-low expression in arsenic-treated A549 cells inhibits cell proliferation by regulating the cell cycle pathway.	Arsenic	49-56	prostaglandin D2 receptor	Homo sapiens	27-30
33621689-0	2021	Prolonged arsenic exposure increases tau phosphorylation in differentiated SH-SY5Y cells: The contribution of GSK3 and ERK1/2.	Arsenic	10-17	microtubule associated protein tau	Homo sapiens	37-40
33621689-0	2021	Prolonged arsenic exposure increases tau phosphorylation in differentiated SH-SY5Y cells: The contribution of GSK3 and ERK1/2.	Arsenic	10-17	mitogen-activated protein kinase 3	Homo sapiens	119-125
33621689-1	2021	Arsenic is a metalloid that has been hypothesized to be an environmental risk factor for Alzheimer"s disease (AD), a disease having hyperphosphorylated tau aggregate as a marker.	Arsenic	0-7	microtubule associated protein tau	Homo sapiens	152-155
33621689-5	2021	These results suggest that arsenic may cause tau hyperphosphorylation in neurons through the activation of GSK3 and ERK1/2.	Arsenic	27-34	microtubule associated protein tau	Homo sapiens	45-48
33621689-5	2021	These results suggest that arsenic may cause tau hyperphosphorylation in neurons through the activation of GSK3 and ERK1/2.	Arsenic	27-34	mitogen-activated protein kinase 3	Homo sapiens	116-122
33621689-10	2021	These results suggest that arsenic induces tau hyperphosphorylation in the membrane fraction which may lead to its redistribution from the membrane fraction to the cytosol, where it promotes neurofibrillary formation.	Arsenic	27-34	microtubule associated protein tau	Homo sapiens	43-46
33621689-11	2021	Collectively, we demonstrate that prolonged arsenic exposure increases tau phosphorylation, partly through GSK3 and ERK1/2 activation, and insoluble tau aggregates, hence possibly contributing to the development of sporadic AD.	Arsenic	44-51	microtubule associated protein tau	Homo sapiens	71-74
33621689-11	2021	Collectively, we demonstrate that prolonged arsenic exposure increases tau phosphorylation, partly through GSK3 and ERK1/2 activation, and insoluble tau aggregates, hence possibly contributing to the development of sporadic AD.	Arsenic	44-51	mitogen-activated protein kinase 3	Homo sapiens	116-122
33621689-11	2021	Collectively, we demonstrate that prolonged arsenic exposure increases tau phosphorylation, partly through GSK3 and ERK1/2 activation, and insoluble tau aggregates, hence possibly contributing to the development of sporadic AD.	Arsenic	44-51	microtubule associated protein tau	Homo sapiens	149-152
34003103-0	2021	[Arsenic: The gold standard for acute promyelocytic leukaemia with FLT3-ITD mutation].	Arsenic	1-8	fms related receptor tyrosine kinase 3	Homo sapiens	67-71
33933676-4	2021	Using a combination of wild type, Nrf2-/-, p62-/-, or Nrf2-/-;p62-/- mice and an arsenic-induced diabetes model, we demonstrate that NRF2 and p62 are essential for promoting insulin resistance and glucose intolerance.	Arsenic	81-88	nuclear factor, erythroid derived 2, like 2	Mus musculus	133-137
33965804-6	2021	In the present investigation, we focused on the roles and mechanisms of miR-21 in EVs on arsenic-induced glycolysis and pulmonary fibrosis through experiments with human populations, experimental animals, and cells.	Arsenic	89-96	microRNA 21	Homo sapiens	72-78
33965804-0	2021	miR-21 in EVs from pulmonary epithelial cells promotes myofibroblast differentiation via glycolysis in arsenic-induced pulmonary fibrosis.	Arsenic	103-110	microRNA 21	Homo sapiens	0-6
33933455-7	2021	Loss of USP7 function attenuated the induction of Nrf1 protein expression in response to treatment with arsenic and other toxic metals, and inhibition of USP7 activity significantly sensitized cells to arsenic treatment.	Arsenic	104-111	ubiquitin specific peptidase 7	Homo sapiens	8-12
33933455-7	2021	Loss of USP7 function attenuated the induction of Nrf1 protein expression in response to treatment with arsenic and other toxic metals, and inhibition of USP7 activity significantly sensitized cells to arsenic treatment.	Arsenic	104-111	nuclear respiratory factor 1	Homo sapiens	50-54
33933455-7	2021	Loss of USP7 function attenuated the induction of Nrf1 protein expression in response to treatment with arsenic and other toxic metals, and inhibition of USP7 activity significantly sensitized cells to arsenic treatment.	Arsenic	202-209	nuclear respiratory factor 1	Homo sapiens	50-54
33933455-7	2021	Loss of USP7 function attenuated the induction of Nrf1 protein expression in response to treatment with arsenic and other toxic metals, and inhibition of USP7 activity significantly sensitized cells to arsenic treatment.	Arsenic	202-209	ubiquitin specific peptidase 7	Homo sapiens	154-158
33921748-0	2021	ATF3 Promotes Arsenic-Induced Apoptosis and Oppositely Regulates DR5 and Bcl-xL Expression in Human Bronchial Epithelial Cells.	Arsenic	14-21	activating transcription factor 3	Homo sapiens	0-4
33957471-7	2021	Thereby, the findings revealed that impregnation of TiO2 in BT/CS is a promising approach for arsenic removal.	Arsenic	94-101	citrate synthase	Homo sapiens	63-65
33995501-6	2021	This work revealed a new role for UBE3A in regulating retinoic acid (RA) signalling downstream genes and hopefully to shed light on the potential drug target of AS.	Arsenic	161-163	ubiquitin protein ligase E3A	Mus musculus	34-39
33891655-0	2021	Association between urinary arsenic, blood cadmium, blood lead, and blood mercury levels and serum prostate-specific antigen in a population-based cohort of men in the United States.	Arsenic	28-35	kallikrein related peptidase 3	Homo sapiens	99-124
33826311-7	2021	Remarkably, a pitcher loaded with a combination of our CeO2@UiO-66@PES granules and activated carbon at standard ratios met the target reduction thresholds set by NSF/ANSI 53-2019 for all the metals tested: As(III), As(V), Cd(II), Cr(III), Cr(VI), Cu(II), Hg(II), and Pb(II).	Arsenic	207-209	N-ethylmaleimide sensitive factor, vesicle fusing ATPase	Homo sapiens	163-166
33921748-4	2021	Arsenic rapidly induced the activating transcription factor ATF3 expression through the JNK and p38 pathways.	Arsenic	0-7	mitogen-activated protein kinase 8	Homo sapiens	88-91
33921748-4	2021	Arsenic rapidly induced the activating transcription factor ATF3 expression through the JNK and p38 pathways.	Arsenic	0-7	mitogen-activated protein kinase 14	Homo sapiens	96-99
33921748-5	2021	The ATF3-deficient BEAS-2B cells were relatively resistant to apoptosis upon arsenic exposure, indicating a facilitatory role of ATF3 in arsenic-induced apoptosis.	Arsenic	77-84	activating transcription factor 3	Homo sapiens	4-8
33921748-5	2021	The ATF3-deficient BEAS-2B cells were relatively resistant to apoptosis upon arsenic exposure, indicating a facilitatory role of ATF3 in arsenic-induced apoptosis.	Arsenic	137-144	activating transcription factor 3	Homo sapiens	4-8
33921748-5	2021	The ATF3-deficient BEAS-2B cells were relatively resistant to apoptosis upon arsenic exposure, indicating a facilitatory role of ATF3 in arsenic-induced apoptosis.	Arsenic	137-144	activating transcription factor 3	Homo sapiens	129-133
33921748-7	2021	Altogether, our findings establish ATF3 as a pro-apoptotic protein in arsenic-induced airway epithelial apoptosis through transcriptionally regulating DR5 and Bcl-xL, highlighting the potential of ATF3 as an early and sensitive biomarker for arsenic-caused lung injury.	Arsenic	70-77	activating transcription factor 3	Homo sapiens	35-39
33921748-7	2021	Altogether, our findings establish ATF3 as a pro-apoptotic protein in arsenic-induced airway epithelial apoptosis through transcriptionally regulating DR5 and Bcl-xL, highlighting the potential of ATF3 as an early and sensitive biomarker for arsenic-caused lung injury.	Arsenic	70-77	TNF receptor superfamily member 10b	Homo sapiens	151-154
33921748-7	2021	Altogether, our findings establish ATF3 as a pro-apoptotic protein in arsenic-induced airway epithelial apoptosis through transcriptionally regulating DR5 and Bcl-xL, highlighting the potential of ATF3 as an early and sensitive biomarker for arsenic-caused lung injury.	Arsenic	70-77	BCL2 like 1	Homo sapiens	159-165
33921748-7	2021	Altogether, our findings establish ATF3 as a pro-apoptotic protein in arsenic-induced airway epithelial apoptosis through transcriptionally regulating DR5 and Bcl-xL, highlighting the potential of ATF3 as an early and sensitive biomarker for arsenic-caused lung injury.	Arsenic	70-77	activating transcription factor 3	Homo sapiens	197-201
33921748-7	2021	Altogether, our findings establish ATF3 as a pro-apoptotic protein in arsenic-induced airway epithelial apoptosis through transcriptionally regulating DR5 and Bcl-xL, highlighting the potential of ATF3 as an early and sensitive biomarker for arsenic-caused lung injury.	Arsenic	242-249	activating transcription factor 3	Homo sapiens	35-39
33933762-6	2021	Under optimal conditions of material (Fe@C-NB) syntheses, both 95% degradation of p-ASA and 86% total arsenic immobilization can be obtained with oxidant (Peroxymonosulfate, PMS) and catalyst (Fe@C-NB) treatment after 60 min.	Arsenic	102-109	proline rich protein BstNI subfamily 1	Homo sapiens	174-177
33866505-6	2021	As a result, PC1 38.5% (As, Cr, Cu, and Ni), PC2 17.3% (Pb and Zn), and PC3 14.7% (Co and Pb) are attributable to coal combustion, vehicle exhaust emission, and resuspension of soil particles, respectively.	Arsenic	0-2	proprotein convertase subtilisin/kexin type 1	Homo sapiens	13-16
33866505-6	2021	As a result, PC1 38.5% (As, Cr, Cu, and Ni), PC2 17.3% (Pb and Zn), and PC3 14.7% (Co and Pb) are attributable to coal combustion, vehicle exhaust emission, and resuspension of soil particles, respectively.	Arsenic	0-2	polycystin 2, transient receptor potential cation channel	Homo sapiens	45-48
33866505-6	2021	As a result, PC1 38.5% (As, Cr, Cu, and Ni), PC2 17.3% (Pb and Zn), and PC3 14.7% (Co and Pb) are attributable to coal combustion, vehicle exhaust emission, and resuspension of soil particles, respectively.	Arsenic	0-2	proprotein convertase subtilisin/kexin type 1	Homo sapiens	72-75
33418518-5	2021	The adsorption and photocatalysis experiments results showed that the efficiency of removing As(III) by biochar/SnS2/phosphotungstic acid (biochar/SnS2/PTA) systems was 1.5 times that of biochar/SnS2 systems, and the concentration of total arsenic in the biochar/SnS2/PTA composite system gradually decreased during the photocatalysis process.	Arsenic	240-247	sodium voltage-gated channel alpha subunit 11	Homo sapiens	112-116
33860893-7	2021	The stability of As and Sb in the sediment was found to be the best at pH 5.	Arsenic	17-19	phenylalanine hydroxylase	Homo sapiens	71-73
33561751-0	2021	Decreases in arsenic accumulation by the plasma membrane intrinsic protein PIP2;2 in Arabidopsis and yeast.	Arsenic	13-20	plasma membrane intrinsic protein 2	Arabidopsis thaliana	75-81
33561751-10	2021	The expression of AtPIP2;2 rescued the As(III)-sensitive phenotype of acr3 mutant yeast by reducing As levels and slightly reduced the As(III)-tolerant phenotype of fps1 mutant yeast by enhancing As content, suggesting that AtPIP2; 2 functions as a bidirectional channel of As(III), while the As(III) exporter activity is higher than the As(III) importer activity.	Arsenic	39-42	plasma membrane intrinsic protein 2A	Arabidopsis thaliana	18-24
33561751-10	2021	The expression of AtPIP2;2 rescued the As(III)-sensitive phenotype of acr3 mutant yeast by reducing As levels and slightly reduced the As(III)-tolerant phenotype of fps1 mutant yeast by enhancing As content, suggesting that AtPIP2; 2 functions as a bidirectional channel of As(III), while the As(III) exporter activity is higher than the As(III) importer activity.	Arsenic	39-42	Arr3p	Saccharomyces cerevisiae S288C	70-74
33860893-0	2021	A study on the effects of anion, cation, organic compounds, and pH on the release behaviors of As and Sb from sediments.	Arsenic	95-97	phenylalanine hydroxylase	Homo sapiens	64-66
33418518-5	2021	The adsorption and photocatalysis experiments results showed that the efficiency of removing As(III) by biochar/SnS2/phosphotungstic acid (biochar/SnS2/PTA) systems was 1.5 times that of biochar/SnS2 systems, and the concentration of total arsenic in the biochar/SnS2/PTA composite system gradually decreased during the photocatalysis process.	Arsenic	240-247	pre T cell antigen receptor alpha	Homo sapiens	152-155
33846348-1	2021	Here we show that FTO as an N6-methyladenosine (m6A) RNA demethylase is degraded by selective autophagy, which is impaired by low-level arsenic exposure to promote tumorigenesis.	Arsenic	136-143	FTO alpha-ketoglutarate dependent dioxygenase	Homo sapiens	18-21
33844876-4	2021	A simple one-pot reaction of [CpMo(CO) 2 ] 2 with ME(SiMe 3 ) 2 (M = Li, K; E = P, As, Sb, Bi) and the subsequent addition of PCl 3 , AsCl 3 , SbCl 3 or BiCl 3 , respectively, give the complexes 1 - 5 .	Arsenic	83-85	PHD finger protein 19	Homo sapiens	126-131
33846348-2	2021	We found that in arsenic-associated human skin lesions, FTO is upregulated, while m6A RNA methylation is downregulated.	Arsenic	17-24	FTO alpha-ketoglutarate dependent dioxygenase	Homo sapiens	56-59
33846348-8	2021	Finally, arsenic stabilizes FTO protein through inhibiting p62-mediated selective autophagy.	Arsenic	9-16	nucleoporin 62	Homo sapiens	59-62
33846348-3	2021	In keratinocytes, chronic relevant low-level arsenic exposure upregulated FTO, downregulated m6A RNA methylation, and induced malignant transformation and tumorigenesis.	Arsenic	45-52	FTO alpha-ketoglutarate dependent dioxygenase	Homo sapiens	74-77
33846348-4	2021	FTO deletion inhibited arsenic-induced tumorigenesis.	Arsenic	23-30	FTO alpha-ketoglutarate dependent dioxygenase	Homo sapiens	0-3
33846348-5	2021	Moreover, in mice, epidermis-specific FTO deletion prevented skin tumorigenesis induced by arsenic and UVB irradiation.	Arsenic	91-98	fat mass and obesity associated	Mus musculus	38-41
33846348-10	2021	Our study reveals FTO-mediated dysregulation of mRNA m6A methylation as an epitranscriptomic mechanism to promote arsenic tumorigenicity.	Arsenic	114-121	fat mass and obesity associated	Mus musculus	18-21
33846348-6	2021	Targeting FTO genetically or pharmacologically inhibits the tumorigenicity of arsenic-transformed tumor cells.	Arsenic	78-85	fat mass and obesity associated	Mus musculus	10-13
33846348-8	2021	Finally, arsenic stabilizes FTO protein through inhibiting p62-mediated selective autophagy.	Arsenic	9-16	fat mass and obesity associated	Mus musculus	28-31
33121781-6	2021	FTIR and XPS showed that the adsorption of As(V) by GT-1 occurred both via complexation with Fe(III) in GT-1 and via coordination of As(V) with free hydroxyl groups on the surface of GT-1.	Arsenic	43-46	beta-1,4-galactosyltransferase 1	Homo sapiens	52-56
33121781-6	2021	FTIR and XPS showed that the adsorption of As(V) by GT-1 occurred both via complexation with Fe(III) in GT-1 and via coordination of As(V) with free hydroxyl groups on the surface of GT-1.	Arsenic	43-46	beta-1,4-galactosyltransferase 1	Homo sapiens	104-108
33121781-6	2021	FTIR and XPS showed that the adsorption of As(V) by GT-1 occurred both via complexation with Fe(III) in GT-1 and via coordination of As(V) with free hydroxyl groups on the surface of GT-1.	Arsenic	43-46	beta-1,4-galactosyltransferase 1	Homo sapiens	104-108
33121781-6	2021	FTIR and XPS showed that the adsorption of As(V) by GT-1 occurred both via complexation with Fe(III) in GT-1 and via coordination of As(V) with free hydroxyl groups on the surface of GT-1.	Arsenic	133-136	beta-1,4-galactosyltransferase 1	Homo sapiens	52-56
33121781-8	2021	Finally, mechanisms for the formation of GT-1 and the removal of As (V) by GT-1 were proposed.	Arsenic	65-69	beta-1,4-galactosyltransferase 1	Homo sapiens	41-45
33121781-8	2021	Finally, mechanisms for the formation of GT-1 and the removal of As (V) by GT-1 were proposed.	Arsenic	65-69	beta-1,4-galactosyltransferase 1	Homo sapiens	75-79
33578085-8	2021	The colloidal mercuric formulation upregulated the expression of TGF-beta, IL-6 and TNF-alpha, due to the presence of arsenic and other organic compounds such as piperine.	Arsenic	118-125	transforming growth factor alpha	Homo sapiens	65-73
33561210-5	2021	Western blot was used to measure the abundance of the inhibitor of NF-kappaB (IKBA), mitofusin-2 (MFN2), mitochondrial electron transport chain complex proteins, and insulin-dependent AKT (Ser473) and AKT substrate 160 (AS 160; Thr642) phosphorylation.	Arsenic	220-222	insulin	Homo sapiens	166-173
33340971-3	2021	Here we characterized the Arabidopsis F-box protein gene AT2G16220 (Arsenic Stress-Related F-box (ASRF)) that we identified in the genome-wide association study.	Arsenic	68-75	F-box and associated interaction domains-containing protein	Arabidopsis thaliana	57-66
33127104-4	2021	Persistent near-basal level of GSH, least increased MDA content and catalase activity portrayed arsenic and fluoride co-exposure as less toxic which was corroborated with far less damage caused in the histoarchitecture of optic tectum region in midbrain.	Arsenic	96-103	catalase	Danio rerio	68-76
33578085-8	2021	The colloidal mercuric formulation upregulated the expression of TGF-beta, IL-6 and TNF-alpha, due to the presence of arsenic and other organic compounds such as piperine.	Arsenic	118-125	interleukin 6	Homo sapiens	75-79
33578085-8	2021	The colloidal mercuric formulation upregulated the expression of TGF-beta, IL-6 and TNF-alpha, due to the presence of arsenic and other organic compounds such as piperine.	Arsenic	118-125	tumor necrosis factor	Homo sapiens	84-93
33410021-11	2021	Our findings revealed the beneficial effects of the flavonoids against the arsenic-induced toxicity, due to their ability to enhance the intracellular antioxidant response system by modulating the Nrf2 signaling pathway.	Arsenic	75-82	nuclear factor, erythroid derived 2, like 2	Mus musculus	197-201
33826413-1	2021	BACKGROUND: Common genetic variation in the arsenic methyltransferase (AS3MT) gene region is known to be associated with arsenic metabolism efficiency (AME), measured as the percentage of dimethylarsinic acid (DMA%) in the urine.	Arsenic	44-51	arsenite methyltransferase	Homo sapiens	71-76
33826413-4	2021	METHODS: We generated targeted DNA sequencing data for the coding regions of AS3MT for three arsenic-exposed cohorts with existing data on arsenic species measured in urine: Health Effects of Arsenic Longitudinal Study (HEALS, n=2,434), Strong Heart Study (SHS, n=868), and New Hampshire Skin Cancer Study (NHSCS, n=666).	Arsenic	93-100	arsenite methyltransferase	Homo sapiens	77-82
33826413-4	2021	METHODS: We generated targeted DNA sequencing data for the coding regions of AS3MT for three arsenic-exposed cohorts with existing data on arsenic species measured in urine: Health Effects of Arsenic Longitudinal Study (HEALS, n=2,434), Strong Heart Study (SHS, n=868), and New Hampshire Skin Cancer Study (NHSCS, n=666).	Arsenic	139-146	arsenite methyltransferase	Homo sapiens	77-82
33826413-4	2021	METHODS: We generated targeted DNA sequencing data for the coding regions of AS3MT for three arsenic-exposed cohorts with existing data on arsenic species measured in urine: Health Effects of Arsenic Longitudinal Study (HEALS, n=2,434), Strong Heart Study (SHS, n=868), and New Hampshire Skin Cancer Study (NHSCS, n=666).	Arsenic	192-199	arsenite methyltransferase	Homo sapiens	77-82
33443393-5	2021	CONCLUSIONS: Our findings suggest that the DNA damage levels of BRCA1 and BRCA2 genes may modulate by genetic variations of GSTT1 and GSTO1 when individuals are exposed to carcinogens, such as arsenic.	Arsenic	193-200	BRCA1 DNA repair associated	Homo sapiens	64-69
33476663-3	2021	One-carbon metabolism (OCM), a biochemical pathway that is influenced by folate and vitamin B12, facilitates the methylation of As.	Arsenic	128-130	NADH:ubiquinone oxidoreductase subunit B3	Homo sapiens	92-95
33443393-0	2021	The Relationship Between GSTT1, GSTM1, GSTO1, GSTP1 and MTHFR Gene Polymorphisms and DNA Damage of BRCA1 and BRCA2 Genes in Arsenic-Exposed Workers.	Arsenic	124-131	glutathione S-transferase theta 1	Homo sapiens	25-30
33497711-7	2021	Arsenic, cadmium and the combination increased caspase-3/7 activity, while mercury reduced it.	Arsenic	0-7	caspase 3	Homo sapiens	47-58
33443393-0	2021	The Relationship Between GSTT1, GSTM1, GSTO1, GSTP1 and MTHFR Gene Polymorphisms and DNA Damage of BRCA1 and BRCA2 Genes in Arsenic-Exposed Workers.	Arsenic	124-131	glutathione S-transferase mu 1	Homo sapiens	32-37
33443393-0	2021	The Relationship Between GSTT1, GSTM1, GSTO1, GSTP1 and MTHFR Gene Polymorphisms and DNA Damage of BRCA1 and BRCA2 Genes in Arsenic-Exposed Workers.	Arsenic	124-131	glutathione S-transferase omega 1	Homo sapiens	39-44
33443393-0	2021	The Relationship Between GSTT1, GSTM1, GSTO1, GSTP1 and MTHFR Gene Polymorphisms and DNA Damage of BRCA1 and BRCA2 Genes in Arsenic-Exposed Workers.	Arsenic	124-131	glutathione S-transferase pi 1	Homo sapiens	46-51
33443393-0	2021	The Relationship Between GSTT1, GSTM1, GSTO1, GSTP1 and MTHFR Gene Polymorphisms and DNA Damage of BRCA1 and BRCA2 Genes in Arsenic-Exposed Workers.	Arsenic	124-131	methylenetetrahydrofolate reductase	Homo sapiens	56-61
33443393-0	2021	The Relationship Between GSTT1, GSTM1, GSTO1, GSTP1 and MTHFR Gene Polymorphisms and DNA Damage of BRCA1 and BRCA2 Genes in Arsenic-Exposed Workers.	Arsenic	124-131	BRCA1 DNA repair associated	Homo sapiens	99-104
33443393-0	2021	The Relationship Between GSTT1, GSTM1, GSTO1, GSTP1 and MTHFR Gene Polymorphisms and DNA Damage of BRCA1 and BRCA2 Genes in Arsenic-Exposed Workers.	Arsenic	124-131	BRCA2 DNA repair associated	Homo sapiens	109-114
33388378-0	2021	TET-mediated DNA demethylation plays an important role in arsenic-induced HBE cells oxidative stress via regulating promoter methylation of OGG1 and GSTP1.	Arsenic	58-65	8-oxoguanine DNA glycosylase	Homo sapiens	140-144
33388378-0	2021	TET-mediated DNA demethylation plays an important role in arsenic-induced HBE cells oxidative stress via regulating promoter methylation of OGG1 and GSTP1.	Arsenic	58-65	glutathione S-transferase pi 1	Homo sapiens	149-154
33388378-10	2021	Taken together, the results indicate that arsenic induced the inhibition of TET-mediated DNA demethylation, which induced promoter hypermethylation, inhibiting the expression of the OGG1 and GSTP1, and increasing oxidative stress in lung cells in vitro.	Arsenic	42-49	8-oxoguanine DNA glycosylase	Homo sapiens	182-186
33388378-10	2021	Taken together, the results indicate that arsenic induced the inhibition of TET-mediated DNA demethylation, which induced promoter hypermethylation, inhibiting the expression of the OGG1 and GSTP1, and increasing oxidative stress in lung cells in vitro.	Arsenic	42-49	glutathione S-transferase pi 1	Homo sapiens	191-196
33443393-5	2021	CONCLUSIONS: Our findings suggest that the DNA damage levels of BRCA1 and BRCA2 genes may modulate by genetic variations of GSTT1 and GSTO1 when individuals are exposed to carcinogens, such as arsenic.	Arsenic	193-200	BRCA2 DNA repair associated	Homo sapiens	74-79
33443393-5	2021	CONCLUSIONS: Our findings suggest that the DNA damage levels of BRCA1 and BRCA2 genes may modulate by genetic variations of GSTT1 and GSTO1 when individuals are exposed to carcinogens, such as arsenic.	Arsenic	193-200	glutathione S-transferase theta 1	Homo sapiens	124-129
33443393-5	2021	CONCLUSIONS: Our findings suggest that the DNA damage levels of BRCA1 and BRCA2 genes may modulate by genetic variations of GSTT1 and GSTO1 when individuals are exposed to carcinogens, such as arsenic.	Arsenic	193-200	glutathione S-transferase omega 1	Homo sapiens	134-139
33352257-5	2021	Results showed that exposure to As induced cell apoptosis and autophagy, which were mediated by the significantly altered expression levels of autophagy markers (mTOR, LC3, PI3K and P62), and apoptosis markers (Bcl-2 and caspase-3).	Arsenic	32-34	mechanistic target of rapamycin kinase	Mus musculus	162-166
33352257-5	2021	Results showed that exposure to As induced cell apoptosis and autophagy, which were mediated by the significantly altered expression levels of autophagy markers (mTOR, LC3, PI3K and P62), and apoptosis markers (Bcl-2 and caspase-3).	Arsenic	32-34	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	168-171
33352257-5	2021	Results showed that exposure to As induced cell apoptosis and autophagy, which were mediated by the significantly altered expression levels of autophagy markers (mTOR, LC3, PI3K and P62), and apoptosis markers (Bcl-2 and caspase-3).	Arsenic	32-34	nucleoporin 62	Mus musculus	182-185
33352257-5	2021	Results showed that exposure to As induced cell apoptosis and autophagy, which were mediated by the significantly altered expression levels of autophagy markers (mTOR, LC3, PI3K and P62), and apoptosis markers (Bcl-2 and caspase-3).	Arsenic	32-34	B cell leukemia/lymphoma 2	Mus musculus	211-216
33352257-5	2021	Results showed that exposure to As induced cell apoptosis and autophagy, which were mediated by the significantly altered expression levels of autophagy markers (mTOR, LC3, PI3K and P62), and apoptosis markers (Bcl-2 and caspase-3).	Arsenic	32-34	caspase 3	Mus musculus	221-230
33781774-14	2021	CONCLUSIONS: In a nationally representative sample of 8-17 year-olds, we found suggestive inverse association of the mixture of low-level Pb, Hg, As, and Cd, with DBP.	Arsenic	146-148	D-box binding PAR bZIP transcription factor	Homo sapiens	163-166
33360458-7	2021	Principal component analysis indicated that variable pH values and humic-like OM could affect Mn, As and Al concentrations at the consumer"s tap.	Arsenic	98-100	nuclear RNA export factor 1	Homo sapiens	141-144
33737636-8	2021	Again, adjusted analysis showed significant association of AA genotype of AS3MT rs10748835 with CVD patients from arsenic affected areas.	Arsenic	114-121	arsenite methyltransferase	Homo sapiens	74-79
33745108-10	2022	The reversal in the reduced level of malondialdehyde and activity of acetylcholinesterase in the hippocampus by Se was observed in As-treated animals, while the activity of antioxidant enzymes in the hippocampus was increased in As+Se than dw+As-treated animals.	Arsenic	131-133	acetylcholinesterase	Rattus norvegicus	69-89
33310327-8	2021	CDK1 and cyclin B1 were reduced in As-exposed GC-1 cells and mouse testes.	Arsenic	35-37	cyclin-dependent kinase 1	Mus musculus	0-4
33310327-8	2021	CDK1 and cyclin B1 were reduced in As-exposed GC-1 cells and mouse testes.	Arsenic	35-37	cyclin B1	Mus musculus	9-18
33310327-9	2021	Additional experiment revealed that p-ATR, a marker of genotoxic stress, was elevated in As-exposed mouse testes and GC-1 cells.	Arsenic	89-91	ataxia telangiectasia and Rad3 related	Mus musculus	38-41
33310327-10	2021	Accordingly, p-p53 and p21, two downstream molecules of ATR, were increased in As-exposed GC-1 cells.	Arsenic	79-81	transformation related protein 53, pseudogene	Mus musculus	15-18
33310327-10	2021	Accordingly, p-p53 and p21, two downstream molecules of ATR, were increased in As-exposed GC-1 cells.	Arsenic	79-81	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	23-26
33310327-10	2021	Accordingly, p-p53 and p21, two downstream molecules of ATR, were increased in As-exposed GC-1 cells.	Arsenic	79-81	ataxia telangiectasia and Rad3 related	Mus musculus	56-59
33740714-1	2021	Arsenite (AsIII) antiporter ACR3 is crucial for arsenic (As) translocation and sequestration in As-hyperaccumulator Pteris vittata, which has potential for phytoremediation of As-contaminated soils.	Arsenic	48-55	Arr3p	Saccharomyces cerevisiae S288C	28-32
33740714-1	2021	Arsenite (AsIII) antiporter ACR3 is crucial for arsenic (As) translocation and sequestration in As-hyperaccumulator Pteris vittata, which has potential for phytoremediation of As-contaminated soils.	Arsenic	10-12	Arr3p	Saccharomyces cerevisiae S288C	28-32
33740714-1	2021	Arsenite (AsIII) antiporter ACR3 is crucial for arsenic (As) translocation and sequestration in As-hyperaccumulator Pteris vittata, which has potential for phytoremediation of As-contaminated soils.	Arsenic	57-59	Arr3p	Saccharomyces cerevisiae S288C	28-32
33740714-1	2021	Arsenite (AsIII) antiporter ACR3 is crucial for arsenic (As) translocation and sequestration in As-hyperaccumulator Pteris vittata, which has potential for phytoremediation of As-contaminated soils.	Arsenic	57-59	Arr3p	Saccharomyces cerevisiae S288C	28-32
32621277-0	2021	Relationship between p38 signaling pathway and arsenic-induced apoptosis: a meta-analysis.	Arsenic	47-54	mitogen-activated protein kinase 14	Homo sapiens	21-24
33884182-8	2021	Our results demonstrated that arsenic accumulated in the brain time-dependently and increased Ser262 tau phosphorylation, which is very important in several tauopathies.	Arsenic	30-37	microtubule associated protein tau	Homo sapiens	101-104
32476085-4	2021	Adding 3 mg/kg arsenic to the diet caused the growth and development of chicken liver to be blocked, resulting in decrease of protein contents in liver tissue, decrease of SOD and GSH-Px activities, increase of MDA contents, decrease of NO contents, decrease of iNOS and TNOs activities, increase of ALT and AST activities, increase of apoptosis rates of liver cells.	Arsenic	15-22	nitric oxide synthase 2	Gallus gallus	262-266
33497687-9	2021	Arsenic increased proinflammatory cytokine (tumor necrosis factor-alpha and interleukin-1beta) levels, enhanced caspase-3 and Bax expression, and reduced Bcl-2 expression.	Arsenic	0-7	tumor necrosis factor	Mus musculus	44-71
33497687-9	2021	Arsenic increased proinflammatory cytokine (tumor necrosis factor-alpha and interleukin-1beta) levels, enhanced caspase-3 and Bax expression, and reduced Bcl-2 expression.	Arsenic	0-7	interleukin 1 beta	Mus musculus	76-93
33497687-9	2021	Arsenic increased proinflammatory cytokine (tumor necrosis factor-alpha and interleukin-1beta) levels, enhanced caspase-3 and Bax expression, and reduced Bcl-2 expression.	Arsenic	0-7	caspase 3	Mus musculus	112-121
33497687-9	2021	Arsenic increased proinflammatory cytokine (tumor necrosis factor-alpha and interleukin-1beta) levels, enhanced caspase-3 and Bax expression, and reduced Bcl-2 expression.	Arsenic	0-7	BCL2-associated X protein	Mus musculus	126-129
33497687-9	2021	Arsenic increased proinflammatory cytokine (tumor necrosis factor-alpha and interleukin-1beta) levels, enhanced caspase-3 and Bax expression, and reduced Bcl-2 expression.	Arsenic	0-7	B cell leukemia/lymphoma 2	Mus musculus	154-159
33497687-10	2021	Furthermore, arsenic-exposure in mice decreased significantly acetylcholinesterase activity and brain-derived neurotrophic factor level in the cerebral cortex.	Arsenic	13-20	brain derived neurotrophic factor	Mus musculus	96-129
32621277-4	2021	Therefore, the relationship between p38 signaling pathway and arsenic-induced apoptosis was systematically reviewed and analyzed by meta-analysis.	Arsenic	62-69	mitogen-activated protein kinase 14	Homo sapiens	36-39
32621277-9	2021	Subgroup analysis showed, when arsenic exposure was >= 5 mumol/l, the expression of Bcl-2 and Bax was down-regulated and the expression of p38 and Caspase-3 was up-regulated.	Arsenic	31-38	BCL2 apoptosis regulator	Homo sapiens	84-89
32621277-9	2021	Subgroup analysis showed, when arsenic exposure was >= 5 mumol/l, the expression of Bcl-2 and Bax was down-regulated and the expression of p38 and Caspase-3 was up-regulated.	Arsenic	31-38	BCL2 associated X, apoptosis regulator	Homo sapiens	94-97
32621277-9	2021	Subgroup analysis showed, when arsenic exposure was >= 5 mumol/l, the expression of Bcl-2 and Bax was down-regulated and the expression of p38 and Caspase-3 was up-regulated.	Arsenic	31-38	mitogen-activated protein kinase 14	Homo sapiens	139-142
33385390-4	2021	PCA analyses revealed three major groups of pollutants: PC1 represented predominantly an assortment of metal(loid)s, namely aluminium, arsenic, chromium, nickel and lead; PC2 included mostly Organochlorine Pesticides (OCPs), such as HCB, beta-HCH and p,p"-DDE; and PC3 gathered mainly a mixture of Polychlorinated Biphenyls (PCB-138, PCB-153 and PCB-180) and metals (cadmium, cobalt and chromium).	Arsenic	135-142	proprotein convertase subtilisin/kexin type 1	Homo sapiens	56-59
32621277-2	2021	It was reported that p38 signaling pathway played a key transcriptional regulatory factor in arsenic-induced apoptosis.	Arsenic	93-100	mitogen-activated protein kinase 14	Homo sapiens	21-24
33884178-9	2021	Therefore, our findings were helpful for further understanding the role of Nrf2/PPARgamma feedback loop in As-induced neurobehavioral toxicity.	Arsenic	107-109	nuclear factor, erythroid derived 2, like 2	Mus musculus	75-79
33650048-1	2021	Environmental arsenic exposure in adults and children has been associated with a reduction in the expression of club cell secretory protein (CC16) and an increase in the expression of matrix metalloproteinase-9 (MMP-9), both biomarkers of lung inflammation and negative respiratory outcomes.	Arsenic	14-21	secretoglobin family 1A member 1	Homo sapiens	141-145
33650048-1	2021	Environmental arsenic exposure in adults and children has been associated with a reduction in the expression of club cell secretory protein (CC16) and an increase in the expression of matrix metalloproteinase-9 (MMP-9), both biomarkers of lung inflammation and negative respiratory outcomes.	Arsenic	14-21	matrix metallopeptidase 9	Homo sapiens	184-210
33650048-1	2021	Environmental arsenic exposure in adults and children has been associated with a reduction in the expression of club cell secretory protein (CC16) and an increase in the expression of matrix metalloproteinase-9 (MMP-9), both biomarkers of lung inflammation and negative respiratory outcomes.	Arsenic	14-21	matrix metallopeptidase 9	Homo sapiens	212-217
33650048-2	2021	The objectives of this study were to determine if the levels of serum CC16 and MMP-9 and subsequent respiratory infections in children are associated with the ingestion of arsenic by drinking water.	Arsenic	172-179	secretoglobin family 1A member 1	Homo sapiens	70-74
33650048-2	2021	The objectives of this study were to determine if the levels of serum CC16 and MMP-9 and subsequent respiratory infections in children are associated with the ingestion of arsenic by drinking water.	Arsenic	172-179	matrix metallopeptidase 9	Homo sapiens	79-84
33650048-10	2021	In conclusion, altered levels of serum CC16 and MMP-9 in the children may be due to the toxic effects of arsenic exposure through drinking water.	Arsenic	105-112	secretoglobin family 1A member 1	Homo sapiens	39-43
33650048-10	2021	In conclusion, altered levels of serum CC16 and MMP-9 in the children may be due to the toxic effects of arsenic exposure through drinking water.	Arsenic	105-112	matrix metallopeptidase 9	Homo sapiens	48-53
33261869-1	2021	In arsenic toxicity, activation of the erythroid 2-related factor 2 (NRF2) pathway is regarded as a driver of cancer development and progression; however, the mechanisms by which NRF2 gene expression regulates cell cycle progression and mediates pathways of cellular proliferation and apoptosis in arsenic-induced lung carcinogenesis are poorly understood.	Arsenic	3-10	NFE2 like bZIP transcription factor 2	Homo sapiens	69-73
33261869-1	2021	In arsenic toxicity, activation of the erythroid 2-related factor 2 (NRF2) pathway is regarded as a driver of cancer development and progression; however, the mechanisms by which NRF2 gene expression regulates cell cycle progression and mediates pathways of cellular proliferation and apoptosis in arsenic-induced lung carcinogenesis are poorly understood.	Arsenic	3-10	NFE2 like bZIP transcription factor 2	Homo sapiens	179-183
32621277-9	2021	Subgroup analysis showed, when arsenic exposure was >= 5 mumol/l, the expression of Bcl-2 and Bax was down-regulated and the expression of p38 and Caspase-3 was up-regulated.	Arsenic	31-38	caspase 3	Homo sapiens	147-156
32621277-10	2021	When arsenic exposure was < 5 mumol/l, the expression of Bcl-2, Bax, p38 and Caspase-3 was up-regulated.	Arsenic	5-12	BCL2 apoptosis regulator	Homo sapiens	57-62
32621277-10	2021	When arsenic exposure was < 5 mumol/l, the expression of Bcl-2, Bax, p38 and Caspase-3 was up-regulated.	Arsenic	5-12	BCL2 associated X, apoptosis regulator	Homo sapiens	64-67
32621277-10	2021	When arsenic exposure was < 5 mumol/l, the expression of Bcl-2, Bax, p38 and Caspase-3 was up-regulated.	Arsenic	5-12	mitogen-activated protein kinase 14	Homo sapiens	69-72
32621277-10	2021	When arsenic exposure was < 5 mumol/l, the expression of Bcl-2, Bax, p38 and Caspase-3 was up-regulated.	Arsenic	5-12	caspase 3	Homo sapiens	77-86
32621277-11	2021	Arsenic exposure time (>= 48 h) or arsenic exposure dose (>= 5 mumol/l or < 5 mumol/l) can promote the expression of p38.	Arsenic	0-7	mitogen-activated protein kinase 14	Homo sapiens	117-120
32621277-11	2021	Arsenic exposure time (>= 48 h) or arsenic exposure dose (>= 5 mumol/l or < 5 mumol/l) can promote the expression of p38.	Arsenic	35-42	mitogen-activated protein kinase 14	Homo sapiens	117-120
32621277-12	2021	Arsenic exposure time was >= 48 h or exposure dose was < 5 mumol/l in cancer cells, arsenic exposure dose was >= 5 mumol/l or exposure time was < 48 h in normal cells, and they are statistically significant in the expression of p38.	Arsenic	0-7	mitogen-activated protein kinase 14	Homo sapiens	228-231
32621277-12	2021	Arsenic exposure time was >= 48 h or exposure dose was < 5 mumol/l in cancer cells, arsenic exposure dose was >= 5 mumol/l or exposure time was < 48 h in normal cells, and they are statistically significant in the expression of p38.	Arsenic	84-91	mitogen-activated protein kinase 14	Homo sapiens	228-231
32621277-13	2021	This study evaluates the role of p38 signaling pathway in arsenic-induced apoptosis, which is helpful to provide theoretical basis for the differentiation of arsenic-induced injury and the therapeutic mechanism of arsenic-induced apoptosis.	Arsenic	58-65	mitogen-activated protein kinase 14	Homo sapiens	33-36
32621277-13	2021	This study evaluates the role of p38 signaling pathway in arsenic-induced apoptosis, which is helpful to provide theoretical basis for the differentiation of arsenic-induced injury and the therapeutic mechanism of arsenic-induced apoptosis.	Arsenic	158-165	mitogen-activated protein kinase 14	Homo sapiens	33-36
32621277-13	2021	This study evaluates the role of p38 signaling pathway in arsenic-induced apoptosis, which is helpful to provide theoretical basis for the differentiation of arsenic-induced injury and the therapeutic mechanism of arsenic-induced apoptosis.	Arsenic	158-165	mitogen-activated protein kinase 14	Homo sapiens	33-36
33884178-9	2021	Therefore, our findings were helpful for further understanding the role of Nrf2/PPARgamma feedback loop in As-induced neurobehavioral toxicity.	Arsenic	107-109	peroxisome proliferator activated receptor gamma	Mus musculus	80-89
33434570-5	2021	This study aimed to explore the activation of the Nrf2 pathway upon treatment of arsenic in various forms, including inorganic and organic arsenic.	Arsenic	81-88	NFE2 like bZIP transcription factor 2	Homo sapiens	50-54
33360347-0	2021	Arsenic suppresses GDF1 expression via ROS-dependent downregulation of specificity protein 1.	Arsenic	0-7	sp1 transcription factor	Danio rerio	71-92
33360347-2	2021	Our previous studies showed that arsenic causes abnormal cardiac development in zebrafish embryos by downregulating Dvr1/GDF1 expression and that folic acid protects against these effects.	Arsenic	33-40	growth differentiation factor 3	Danio rerio	116-120
33360347-3	2021	However, the mechanism by which arsenic represses Dvr1/GDF1 expression remains unknown.	Arsenic	32-39	growth differentiation factor 3	Danio rerio	50-54
33360347-5	2021	Arsenic treatment downregulated Sp1 at both the mRNA and protein level and its downstream targets GDF1 and SIRT1.	Arsenic	0-7	sirtuin 1	Danio rerio	107-112
33360347-7	2021	Further investigation showed that Sp1 overexpression inhibited the arsenic-mediated decrease in GDF1 and SIRT1, while Sp1 knockdown had the opposite effect.	Arsenic	67-74	sirtuin 1	Danio rerio	105-110
33360347-10	2021	Both the antioxidants N-acetylcysteine and folic acid reversed the arsenic-mediated repression of Sp1, GDF1 and SIRT1.	Arsenic	67-74	sirtuin 1	Danio rerio	112-117
33360347-11	2021	Moreover, wild-type p66shc overexpression enhanced the arsenic-mediated repression of Sp1, GDF1 and SIRT1, which was accompanied by an increase in intracellular reactive oxygen species (ROS) levels, while both overexpression of a dominant negative p66shcSer36Ala mutant and deficiency in p66shc reversed these effects.	Arsenic	55-62	sirtuin 1	Danio rerio	100-105
33360347-12	2021	Taken together, our results revealed that arsenic suppresses GDF1 expression via the ROS-dependent downregulation of the Sp1/SIRT1 axis, which forms a negative feedback loop with p66shc to regulate oxidative stress.	Arsenic	42-49	sirtuin 1	Danio rerio	125-130
33434570-0	2021	Differential effects of arsenic species on Nrf2 and Bach1 nuclear localization in cultured hepatocytes.	Arsenic	24-31	NFE2 like bZIP transcription factor 2	Homo sapiens	43-47
33434570-0	2021	Differential effects of arsenic species on Nrf2 and Bach1 nuclear localization in cultured hepatocytes.	Arsenic	24-31	BTB domain and CNC homolog 1	Homo sapiens	52-57
33434570-5	2021	This study aimed to explore the activation of the Nrf2 pathway upon treatment of arsenic in various forms, including inorganic and organic arsenic.	Arsenic	139-146	NFE2 like bZIP transcription factor 2	Homo sapiens	50-54
33434570-6	2021	Our results showed that inorganic arsenic-both As2O3 and Na2HAsO4 significantly induced the expression of Nrf2 protein and mRNA, enhanced the transcription activity of Nrf2, and induced the expression of downstream target genes.	Arsenic	34-41	NFE2 like bZIP transcription factor 2	Homo sapiens	106-110
33434570-6	2021	Our results showed that inorganic arsenic-both As2O3 and Na2HAsO4 significantly induced the expression of Nrf2 protein and mRNA, enhanced the transcription activity of Nrf2, and induced the expression of downstream target genes.	Arsenic	34-41	NFE2 like bZIP transcription factor 2	Homo sapiens	168-172
33434570-7	2021	These results confirmed the inorganic arsenic-induced Nrf2 pathway activation in hepatocytes.	Arsenic	38-45	NFE2 like bZIP transcription factor 2	Homo sapiens	54-58
33434570-10	2021	Mechanistically, our results confirmed inorganic arsenic-induced both the nuclear import of Nrf2 and export of Bach1 (BTB and CNC homology 1), which is an Nrf2 transcriptional repressor, while organic arsenic only induced Nrf2 translocation.	Arsenic	49-56	NFE2 like bZIP transcription factor 2	Homo sapiens	92-96
33434570-10	2021	Mechanistically, our results confirmed inorganic arsenic-induced both the nuclear import of Nrf2 and export of Bach1 (BTB and CNC homology 1), which is an Nrf2 transcriptional repressor, while organic arsenic only induced Nrf2 translocation.	Arsenic	49-56	BTB domain and CNC homolog 1	Homo sapiens	111-116
33434570-10	2021	Mechanistically, our results confirmed inorganic arsenic-induced both the nuclear import of Nrf2 and export of Bach1 (BTB and CNC homology 1), which is an Nrf2 transcriptional repressor, while organic arsenic only induced Nrf2 translocation.	Arsenic	49-56	BTB domain and CNC homolog 1	Homo sapiens	118-140
33434570-10	2021	Mechanistically, our results confirmed inorganic arsenic-induced both the nuclear import of Nrf2 and export of Bach1 (BTB and CNC homology 1), which is an Nrf2 transcriptional repressor, while organic arsenic only induced Nrf2 translocation.	Arsenic	49-56	NFE2 like bZIP transcription factor 2	Homo sapiens	155-159
33434570-10	2021	Mechanistically, our results confirmed inorganic arsenic-induced both the nuclear import of Nrf2 and export of Bach1 (BTB and CNC homology 1), which is an Nrf2 transcriptional repressor, while organic arsenic only induced Nrf2 translocation.	Arsenic	49-56	NFE2 like bZIP transcription factor 2	Homo sapiens	155-159
33434570-11	2021	The unique pattern of Nrf2 regulation by organic arsenic underlines the critical role of Nrf2 and Bach1 in the arsenic toxicology.	Arsenic	49-56	NFE2 like bZIP transcription factor 2	Homo sapiens	22-26
33434570-11	2021	The unique pattern of Nrf2 regulation by organic arsenic underlines the critical role of Nrf2 and Bach1 in the arsenic toxicology.	Arsenic	49-56	NFE2 like bZIP transcription factor 2	Homo sapiens	89-93
33434570-11	2021	The unique pattern of Nrf2 regulation by organic arsenic underlines the critical role of Nrf2 and Bach1 in the arsenic toxicology.	Arsenic	49-56	BTB domain and CNC homolog 1	Homo sapiens	98-103
33434570-11	2021	The unique pattern of Nrf2 regulation by organic arsenic underlines the critical role of Nrf2 and Bach1 in the arsenic toxicology.	Arsenic	111-118	NFE2 like bZIP transcription factor 2	Homo sapiens	22-26
33434570-11	2021	The unique pattern of Nrf2 regulation by organic arsenic underlines the critical role of Nrf2 and Bach1 in the arsenic toxicology.	Arsenic	111-118	NFE2 like bZIP transcription factor 2	Homo sapiens	89-93
33434570-11	2021	The unique pattern of Nrf2 regulation by organic arsenic underlines the critical role of Nrf2 and Bach1 in the arsenic toxicology.	Arsenic	111-118	BTB domain and CNC homolog 1	Homo sapiens	98-103
33568718-4	2021	The D3 domain of Salmonella typhimurium flagellin was replaced with an arsenic-binding peptide motif of different bacterial ArsR transcriptional repressor factors.	Arsenic	71-78	DNA-binding transcriptional repressor ArsR	Salmonella enterica subsp. enterica serovar Typhimurium	124-128
33357454-4	2021	Crystal structures of arsenic-bound p53 mutants reveal a cryptic allosteric site involving three arsenic-coordinating cysteines within the DNA-binding domain, distal to the zinc-binding site.	Arsenic	22-29	tumor protein p53	Homo sapiens	36-39
33357454-4	2021	Crystal structures of arsenic-bound p53 mutants reveal a cryptic allosteric site involving three arsenic-coordinating cysteines within the DNA-binding domain, distal to the zinc-binding site.	Arsenic	97-104	tumor protein p53	Homo sapiens	36-39
33561393-0	2021	Arsenic and an Old Place: Rescuing p53 Mutants in Cancer.	Arsenic	0-7	tumor protein p53	Homo sapiens	35-38
33561393-4	2021	The arsenic atom binds in a conserved, cryptic site and reactivates multiple p53 mutants.	Arsenic	4-11	tumor protein p53	Homo sapiens	77-80
33357454-5	2021	Arsenic binding stabilizes the DNA-binding loop-sheet-helix motif alongside the overall beta-sandwich fold, endowing p53 mutants with thermostability and transcriptional activity.	Arsenic	0-7	tumor protein p53	Homo sapiens	117-120
33549147-6	2021	Eighteen single nucleotide polymorphisms (SNPs) of the arsenic (+ 3 oxidative state) methylation transferase (AS3MT) gene, which was known as the main catalyzer for arsenic methylation, were tested with the polymerase chain reaction method.	Arsenic	55-62	arsenite methyltransferase	Homo sapiens	110-115
33549147-6	2021	Eighteen single nucleotide polymorphisms (SNPs) of the arsenic (+ 3 oxidative state) methylation transferase (AS3MT) gene, which was known as the main catalyzer for arsenic methylation, were tested with the polymerase chain reaction method.	Arsenic	165-172	arsenite methyltransferase	Homo sapiens	110-115
32810714-6	2021	Modulated spatio-temporal expression of various TaCAT genes and alteration in total catalase enzyme activity during heat, drought, salt and arsenic (AsIII and AsV) treatment suggested their roles in abiotic stress response and arsenic tolerance.	Arsenic	140-147	catalase-1	Triticum aestivum	48-53
32810714-6	2021	Modulated spatio-temporal expression of various TaCAT genes and alteration in total catalase enzyme activity during heat, drought, salt and arsenic (AsIII and AsV) treatment suggested their roles in abiotic stress response and arsenic tolerance.	Arsenic	227-234	catalase-1	Triticum aestivum	48-53
32930475-3	2021	In this study, we found that the AS3MT was overexpressed in arsenic exposed population, non-small cell lung cancer (NSCLC) tissues, and A549 cells with sodium arsenite (NaAsO2 ) treatment for 48 hours.	Arsenic	60-67	arsenite methyltransferase	Homo sapiens	33-38
33038235-1	2021	High Arsenic Concentration 1 (HAC1), an Arabidopsis thaliana arsenate reductase, plays a key role in arsenate [As(V)] tolerance.	Arsenic	5-12	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	61-79
33038235-1	2021	High Arsenic Concentration 1 (HAC1), an Arabidopsis thaliana arsenate reductase, plays a key role in arsenate [As(V)] tolerance.	Arsenic	111-114	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	61-79
33049506-0	2021	Heme oxygenase-1 (HO-1) assists inorganic arsenic-induced immune tolerance in murine dendritic cells.	Arsenic	42-49	heme oxygenase 1	Mus musculus	0-16
33049506-0	2021	Heme oxygenase-1 (HO-1) assists inorganic arsenic-induced immune tolerance in murine dendritic cells.	Arsenic	42-49	heme oxygenase 1	Mus musculus	18-22
33049506-7	2021	Based on these experimental findings, we postulated the immunosuppressive property of inorganic arsenic might be mediated partially by HO-1 in DCs, thus contributing to the interactions of DCs-polarized differentiation of T-lymphocyte subtype as well as the development of infections and malignant diseases.	Arsenic	96-103	heme oxygenase 1	Mus musculus	135-139
32735355-1	2021	The aim of the present study is to determine four anionic alkyl sulfate (AS) surfactants with different alkyl chains, namely, C8, C10, C12 and C14, in wastewater by capillary electrophoresis with contactless conductivity detection (CE-C4 D).	Arsenic	73-75	chromosome 12 open reading frame 57	Homo sapiens	130-133
33321388-7	2021	RESULTS: Arsenic blood concentrations were significantly associated with increased levels in CRH (%Delta: 23.0, 95%CI: 8.4-39.6) and decreased levels in testosterone (%Delta: -16.3, 95%CI: -26.2--5.1).	Arsenic	9-16	corticotropin releasing hormone	Homo sapiens	93-96
32989703-4	2021	Arsenic exposure resulted in hepatic oxidative damage which was evidenced by marked decreases in antioxidant parameters (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH)) concomitant with high malondialdehyde (MDA) level.	Arsenic	0-7	catalase	Rattus norvegicus	149-157
32989703-4	2021	Arsenic exposure resulted in hepatic oxidative damage which was evidenced by marked decreases in antioxidant parameters (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH)) concomitant with high malondialdehyde (MDA) level.	Arsenic	0-7	catalase	Rattus norvegicus	159-162
32989703-4	2021	Arsenic exposure resulted in hepatic oxidative damage which was evidenced by marked decreases in antioxidant parameters (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH)) concomitant with high malondialdehyde (MDA) level.	Arsenic	0-7	glutathione-disulfide reductase	Rattus norvegicus	195-216
32930475-7	2021	Therefore, arsenic increased AS3MT expression in vivo and in vitro, which could directly act on the cell and affect the progression of NSCLC by regulating cell cycle genes.	Arsenic	11-18	arsenite methyltransferase	Homo sapiens	29-34
32989703-4	2021	Arsenic exposure resulted in hepatic oxidative damage which was evidenced by marked decreases in antioxidant parameters (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH)) concomitant with high malondialdehyde (MDA) level.	Arsenic	0-7	glutathione-disulfide reductase	Rattus norvegicus	218-220
32930475-4	2021	Besides, the level of AS3MT expression was positively correlated with the concentrations of urinary total arsenic (tAs), inorganic arsenic (iAs), methanearsonic acid (MMA), and dimethylarsinic acid (DMA) in all subjects.	Arsenic	106-113	arsenite methyltransferase	Homo sapiens	22-27
32989703-5	2021	Furthermore, As toxicity induced significant elevations in liver accumulation of As, serum hepatic indices (aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and total bilirubin (TB)), and apoptotic marker (B cell lymphoma 2(Bcl2), Bcl-2-associated X protein (Bax), and caspase 3) levels.	Arsenic	13-15	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	108-134
33026618-10	2021	Immunohistological results demonstrated the reduction of renal eNOS expression in arsenic treated rats.	Arsenic	82-89	nitric oxide synthase 3	Rattus norvegicus	63-67
33075130-0	2021	JAK2V617F myeloproliferative neoplasm eradication by a novel interferon/arsenic therapy involves PML.	Arsenic	72-79	Janus kinase 2	Mus musculus	0-4
33026618-11	2021	Notably, treatment with bosentan attenuated arsenic-induced renal damage and resisted arsenic-led reduction in renal eNOS expression.	Arsenic	86-93	nitric oxide synthase 3	Rattus norvegicus	117-121
32989703-5	2021	Furthermore, As toxicity induced significant elevations in liver accumulation of As, serum hepatic indices (aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and total bilirubin (TB)), and apoptotic marker (B cell lymphoma 2(Bcl2), Bcl-2-associated X protein (Bax), and caspase 3) levels.	Arsenic	13-15	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	136-139
32989703-5	2021	Furthermore, As toxicity induced significant elevations in liver accumulation of As, serum hepatic indices (aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and total bilirubin (TB)), and apoptotic marker (B cell lymphoma 2(Bcl2), Bcl-2-associated X protein (Bax), and caspase 3) levels.	Arsenic	13-15	BCL2, apoptosis regulator	Rattus norvegicus	269-273
32989703-5	2021	Furthermore, As toxicity induced significant elevations in liver accumulation of As, serum hepatic indices (aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and total bilirubin (TB)), and apoptotic marker (B cell lymphoma 2(Bcl2), Bcl-2-associated X protein (Bax), and caspase 3) levels.	Arsenic	13-15	BCL2 associated X, apoptosis regulator	Rattus norvegicus	276-302
32989703-5	2021	Furthermore, As toxicity induced significant elevations in liver accumulation of As, serum hepatic indices (aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and total bilirubin (TB)), and apoptotic marker (B cell lymphoma 2(Bcl2), Bcl-2-associated X protein (Bax), and caspase 3) levels.	Arsenic	13-15	BCL2 associated X, apoptosis regulator	Rattus norvegicus	304-307
32989703-5	2021	Furthermore, As toxicity induced significant elevations in liver accumulation of As, serum hepatic indices (aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and total bilirubin (TB)), and apoptotic marker (B cell lymphoma 2(Bcl2), Bcl-2-associated X protein (Bax), and caspase 3) levels.	Arsenic	13-15	caspase 3	Rattus norvegicus	314-323
32776539-8	2021	In conclusion, the present study manifested that inorganic arsenic exposure could activate HSCs through IRE1alpha/NOX4-mediated ROS generation.	Arsenic	59-66	NADPH oxidase 4	Rattus norvegicus	114-118
33279052-0	2021	Stability of Fe-As composites formed with As(V) and aged ferrihydrite.	Arsenic	16-18	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	42-47
33075130-0	2021	JAK2V617F myeloproliferative neoplasm eradication by a novel interferon/arsenic therapy involves PML.	Arsenic	72-79	promyelocytic leukemia	Mus musculus	97-100
32878582-8	2021	In the first optimization application, the optimal point is obtained for input variables in composite as 21.91% MU, 37.10% SR, and 13.54% CP.	Arsenic	102-104	ceruloplasmin	Homo sapiens	138-140
33396024-0	2021	HER2 overexpression triggers the IL-8 to promote arsenic-induced EMT and stem cell-like phenotypes in human bladder epithelial cells.	Arsenic	49-56	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-4
33552384-0	2021	Retracted: Proanthocyanidins Antagonize Arsenic-Induced Oxidative Damage and Promote Arsenic Methylation through Activation of the Nrf2 Signaling Pathway.	Arsenic	85-92	NFE2 like bZIP transcription factor 2	Homo sapiens	131-135
33396077-9	2021	Growth factor regulator proteins such as c-Jun, c-fos and c-myc are influenced by chronic arsenic exposure.	Arsenic	90-97	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	41-46
33501840-0	2021	Role of inhibiting Chk1-p53 pathway in hepatotoxicity caused by chronic arsenic exposure from coal-burning.	Arsenic	72-79	checkpoint kinase 1	Homo sapiens	19-23
33501840-0	2021	Role of inhibiting Chk1-p53 pathway in hepatotoxicity caused by chronic arsenic exposure from coal-burning.	Arsenic	72-79	tumor protein p53	Homo sapiens	24-27
33501840-5	2021	The results showed that arsenic induced liver damage, increased hepatocyte apoptosis and elevated the expression level of Chk1 and the ratios of p-p53/p53 and Bax/Bcl-2 in liver tissues, which were significantly attenuated by GBE.	Arsenic	24-31	checkpoint kinase 1	Homo sapiens	122-126
33501840-5	2021	The results showed that arsenic induced liver damage, increased hepatocyte apoptosis and elevated the expression level of Chk1 and the ratios of p-p53/p53 and Bax/Bcl-2 in liver tissues, which were significantly attenuated by GBE.	Arsenic	24-31	tumor protein p53	Homo sapiens	147-150
33501840-5	2021	The results showed that arsenic induced liver damage, increased hepatocyte apoptosis and elevated the expression level of Chk1 and the ratios of p-p53/p53 and Bax/Bcl-2 in liver tissues, which were significantly attenuated by GBE.	Arsenic	24-31	tumor protein p53	Homo sapiens	151-154
33501840-5	2021	The results showed that arsenic induced liver damage, increased hepatocyte apoptosis and elevated the expression level of Chk1 and the ratios of p-p53/p53 and Bax/Bcl-2 in liver tissues, which were significantly attenuated by GBE.	Arsenic	24-31	BCL2 associated X, apoptosis regulator	Homo sapiens	159-162
33501840-5	2021	The results showed that arsenic induced liver damage, increased hepatocyte apoptosis and elevated the expression level of Chk1 and the ratios of p-p53/p53 and Bax/Bcl-2 in liver tissues, which were significantly attenuated by GBE.	Arsenic	24-31	BCL2 apoptosis regulator	Homo sapiens	163-168
33501841-0	2021	Urinary leucine aminopeptidase 3 in population environmentally exposed to airborne arsenic.	Arsenic	83-90	leucine aminopeptidase 3	Homo sapiens	8-32
33501841-12	2021	CONCLUSIONS: These data suggest that urinary LAP3 may be a potential biomarker of arsenic exposure, which warrants further study.	Arsenic	82-89	leucine aminopeptidase 3	Homo sapiens	45-49
33331839-1	2021	A new design of a membraneless vaporization (MBL-VP) unit coupled with a specific flow system is presented for the determination of arsenic at trace levels using a hydride generation process.	Arsenic	132-139	mannose-binding lectin family member 3, pseudogene	Homo sapiens	45-48
33468231-0	2021	Correction to: Arsenic nano complex induced degradation of YAP sensitized ESCC cancer cells to radiation and chemotherapy.	Arsenic	15-22	Yes1 associated transcriptional regulator	Homo sapiens	59-62
33396077-9	2021	Growth factor regulator proteins such as c-Jun, c-fos and c-myc are influenced by chronic arsenic exposure.	Arsenic	90-97	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	48-53
33396077-9	2021	Growth factor regulator proteins such as c-Jun, c-fos and c-myc are influenced by chronic arsenic exposure.	Arsenic	90-97	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	58-63
33396024-0	2021	HER2 overexpression triggers the IL-8 to promote arsenic-induced EMT and stem cell-like phenotypes in human bladder epithelial cells.	Arsenic	49-56	C-X-C motif chemokine ligand 8	Homo sapiens	33-37
33396077-10	2021	In this review we have delineated arsenic induced ROS regulations of epidermal growth factor receptor (EGFR), NF-kbeta, MAP kinase, matrix-metalloproteinases (MMPs).	Arsenic	34-41	epidermal growth factor receptor	Homo sapiens	69-101
33396077-10	2021	In this review we have delineated arsenic induced ROS regulations of epidermal growth factor receptor (EGFR), NF-kbeta, MAP kinase, matrix-metalloproteinases (MMPs).	Arsenic	34-41	epidermal growth factor receptor	Homo sapiens	103-107
33396024-4	2021	Here, we reported that chronic exposure to arsenic resulted in EMT and increased levels of the CSC marker CD44 in human uroepithelial cells.	Arsenic	43-50	CD44 molecule (Indian blood group)	Homo sapiens	106-110
33396024-6	2021	Phosphorylation of the human epidermal growth factor receptor 2 (HER2) was key for arsenic-induced IL-8 overexpression and depended on the simultaneous activation of the MAPK, JNK, PI3K/AKT and GSK3beta signaling pathways.	Arsenic	83-90	erb-b2 receptor tyrosine kinase 2	Homo sapiens	29-63
33396024-6	2021	Phosphorylation of the human epidermal growth factor receptor 2 (HER2) was key for arsenic-induced IL-8 overexpression and depended on the simultaneous activation of the MAPK, JNK, PI3K/AKT and GSK3beta signaling pathways.	Arsenic	83-90	erb-b2 receptor tyrosine kinase 2	Homo sapiens	65-69
33396024-6	2021	Phosphorylation of the human epidermal growth factor receptor 2 (HER2) was key for arsenic-induced IL-8 overexpression and depended on the simultaneous activation of the MAPK, JNK, PI3K/AKT and GSK3beta signaling pathways.	Arsenic	83-90	C-X-C motif chemokine ligand 8	Homo sapiens	99-103
33396024-6	2021	Phosphorylation of the human epidermal growth factor receptor 2 (HER2) was key for arsenic-induced IL-8 overexpression and depended on the simultaneous activation of the MAPK, JNK, PI3K/AKT and GSK3beta signaling pathways.	Arsenic	83-90	mitogen-activated protein kinase 8	Homo sapiens	176-179
33396024-6	2021	Phosphorylation of the human epidermal growth factor receptor 2 (HER2) was key for arsenic-induced IL-8 overexpression and depended on the simultaneous activation of the MAPK, JNK, PI3K/AKT and GSK3beta signaling pathways.	Arsenic	83-90	AKT serine/threonine kinase 1	Homo sapiens	186-189
32712355-10	2021	Analysis of genes involved in As-resistance showed that recovered isolates possess the genes encoding the ArsB, Acr3(1) and Acr3(2) proteins, indicating that at least a part of their resistance could be ascribed to As-efflux systems described in isolates obtained from human-polluted environments.	Arsenic	30-32	arylsulfatase B	Homo sapiens	106-110
33396024-6	2021	Phosphorylation of the human epidermal growth factor receptor 2 (HER2) was key for arsenic-induced IL-8 overexpression and depended on the simultaneous activation of the MAPK, JNK, PI3K/AKT and GSK3beta signaling pathways.	Arsenic	83-90	glycogen synthase kinase 3 alpha	Homo sapiens	194-202
33396024-7	2021	We also found that genistein inhibited arsenic-induced HER2 phosphorylation and downregulated its downstream signaling pathways, thereby inhibiting progression of EMT, and reducing CD44 expression levels.	Arsenic	39-46	erb-b2 receptor tyrosine kinase 2	Homo sapiens	55-59
33396024-7	2021	We also found that genistein inhibited arsenic-induced HER2 phosphorylation and downregulated its downstream signaling pathways, thereby inhibiting progression of EMT, and reducing CD44 expression levels.	Arsenic	39-46	CD44 molecule (Indian blood group)	Homo sapiens	181-185
33396024-8	2021	These results demonstrate that the HER2/IL-8 axis is related to the acquisition of an EMT phenotype and CSCs in arsenic-treated cells.	Arsenic	112-119	erb-b2 receptor tyrosine kinase 2	Homo sapiens	35-39
32763770-2	2021	This study shows that less toxic ROX is completely converted into highly toxic As(III) and As(V) in the HTL reaction with temperature more than 240  C. Moreover, more than 81.5% of As is distributed in the liquid phase generated by the livestock manure HTL reaction.	Arsenic	79-81	MAX network transcriptional repressor	Homo sapiens	33-36
33396024-8	2021	These results demonstrate that the HER2/IL-8 axis is related to the acquisition of an EMT phenotype and CSCs in arsenic-treated cells.	Arsenic	112-119	C-X-C motif chemokine ligand 8	Homo sapiens	40-44
33396050-6	2021	The results found that a decrease in Se was a risk factor for arsenic-induced skin and liver damage (OR = 8.33 and 1.92, respectively).	Arsenic	62-69	squalene epoxidase	Homo sapiens	37-39
33396050-8	2021	In addition, the results found that Se and Al possessed certain diagnostic values for arsenic-induced skin damage (AUC = 0.93, 0.80), that Se possessed a diagnostic value for liver damage (AUC = 0.93), and that the combination of Se and Al increased the diagnostic value for skin damage (AUC = 0.96).	Arsenic	86-93	squalene epoxidase	Homo sapiens	36-38
33279514-1	2021	Arsenic exposure is well established to impair the function of zinc finger proteins, including PARP-1.	Arsenic	0-7	poly (ADP-ribose) polymerase family, member 1	Mus musculus	95-101
33641653-0	2021	Arsenic Dispensing Powder Promotes Erythropoiesis in Myelodysplastic Syndromes via Downregulation of HIF1A and Upregulation of GATA Factors.	Arsenic	0-7	hypoxia inducible factor 1 subunit alpha	Homo sapiens	101-106
33406855-0	2022	Transgenerational male reproductive effect of prenatal arsenic exposure: abnormal spermatogenesis with Igf2/H19 epigenetic alteration in CD1 mouse.	Arsenic	55-62	insulin-like growth factor 2	Mus musculus	103-107
33406855-0	2022	Transgenerational male reproductive effect of prenatal arsenic exposure: abnormal spermatogenesis with Igf2/H19 epigenetic alteration in CD1 mouse.	Arsenic	55-62	H19, imprinted maternally expressed transcript	Mus musculus	108-111
33406855-0	2022	Transgenerational male reproductive effect of prenatal arsenic exposure: abnormal spermatogenesis with Igf2/H19 epigenetic alteration in CD1 mouse.	Arsenic	55-62	CD1 antigen complex	Mus musculus	137-140
33406855-5	2022	The overall methylation status of Igf2 DMR2 and H19 DMR was significantly lower in the arsenic-exposed group than that of the control group in both F1 and F3.	Arsenic	87-94	insulin-like growth factor 2	Mus musculus	34-38
33406855-5	2022	The overall methylation status of Igf2 DMR2 and H19 DMR was significantly lower in the arsenic-exposed group than that of the control group in both F1 and F3.	Arsenic	87-94	H19, imprinted maternally expressed transcript	Mus musculus	48-51
33406855-6	2022	The relative mRNA expression levels of Igf2 and H19 in arsenic-exposed males were significantly increased in both F1 and F3.	Arsenic	55-62	insulin-like growth factor 2	Mus musculus	39-43
33406855-6	2022	The relative mRNA expression levels of Igf2 and H19 in arsenic-exposed males were significantly increased in both F1 and F3.	Arsenic	55-62	H19, imprinted maternally expressed transcript	Mus musculus	48-51
33406855-7	2022	This study indicates that ancestral exposure to arsenic may result in transgenerational inheritance of an impaired spermatogenesis phenotyping involving both epigenetic alterations and the abnormal expression of Igf2 and H19.	Arsenic	48-55	insulin-like growth factor 2	Mus musculus	212-216
33406855-7	2022	This study indicates that ancestral exposure to arsenic may result in transgenerational inheritance of an impaired spermatogenesis phenotyping involving both epigenetic alterations and the abnormal expression of Igf2 and H19.	Arsenic	48-55	H19, imprinted maternally expressed transcript	Mus musculus	221-224
33445796-4	2021	The as-synthesized SI-PBP membranes provide enhanced proton conductivity (107.07 mS/cm) compared to Nafion 211  (104.5 mS/cm).	Arsenic	4-6	dedicator of cytokinesis 3	Homo sapiens	22-25
33490807-0	2021	Simultaneous Oxidation and Sequestration of Arsenic(III) from Aqueous Solution by Copper Aluminate with Peroxymonosulfate: A Fast and Efficient Heterogeneous Process.	Arsenic	44-51	Fas activated serine/threonine kinase	Homo sapiens	125-129
33242462-9	2021	However, pretreatment of mice with CGA resulted in noteworthy improvements in testicular damage induced by arsenic in a dose-dependent manner possibly mediated by the Nrf2 signaling pathway.	Arsenic	107-114	nuclear factor, erythroid derived 2, like 2	Mus musculus	167-171
33389622-7	2021	In the liver, exposure to arsenic reduced the levels of reduced glutathione (GSH), total glutathione (TG), redox ratio, and the activity of superoxide dismutase (SOD), whereas lipid peroxidation (LPO), inflammation markers, and nitric oxide (NO) levels were elevated with no significant change in catalase (CAT) activity.	Arsenic	26-33	catalase	Rattus norvegicus	297-305
33389622-7	2021	In the liver, exposure to arsenic reduced the levels of reduced glutathione (GSH), total glutathione (TG), redox ratio, and the activity of superoxide dismutase (SOD), whereas lipid peroxidation (LPO), inflammation markers, and nitric oxide (NO) levels were elevated with no significant change in catalase (CAT) activity.	Arsenic	26-33	catalase	Rattus norvegicus	307-310
33641653-0	2021	Arsenic Dispensing Powder Promotes Erythropoiesis in Myelodysplastic Syndromes via Downregulation of HIF1A and Upregulation of GATA Factors.	Arsenic	0-7	glutaminyl-tRNA amidotransferase subunit QRSL1	Homo sapiens	127-131
33044731-7	2021	Arsenic (As) is probably derived from the dissolution of Fe oxide and hydroxide (i.e., Fe(OH)3, goethite, maghemite, and magnetite).	Arsenic	0-7	general transcription factor IIE subunit 1	Homo sapiens	87-94
32739679-0	2021	A 3D ecotoxi-topological profile: Using concentration-time-response surfaces to show peroxidase activity in Zea mays (L.) exposed to aluminium or arsenic in hydroponic conditions.	Arsenic	146-153	peroxidase 1	Zea mays	85-95
32916524-5	2021	Given that the wildtype ArsR did not respond to arsenic and activate GFP expression in vitro, we found, after screening, an evolved ArsR mutant ep3 could respond to arsenic and exhibited an approximately 3.4-fold fluorescence increase.	Arsenic	165-172	prostaglandin E receptor 3	Homo sapiens	144-147
32916524-6	2021	Arsenic induced expression of both wildtype ArsR and ep3 mutant in vitro, however, only ep3 mutant regulated the expression of reporter gene.	Arsenic	0-7	prostaglandin E receptor 3	Homo sapiens	53-56
33044731-7	2021	Arsenic (As) is probably derived from the dissolution of Fe oxide and hydroxide (i.e., Fe(OH)3, goethite, maghemite, and magnetite).	Arsenic	9-11	general transcription factor IIE subunit 1	Homo sapiens	87-94
32816178-0	2021	Arsenic exposure increased expression of HOTAIR and LincRNA-p21 in vivo and vitro.	Arsenic	0-7	HOX transcript antisense RNA	Homo sapiens	41-47
32816178-6	2021	HOTAIR and LincRNA-p21 expression were positively linked to monomethylarsenic acid (MMA), dimethylarsenic acid (DMA), inorganic arsenic (iAs), total arsenic (tAs), and MMA% and negatively linked to secondary methylation index (SMI).	Arsenic	70-77	HOX transcript antisense RNA	Homo sapiens	0-6
32816178-6	2021	HOTAIR and LincRNA-p21 expression were positively linked to monomethylarsenic acid (MMA), dimethylarsenic acid (DMA), inorganic arsenic (iAs), total arsenic (tAs), and MMA% and negatively linked to secondary methylation index (SMI).	Arsenic	70-77	tumor protein p53 pathway corepressor 1	Homo sapiens	11-22
32816178-0	2021	Arsenic exposure increased expression of HOTAIR and LincRNA-p21 in vivo and vitro.	Arsenic	0-7	tumor protein p53 pathway corepressor 1	Homo sapiens	52-63
32816178-4	2021	This study investigated the association between arsenic and the expression of HOTAIR and LincRNA-p21 in vivo and vitro.	Arsenic	48-55	HOX transcript antisense RNA	Homo sapiens	78-84
33162208-0	2021	LncRNA H19-mediated M2 polarization of macrophages promotes myofibroblast differentiation in pulmonary fibrosis induced by arsenic exposure.	Arsenic	123-130	H19 imprinted maternally expressed transcript	Homo sapiens	7-10
32816178-7	2021	In A549 cells, arsenic exposure resulted in enhanced HOTAIR and LincRNA-p21 expression dose-dependently.	Arsenic	15-22	HOX transcript antisense RNA	Homo sapiens	53-59
33162208-5	2021	We have found that, in lung tissues of mice, arsenite, a biologically active form of arsenic, elevated H19, c-Myc, and Arg1; decreased let-7a; and caused pulmonary fibrosis.	Arsenic	85-92	H19, imprinted maternally expressed transcript	Mus musculus	103-106
32816178-4	2021	This study investigated the association between arsenic and the expression of HOTAIR and LincRNA-p21 in vivo and vitro.	Arsenic	48-55	tumor protein p53 pathway corepressor 1	Homo sapiens	89-100
32816178-7	2021	In A549 cells, arsenic exposure resulted in enhanced HOTAIR and LincRNA-p21 expression dose-dependently.	Arsenic	15-22	tumor protein p53 pathway corepressor 1	Homo sapiens	64-75
32816178-5	2021	In epidemiological studies, the expression of HOTAIR and LincRNA-p21 was increased after long-term arsenic exposure.	Arsenic	99-106	HOX transcript antisense RNA	Homo sapiens	46-52
32816178-5	2021	In epidemiological studies, the expression of HOTAIR and LincRNA-p21 was increased after long-term arsenic exposure.	Arsenic	99-106	tumor protein p53 pathway corepressor 1	Homo sapiens	57-68
32816178-13	2021	Besides, in the presence of arsenic, both of HOTAIR and LincRNA-p21 were upregulated significantly when P53 was knocked down.	Arsenic	28-35	HOX transcript antisense RNA	Homo sapiens	45-51
32816178-13	2021	Besides, in the presence of arsenic, both of HOTAIR and LincRNA-p21 were upregulated significantly when P53 was knocked down.	Arsenic	28-35	tumor protein p53 pathway corepressor 1	Homo sapiens	56-67
32816178-13	2021	Besides, in the presence of arsenic, both of HOTAIR and LincRNA-p21 were upregulated significantly when P53 was knocked down.	Arsenic	28-35	tumor protein p53	Homo sapiens	104-107
32816178-14	2021	We revealed that inorganic arsenic, its methylated metabolites, and arsenic metabolism efficiency affect the expression of HOTAIR and LincRNA-p21.	Arsenic	27-34	HOX transcript antisense RNA	Homo sapiens	123-129
32816178-14	2021	We revealed that inorganic arsenic, its methylated metabolites, and arsenic metabolism efficiency affect the expression of HOTAIR and LincRNA-p21.	Arsenic	27-34	tumor protein p53 pathway corepressor 1	Homo sapiens	134-145
32816178-14	2021	We revealed that inorganic arsenic, its methylated metabolites, and arsenic metabolism efficiency affect the expression of HOTAIR and LincRNA-p21.	Arsenic	68-75	HOX transcript antisense RNA	Homo sapiens	123-129
32816178-14	2021	We revealed that inorganic arsenic, its methylated metabolites, and arsenic metabolism efficiency affect the expression of HOTAIR and LincRNA-p21.	Arsenic	68-75	tumor protein p53 pathway corepressor 1	Homo sapiens	134-145
33164855-0	2021	Effect of gene-environment interaction (arsenic exposure - PON1 Q192R polymorphism) on cardiovascular disease biomarkers in Mexican population.	Arsenic	40-47	paraoxonase 1	Homo sapiens	59-63
32735129-4	2021	Moreover, our results revealed that arsenic can reduce global acetylation of histone H4 at K16 (H4K16 ac) in lymphocytes via decreasing the level of males absent on the first but upregulates mRNA and protein levels of the forkhead/winged-helix box P3 (Foxp3) gene by increasing the acetylation of histone H4 at K16 (H4K16) at the promoter of Foxp3.	Arsenic	36-43	forkhead box P3	Homo sapiens	342-347
32735129-6	2021	Our research indicates that arsenic-induced immunosuppressive effect in human lymphocytes may be related to the acetylation of H4K16 at the promoter of Foxp3 and that histone deacetylase inhibitors may play a role in the prevention and treatment of immune injury caused by arsenic.	Arsenic	28-35	forkhead box P3	Homo sapiens	152-157
32735129-4	2021	Moreover, our results revealed that arsenic can reduce global acetylation of histone H4 at K16 (H4K16 ac) in lymphocytes via decreasing the level of males absent on the first but upregulates mRNA and protein levels of the forkhead/winged-helix box P3 (Foxp3) gene by increasing the acetylation of histone H4 at K16 (H4K16) at the promoter of Foxp3.	Arsenic	36-43	forkhead box P3	Homo sapiens	222-250
33290778-0	2021	Semaphorin 4A antibody alleviates arsenic-induced hepatotoxicity in mice via inhibition of AKT2/NF-kappaB inflammatory signaling.	Arsenic	34-41	sema domain, immunoglobulin domain (Ig), transmembrane domain (TM) and short cytoplasmic domain, (semaphorin) 4A	Mus musculus	0-13
32735129-4	2021	Moreover, our results revealed that arsenic can reduce global acetylation of histone H4 at K16 (H4K16 ac) in lymphocytes via decreasing the level of males absent on the first but upregulates mRNA and protein levels of the forkhead/winged-helix box P3 (Foxp3) gene by increasing the acetylation of histone H4 at K16 (H4K16) at the promoter of Foxp3.	Arsenic	36-43	forkhead box P3	Homo sapiens	252-257
33176587-1	2021	A transgenic Acute Promyelocytic Leukemia (APL) murine model established by Michael Bishop by cloning a human PML-RARalpha cDNA into the hMRP8 expression cassette has been widely used in the all-trans retinoid acid and arsenic preparations for the research of APL.	Arsenic	219-226	S100 calcium binding protein A8	Homo sapiens	137-142
33290778-5	2021	Arsenic exposure induced hepatic injury and resulted in the activations of p-AKT2, NF-kappaB p65, and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, downregulation of Sema 3A, and upregulation of Sema 4A or NRP-1.	Arsenic	0-7	thymoma viral proto-oncogene 2	Mus musculus	77-81
33290778-5	2021	Arsenic exposure induced hepatic injury and resulted in the activations of p-AKT2, NF-kappaB p65, and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, downregulation of Sema 3A, and upregulation of Sema 4A or NRP-1.	Arsenic	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	83-92
33290778-5	2021	Arsenic exposure induced hepatic injury and resulted in the activations of p-AKT2, NF-kappaB p65, and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, downregulation of Sema 3A, and upregulation of Sema 4A or NRP-1.	Arsenic	0-7	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	93-96
33290778-5	2021	Arsenic exposure induced hepatic injury and resulted in the activations of p-AKT2, NF-kappaB p65, and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, downregulation of Sema 3A, and upregulation of Sema 4A or NRP-1.	Arsenic	0-7	NLR family, pyrin domain containing 3	Mus musculus	102-152
33290778-5	2021	Arsenic exposure induced hepatic injury and resulted in the activations of p-AKT2, NF-kappaB p65, and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, downregulation of Sema 3A, and upregulation of Sema 4A or NRP-1.	Arsenic	0-7	NLR family, pyrin domain containing 3	Mus musculus	154-159
33290778-5	2021	Arsenic exposure induced hepatic injury and resulted in the activations of p-AKT2, NF-kappaB p65, and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, downregulation of Sema 3A, and upregulation of Sema 4A or NRP-1.	Arsenic	0-7	sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3A	Mus musculus	193-200
33290778-5	2021	Arsenic exposure induced hepatic injury and resulted in the activations of p-AKT2, NF-kappaB p65, and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, downregulation of Sema 3A, and upregulation of Sema 4A or NRP-1.	Arsenic	0-7	sema domain, immunoglobulin domain (Ig), transmembrane domain (TM) and short cytoplasmic domain, (semaphorin) 4A	Mus musculus	222-229
33290778-5	2021	Arsenic exposure induced hepatic injury and resulted in the activations of p-AKT2, NF-kappaB p65, and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, downregulation of Sema 3A, and upregulation of Sema 4A or NRP-1.	Arsenic	0-7	neuropilin 1	Mus musculus	233-238
33290778-6	2021	Interestingly, intervention with anti-Sema 4A antibody showed the mitigation of arsenic-induced hepatotoxicity, accompanied by the downregulation of Sema 4A, rebound of Sema 3A, and upregulation of NRP-1.	Arsenic	80-87	sema domain, immunoglobulin domain (Ig), transmembrane domain (TM) and short cytoplasmic domain, (semaphorin) 4A	Mus musculus	38-45
33290778-6	2021	Interestingly, intervention with anti-Sema 4A antibody showed the mitigation of arsenic-induced hepatotoxicity, accompanied by the downregulation of Sema 4A, rebound of Sema 3A, and upregulation of NRP-1.	Arsenic	80-87	sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3A	Mus musculus	169-176
33290778-6	2021	Interestingly, intervention with anti-Sema 4A antibody showed the mitigation of arsenic-induced hepatotoxicity, accompanied by the downregulation of Sema 4A, rebound of Sema 3A, and upregulation of NRP-1.	Arsenic	80-87	neuropilin 1	Mus musculus	198-203
33290778-7	2021	And, the inflammatory signaling p-AKT2 or NF-kappaB p65, and NLRP3 inflammasome showed a downregulation compared with arsenic treatment group.	Arsenic	118-125	thymoma viral proto-oncogene 2	Mus musculus	34-38
33290778-7	2021	And, the inflammatory signaling p-AKT2 or NF-kappaB p65, and NLRP3 inflammasome showed a downregulation compared with arsenic treatment group.	Arsenic	118-125	NLR family, pyrin domain containing 3	Mus musculus	61-66
33290778-9	2021	In conclusion, the anti-Sema 4A antibody antagonizes arsenic-induced hepatotoxicity in mice and may be involved in the inhibitions of AKT2/NF-kappaB and NLRP3 inflammatory signaling mediated synergistically by Sema 4A or Sema 3A and their receptor NRP-1.	Arsenic	53-60	sema domain, immunoglobulin domain (Ig), transmembrane domain (TM) and short cytoplasmic domain, (semaphorin) 4A	Mus musculus	24-31
33400797-0	2020	Divergent molecular profile of PIK3CA gene in arsenic-associated bladder carcinoma.	Arsenic	46-53	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	31-37
33400797-3	2020	Therefore, we aimed to analyse the effect of arsenic on the genetic (copy number variation/mutation) and expression profiles of PIK3CA in primary BlCa samples.	Arsenic	45-52	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	128-134
33400797-4	2020	Infrequent amplification (16%) of the PIK3CA locus was observed, with higher frequency among the arsenic-high (AsH) than arsenic-low (AsL) samples.	Arsenic	97-104	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	38-44
33400797-4	2020	Infrequent amplification (16%) of the PIK3CA locus was observed, with higher frequency among the arsenic-high (AsH) than arsenic-low (AsL) samples.	Arsenic	121-128	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	38-44
33400797-12	2020	Finally, AsH patients with the overexpression of PIK3CA or NFkappaB had the worst overall survival, signifying a strong impact of arsenic on this pathway and outcome of the patients.	Arsenic	130-137	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	49-55
33400797-12	2020	Finally, AsH patients with the overexpression of PIK3CA or NFkappaB had the worst overall survival, signifying a strong impact of arsenic on this pathway and outcome of the patients.	Arsenic	130-137	nuclear factor kappa B subunit 1	Homo sapiens	59-67
33400797-13	2020	Thus, our study showed that the arsenic-associated differential molecular profile of PIK3CA/AKT1/NFkB in BlCa has an important role in the molecular pathogenesis of the disease.	Arsenic	32-39	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	85-91
33400797-13	2020	Thus, our study showed that the arsenic-associated differential molecular profile of PIK3CA/AKT1/NFkB in BlCa has an important role in the molecular pathogenesis of the disease.	Arsenic	32-39	AKT serine/threonine kinase 1	Homo sapiens	92-96
33374180-0	2020	In Silico and In Vitro Analysis of Major Cannabis-Derived Compounds as Fatty Acid Amide Hydrolase Inhibitors.	Arsenic	68-70	fatty acid amide hydrolase	Homo sapiens	71-97
33353561-0	2020	Arsenic nano complex induced degradation of YAP sensitized ESCC cancer cells to radiation and chemotherapy.	Arsenic	0-7	Yes1 associated transcriptional regulator	Homo sapiens	44-47
33313624-0	2020	FRA1 is essential for the maintenance of the oncogenic phenotype induced by in vitro long-term arsenic exposure.	Arsenic	95-102	FOS like 1, AP-1 transcription factor subunit	Homo sapiens	0-4
33313624-4	2020	Accordingly, FRA1 could play an essential role in the in vitro cell transformation induced by arsenic.	Arsenic	94-101	FOS like 1, AP-1 transcription factor subunit	Homo sapiens	13-17
33313624-5	2020	FRA1 levels were monitored in MEF cells throughout their transformation stages during 40 weeks of long-term 2 muM arsenic exposure.	Arsenic	114-121	FOS like 1, AP-1 transcription factor subunit	Homo sapiens	0-4
33313624-7	2020	The levels of MAPKs (ERK, p38, and JNK) and other known players upstream from FRA1 were assessed at equivalent time-points, and ERK, p38 and RAS were pinpointed as potential candidates involved in arsenic-induced FRA1 activation.	Arsenic	197-204	FOS like 1, AP-1 transcription factor subunit	Homo sapiens	213-217
33313624-8	2020	Furthermore, FRA1 stable knockdown under chronic arsenic exposure settings elicits a remarkable impact on the features relative to the cells" oncogenic phenotype.	Arsenic	49-56	FOS like 1, AP-1 transcription factor subunit	Homo sapiens	13-17
33313624-10	2020	This work is the first to demonstrate the important role of FRA1 in the development and aggressiveness of the in vitro transformed phenotype induced by long-term arsenic exposure.	Arsenic	162-169	FOS like 1, AP-1 transcription factor subunit	Homo sapiens	60-64
33353561-8	2020	Mechanistically we proved PML physically interacted with YAP, and arsenic induced degradation PML mediated the degradation of YAP in ESCC cells.	Arsenic	66-73	PML nuclear body scaffold	Homo sapiens	94-97
33353561-8	2020	Mechanistically we proved PML physically interacted with YAP, and arsenic induced degradation PML mediated the degradation of YAP in ESCC cells.	Arsenic	66-73	Yes1 associated transcriptional regulator	Homo sapiens	126-129
33353561-13	2020	CONCLUSIONS: Together, these findings suggested besides ROS, YAP is a potential target for arsenic based therapy in ESCC, which should play an important role in the synthetic effects of arsenic nano complex with chemo and radiation therapy.	Arsenic	91-98	yes-associated protein 1	Mus musculus	61-64
33353561-13	2020	CONCLUSIONS: Together, these findings suggested besides ROS, YAP is a potential target for arsenic based therapy in ESCC, which should play an important role in the synthetic effects of arsenic nano complex with chemo and radiation therapy.	Arsenic	186-193	yes-associated protein 1	Mus musculus	61-64
33340130-3	2021	Among the risk factors for cancer, arsenic methylation efficiency (As3MT) and the clearance of arsenic from cells by two members of the ATP-binding cassette (ABC) transporter family (multidrug resistance protein 1 [MRP1] and P-glycoprotein [P-gp]) play an important role in processing of arsenic and decreasing its intracellular levels.	Arsenic	35-42	ATP binding cassette subfamily B member 1	Homo sapiens	215-219
33156617-0	2020	Predicted AS3MT Proteins Methylate Arsenic and Support Two Major Phylogenetic AS3MT Groups.	Arsenic	35-42	arsenite methyltransferase	Homo sapiens	10-15
33156617-0	2020	Predicted AS3MT Proteins Methylate Arsenic and Support Two Major Phylogenetic AS3MT Groups.	Arsenic	35-42	arsenite methyltransferase	Homo sapiens	78-83
33156617-4	2020	In this study, we evaluated whether 55 (out of which 47 were predicted based on protein sequence similarity) sequences encoding putative AS3MT orthologues in 47 species from different kingdoms can indeed methylate arsenic.	Arsenic	214-221	arsenite methyltransferase	Homo sapiens	137-142
33156617-6	2020	For example, the predicted AS3MT of the human gut bacterium Faecalibacterium prausnitzii methylated arsenic efficiently.	Arsenic	100-107	arsenite methyltransferase	Homo sapiens	27-32
33156617-10	2020	Further, it shows that humans carry two bacterial systems for arsenic methylation: one bacterium-derived AS3MT from Group 1 incorporated in the human genome and one from Group 2 in F. prausnitzii present in the gut microbiome.	Arsenic	62-69	arsenite methyltransferase	Homo sapiens	105-110
33340130-0	2021	Association between the polymorphism of three genes involved in the methylation and efflux of arsenic (As3MT, MRP1, and P-gp) with lung cancer in a Mexican cohort.	Arsenic	94-101	arsenite methyltransferase	Homo sapiens	103-108
33340130-0	2021	Association between the polymorphism of three genes involved in the methylation and efflux of arsenic (As3MT, MRP1, and P-gp) with lung cancer in a Mexican cohort.	Arsenic	94-101	ATP binding cassette subfamily B member 1	Homo sapiens	110-114
33340130-3	2021	Among the risk factors for cancer, arsenic methylation efficiency (As3MT) and the clearance of arsenic from cells by two members of the ATP-binding cassette (ABC) transporter family (multidrug resistance protein 1 [MRP1] and P-glycoprotein [P-gp]) play an important role in processing of arsenic and decreasing its intracellular levels.	Arsenic	35-42	ATP binding cassette subfamily B member 1	Homo sapiens	241-245
33340130-0	2021	Association between the polymorphism of three genes involved in the methylation and efflux of arsenic (As3MT, MRP1, and P-gp) with lung cancer in a Mexican cohort.	Arsenic	94-101	ATP binding cassette subfamily B member 1	Homo sapiens	120-124
33340130-3	2021	Among the risk factors for cancer, arsenic methylation efficiency (As3MT) and the clearance of arsenic from cells by two members of the ATP-binding cassette (ABC) transporter family (multidrug resistance protein 1 [MRP1] and P-glycoprotein [P-gp]) play an important role in processing of arsenic and decreasing its intracellular levels.	Arsenic	35-42	arsenite methyltransferase	Homo sapiens	67-72
33340130-3	2021	Among the risk factors for cancer, arsenic methylation efficiency (As3MT) and the clearance of arsenic from cells by two members of the ATP-binding cassette (ABC) transporter family (multidrug resistance protein 1 [MRP1] and P-glycoprotein [P-gp]) play an important role in processing of arsenic and decreasing its intracellular levels.	Arsenic	95-102	ATP binding cassette subfamily B member 1	Homo sapiens	183-213
33340130-3	2021	Among the risk factors for cancer, arsenic methylation efficiency (As3MT) and the clearance of arsenic from cells by two members of the ATP-binding cassette (ABC) transporter family (multidrug resistance protein 1 [MRP1] and P-glycoprotein [P-gp]) play an important role in processing of arsenic and decreasing its intracellular levels.	Arsenic	95-102	ATP binding cassette subfamily B member 1	Homo sapiens	215-219
33340130-3	2021	Among the risk factors for cancer, arsenic methylation efficiency (As3MT) and the clearance of arsenic from cells by two members of the ATP-binding cassette (ABC) transporter family (multidrug resistance protein 1 [MRP1] and P-glycoprotein [P-gp]) play an important role in processing of arsenic and decreasing its intracellular levels.	Arsenic	95-102	ATP binding cassette subfamily B member 1	Homo sapiens	225-239
33340130-3	2021	Among the risk factors for cancer, arsenic methylation efficiency (As3MT) and the clearance of arsenic from cells by two members of the ATP-binding cassette (ABC) transporter family (multidrug resistance protein 1 [MRP1] and P-glycoprotein [P-gp]) play an important role in processing of arsenic and decreasing its intracellular levels.	Arsenic	95-102	ATP binding cassette subfamily B member 1	Homo sapiens	241-245
33340130-3	2021	Among the risk factors for cancer, arsenic methylation efficiency (As3MT) and the clearance of arsenic from cells by two members of the ATP-binding cassette (ABC) transporter family (multidrug resistance protein 1 [MRP1] and P-glycoprotein [P-gp]) play an important role in processing of arsenic and decreasing its intracellular levels.	Arsenic	95-102	ATP binding cassette subfamily B member 1	Homo sapiens	183-213
33340130-3	2021	Among the risk factors for cancer, arsenic methylation efficiency (As3MT) and the clearance of arsenic from cells by two members of the ATP-binding cassette (ABC) transporter family (multidrug resistance protein 1 [MRP1] and P-glycoprotein [P-gp]) play an important role in processing of arsenic and decreasing its intracellular levels.	Arsenic	95-102	ATP binding cassette subfamily B member 1	Homo sapiens	215-219
33340130-3	2021	Among the risk factors for cancer, arsenic methylation efficiency (As3MT) and the clearance of arsenic from cells by two members of the ATP-binding cassette (ABC) transporter family (multidrug resistance protein 1 [MRP1] and P-glycoprotein [P-gp]) play an important role in processing of arsenic and decreasing its intracellular levels.	Arsenic	95-102	ATP binding cassette subfamily B member 1	Homo sapiens	225-239
33340130-3	2021	Among the risk factors for cancer, arsenic methylation efficiency (As3MT) and the clearance of arsenic from cells by two members of the ATP-binding cassette (ABC) transporter family (multidrug resistance protein 1 [MRP1] and P-glycoprotein [P-gp]) play an important role in processing of arsenic and decreasing its intracellular levels.	Arsenic	95-102	ATP binding cassette subfamily B member 1	Homo sapiens	241-245
33340130-5	2021	Polymorphism in As3MT, MRP1, and P-gp modified the arsenic metabolism increasing significantly the AsV urinary levels.	Arsenic	51-58	arsenite methyltransferase	Homo sapiens	16-21
33391994-6	2021	Arsenic exposed rats after supplementation showed relatively less severe effects of toxicity evident by significantly higher amount of (p<0.05) mtDNA copy number and reduced occurrence of deletion containing mtDNA as well as lower levels of methylation in p53 gene promoter.	Arsenic	0-7	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	256-259
33340130-5	2021	Polymorphism in As3MT, MRP1, and P-gp modified the arsenic metabolism increasing significantly the AsV urinary levels.	Arsenic	51-58	ATP binding cassette subfamily B member 1	Homo sapiens	23-27
33340130-5	2021	Polymorphism in As3MT, MRP1, and P-gp modified the arsenic metabolism increasing significantly the AsV urinary levels.	Arsenic	51-58	ATP binding cassette subfamily B member 1	Homo sapiens	33-37
33340130-7	2021	The high inorganic arsenic urinary levels registered in the studied subjects suggest a reduction in the efficiency of As3MT, MRP1, and P-gp firstly because of gene polymorphisms and secondarily because of high internal inorganic arsenic levels.	Arsenic	19-26	arsenite methyltransferase	Homo sapiens	118-123
33340130-7	2021	The high inorganic arsenic urinary levels registered in the studied subjects suggest a reduction in the efficiency of As3MT, MRP1, and P-gp firstly because of gene polymorphisms and secondarily because of high internal inorganic arsenic levels.	Arsenic	19-26	ATP binding cassette subfamily B member 1	Homo sapiens	125-129
33340130-7	2021	The high inorganic arsenic urinary levels registered in the studied subjects suggest a reduction in the efficiency of As3MT, MRP1, and P-gp firstly because of gene polymorphisms and secondarily because of high internal inorganic arsenic levels.	Arsenic	19-26	ATP binding cassette subfamily B member 1	Homo sapiens	135-139
33141059-2	2020	The arsenic biotransformation enzyme AS3MT is known to participate in the generation of ROS after arsenic exposure, whereas MTH1 sanitizes oxidized dNTP pools to prevent the incorporation of damaged bases into DNA.	Arsenic	4-11	arsenite methyltransferase	Homo sapiens	37-42
33141059-2	2020	The arsenic biotransformation enzyme AS3MT is known to participate in the generation of ROS after arsenic exposure, whereas MTH1 sanitizes oxidized dNTP pools to prevent the incorporation of damaged bases into DNA.	Arsenic	98-105	arsenite methyltransferase	Homo sapiens	37-42
33129825-0	2020	Inorganic arsenic and its methylated metabolites as endocrine disruptors in the placenta: Mechanisms underpinning glucocorticoid receptor (GR) pathway perturbations.	Arsenic	10-17	nuclear receptor subfamily 3 group C member 1	Homo sapiens	114-137
33254717-0	2020	The role of Hipk2-p53 pathways in arsenic-induced autistic behaviors: A translational study from rats to humans.	Arsenic	34-41	homeodomain interacting protein kinase 2	Rattus norvegicus	12-17
33129825-0	2020	Inorganic arsenic and its methylated metabolites as endocrine disruptors in the placenta: Mechanisms underpinning glucocorticoid receptor (GR) pathway perturbations.	Arsenic	10-17	nuclear receptor subfamily 3 group C member 1	Homo sapiens	139-141
32124230-0	2020	The Mechanism of Trivalent Inorganic Arsenic on HIF-1alpha: a Systematic Review and Meta-analysis.	Arsenic	37-44	hypoxia inducible factor 1 subunit alpha	Homo sapiens	48-58
32124230-3	2020	The results showed that low-dose exposure to arsenic (<= 10 mumol/L) could promote the expression of phosphatidylinositol 3-kinase (PI3K) and phosphorylation-protein kinase B (p-AKT).	Arsenic	45-52	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	101-130
33026605-10	2020	Arsenic induced rats had significantly (p < 0.0001) altered biochemical serum levels of SGPT, SGOT, ALP, total bilirubin, urea, uric acid, creatinine and albumin; But, after the administration of T. cordifolia there was significant (p < 0.0001) restoration observed in these liver and kidney function parameters.	Arsenic	0-7	PDZ and LIM domain 3	Rattus norvegicus	100-103
32725557-6	2020	Furthermore, ligand exchange between the hydroxyl groups of the adsorbent and As(V) and the formation of inner-sphere surface complexes could play a central role in arsenic removal which needs further investigation.	Arsenic	165-172	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	78-83
32124230-4	2020	High-dose arsenic exposure (> 10 mumol/L) promoted the expression of PI3K, HIF-1alpha, vascular endothelial growth factor (VEGF), and p38MAPK (P38).	Arsenic	10-17	hypoxia inducible factor 1 subunit alpha	Homo sapiens	75-85
32124230-4	2020	High-dose arsenic exposure (> 10 mumol/L) promoted the expression of PI3K, HIF-1alpha, vascular endothelial growth factor (VEGF), and p38MAPK (P38).	Arsenic	10-17	vascular endothelial growth factor A	Homo sapiens	87-121
32124230-4	2020	High-dose arsenic exposure (> 10 mumol/L) promoted the expression of PI3K, HIF-1alpha, vascular endothelial growth factor (VEGF), and p38MAPK (P38).	Arsenic	10-17	vascular endothelial growth factor A	Homo sapiens	123-127
32124230-4	2020	High-dose arsenic exposure (> 10 mumol/L) promoted the expression of PI3K, HIF-1alpha, vascular endothelial growth factor (VEGF), and p38MAPK (P38).	Arsenic	10-17	mitogen-activated protein kinase 14	Homo sapiens	134-141
32124230-4	2020	High-dose arsenic exposure (> 10 mumol/L) promoted the expression of PI3K, HIF-1alpha, vascular endothelial growth factor (VEGF), and p38MAPK (P38).	Arsenic	10-17	mitogen-activated protein kinase 14	Homo sapiens	143-146
32124230-5	2020	Acute arsenic exposure (< 24 h) promoted the expression of PI3K, HIF-1alpha, and VEGF.	Arsenic	6-13	hypoxia inducible factor 1 subunit alpha	Homo sapiens	65-75
32124230-5	2020	Acute arsenic exposure (< 24 h) promoted the expression of PI3K, HIF-1alpha, and VEGF.	Arsenic	6-13	vascular endothelial growth factor A	Homo sapiens	81-85
32124230-6	2020	Chronic arsenic exposure (>= 24 h) promoted the expression of PI3K, p-AKT, and P38.	Arsenic	8-15	mitogen-activated protein kinase 14	Homo sapiens	79-82
32124230-7	2020	Moreover, for normal tissue-derived cells, arsenic could induce the increased expression of PI3K, p-AKT, HIF-1alpha, and VEGF.	Arsenic	43-50	hypoxia inducible factor 1 subunit alpha	Homo sapiens	105-115
32124230-7	2020	Moreover, for normal tissue-derived cells, arsenic could induce the increased expression of PI3K, p-AKT, HIF-1alpha, and VEGF.	Arsenic	43-50	vascular endothelial growth factor A	Homo sapiens	121-125
32124230-8	2020	For tumor tissue-derived cells, arsenic could induce the expression of PI3K, p-AKT, and P38.	Arsenic	32-39	mitogen-activated protein kinase 14	Homo sapiens	88-91
32124230-9	2020	We found that arsenic exposure could activate the PI3K/AKT pathway, further induce the high expression of HIF-1alpha, and then upregulate the levels of miRNA-21 and VEGF, promote the expression of proliferating cell nuclear antigen (PCNA), and ultimately lead to malignant cell proliferation.	Arsenic	14-21	AKT serine/threonine kinase 1	Homo sapiens	55-58
32124230-9	2020	We found that arsenic exposure could activate the PI3K/AKT pathway, further induce the high expression of HIF-1alpha, and then upregulate the levels of miRNA-21 and VEGF, promote the expression of proliferating cell nuclear antigen (PCNA), and ultimately lead to malignant cell proliferation.	Arsenic	14-21	hypoxia inducible factor 1 subunit alpha	Homo sapiens	106-116
32124230-9	2020	We found that arsenic exposure could activate the PI3K/AKT pathway, further induce the high expression of HIF-1alpha, and then upregulate the levels of miRNA-21 and VEGF, promote the expression of proliferating cell nuclear antigen (PCNA), and ultimately lead to malignant cell proliferation.	Arsenic	14-21	microRNA 21	Homo sapiens	152-160
32124230-9	2020	We found that arsenic exposure could activate the PI3K/AKT pathway, further induce the high expression of HIF-1alpha, and then upregulate the levels of miRNA-21 and VEGF, promote the expression of proliferating cell nuclear antigen (PCNA), and ultimately lead to malignant cell proliferation.	Arsenic	14-21	vascular endothelial growth factor A	Homo sapiens	165-169
32124230-9	2020	We found that arsenic exposure could activate the PI3K/AKT pathway, further induce the high expression of HIF-1alpha, and then upregulate the levels of miRNA-21 and VEGF, promote the expression of proliferating cell nuclear antigen (PCNA), and ultimately lead to malignant cell proliferation.	Arsenic	14-21	proliferating cell nuclear antigen	Homo sapiens	197-231
32124230-9	2020	We found that arsenic exposure could activate the PI3K/AKT pathway, further induce the high expression of HIF-1alpha, and then upregulate the levels of miRNA-21 and VEGF, promote the expression of proliferating cell nuclear antigen (PCNA), and ultimately lead to malignant cell proliferation.	Arsenic	14-21	proliferating cell nuclear antigen	Homo sapiens	233-237
32124230-10	2020	Our findings indicated that arsenic could increase the expression of HIF-1alpha by activating the PI3K/AKT pathway and eventually induce malignant cell proliferation.	Arsenic	28-35	hypoxia inducible factor 1 subunit alpha	Homo sapiens	69-79
32124230-10	2020	Our findings indicated that arsenic could increase the expression of HIF-1alpha by activating the PI3K/AKT pathway and eventually induce malignant cell proliferation.	Arsenic	28-35	AKT serine/threonine kinase 1	Homo sapiens	103-106
32770468-8	2020	Moreover, the enzyme activities of AKP, GSTs, and MTs were inhibited with increasing As(V) levels under both IP and GP conditions.	Arsenic	85-88	glutathione S-transferase kappa 1	Homo sapiens	40-44
33254717-0	2020	The role of Hipk2-p53 pathways in arsenic-induced autistic behaviors: A translational study from rats to humans.	Arsenic	34-41	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	18-21
33254717-6	2020	In animals, we found that arsenic exposures caused difficulties of social interaction and increased stereotypic behaviors in a dose-dependent manner, accompanied by increased neuronal apoptosis and upregulation of Hipk2-p53 pathway in the frontal cortex.	Arsenic	26-33	homeodomain interacting protein kinase 2	Homo sapiens	214-219
33254717-6	2020	In animals, we found that arsenic exposures caused difficulties of social interaction and increased stereotypic behaviors in a dose-dependent manner, accompanied by increased neuronal apoptosis and upregulation of Hipk2-p53 pathway in the frontal cortex.	Arsenic	26-33	tumor protein p53	Homo sapiens	220-223
33254717-8	2020	ASD children had significantly higher serum levels of 15 elements, among which arsenic, silicon, strontium, and vanadium were positively associated with both Hipk2 and p53.	Arsenic	79-86	homeodomain interacting protein kinase 2	Homo sapiens	158-163
33254717-8	2020	ASD children had significantly higher serum levels of 15 elements, among which arsenic, silicon, strontium, and vanadium were positively associated with both Hipk2 and p53.	Arsenic	79-86	tumor protein p53	Homo sapiens	168-171
33254717-9	2020	Results from both the rat arsenic exposure and human case-control studies suggest a likely role of Hipk2-p53 pathway in ASD development induced by exposures to environmental pollutants such as arsenic.	Arsenic	26-33	homeodomain interacting protein kinase 2	Homo sapiens	99-104
33254717-9	2020	Results from both the rat arsenic exposure and human case-control studies suggest a likely role of Hipk2-p53 pathway in ASD development induced by exposures to environmental pollutants such as arsenic.	Arsenic	26-33	tumor protein p53	Homo sapiens	105-108
33254717-9	2020	Results from both the rat arsenic exposure and human case-control studies suggest a likely role of Hipk2-p53 pathway in ASD development induced by exposures to environmental pollutants such as arsenic.	Arsenic	193-200	homeodomain interacting protein kinase 2	Homo sapiens	99-104
33254717-9	2020	Results from both the rat arsenic exposure and human case-control studies suggest a likely role of Hipk2-p53 pathway in ASD development induced by exposures to environmental pollutants such as arsenic.	Arsenic	193-200	tumor protein p53	Homo sapiens	105-108
33125114-0	2020	Arsenic compounds activate the MAPK and caspase pathways to induce apoptosis in OEC-M1 gingival epidermal carcinoma.	Arsenic	0-7	caspase 8	Homo sapiens	40-47
32608101-0	2020	Histone demethylase JHDM2A regulates H3K9 dimethylation in response to arsenic-induced DNA damage and repair in normal human liver cells.	Arsenic	71-78	lysine demethylase 3A	Homo sapiens	20-26
32608101-4	2020	In this study, we conducted experiments in vitro using normal human liver cells (L-02) to explore the mechanism by which the histone demethylase JHDM2A regulates H3K9 dimethylation (me2) in response to arsenic-induced DNA damage.	Arsenic	202-209	lysine demethylase 3A	Homo sapiens	145-151
32608101-5	2020	Our results indicated that arsenic exposure upregulated the expression of JHDM2A, downregulated global H3K9me2 modification levels, increased the H3K9me2 levels at the promoters of base excision repair (BER) genes (N-methylpurine-DNA glycosylase [MPG], XRCC1 and poly(ADP-ribose)polymerase 1) and inhibited their expression levels, causing DNA damage in cells.	Arsenic	27-34	lysine demethylase 3A	Homo sapiens	74-80
32663744-0	2020	Screening of hub genes and prediction of putative drugs in arsenic-related bladder carcinoma: An in silico study.	Arsenic	59-66	ELAV like RNA binding protein 2	Homo sapiens	13-16
33378035-8	2020	The level of autophagy was decreased in AS, which was reversed by overexpression of circHIPK3.	Arsenic	40-42	homeodomain interacting protein kinase 3	Mus musculus	84-93
32608101-5	2020	Our results indicated that arsenic exposure upregulated the expression of JHDM2A, downregulated global H3K9me2 modification levels, increased the H3K9me2 levels at the promoters of base excision repair (BER) genes (N-methylpurine-DNA glycosylase [MPG], XRCC1 and poly(ADP-ribose)polymerase 1) and inhibited their expression levels, causing DNA damage in cells.	Arsenic	27-34	N-methylpurine DNA glycosylase	Homo sapiens	215-245
32608101-5	2020	Our results indicated that arsenic exposure upregulated the expression of JHDM2A, downregulated global H3K9me2 modification levels, increased the H3K9me2 levels at the promoters of base excision repair (BER) genes (N-methylpurine-DNA glycosylase [MPG], XRCC1 and poly(ADP-ribose)polymerase 1) and inhibited their expression levels, causing DNA damage in cells.	Arsenic	27-34	N-methylpurine DNA glycosylase	Homo sapiens	247-250
32608101-5	2020	Our results indicated that arsenic exposure upregulated the expression of JHDM2A, downregulated global H3K9me2 modification levels, increased the H3K9me2 levels at the promoters of base excision repair (BER) genes (N-methylpurine-DNA glycosylase [MPG], XRCC1 and poly(ADP-ribose)polymerase 1) and inhibited their expression levels, causing DNA damage in cells.	Arsenic	27-34	X-ray repair cross complementing 1	Homo sapiens	253-258
32608101-5	2020	Our results indicated that arsenic exposure upregulated the expression of JHDM2A, downregulated global H3K9me2 modification levels, increased the H3K9me2 levels at the promoters of base excision repair (BER) genes (N-methylpurine-DNA glycosylase [MPG], XRCC1 and poly(ADP-ribose)polymerase 1) and inhibited their expression levels, causing DNA damage in cells.	Arsenic	27-34	poly(ADP-ribose) polymerase 1	Homo sapiens	263-291
32608101-6	2020	In addition, we studied the effects of overexpression and inhibition of JHDM2A and found that JHDM2A can participate in the molecular mechanism of arsenic-induced DNA damage via the BER pathway, which may not be involved in the BER process because H3K9me2 levels at the promoter region of the BER genes were unchanged following JHDM2A interference.	Arsenic	147-154	lysine demethylase 3A	Homo sapiens	72-78
32608101-6	2020	In addition, we studied the effects of overexpression and inhibition of JHDM2A and found that JHDM2A can participate in the molecular mechanism of arsenic-induced DNA damage via the BER pathway, which may not be involved in the BER process because H3K9me2 levels at the promoter region of the BER genes were unchanged following JHDM2A interference.	Arsenic	147-154	lysine demethylase 3A	Homo sapiens	94-100
32608101-6	2020	In addition, we studied the effects of overexpression and inhibition of JHDM2A and found that JHDM2A can participate in the molecular mechanism of arsenic-induced DNA damage via the BER pathway, which may not be involved in the BER process because H3K9me2 levels at the promoter region of the BER genes were unchanged following JHDM2A interference.	Arsenic	147-154	lysine demethylase 3A	Homo sapiens	94-100
32608101-7	2020	These results suggest a potential mechanism by which JHDM2A can regulate the MPG and XRCC1 genes in the process of responding to DNA damage induced by arsenic exposure and can participate in the process of DNA damage repair, which provides a scientific basis for understanding the epigenetic mechanisms and treatments for endemic arsenic poisoning.	Arsenic	151-158	lysine demethylase 3A	Homo sapiens	53-59
32608101-7	2020	These results suggest a potential mechanism by which JHDM2A can regulate the MPG and XRCC1 genes in the process of responding to DNA damage induced by arsenic exposure and can participate in the process of DNA damage repair, which provides a scientific basis for understanding the epigenetic mechanisms and treatments for endemic arsenic poisoning.	Arsenic	151-158	N-methylpurine DNA glycosylase	Homo sapiens	77-80
32608101-7	2020	These results suggest a potential mechanism by which JHDM2A can regulate the MPG and XRCC1 genes in the process of responding to DNA damage induced by arsenic exposure and can participate in the process of DNA damage repair, which provides a scientific basis for understanding the epigenetic mechanisms and treatments for endemic arsenic poisoning.	Arsenic	151-158	X-ray repair cross complementing 1	Homo sapiens	85-90
33125114-8	2020	Annexin V/PI double staining analysis further confirmed that both arsenic compounds induced apoptosis of OEC-M1 cells.	Arsenic	66-73	annexin A5	Homo sapiens	0-9
33125114-10	2020	Furthermore, both arsenic compounds significantly activated the cleavage of caspase-8, -9, -3 and PARP, and the phosphorylation of JNK, ERK1/2 and p38 in OEC-M1 cells (P<0.05).	Arsenic	18-25	caspase 8	Homo sapiens	76-93
33125114-10	2020	Furthermore, both arsenic compounds significantly activated the cleavage of caspase-8, -9, -3 and PARP, and the phosphorylation of JNK, ERK1/2 and p38 in OEC-M1 cells (P<0.05).	Arsenic	18-25	collagen type XI alpha 2 chain	Homo sapiens	98-102
33125114-10	2020	Furthermore, both arsenic compounds significantly activated the cleavage of caspase-8, -9, -3 and PARP, and the phosphorylation of JNK, ERK1/2 and p38 in OEC-M1 cells (P<0.05).	Arsenic	18-25	mitogen-activated protein kinase 8	Homo sapiens	131-134
33125114-10	2020	Furthermore, both arsenic compounds significantly activated the cleavage of caspase-8, -9, -3 and PARP, and the phosphorylation of JNK, ERK1/2 and p38 in OEC-M1 cells (P<0.05).	Arsenic	18-25	mitogen-activated protein kinase 3	Homo sapiens	136-142
33125114-10	2020	Furthermore, both arsenic compounds significantly activated the cleavage of caspase-8, -9, -3 and PARP, and the phosphorylation of JNK, ERK1/2 and p38 in OEC-M1 cells (P<0.05).	Arsenic	18-25	mitogen-activated protein kinase 1	Homo sapiens	147-150
32077013-1	2020	Inorganic arsenic [iAs, As(III) + As(V)] is considered a human carcinogen.	Arsenic	10-17	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	34-39
33238896-15	2020	Thus, the total dissolved solids and arsenic in drinking water may have positive correlation with the occurrence of CKDu in Thunukkai region in the Mullaitivu District of Sri Lanka.	Arsenic	37-44	sorcin	Homo sapiens	171-174
32860851-0	2020	Integrin alpha4 up-regulation activates the hedgehog pathway to promote arsenic and benzo[alpha]pyrene co-exposure-induced cancer stem cell-like property and tumorigenesis.	Arsenic	72-79	integrin subunit alpha 4	Homo sapiens	0-15
32860851-4	2020	It was found that integrin alpha4 (ITGA4) expression levels are significantly up-regulated and the Hedgehog pathway is highly activated in arsenic plus BaP co-exposure-transformed human bronchial epithelial cells.	Arsenic	139-146	integrin subunit alpha 4	Homo sapiens	18-33
32860851-4	2020	It was found that integrin alpha4 (ITGA4) expression levels are significantly up-regulated and the Hedgehog pathway is highly activated in arsenic plus BaP co-exposure-transformed human bronchial epithelial cells.	Arsenic	139-146	integrin subunit alpha 4	Homo sapiens	35-40
32860851-8	2020	These findings indicate that ITGA4 up-regulation activates the Hedgehog pathway to enhance the CSC-like property and tumorigenicity of arsenic and BaP co-exposure-transformed cells, offering new mechanistic insight for the synergistic carcinogenic effect of arsenic and BaP co-exposure.	Arsenic	135-142	integrin subunit alpha 4	Homo sapiens	29-34
32860851-8	2020	These findings indicate that ITGA4 up-regulation activates the Hedgehog pathway to enhance the CSC-like property and tumorigenicity of arsenic and BaP co-exposure-transformed cells, offering new mechanistic insight for the synergistic carcinogenic effect of arsenic and BaP co-exposure.	Arsenic	258-265	integrin subunit alpha 4	Homo sapiens	29-34
33053406-2	2020	Considering that arsenic has the potential to inhibit autophagic flux, it was hypothesized that arsenite (NaAsO2) may interplay with LRRK2 and alpha-Synuclein, affecting their phosphorylation in brain regions prone to neurodegeneration.	Arsenic	17-24	leucine-rich repeat kinase 2	Mus musculus	133-138
33053406-2	2020	Considering that arsenic has the potential to inhibit autophagic flux, it was hypothesized that arsenite (NaAsO2) may interplay with LRRK2 and alpha-Synuclein, affecting their phosphorylation in brain regions prone to neurodegeneration.	Arsenic	17-24	synuclein, alpha	Mus musculus	143-158
32980394-7	2020	L-Nrf1-silenced mBM-MSCs showed decreased arsenic efflux with reduced expression of arsenic transporter ATP-binding cassette subfamily C member 4 (ABCC4), as well as compromised NRF2-mediated antioxidative defense with elevated level of mitochondrial reactive oxygen species (mtROS) under arsenite-exposed conditions.	Arsenic	42-49	nuclear respiratory factor 1	Mus musculus	2-6
32544768-0	2020	Arsenic induces hepatic insulin resistance via mtROS-NLRP3 inflammasome pathway.	Arsenic	0-7	NLR family, pyrin domain containing 3	Rattus norvegicus	53-58
32544768-3	2020	The current study determined the role of NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation in arsenic-induced IR and revealed the underlying mechanism.	Arsenic	127-134	NLR family, pyrin domain containing 3	Rattus norvegicus	41-91
32544768-3	2020	The current study determined the role of NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation in arsenic-induced IR and revealed the underlying mechanism.	Arsenic	127-134	NLR family, pyrin domain containing 3	Rattus norvegicus	93-98
32544768-9	2020	Taken together, these data demonstrated that mtROS-triggered ox-mtDNA, mitophagy, and the activation of NLRP3 inflammasome was involved in arsenic-induced hepatic IR.	Arsenic	139-146	NLR family, pyrin domain containing 3	Rattus norvegicus	104-109
32980394-0	2020	Long-isoform NRF1 protects against arsenic cytotoxicity in mouse bone marrow-derived mesenchymal stem cells by suppressing mitochondrial ROS and facilitating arsenic efflux.	Arsenic	35-42	nuclear respiratory factor 1	Mus musculus	13-17
32980394-9	2020	Taken together, these findings suggest that L-NRF1 protects mBM-MSCs from arsenite-induced cytotoxicity via suppressing mtROS in addition to facilitating cellular arsenic efflux.	Arsenic	163-170	nuclear respiratory factor 1	Mus musculus	46-50
32516727-3	2020	Tara) plant to metalloid arsenic (As) toxicity.	Arsenic	25-32	TRIO and F-actin binding protein	Homo sapiens	0-4
32768839-10	2020	As experimentally observed, AsCl3 is the main arsenic product produced almost in one-to-one yield, whereas acetylene is an important hydrocarbon product in pyrolysis.	Arsenic	46-53	achaete-scute family bHLH transcription factor 3	Homo sapiens	28-33
32516727-3	2020	Tara) plant to metalloid arsenic (As) toxicity.	Arsenic	34-36	TRIO and F-actin binding protein	Homo sapiens	0-4
33153165-2	2020	Previously, we reported that the overexpression of NtCyc07 enhanced As(III) tolerance and reduced As(III) accumulation in yeast (Saccharomyces cerevisiae) and tobacco (Nicotiana tabacum).	Arsenic	68-70	40S ribosomal protein S3a	Nicotiana tabacum	51-58
33149232-0	2020	Inhibition of red blood cell development by arsenic-induced disruption of GATA-1.	Arsenic	44-51	GATA binding protein 1	Homo sapiens	74-80
33149232-5	2020	Herein, we utilize a combination of in vitro and in vivo studies to provide evidence that arsenic, a widespread environmental toxicant, inhibits erythropoiesis likely through replacing zinc within the zinc fingers of the critical transcription factor GATA-1.	Arsenic	90-97	GATA binding protein 1	Homo sapiens	251-257
33149232-6	2020	We found that arsenic interacts with the N- and C-terminal zinc finger motifs of GATA-1, causing zinc loss and inhibition of DNA and protein binding activities, leading to dyserythropoiesis and an imbalance of hematopoietic differentiation.	Arsenic	14-21	GATA binding protein 1	Homo sapiens	81-87
33153165-7	2020	Taken together, the overexpression of NtCyc07 enhances As(III) tolerance by reducing As(III) accumulation through modulation of expressions of putative As(III) transporters in tobacco.	Arsenic	55-57	40S ribosomal protein S3a	Nicotiana tabacum	38-45
32452228-0	2020	The relationship between PNP, GSTO-1, AS3MT and ADRB3 gene polymorphisms and urinary arsenic concentration among copper smelter and refinery employers.	Arsenic	85-92	adrenoceptor beta 3	Homo sapiens	48-53
32739672-8	2020	In the human study, the serum lactate and TGF-beta levels were higher in arsenic-exposed subjects than that in reference subjects (t= 4.50, 6.24, both p < 0.05), while FVC and FEV1 were both lower (t= 5.47, 7.59, both p < 0.05).	Arsenic	73-80	transforming growth factor alpha	Homo sapiens	42-50
32739672-10	2020	In mediation analyses, lactate and TGF-beta significantly mediated 24.3% and 9.0%, respectively, of the association between arsenic and FVC (pmediation<0.05), while lactate and TGF-beta significantly mediated 22.2% and 12.5%, respectively, of the association between arsenic and FEV1 (pmediation<0.05).	Arsenic	124-131	transforming growth factor alpha	Homo sapiens	35-43
32871193-8	2020	The present study indicates that CSLE containing (E)-2-alkenals activates Nrf2, leading to a reduction in arsenic accumulation in vivo.	Arsenic	106-113	nuclear factor, erythroid derived 2, like 2	Mus musculus	74-78
32781346-9	2020	A dose-dependent increment in the gene expression of PDK1, PI3K, TSC2, AMPK, ULK1, ATG13, Beclin1, ATG12, ATG5, LC3, P62, ATG3, ATG7, and p62, as well as protein expression of Beclin1, and LC3- I, II, was evident in the ovaries of the As-treated animals.	Arsenic	235-237	pyruvate dehydrogenase kinase, isoenzyme 1	Mus musculus	53-57
32781346-10	2020	Moreover, a dose-dependent decrease in the expression of mTOR and Bcl-2 genes, and mTOR protein was detected with increasing doses of As, suggesting that As treatment-induced autophagy.	Arsenic	134-136	mechanistic target of rapamycin kinase	Mus musculus	57-61
32781346-10	2020	Moreover, a dose-dependent decrease in the expression of mTOR and Bcl-2 genes, and mTOR protein was detected with increasing doses of As, suggesting that As treatment-induced autophagy.	Arsenic	134-136	mechanistic target of rapamycin kinase	Mus musculus	83-87
32781346-10	2020	Moreover, a dose-dependent decrease in the expression of mTOR and Bcl-2 genes, and mTOR protein was detected with increasing doses of As, suggesting that As treatment-induced autophagy.	Arsenic	154-156	mechanistic target of rapamycin kinase	Mus musculus	57-61
32781346-10	2020	Moreover, a dose-dependent decrease in the expression of mTOR and Bcl-2 genes, and mTOR protein was detected with increasing doses of As, suggesting that As treatment-induced autophagy.	Arsenic	154-156	B cell leukemia/lymphoma 2	Mus musculus	66-71
32781346-10	2020	Moreover, a dose-dependent decrease in the expression of mTOR and Bcl-2 genes, and mTOR protein was detected with increasing doses of As, suggesting that As treatment-induced autophagy.	Arsenic	154-156	mechanistic target of rapamycin kinase	Mus musculus	83-87
32452228-6	2020	RESULTS: Individuals occupationally exposed to arsenic compounds, who have allele T in homozygous constellation in locus rs 1130650 of PNP gene, are predisposed to lower urinary arsenic concentration, while AA homozygosity in locus rs 4925 of GSTO-1 gene may result in statistically significant higher urinary arsenic concentration.	Arsenic	47-54	purine nucleoside phosphorylase	Homo sapiens	135-138
32452228-6	2020	RESULTS: Individuals occupationally exposed to arsenic compounds, who have allele T in homozygous constellation in locus rs 1130650 of PNP gene, are predisposed to lower urinary arsenic concentration, while AA homozygosity in locus rs 4925 of GSTO-1 gene may result in statistically significant higher urinary arsenic concentration.	Arsenic	47-54	glutathione S-transferase omega 1	Homo sapiens	243-249
32452228-6	2020	RESULTS: Individuals occupationally exposed to arsenic compounds, who have allele T in homozygous constellation in locus rs 1130650 of PNP gene, are predisposed to lower urinary arsenic concentration, while AA homozygosity in locus rs 4925 of GSTO-1 gene may result in statistically significant higher urinary arsenic concentration.	Arsenic	178-185	purine nucleoside phosphorylase	Homo sapiens	135-138
32452228-6	2020	RESULTS: Individuals occupationally exposed to arsenic compounds, who have allele T in homozygous constellation in locus rs 1130650 of PNP gene, are predisposed to lower urinary arsenic concentration, while AA homozygosity in locus rs 4925 of GSTO-1 gene may result in statistically significant higher urinary arsenic concentration.	Arsenic	178-185	purine nucleoside phosphorylase	Homo sapiens	135-138
32452228-7	2020	Polymorphisms of AS3MT and ADRB3 genes showed no statistically significant correlation with urinary arsenic, however, there was a tendency to higher arsenic concentration in allele A carriers in locus rs4994 of ADRB3 gene and in allele T carriers in rs 11191439 of AS3MT gene.	Arsenic	149-156	arsenite methyltransferase	Homo sapiens	17-22
32452228-7	2020	Polymorphisms of AS3MT and ADRB3 genes showed no statistically significant correlation with urinary arsenic, however, there was a tendency to higher arsenic concentration in allele A carriers in locus rs4994 of ADRB3 gene and in allele T carriers in rs 11191439 of AS3MT gene.	Arsenic	149-156	adrenoceptor beta 3	Homo sapiens	211-216
32452228-8	2020	CONCLUSION: This study indicates that arsenic absorption and metabolism depend on polymorphisms of genes encoding PNP and GSTO-1.	Arsenic	38-45	purine nucleoside phosphorylase	Homo sapiens	114-117
32452228-8	2020	CONCLUSION: This study indicates that arsenic absorption and metabolism depend on polymorphisms of genes encoding PNP and GSTO-1.	Arsenic	38-45	glutathione S-transferase omega 1	Homo sapiens	122-128
33135229-3	2020	Arsenic retention can be affected by changes in soil pH and the presence of competing anions, like phosphate.	Arsenic	0-7	phenylalanine hydroxylase	Homo sapiens	53-55
33312665-1	2020	The research focused on assessing the risk to human health resulting from the content of selected Cr, Co, Mn, Cu, Ni, Pb, As, Zn and Sr metals in tap water supplied by Upper Silesia Water Plant to the inhabitants of the Upper Silesia region (Poland).	Arsenic	122-124	nuclear RNA export factor 1	Homo sapiens	146-149
32949585-6	2020	Here, we attempted to elucidate the role of arsenic in redox imbalance on increased oxidative stress (elevated level of ROS, MDA and NO) and decreased antioxidant levels such as reduced GSH, catalase, and SOD.	Arsenic	44-51	catalase	Homo sapiens	191-199
32949585-6	2020	Here, we attempted to elucidate the role of arsenic in redox imbalance on increased oxidative stress (elevated level of ROS, MDA and NO) and decreased antioxidant levels such as reduced GSH, catalase, and SOD.	Arsenic	44-51	superoxide dismutase 1	Homo sapiens	205-208
32949585-8	2020	Along with that, arsenic activates caspases and Bax, decreases Bcl2 through mitochondrial dysfunction, and induces apoptosis regulatory mechanism.	Arsenic	17-24	BCL2 associated X, apoptosis regulator	Homo sapiens	48-51
32949585-8	2020	Along with that, arsenic activates caspases and Bax, decreases Bcl2 through mitochondrial dysfunction, and induces apoptosis regulatory mechanism.	Arsenic	17-24	BCL2 apoptosis regulator	Homo sapiens	63-67
33312665-10	2020	The concentration of As, Cr, Cu, Mn and Ni in analyzed tap water is in accordance with Polish and international requirements.	Arsenic	21-23	nuclear RNA export factor 1	Homo sapiens	55-58
33150055-13	2020	The diffused distribution of pEGFP-C3-MAP1LC3B green fluorescence were become the punctuate pattern fluorescence after treatment with RQDs in cells transfected with pEGFP-C3-MAP1LC3B plasmid RQDs increased the expression of autophagyregulatory proteins LC3 I/II, Beclin-1, p62 and Atg12 in a concentration-dependent manner, similar to autophagy induced by serum starvation, except for p62, as induction of p62 is a characteristic of arsenic compounds.	Arsenic	433-440	microtubule associated protein 1 light chain 3 beta	Homo sapiens	38-46
33124703-6	2021	Sox2 and Oct4 mRNA expression were increased by 1.9- to 2.5-fold in the arsenic-exposed cells, beginning at Week 12.	Arsenic	72-79	SRY (sex determining region Y)-box 2	Mus musculus	0-4
33124703-6	2021	Sox2 and Oct4 mRNA expression were increased by 1.9- to 2.5-fold in the arsenic-exposed cells, beginning at Week 12.	Arsenic	72-79	POU domain, class 5, transcription factor 1	Mus musculus	9-13
33124703-9	2021	Exposure to arsenic significantly increased N-cadherin protein levels beginning at Week 20, concurrent with increased grouping of N-cadherin positive cells at the perimeter of the embryoid body.	Arsenic	12-19	cadherin 2	Mus musculus	44-54
33124703-9	2021	Exposure to arsenic significantly increased N-cadherin protein levels beginning at Week 20, concurrent with increased grouping of N-cadherin positive cells at the perimeter of the embryoid body.	Arsenic	12-19	cadherin 2	Mus musculus	130-140
33116153-6	2020	Arsenic mass flux exceeded 8 kg/day near the confluence of the Trujaca River with the Nysa Klodzka, a main tributary of the Oder River.	Arsenic	0-7	NYS2	Homo sapiens	86-90
33150055-13	2020	The diffused distribution of pEGFP-C3-MAP1LC3B green fluorescence were become the punctuate pattern fluorescence after treatment with RQDs in cells transfected with pEGFP-C3-MAP1LC3B plasmid RQDs increased the expression of autophagyregulatory proteins LC3 I/II, Beclin-1, p62 and Atg12 in a concentration-dependent manner, similar to autophagy induced by serum starvation, except for p62, as induction of p62 is a characteristic of arsenic compounds.	Arsenic	433-440	microtubule associated protein 1 light chain 3 beta	Homo sapiens	174-182
33150055-13	2020	The diffused distribution of pEGFP-C3-MAP1LC3B green fluorescence were become the punctuate pattern fluorescence after treatment with RQDs in cells transfected with pEGFP-C3-MAP1LC3B plasmid RQDs increased the expression of autophagyregulatory proteins LC3 I/II, Beclin-1, p62 and Atg12 in a concentration-dependent manner, similar to autophagy induced by serum starvation, except for p62, as induction of p62 is a characteristic of arsenic compounds.	Arsenic	433-440	beclin 1	Homo sapiens	263-271
33150055-13	2020	The diffused distribution of pEGFP-C3-MAP1LC3B green fluorescence were become the punctuate pattern fluorescence after treatment with RQDs in cells transfected with pEGFP-C3-MAP1LC3B plasmid RQDs increased the expression of autophagyregulatory proteins LC3 I/II, Beclin-1, p62 and Atg12 in a concentration-dependent manner, similar to autophagy induced by serum starvation, except for p62, as induction of p62 is a characteristic of arsenic compounds.	Arsenic	433-440	nucleoporin 62	Homo sapiens	273-276
33150055-13	2020	The diffused distribution of pEGFP-C3-MAP1LC3B green fluorescence were become the punctuate pattern fluorescence after treatment with RQDs in cells transfected with pEGFP-C3-MAP1LC3B plasmid RQDs increased the expression of autophagyregulatory proteins LC3 I/II, Beclin-1, p62 and Atg12 in a concentration-dependent manner, similar to autophagy induced by serum starvation, except for p62, as induction of p62 is a characteristic of arsenic compounds.	Arsenic	433-440	autophagy related 12	Homo sapiens	281-286
33150055-13	2020	The diffused distribution of pEGFP-C3-MAP1LC3B green fluorescence were become the punctuate pattern fluorescence after treatment with RQDs in cells transfected with pEGFP-C3-MAP1LC3B plasmid RQDs increased the expression of autophagyregulatory proteins LC3 I/II, Beclin-1, p62 and Atg12 in a concentration-dependent manner, similar to autophagy induced by serum starvation, except for p62, as induction of p62 is a characteristic of arsenic compounds.	Arsenic	433-440	nucleoporin 62	Homo sapiens	385-388
33150055-13	2020	The diffused distribution of pEGFP-C3-MAP1LC3B green fluorescence were become the punctuate pattern fluorescence after treatment with RQDs in cells transfected with pEGFP-C3-MAP1LC3B plasmid RQDs increased the expression of autophagyregulatory proteins LC3 I/II, Beclin-1, p62 and Atg12 in a concentration-dependent manner, similar to autophagy induced by serum starvation, except for p62, as induction of p62 is a characteristic of arsenic compounds.	Arsenic	433-440	nucleoporin 62	Homo sapiens	385-388
32506763-10	2020	Taken together, the results indicate that ROS-mediated PERK-eIF2alpha-ATF4 pathway activated by NaAsO2 is the critical upstream event for subsequent apoptosis induction via regulating CHOP-DR5 signaling in L-02 cells when chronic exposure to arsenic, and support that antioxidants might be potential therapeutic agents for preventing or delaying the onset and progress of arsenic-induced hepatotoxicity.	Arsenic	242-249	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	55-59
33075241-5	2020	IC50 values narcissoside, as 11.54 nM for AChE and 65.58 nM for alpha-glucosidase were calculated with % Activity-[Inhibitory] graphs.	Arsenic	26-28	acetylcholinesterase (Cartwright blood group)	Homo sapiens	42-46
33178028-0	2020	Ursodeoxycholic Acid Protects Against Arsenic Induced Hepatotoxicity by the Nrf2 Signaling Pathway.	Arsenic	38-45	NFE2 like bZIP transcription factor 2	Homo sapiens	76-80
33178028-9	2020	Moreover, UDCA promoted the expression of nuclear Nrf2, HO-1, and NQO1, although arsenic regulated nuclear translocation of Nrf2 positively.	Arsenic	81-88	NFE2 like bZIP transcription factor 2	Homo sapiens	124-128
32678762-5	2020	The test results showed that excessive intake of As or/and Cu led to a significant reduction in the total antioxidant capacity (T-AOC), catalase (CAT) and hydroxyl radicals.	Arsenic	49-51	catalase	Gallus gallus	136-144
32678762-5	2020	The test results showed that excessive intake of As or/and Cu led to a significant reduction in the total antioxidant capacity (T-AOC), catalase (CAT) and hydroxyl radicals.	Arsenic	49-51	catalase	Gallus gallus	146-149
32736004-4	2020	Arsenite decreased the expression of Aqp3, Mrp1, Mrp4, and Mdr1b (i.e., transporters and channels used by arsenic), but not that of Aqp7, Glut1, Mrp2, and Mdr1a.	Arsenic	106-113	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	59-64
32534297-9	2020	Anti-inflammatory IL-1RA concentration was negatively related with Pb, Cd, Hg and As, while pro-inflammatory IL-1beta and IL-6 were positively correlated with Pb.	Arsenic	82-84	interleukin 1 receptor antagonist	Homo sapiens	18-24
32506763-10	2020	Taken together, the results indicate that ROS-mediated PERK-eIF2alpha-ATF4 pathway activated by NaAsO2 is the critical upstream event for subsequent apoptosis induction via regulating CHOP-DR5 signaling in L-02 cells when chronic exposure to arsenic, and support that antioxidants might be potential therapeutic agents for preventing or delaying the onset and progress of arsenic-induced hepatotoxicity.	Arsenic	242-249	activating transcription factor 4	Homo sapiens	70-74
32506763-10	2020	Taken together, the results indicate that ROS-mediated PERK-eIF2alpha-ATF4 pathway activated by NaAsO2 is the critical upstream event for subsequent apoptosis induction via regulating CHOP-DR5 signaling in L-02 cells when chronic exposure to arsenic, and support that antioxidants might be potential therapeutic agents for preventing or delaying the onset and progress of arsenic-induced hepatotoxicity.	Arsenic	372-379	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	55-59
32506763-10	2020	Taken together, the results indicate that ROS-mediated PERK-eIF2alpha-ATF4 pathway activated by NaAsO2 is the critical upstream event for subsequent apoptosis induction via regulating CHOP-DR5 signaling in L-02 cells when chronic exposure to arsenic, and support that antioxidants might be potential therapeutic agents for preventing or delaying the onset and progress of arsenic-induced hepatotoxicity.	Arsenic	372-379	eukaryotic translation initiation factor 2A	Homo sapiens	60-69
32645460-0	2020	Autophagy mediates bronchial cell malignant transformation induced by chronic arsenic exposure via MEK/ERK1/2 pathway.	Arsenic	78-85	mitogen-activated protein kinase kinase 7	Homo sapiens	99-102
32645460-0	2020	Autophagy mediates bronchial cell malignant transformation induced by chronic arsenic exposure via MEK/ERK1/2 pathway.	Arsenic	78-85	mitogen-activated protein kinase 3	Homo sapiens	103-109
32683294-2	2020	In this study, we identified changes in occludin in arsenic-induced lung injury in vivo and in vitro.	Arsenic	52-59	occludin	Homo sapiens	40-48
32619914-0	2020	Arsenic exposure-related hyperglycemia is linked to insulin resistance with concomitant reduction of skeletal muscle mass.	Arsenic	0-7	insulin	Homo sapiens	52-59
32619914-2	2020	OBJECTIVE: We explored the association between arsenic exposure and the reduction of skeletal muscle mass as a potential mechanism of insulin resistance for developing arsenic-related hyperglycemia.	Arsenic	47-54	insulin	Homo sapiens	134-141
32619914-2	2020	OBJECTIVE: We explored the association between arsenic exposure and the reduction of skeletal muscle mass as a potential mechanism of insulin resistance for developing arsenic-related hyperglycemia.	Arsenic	168-175	insulin	Homo sapiens	134-141
32619914-7	2020	RESULTS: Water, hair and nail arsenic concentrations showed significant positive associations with FBG, serum insulin and HOMA-IR and inverse associations with serum creatinine and LBM in a dose-dependent manner both in males and females.	Arsenic	30-37	insulin	Homo sapiens	110-117
32506763-10	2020	Taken together, the results indicate that ROS-mediated PERK-eIF2alpha-ATF4 pathway activated by NaAsO2 is the critical upstream event for subsequent apoptosis induction via regulating CHOP-DR5 signaling in L-02 cells when chronic exposure to arsenic, and support that antioxidants might be potential therapeutic agents for preventing or delaying the onset and progress of arsenic-induced hepatotoxicity.	Arsenic	242-249	eukaryotic translation initiation factor 2A	Homo sapiens	60-69
32619914-13	2020	CONCLUSION: Arsenic exposure elevates FBG levels and the risk of hyperglycemia through increasing insulin resistance with greater susceptibility in females than males.	Arsenic	12-19	insulin	Homo sapiens	98-105
32598327-10	2020	As many as 49 of 52 people living around Kao Bay have a risk from mercury and arsenic exposure via fish consumption.	Arsenic	78-85	amine oxidase copper containing 1	Homo sapiens	41-44
32619914-14	2020	Additionally, arsenic exposure-related reduction of skeletal muscle mass may be a mechanism underlying the development of insulin resistance and hyperglycemia.	Arsenic	14-21	insulin	Homo sapiens	122-129
32647881-0	2020	Arsenic Directs Stem Cell Fate by Imparting Notch Signaling into the Extracellular Matrix Niche.	Arsenic	0-7	notch 1	Mus musculus	44-49
32647881-7	2020	SS-31 treatment also reversed arsenic-induced Notch1 expression, resulting in an improved muscle regeneration after injury.	Arsenic	30-37	notch 1	Mus musculus	46-52
32647881-8	2020	We found that persistent arsenic-induced CTF Notch1 expression caused the elaboration of dysfunctional ECM with increased expression of the Notch ligand DLL4.	Arsenic	25-32	notch 1	Mus musculus	45-51
32647881-8	2020	We found that persistent arsenic-induced CTF Notch1 expression caused the elaboration of dysfunctional ECM with increased expression of the Notch ligand DLL4.	Arsenic	25-32	notch 1	Mus musculus	45-50
32647881-8	2020	We found that persistent arsenic-induced CTF Notch1 expression caused the elaboration of dysfunctional ECM with increased expression of the Notch ligand DLL4.	Arsenic	25-32	delta like canonical Notch ligand 4	Mus musculus	153-157
33148380-1	2020	Objective To investigate the effects of inorganic arsenic exposure on the differentiation of renal CD4+T lymphocytes and the possible mechanism.	Arsenic	50-57	CD4 antigen	Mus musculus	99-102
33148380-8	2020	Serum CAT activity and T-AOC level in the arsenic-treated mice dropped greatly.	Arsenic	42-49	catalase	Mus musculus	6-9
32506763-10	2020	Taken together, the results indicate that ROS-mediated PERK-eIF2alpha-ATF4 pathway activated by NaAsO2 is the critical upstream event for subsequent apoptosis induction via regulating CHOP-DR5 signaling in L-02 cells when chronic exposure to arsenic, and support that antioxidants might be potential therapeutic agents for preventing or delaying the onset and progress of arsenic-induced hepatotoxicity.	Arsenic	372-379	activating transcription factor 4	Homo sapiens	70-74
33071297-12	2020	Arsenic release during arsenopyrite oxidation resulted in both downward translocation and As(V) attenuation by stable Fe(III)(oxyhydr)oxide and Fe(III) (hydroxy)sulfate minerals over time, highlighting the need for sampling at multiple depths and time points for accurate interpretation of arsenic speciation, lability, and translocation in weathering profiles.	Arsenic	0-7	general transcription factor IIE subunit 1	Homo sapiens	118-125
33071297-12	2020	Arsenic release during arsenopyrite oxidation resulted in both downward translocation and As(V) attenuation by stable Fe(III)(oxyhydr)oxide and Fe(III) (hydroxy)sulfate minerals over time, highlighting the need for sampling at multiple depths and time points for accurate interpretation of arsenic speciation, lability, and translocation in weathering profiles.	Arsenic	0-7	general transcription factor IIE subunit 1	Homo sapiens	144-151
32812591-5	2020	The review is devoted to recent advances of using isolable silylenes and corresponding silylene-metal complexes for the activation of fundamental but inert molecules such as H2, COx, N2O, O2, H2O, NH3, C2H4 and E4 (E = P, As).	Arsenic	222-224	cytochrome c oxidase subunit 8A	Homo sapiens	178-181
32971865-9	2020	An altered ability to methylate arsenic is dependent on specific single nucleotide polymorphisms (SNPs) in AS3MT.	Arsenic	32-39	arsenite methyltransferase	Homo sapiens	107-112
32971865-14	2020	NRF2 may be partly responsible for the biotransformation of iAs and the generation of methylated arsenic species via AS3MT.	Arsenic	97-104	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
32971865-14	2020	NRF2 may be partly responsible for the biotransformation of iAs and the generation of methylated arsenic species via AS3MT.	Arsenic	97-104	arsenite methyltransferase	Homo sapiens	117-122
32661532-4	2020	MTF-1 biomarker genes were identified that exhibited consistent, robust expression across 10 microarray comparisons examining the effects of metals (zinc, nickel, lead, arsenic, mercury, and silver) on gene expression in human cells.	Arsenic	169-176	metal regulatory transcription factor 1	Homo sapiens	0-5
32460071-7	2020	Furthermore, arsenic decreased the mRNA expressions of 11 out of 13 genes associated with acrosome biosynthesis and 11 out of 12 genes related to flagellum formation in testes, particularly, down-regulated DPY19L2, AKAP3, AKAP4, CFAP44 and SPAG16 were further confirmed at the protein levels by western blotting.	Arsenic	13-20	dpy-19-like 2 (C. elegans)	Mus musculus	206-213
32939585-1	2020	An electrochemical sensor has been developed based on ion imprinted polymer (IIP) and nanoporous gold (NPG) modified gold electrode (IIP/NPG/GE) for determination of arsenic ion (As3+) in different kinds of water.	Arsenic	166-173	PDS5 cohesin associated factor B	Homo sapiens	179-182
32531573-0	2020	Assessment of arsenic-induced modifications in the DNA methylation of insulin-related genes in rat pancreatic islets.	Arsenic	14-21	pancreatic and duodenal homeobox 1	Rattus norvegicus	99-109
32738329-8	2020	Additionally, BNP was positively associated with arsenic methylated metabolites (U-MAs and U-DMAs).	Arsenic	49-56	natriuretic peptide B	Homo sapiens	14-17
32738329-12	2020	CONCLUSIONS: In this study, we showed associations between plasma BNP and arsenic exposure.	Arsenic	74-81	natriuretic peptide B	Homo sapiens	66-69
32460071-7	2020	Furthermore, arsenic decreased the mRNA expressions of 11 out of 13 genes associated with acrosome biosynthesis and 11 out of 12 genes related to flagellum formation in testes, particularly, down-regulated DPY19L2, AKAP3, AKAP4, CFAP44 and SPAG16 were further confirmed at the protein levels by western blotting.	Arsenic	13-20	A kinase (PRKA) anchor protein 3	Mus musculus	215-220
32460071-7	2020	Furthermore, arsenic decreased the mRNA expressions of 11 out of 13 genes associated with acrosome biosynthesis and 11 out of 12 genes related to flagellum formation in testes, particularly, down-regulated DPY19L2, AKAP3, AKAP4, CFAP44 and SPAG16 were further confirmed at the protein levels by western blotting.	Arsenic	13-20	A kinase (PRKA) anchor protein 4	Mus musculus	222-227
32460071-7	2020	Furthermore, arsenic decreased the mRNA expressions of 11 out of 13 genes associated with acrosome biosynthesis and 11 out of 12 genes related to flagellum formation in testes, particularly, down-regulated DPY19L2, AKAP3, AKAP4, CFAP44 and SPAG16 were further confirmed at the protein levels by western blotting.	Arsenic	13-20	cilia and flagella associated protein 44	Mus musculus	229-235
32460071-7	2020	Furthermore, arsenic decreased the mRNA expressions of 11 out of 13 genes associated with acrosome biosynthesis and 11 out of 12 genes related to flagellum formation in testes, particularly, down-regulated DPY19L2, AKAP3, AKAP4, CFAP44 and SPAG16 were further confirmed at the protein levels by western blotting.	Arsenic	13-20	sperm associated antigen 16	Mus musculus	240-246
32804029-3	2022	In the CSRT, Nat-Peat achieved higher removal of Ni (<80%) and As (~61%) than M-Peat (72% and 26% for Ni and As, respectively).	Arsenic	63-65	bromodomain containing 2	Homo sapiens	13-16
32484980-1	2020	Treatment of [Ph3EMe][I] with [Na{N(SiMe3)2}] affords the ylides [Ph3E=CH2] (E = As, 1As; P, 1P).	Arsenic	81-83	H3 histone pseudogene 26	Homo sapiens	14-18
32804029-3	2022	In the CSRT, Nat-Peat achieved higher removal of Ni (<80%) and As (~61%) than M-Peat (72% and 26% for Ni and As, respectively).	Arsenic	109-111	bromodomain containing 2	Homo sapiens	13-16
32804029-4	2022	In the HFF, Nat-Peat achieved slightly lower maximum removal of Ni (<96%) than M-Peat (<98%) and higher removal of As and Sb (<87% and 8%) than M-Peat (<35% and 7%).	Arsenic	115-117	bromodomain containing 2	Homo sapiens	12-15
32417510-5	2020	Detailed analysis of oral bioaccessible fraction (BAF i.e. ratio of bioaccessible concentrations to total concentrations on <250 mum fraction) indicated BAF of As (5-33%), Cd (72-98%), Co (24-42%), Cr (3-11%), Cu (25-90%), Ni (17-60%), Pb (16-88%) and Zn (73-94%).	Arsenic	160-162	BAF nuclear assembly factor 1	Homo sapiens	50-53
31768761-7	2020	The mRNA expression levels of PERK, GRP78, EIF2alpha, ATF4, and CHOP as well as the protein levels of CHOP was significantly increased in the As + F group compared with the control group.	Arsenic	142-144	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	36-41
31768761-7	2020	The mRNA expression levels of PERK, GRP78, EIF2alpha, ATF4, and CHOP as well as the protein levels of CHOP was significantly increased in the As + F group compared with the control group.	Arsenic	142-144	eukaryotic translation initiation factor 2A	Rattus norvegicus	43-52
31768761-7	2020	The mRNA expression levels of PERK, GRP78, EIF2alpha, ATF4, and CHOP as well as the protein levels of CHOP was significantly increased in the As + F group compared with the control group.	Arsenic	142-144	activating transcription factor 4	Rattus norvegicus	54-58
31768761-7	2020	The mRNA expression levels of PERK, GRP78, EIF2alpha, ATF4, and CHOP as well as the protein levels of CHOP was significantly increased in the As + F group compared with the control group.	Arsenic	142-144	DNA-damage inducible transcript 3	Rattus norvegicus	64-68
31768761-7	2020	The mRNA expression levels of PERK, GRP78, EIF2alpha, ATF4, and CHOP as well as the protein levels of CHOP was significantly increased in the As + F group compared with the control group.	Arsenic	142-144	DNA-damage inducible transcript 3	Rattus norvegicus	102-106
32417510-5	2020	Detailed analysis of oral bioaccessible fraction (BAF i.e. ratio of bioaccessible concentrations to total concentrations on <250 mum fraction) indicated BAF of As (5-33%), Cd (72-98%), Co (24-42%), Cr (3-11%), Cu (25-90%), Ni (17-60%), Pb (16-88%) and Zn (73-94%).	Arsenic	160-162	BAF nuclear assembly factor 1	Homo sapiens	153-156
32417511-2	2020	The transformation follows the route of "dissolution-recrystallization", during which the arsenic pollutant in gypsum is released into the solution, and hence raises the possibility of being distributed into the product of alpha-HH, a potential harm that has always been neglected.	Arsenic	90-97	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	223-231
32563749-5	2020	The adsorption ability of Fe-C-CO2 for both As(V) and Ni(II) was further enhanced in binary adsorption mode (As(V): 13.4 mg g-1, Ni(II):17.6 mg g-1) through additional removal of those ions by Ni(II)-As(V) complexation.	Arsenic	44-46	complement C2	Homo sapiens	31-34
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	43-50	caspase 9	Rattus norvegicus	227-236
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	43-50	caspase 3	Rattus norvegicus	249-258
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	75-82	mechanistic target of rapamycin kinase	Rattus norvegicus	157-161
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	75-82	annexin A3	Rattus norvegicus	198-201
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	75-82	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	203-206
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	75-82	BCL2 associated X, apoptosis regulator	Rattus norvegicus	208-211
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	75-82	caspase 9	Rattus norvegicus	227-236
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	75-82	caspase 3	Rattus norvegicus	249-258
32593899-0	2020	Ferroptosis mediated by the interaction between Mfn2 and IREalpha promotes arsenic-induced nonalcoholic steatohepatitis.	Arsenic	75-82	mitofusin 2	Homo sapiens	48-52
32593899-5	2020	Simultaneously, the expression of ACSL4 (acyl-CoA synthetase long-chain family member 4) was upregulated in rat"s liver and L-02 cells exposed to arsenic.	Arsenic	146-153	acyl-CoA synthetase long-chain family member 4	Rattus norvegicus	34-39
32593899-5	2020	Simultaneously, the expression of ACSL4 (acyl-CoA synthetase long-chain family member 4) was upregulated in rat"s liver and L-02 cells exposed to arsenic.	Arsenic	146-153	acyl-CoA synthetase long-chain family member 4	Rattus norvegicus	41-87
32464442-7	2020	Moreover, arsenic (10 muM) treatment significantly down-regulated the inhibition factors of autophagy/apoptosis; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap protein expressions, up-regulated the enhanced factors of autophagy/apoptosis; ULK, LC3, p53, Bax, cytochrome c, caspase 9, cleaved caspase 3 proteins and eventually caused autophagic and apoptotic cell death.	Arsenic	10-17	mechanistic target of rapamycin kinase	Rattus norvegicus	113-117
32464442-7	2020	Moreover, arsenic (10 muM) treatment significantly down-regulated the inhibition factors of autophagy/apoptosis; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap protein expressions, up-regulated the enhanced factors of autophagy/apoptosis; ULK, LC3, p53, Bax, cytochrome c, caspase 9, cleaved caspase 3 proteins and eventually caused autophagic and apoptotic cell death.	Arsenic	10-17	AKT serine/threonine kinase 1	Rattus norvegicus	119-122
32464442-7	2020	Moreover, arsenic (10 muM) treatment significantly down-regulated the inhibition factors of autophagy/apoptosis; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap protein expressions, up-regulated the enhanced factors of autophagy/apoptosis; ULK, LC3, p53, Bax, cytochrome c, caspase 9, cleaved caspase 3 proteins and eventually caused autophagic and apoptotic cell death.	Arsenic	10-17	NFE2 like bZIP transcription factor 2	Rattus norvegicus	124-128
32464442-7	2020	Moreover, arsenic (10 muM) treatment significantly down-regulated the inhibition factors of autophagy/apoptosis; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap protein expressions, up-regulated the enhanced factors of autophagy/apoptosis; ULK, LC3, p53, Bax, cytochrome c, caspase 9, cleaved caspase 3 proteins and eventually caused autophagic and apoptotic cell death.	Arsenic	10-17	mitogen activated protein kinase 3	Rattus norvegicus	130-134
32464442-7	2020	Moreover, arsenic (10 muM) treatment significantly down-regulated the inhibition factors of autophagy/apoptosis; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap protein expressions, up-regulated the enhanced factors of autophagy/apoptosis; ULK, LC3, p53, Bax, cytochrome c, caspase 9, cleaved caspase 3 proteins and eventually caused autophagic and apoptotic cell death.	Arsenic	10-17	Bcl2-like 1	Rattus norvegicus	136-141
32464442-7	2020	Moreover, arsenic (10 muM) treatment significantly down-regulated the inhibition factors of autophagy/apoptosis; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap protein expressions, up-regulated the enhanced factors of autophagy/apoptosis; ULK, LC3, p53, Bax, cytochrome c, caspase 9, cleaved caspase 3 proteins and eventually caused autophagic and apoptotic cell death.	Arsenic	10-17	X-linked inhibitor of apoptosis	Rattus norvegicus	143-147
32464442-7	2020	Moreover, arsenic (10 muM) treatment significantly down-regulated the inhibition factors of autophagy/apoptosis; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap protein expressions, up-regulated the enhanced factors of autophagy/apoptosis; ULK, LC3, p53, Bax, cytochrome c, caspase 9, cleaved caspase 3 proteins and eventually caused autophagic and apoptotic cell death.	Arsenic	10-17	annexin A3	Rattus norvegicus	232-235
32464442-7	2020	Moreover, arsenic (10 muM) treatment significantly down-regulated the inhibition factors of autophagy/apoptosis; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap protein expressions, up-regulated the enhanced factors of autophagy/apoptosis; ULK, LC3, p53, Bax, cytochrome c, caspase 9, cleaved caspase 3 proteins and eventually caused autophagic and apoptotic cell death.	Arsenic	10-17	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	237-240
32464442-7	2020	Moreover, arsenic (10 muM) treatment significantly down-regulated the inhibition factors of autophagy/apoptosis; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap protein expressions, up-regulated the enhanced factors of autophagy/apoptosis; ULK, LC3, p53, Bax, cytochrome c, caspase 9, cleaved caspase 3 proteins and eventually caused autophagic and apoptotic cell death.	Arsenic	10-17	BCL2 associated X, apoptosis regulator	Rattus norvegicus	242-245
32464442-7	2020	Moreover, arsenic (10 muM) treatment significantly down-regulated the inhibition factors of autophagy/apoptosis; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap protein expressions, up-regulated the enhanced factors of autophagy/apoptosis; ULK, LC3, p53, Bax, cytochrome c, caspase 9, cleaved caspase 3 proteins and eventually caused autophagic and apoptotic cell death.	Arsenic	10-17	caspase 9	Rattus norvegicus	261-270
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	43-50	mechanistic target of rapamycin kinase	Rattus norvegicus	157-161
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	43-50	AKT serine/threonine kinase 1	Rattus norvegicus	163-166
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	43-50	NFE2 like bZIP transcription factor 2	Rattus norvegicus	168-172
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	43-50	mitogen activated protein kinase 3	Rattus norvegicus	174-178
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	43-50	Bcl2-like 1	Rattus norvegicus	180-185
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	43-50	X-linked inhibitor of apoptosis	Rattus norvegicus	187-191
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	43-50	annexin A3	Rattus norvegicus	198-201
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	43-50	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	203-206
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	43-50	BCL2 associated X, apoptosis regulator	Rattus norvegicus	208-211
32593899-6	2020	While, suppression of ACSL4 with rosiglitazone or ACSL4 siRNA remarkably alleviated arsenic-induced NASH and ferroptosis through diminishing 5-hydroxyeicosatetraenoic acid (5-HETE) content.	Arsenic	84-91	acyl-CoA synthetase long chain family member 4	Homo sapiens	22-27
32593899-6	2020	While, suppression of ACSL4 with rosiglitazone or ACSL4 siRNA remarkably alleviated arsenic-induced NASH and ferroptosis through diminishing 5-hydroxyeicosatetraenoic acid (5-HETE) content.	Arsenic	84-91	acyl-CoA synthetase long chain family member 4	Homo sapiens	50-55
32563749-5	2020	The adsorption ability of Fe-C-CO2 for both As(V) and Ni(II) was further enhanced in binary adsorption mode (As(V): 13.4 mg g-1, Ni(II):17.6 mg g-1) through additional removal of those ions by Ni(II)-As(V) complexation.	Arsenic	109-111	complement C2	Homo sapiens	31-34
32563749-5	2020	The adsorption ability of Fe-C-CO2 for both As(V) and Ni(II) was further enhanced in binary adsorption mode (As(V): 13.4 mg g-1, Ni(II):17.6 mg g-1) through additional removal of those ions by Ni(II)-As(V) complexation.	Arsenic	109-111	complement C2	Homo sapiens	31-34
32853281-12	2020	The activity of sAA decreased after EW and after AS (P<0.05) but not after NI condition.	Arsenic	49-51	serum amyloid A1 cluster	Homo sapiens	16-19
32031413-5	2020	To investigate the role of acetylated histone H3K18 (H3K18 ac) in arsenic-induced DNA damage, HaCaT cells were exposed to sodium arsenite (NaAsO2) for 24 h. It was found that arsenic induced the downregulation of xeroderma pigmentosum A, D, and F (XPA, XPD, and XPF-nucleotide excision repair (NER)-related genes) expression, as well as histone H3K18 ac expression, and aggravated DNA damage.	Arsenic	66-73	XPA, DNA damage recognition and repair factor	Homo sapiens	248-251
32031413-5	2020	To investigate the role of acetylated histone H3K18 (H3K18 ac) in arsenic-induced DNA damage, HaCaT cells were exposed to sodium arsenite (NaAsO2) for 24 h. It was found that arsenic induced the downregulation of xeroderma pigmentosum A, D, and F (XPA, XPD, and XPF-nucleotide excision repair (NER)-related genes) expression, as well as histone H3K18 ac expression, and aggravated DNA damage.	Arsenic	66-73	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	253-256
32031413-5	2020	To investigate the role of acetylated histone H3K18 (H3K18 ac) in arsenic-induced DNA damage, HaCaT cells were exposed to sodium arsenite (NaAsO2) for 24 h. It was found that arsenic induced the downregulation of xeroderma pigmentosum A, D, and F (XPA, XPD, and XPF-nucleotide excision repair (NER)-related genes) expression, as well as histone H3K18 ac expression, and aggravated DNA damage.	Arsenic	66-73	ERCC excision repair 4, endonuclease catalytic subunit	Homo sapiens	262-265
32599262-0	2020	Chronic and acute arsenic exposure enhance EGFR expression via distinct molecular mechanisms.	Arsenic	18-25	epidermal growth factor receptor	Homo sapiens	43-47
32599262-4	2020	Both acute versus chronic arsenic exposure increase EGFR expression, but do so via distinct molecular mechanisms.	Arsenic	26-33	epidermal growth factor receptor	Homo sapiens	52-56
32599262-6	2020	Cells treated with acute arsenic exhibited a decrease in viability, changes in morphology, and increased mRNA level of BTC.	Arsenic	25-32	betacellulin	Homo sapiens	119-122
32599262-7	2020	In contrast, during 24 weeks of arsenic exposure, the cells had increased EGFR expression and activity, and increased mRNA and protein levels of TGFalpha.	Arsenic	32-39	epidermal growth factor receptor	Homo sapiens	74-78
32599262-7	2020	In contrast, during 24 weeks of arsenic exposure, the cells had increased EGFR expression and activity, and increased mRNA and protein levels of TGFalpha.	Arsenic	32-39	transforming growth factor alpha	Homo sapiens	145-153
32599262-10	2020	We propose that lung epithelial cells chronically exposed to low level arsenic increases EGFR signaling via TGFalpha production to enhance ligand-independent cell migration.	Arsenic	71-78	epidermal growth factor receptor	Homo sapiens	89-93
32599262-10	2020	We propose that lung epithelial cells chronically exposed to low level arsenic increases EGFR signaling via TGFalpha production to enhance ligand-independent cell migration.	Arsenic	71-78	transforming growth factor alpha	Homo sapiens	108-116
32599264-7	2020	In contrast, exposure of prepubertal testis to high arsenic concentrations (10, 50 or 100 muM) induced drastic changes: severe destruction of testicular morphology, with loss of seminiferous tubule integrity; a dose-dependent decrease in germ cell density, and a hundred-fold increase in CC3 expression after 50 muM arsenic exposure.	Arsenic	52-59	caspase 3	Mus musculus	288-291
32920490-2	2020	We previously demonstrated that exposure to arsenic, an environmental carcinogen, induces polyadenylation of canonical histone H3.1 mRNA, causing transformation of human cells in vitro.	Arsenic	44-51	H3 clustered histone 1	Homo sapiens	119-131
32920490-6	2020	These data suggest that H3.3 displacement might be central to carcinogenesis caused by polyadenylation of H3.1 mRNA upon arsenic exposure.	Arsenic	121-128	H3 clustered histone 3	Homo sapiens	106-110
32682831-0	2020	Chronic arsenic exposure enhances metastatic potential via NRF2-mediated upregulation of SOX9.	Arsenic	8-15	NFE2 like bZIP transcription factor 2	Homo sapiens	59-63
32682831-0	2020	Chronic arsenic exposure enhances metastatic potential via NRF2-mediated upregulation of SOX9.	Arsenic	8-15	SRY-box transcription factor 9	Homo sapiens	89-93
32682831-4	2020	Here, we demonstrate that chronic arsenic exposure enhances the invasive and migratory capacity of immortalized lung epithelial cells via NRF2-dependent upregulation of SRY-box 9 (SOX9), another transcription factor linked with cell proliferation, epithelial-mesenchymal transition, and metastasis.	Arsenic	34-41	NFE2 like bZIP transcription factor 2	Homo sapiens	138-142
32682831-4	2020	Here, we demonstrate that chronic arsenic exposure enhances the invasive and migratory capacity of immortalized lung epithelial cells via NRF2-dependent upregulation of SRY-box 9 (SOX9), another transcription factor linked with cell proliferation, epithelial-mesenchymal transition, and metastasis.	Arsenic	34-41	SRY-box transcription factor 9	Homo sapiens	169-178
32682831-4	2020	Here, we demonstrate that chronic arsenic exposure enhances the invasive and migratory capacity of immortalized lung epithelial cells via NRF2-dependent upregulation of SRY-box 9 (SOX9), another transcription factor linked with cell proliferation, epithelial-mesenchymal transition, and metastasis.	Arsenic	34-41	SRY-box transcription factor 9	Homo sapiens	180-184
32929351-9	2020	Although arsenic/ATRA therapy degraded PML-RARalpha and restored PPARgamma expression, it exacerbated dyslipidemia in APL patients.	Arsenic	9-16	peroxisome proliferator activated receptor gamma	Homo sapiens	65-74
32519707-0	2020	Arsenic induces mTOR-dependent autophagy, whereas it impairs the autophagy-lysosome pathway and the potential role of TFEB in cultured dendritic cells.	Arsenic	0-7	mechanistic target of rapamycin kinase	Homo sapiens	16-20
32519707-0	2020	Arsenic induces mTOR-dependent autophagy, whereas it impairs the autophagy-lysosome pathway and the potential role of TFEB in cultured dendritic cells.	Arsenic	0-7	transcription factor EB	Homo sapiens	118-122
32519707-6	2020	Initially, we observed that arsenic induced autophagosome accumulation, significantly enhanced the LC3 II and p62 expressions and down-regulated the p-mTOR protein levels.	Arsenic	28-35	nucleoporin 62	Homo sapiens	110-113
32519707-6	2020	Initially, we observed that arsenic induced autophagosome accumulation, significantly enhanced the LC3 II and p62 expressions and down-regulated the p-mTOR protein levels.	Arsenic	28-35	mechanistic target of rapamycin kinase	Homo sapiens	151-155
32519707-7	2020	We also determined that arsenic-induced autophagy occurred via an mTOR pathway.	Arsenic	24-31	mechanistic target of rapamycin kinase	Homo sapiens	66-70
32519707-9	2020	Meanwhile, arsenic significantly decreased the number of lysosomes, protein expression of lysosomal-specific markers LAMP1 and LAMP2, and the protein levels of lysosomal cysteine cathepsins (CTSD and CTSL).	Arsenic	11-18	lysosomal associated membrane protein 1	Homo sapiens	117-122
32519707-9	2020	Meanwhile, arsenic significantly decreased the number of lysosomes, protein expression of lysosomal-specific markers LAMP1 and LAMP2, and the protein levels of lysosomal cysteine cathepsins (CTSD and CTSL).	Arsenic	11-18	lysosomal associated membrane protein 2	Homo sapiens	127-132
32519707-9	2020	Meanwhile, arsenic significantly decreased the number of lysosomes, protein expression of lysosomal-specific markers LAMP1 and LAMP2, and the protein levels of lysosomal cysteine cathepsins (CTSD and CTSL).	Arsenic	11-18	cathepsin D	Homo sapiens	191-195
32519707-9	2020	Meanwhile, arsenic significantly decreased the number of lysosomes, protein expression of lysosomal-specific markers LAMP1 and LAMP2, and the protein levels of lysosomal cysteine cathepsins (CTSD and CTSL).	Arsenic	11-18	cathepsin L	Homo sapiens	200-204
32519707-10	2020	Moreover, the overexpression of transcription factor EB (TFEB), the master transcriptional regulator of autophagy and lysosome biogenesis, partially relieved arsenic-inhibited lysosomal CTSD and CTSL expressions, recovered the disorder of autophagic flux, promoted the production of pro-inflammatory cytokines TNF-alpha, IL-1beta, IL-6, and IL-12, and reduced anti-inflammatory cytokine IL-10 secretion.	Arsenic	158-165	transcription factor EB	Homo sapiens	32-55
32519707-10	2020	Moreover, the overexpression of transcription factor EB (TFEB), the master transcriptional regulator of autophagy and lysosome biogenesis, partially relieved arsenic-inhibited lysosomal CTSD and CTSL expressions, recovered the disorder of autophagic flux, promoted the production of pro-inflammatory cytokines TNF-alpha, IL-1beta, IL-6, and IL-12, and reduced anti-inflammatory cytokine IL-10 secretion.	Arsenic	158-165	transcription factor EB	Homo sapiens	57-61
32519707-10	2020	Moreover, the overexpression of transcription factor EB (TFEB), the master transcriptional regulator of autophagy and lysosome biogenesis, partially relieved arsenic-inhibited lysosomal CTSD and CTSL expressions, recovered the disorder of autophagic flux, promoted the production of pro-inflammatory cytokines TNF-alpha, IL-1beta, IL-6, and IL-12, and reduced anti-inflammatory cytokine IL-10 secretion.	Arsenic	158-165	cathepsin D	Homo sapiens	186-190
32519707-10	2020	Moreover, the overexpression of transcription factor EB (TFEB), the master transcriptional regulator of autophagy and lysosome biogenesis, partially relieved arsenic-inhibited lysosomal CTSD and CTSL expressions, recovered the disorder of autophagic flux, promoted the production of pro-inflammatory cytokines TNF-alpha, IL-1beta, IL-6, and IL-12, and reduced anti-inflammatory cytokine IL-10 secretion.	Arsenic	158-165	cathepsin L	Homo sapiens	195-199
32519707-10	2020	Moreover, the overexpression of transcription factor EB (TFEB), the master transcriptional regulator of autophagy and lysosome biogenesis, partially relieved arsenic-inhibited lysosomal CTSD and CTSL expressions, recovered the disorder of autophagic flux, promoted the production of pro-inflammatory cytokines TNF-alpha, IL-1beta, IL-6, and IL-12, and reduced anti-inflammatory cytokine IL-10 secretion.	Arsenic	158-165	tumor necrosis factor	Homo sapiens	310-319
32519707-10	2020	Moreover, the overexpression of transcription factor EB (TFEB), the master transcriptional regulator of autophagy and lysosome biogenesis, partially relieved arsenic-inhibited lysosomal CTSD and CTSL expressions, recovered the disorder of autophagic flux, promoted the production of pro-inflammatory cytokines TNF-alpha, IL-1beta, IL-6, and IL-12, and reduced anti-inflammatory cytokine IL-10 secretion.	Arsenic	158-165	interleukin 1 alpha	Homo sapiens	321-329
32519707-10	2020	Moreover, the overexpression of transcription factor EB (TFEB), the master transcriptional regulator of autophagy and lysosome biogenesis, partially relieved arsenic-inhibited lysosomal CTSD and CTSL expressions, recovered the disorder of autophagic flux, promoted the production of pro-inflammatory cytokines TNF-alpha, IL-1beta, IL-6, and IL-12, and reduced anti-inflammatory cytokine IL-10 secretion.	Arsenic	158-165	interleukin 6	Homo sapiens	331-335
32519707-10	2020	Moreover, the overexpression of transcription factor EB (TFEB), the master transcriptional regulator of autophagy and lysosome biogenesis, partially relieved arsenic-inhibited lysosomal CTSD and CTSL expressions, recovered the disorder of autophagic flux, promoted the production of pro-inflammatory cytokines TNF-alpha, IL-1beta, IL-6, and IL-12, and reduced anti-inflammatory cytokine IL-10 secretion.	Arsenic	158-165	interleukin 10	Homo sapiens	387-392
32519707-11	2020	In summary, our results support the idea that arsenic induces autophagy through an mTOR-dependent pathway in cultured BMDCs.	Arsenic	46-53	mechanistic target of rapamycin kinase	Homo sapiens	83-87
32422455-9	2020	Geogenic materials (topsoil and mining tailings), and water samples could contain extremely high arsenic concentrations, i.e. 21,000 mg kg-1 or 1,700,000 mug L-1, respectively, have been found mainly at the "Iron Quadrangle".	Arsenic	97-104	L1 cell adhesion molecule	Homo sapiens	158-161
32929351-12	2020	Conclusion: Our work reveals the critical role of the PML-RARalpha/PPARgamma/TRIB3 axis in the development of dyslipidemia in APL patients, potentially conferring a rationale for combining ATRA/arsenic with the PPAR activator for APL treatment.	Arsenic	194-201	retinoic acid receptor alpha	Homo sapiens	58-66
32929351-12	2020	Conclusion: Our work reveals the critical role of the PML-RARalpha/PPARgamma/TRIB3 axis in the development of dyslipidemia in APL patients, potentially conferring a rationale for combining ATRA/arsenic with the PPAR activator for APL treatment.	Arsenic	194-201	peroxisome proliferator activated receptor gamma	Homo sapiens	67-76
32929351-12	2020	Conclusion: Our work reveals the critical role of the PML-RARalpha/PPARgamma/TRIB3 axis in the development of dyslipidemia in APL patients, potentially conferring a rationale for combining ATRA/arsenic with the PPAR activator for APL treatment.	Arsenic	194-201	tribbles pseudokinase 3	Homo sapiens	77-82
32929351-10	2020	The elevated TRIB3 expression in response to arsenic/ATRA therapy suppressed PPARgamma activity by disrupting the PPARgamma/RXR dimer, which resulted in dyslipidemia in APL patients undergoing therapy.	Arsenic	45-52	tribbles pseudokinase 3	Homo sapiens	13-18
32929351-10	2020	The elevated TRIB3 expression in response to arsenic/ATRA therapy suppressed PPARgamma activity by disrupting the PPARgamma/RXR dimer, which resulted in dyslipidemia in APL patients undergoing therapy.	Arsenic	45-52	peroxisome proliferator activated receptor gamma	Homo sapiens	77-86
32929351-10	2020	The elevated TRIB3 expression in response to arsenic/ATRA therapy suppressed PPARgamma activity by disrupting the PPARgamma/RXR dimer, which resulted in dyslipidemia in APL patients undergoing therapy.	Arsenic	45-52	peroxisome proliferator activated receptor gamma	Homo sapiens	114-123
32929351-10	2020	The elevated TRIB3 expression in response to arsenic/ATRA therapy suppressed PPARgamma activity by disrupting the PPARgamma/RXR dimer, which resulted in dyslipidemia in APL patients undergoing therapy.	Arsenic	45-52	retinoid X receptor alpha	Homo sapiens	124-127
32929351-11	2020	Indeed, the PPAR activator not only enhanced the anti-APL effects of arsenic/ATRA by suppressing TRIB3 expression but also reduced therapy-induced dyslipidemia in APL patients.	Arsenic	69-76	peroxisome proliferator activated receptor alpha	Homo sapiens	12-16
32929351-11	2020	Indeed, the PPAR activator not only enhanced the anti-APL effects of arsenic/ATRA by suppressing TRIB3 expression but also reduced therapy-induced dyslipidemia in APL patients.	Arsenic	69-76	tribbles pseudokinase 3	Homo sapiens	97-102
32929351-12	2020	Conclusion: Our work reveals the critical role of the PML-RARalpha/PPARgamma/TRIB3 axis in the development of dyslipidemia in APL patients, potentially conferring a rationale for combining ATRA/arsenic with the PPAR activator for APL treatment.	Arsenic	194-201	PML nuclear body scaffold	Homo sapiens	54-57
32905139-0	2020	DNMT1-mediated Foxp3 gene promoter hypermethylation involved in immune dysfunction caused by arsenic in human lymphocytes.	Arsenic	93-100	DNA methyltransferase 1	Homo sapiens	0-5
32905139-4	2020	In this study, after primary human lymphocytes were treated with different doses of NaAsO2, our results showed that arsenic induced the high expression of DNMT1 and Foxp3 gene promoter methylation level, thereby inhibiting the expression levels of Foxp3, followed by decreasing Tregs and reducing related anti-inflammatory cytokines, such as interleukin 10 (IL-10) and interleukin 10 (IL-35), and increasing the ratio of CD4+/CD8+ T cells in lymphocytes.	Arsenic	116-123	DNA methyltransferase 1	Homo sapiens	155-160
32905139-0	2020	DNMT1-mediated Foxp3 gene promoter hypermethylation involved in immune dysfunction caused by arsenic in human lymphocytes.	Arsenic	93-100	forkhead box P3	Homo sapiens	15-20
32905139-4	2020	In this study, after primary human lymphocytes were treated with different doses of NaAsO2, our results showed that arsenic induced the high expression of DNMT1 and Foxp3 gene promoter methylation level, thereby inhibiting the expression levels of Foxp3, followed by decreasing Tregs and reducing related anti-inflammatory cytokines, such as interleukin 10 (IL-10) and interleukin 10 (IL-35), and increasing the ratio of CD4+/CD8+ T cells in lymphocytes.	Arsenic	116-123	forkhead box P3	Homo sapiens	165-170
32905139-4	2020	In this study, after primary human lymphocytes were treated with different doses of NaAsO2, our results showed that arsenic induced the high expression of DNMT1 and Foxp3 gene promoter methylation level, thereby inhibiting the expression levels of Foxp3, followed by decreasing Tregs and reducing related anti-inflammatory cytokines, such as interleukin 10 (IL-10) and interleukin 10 (IL-35), and increasing the ratio of CD4+/CD8+ T cells in lymphocytes.	Arsenic	116-123	forkhead box P3	Homo sapiens	248-253
32905139-3	2020	While evidence suggests that epigenetic regulated Foxp3 is involved in the immune disorders caused by arsenic exposure, the specific mechanism remains unclear.	Arsenic	102-109	forkhead box P3	Homo sapiens	50-55
32905139-4	2020	In this study, after primary human lymphocytes were treated with different doses of NaAsO2, our results showed that arsenic induced the high expression of DNMT1 and Foxp3 gene promoter methylation level, thereby inhibiting the expression levels of Foxp3, followed by decreasing Tregs and reducing related anti-inflammatory cytokines, such as interleukin 10 (IL-10) and interleukin 10 (IL-35), and increasing the ratio of CD4+/CD8+ T cells in lymphocytes.	Arsenic	116-123	interleukin 10	Homo sapiens	342-356
32203783-6	2020	Arsenic exposure inhibited the growth (body length, body width, and body area) in P C. elegans from 24 h to 60 h, however there was no difference between treatments groups and the control at 72 h. Arsenic led to a dose-dependent degeneration of dopaminergic neurons in C. elegans, and inhibition of BAS-1 and CAT-2 expressions.	Arsenic	0-7	Biogenic Amine Synthesis related	Caenorhabditis elegans	299-304
32905139-4	2020	In this study, after primary human lymphocytes were treated with different doses of NaAsO2, our results showed that arsenic induced the high expression of DNMT1 and Foxp3 gene promoter methylation level, thereby inhibiting the expression levels of Foxp3, followed by decreasing Tregs and reducing related anti-inflammatory cytokines, such as interleukin 10 (IL-10) and interleukin 10 (IL-35), and increasing the ratio of CD4+/CD8+ T cells in lymphocytes.	Arsenic	116-123	interleukin 10	Homo sapiens	358-363
32905139-4	2020	In this study, after primary human lymphocytes were treated with different doses of NaAsO2, our results showed that arsenic induced the high expression of DNMT1 and Foxp3 gene promoter methylation level, thereby inhibiting the expression levels of Foxp3, followed by decreasing Tregs and reducing related anti-inflammatory cytokines, such as interleukin 10 (IL-10) and interleukin 10 (IL-35), and increasing the ratio of CD4+/CD8+ T cells in lymphocytes.	Arsenic	116-123	interleukin 10	Homo sapiens	369-383
32905139-4	2020	In this study, after primary human lymphocytes were treated with different doses of NaAsO2, our results showed that arsenic induced the high expression of DNMT1 and Foxp3 gene promoter methylation level, thereby inhibiting the expression levels of Foxp3, followed by decreasing Tregs and reducing related anti-inflammatory cytokines, such as interleukin 10 (IL-10) and interleukin 10 (IL-35), and increasing the ratio of CD4+/CD8+ T cells in lymphocytes.	Arsenic	116-123	CD4 molecule	Homo sapiens	421-424
32905139-4	2020	In this study, after primary human lymphocytes were treated with different doses of NaAsO2, our results showed that arsenic induced the high expression of DNMT1 and Foxp3 gene promoter methylation level, thereby inhibiting the expression levels of Foxp3, followed by decreasing Tregs and reducing related anti-inflammatory cytokines, such as interleukin 10 (IL-10) and interleukin 10 (IL-35), and increasing the ratio of CD4+/CD8+ T cells in lymphocytes.	Arsenic	116-123	CD8a molecule	Homo sapiens	426-429
32905139-7	2020	In conclusion, our study provides limited evidence that DNMT1-mediated Foxp3 gene promoter hypermethylation is involved in immune dysfunction caused by arsenic in primary human lymphocytes.	Arsenic	152-159	DNA methyltransferase 1	Homo sapiens	56-61
32905139-7	2020	In conclusion, our study provides limited evidence that DNMT1-mediated Foxp3 gene promoter hypermethylation is involved in immune dysfunction caused by arsenic in primary human lymphocytes.	Arsenic	152-159	forkhead box P3	Homo sapiens	71-76
32474354-11	2020	CONCLUSION: Early signs of urinary bladder carcinogenesis were observed in arsenic and DMA exposed rats which were linked to metal accumulation, oxidative/ nitrosative stress, 8-OHdG, MMP-9 and survivin which were reduced by MiADMSA possibly via its efficient chelation abilities in vivo and in vitro.	Arsenic	75-82	matrix metallopeptidase 9	Rattus norvegicus	184-189
32203783-6	2020	Arsenic exposure inhibited the growth (body length, body width, and body area) in P C. elegans from 24 h to 60 h, however there was no difference between treatments groups and the control at 72 h. Arsenic led to a dose-dependent degeneration of dopaminergic neurons in C. elegans, and inhibition of BAS-1 and CAT-2 expressions.	Arsenic	0-7	BH4_AAA_HYDROXYL_2 domain-containing protein;Tyrosine 3-hydroxylase;Tyrosine 3-monooxygenase	Caenorhabditis elegans	309-314
32203783-6	2020	Arsenic exposure inhibited the growth (body length, body width, and body area) in P C. elegans from 24 h to 60 h, however there was no difference between treatments groups and the control at 72 h. Arsenic led to a dose-dependent degeneration of dopaminergic neurons in C. elegans, and inhibition of BAS-1 and CAT-2 expressions.	Arsenic	197-204	Biogenic Amine Synthesis related	Caenorhabditis elegans	299-304
32203783-6	2020	Arsenic exposure inhibited the growth (body length, body width, and body area) in P C. elegans from 24 h to 60 h, however there was no difference between treatments groups and the control at 72 h. Arsenic led to a dose-dependent degeneration of dopaminergic neurons in C. elegans, and inhibition of BAS-1 and CAT-2 expressions.	Arsenic	197-204	BH4_AAA_HYDROXYL_2 domain-containing protein;Tyrosine 3-hydroxylase;Tyrosine 3-monooxygenase	Caenorhabditis elegans	309-314
32203783-7	2020	The expressions of GCS-1, GSS-1, and SKN-1 were induced by arsenic exposure.	Arsenic	59-66	Glutamate--cysteine ligase	Caenorhabditis elegans	19-24
32203783-7	2020	The expressions of GCS-1, GSS-1, and SKN-1 were induced by arsenic exposure.	Arsenic	59-66	Glutathione synthetase	Caenorhabditis elegans	26-31
32203783-7	2020	The expressions of GCS-1, GSS-1, and SKN-1 were induced by arsenic exposure.	Arsenic	59-66	BZIP domain-containing protein;Protein skinhead-1	Caenorhabditis elegans	37-42
32402895-5	2020	Arsenic intoxicated group exhibited a comparable inactivation of antioxidant enzymes superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) due to oxidative stress in reproductive organs along with a simultaneous elevation of lipid peroxidation state and decline in non-protein soluble thiols (NPSH) level in female reproductive organs.	Arsenic	0-7	catalase	Rattus norvegicus	113-121
32467084-0	2020	Retraction notice to "Diallyl trisulfide, a garlic polysulfide protects against As-induced renal oxidative nephrotoxicity, apoptosis and inflammation in rats by activating the Nrf2/ARE signaling pathway" [Int.	Arsenic	80-82	NFE2 like bZIP transcription factor 2	Rattus norvegicus	176-180
32402895-6	2020	Arsenic intoxication also accomplished with the up-regulation of inflammatory markers tumour necrosis factor (TNF alpha) and nuclear factor kappaB (NF kappaB).	Arsenic	0-7	tumor necrosis factor	Rattus norvegicus	110-119
32436094-1	2020	This study aimed to evaluate biomarkers of exposure to cholinesterase inhibitors insecticides (AChE and BuChE activities) and metals (As, Cd, Cr, Mn, Ni, and Pb blood levels) and their associations with biochemical, hematological, and immunological parameters in farmers from Southern Brazil.	Arsenic	134-136	butyrylcholinesterase	Homo sapiens	55-69
32436094-8	2020	Inverse associations were found between LFA-1 and blood As, Cr, and Ni levels (p < 0.05).	Arsenic	56-58	integrin subunit alpha L	Homo sapiens	40-45
31842638-6	2020	As neuronal apoptosis is the most crucial event in ICH disease, the expression of active caspase-3 and p53 is also enhanced around the hematoma, which is consistent with Triad1 in expression tendency.	Arsenic	0-2	ariadne RBR E3 ubiquitin protein ligase 2	Rattus norvegicus	170-176
32779937-0	2020	Arsenic Metabolism in Mice Carrying a BORCS7/AS3MT Locus Humanized by Syntenic Replacement.	Arsenic	0-7	BLOC-1 related complex subunit 7	Mus musculus	38-44
32779937-0	2020	Arsenic Metabolism in Mice Carrying a BORCS7/AS3MT Locus Humanized by Syntenic Replacement.	Arsenic	0-7	arsenite methyltransferase	Mus musculus	45-50
31842638-6	2020	As neuronal apoptosis is the most crucial event in ICH disease, the expression of active caspase-3 and p53 is also enhanced around the hematoma, which is consistent with Triad1 in expression tendency.	Arsenic	0-2	caspase 3	Rattus norvegicus	89-98
31842638-6	2020	As neuronal apoptosis is the most crucial event in ICH disease, the expression of active caspase-3 and p53 is also enhanced around the hematoma, which is consistent with Triad1 in expression tendency.	Arsenic	0-2	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	103-106
32433756-3	2020	Arsenic metabolism involves the AS3MT (arsenic methyltransferase) gene, and arsenic metabolism efficiency (AME, measured as relative concentrations of arsenic metabolites in urine) varies among individuals.	Arsenic	0-7	arsenite methyltransferase	Homo sapiens	32-37
32718300-0	2021	In Silico Identification of a Potent Arsenic Based Approved Drug Darinaparsin against SARS-CoV-2: Inhibitor of RNA Dependent RNA polymerase (RdRp) and Essential Proteases.	Arsenic	37-44	ORF1a polyprotein;ORF1ab polyprotein	Severe acute respiratory syndrome coronavirus 2	141-145
32760496-9	2020	Results: Our results shown that NF-kappaB were continuously activated with treatment of 25 mg/L arsenic from 1, 3 to 12 months and 50 mg/L arsenic for 12 months.	Arsenic	96-103	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	32-41
32760496-9	2020	Results: Our results shown that NF-kappaB were continuously activated with treatment of 25 mg/L arsenic from 1, 3 to 12 months and 50 mg/L arsenic for 12 months.	Arsenic	139-146	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	32-41
32760496-10	2020	The transcription factor Foxp3 increased at 1 month but decreased at 3 and 12 months no matter 25 or 50 mg/L arsenic exposure.	Arsenic	109-116	forkhead box P3	Mus musculus	25-30
32760496-11	2020	However, cytokine Il-10 always showed increased trend in mice treated with 25 or 50 mg/L arsenic for 1, 3 and 12 months.	Arsenic	89-96	interleukin 10	Mus musculus	18-23
32760496-13	2020	In addition, the sustained activation of inflammatory MAPK and anti-oxidative Nrf2 signaling pathways were observed in mice exposed to arsenic for 1, 3 and 12 months.	Arsenic	135-142	nuclear factor, erythroid derived 2, like 2	Mus musculus	78-82
32760496-14	2020	Conclusion: In summary, our experiment in vivo suggested chronic arsenic exposure induces the time-dependent modulation of the inflammation and immunosuppression in spleen, which may be related to the activation of Tregs induced by MAPK/NF-kappaB as well as the increased transcription level of Foxp3 and Il-10.	Arsenic	65-72	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	237-246
32760496-14	2020	Conclusion: In summary, our experiment in vivo suggested chronic arsenic exposure induces the time-dependent modulation of the inflammation and immunosuppression in spleen, which may be related to the activation of Tregs induced by MAPK/NF-kappaB as well as the increased transcription level of Foxp3 and Il-10.	Arsenic	65-72	forkhead box P3	Mus musculus	295-300
32760496-14	2020	Conclusion: In summary, our experiment in vivo suggested chronic arsenic exposure induces the time-dependent modulation of the inflammation and immunosuppression in spleen, which may be related to the activation of Tregs induced by MAPK/NF-kappaB as well as the increased transcription level of Foxp3 and Il-10.	Arsenic	65-72	interleukin 10	Mus musculus	305-310
32849333-6	2020	When exposed to 100 ppm As, Cd, or Pb, HFD-fed mice accumulated more heavy metals in the liver and kidney along with more severe functional damage than ND-fed mice, indicated by a more dramatic increase of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and urinary total protein (TPU), urinary uric acid (UUA), and urinary creatinine (Ucrea) content.	Arsenic	24-26	glutamic pyruvic transaminase, soluble	Mus musculus	206-230
32849333-6	2020	When exposed to 100 ppm As, Cd, or Pb, HFD-fed mice accumulated more heavy metals in the liver and kidney along with more severe functional damage than ND-fed mice, indicated by a more dramatic increase of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and urinary total protein (TPU), urinary uric acid (UUA), and urinary creatinine (Ucrea) content.	Arsenic	24-26	glutamic pyruvic transaminase, soluble	Mus musculus	232-235
32849333-6	2020	When exposed to 100 ppm As, Cd, or Pb, HFD-fed mice accumulated more heavy metals in the liver and kidney along with more severe functional damage than ND-fed mice, indicated by a more dramatic increase of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and urinary total protein (TPU), urinary uric acid (UUA), and urinary creatinine (Ucrea) content.	Arsenic	24-26	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	241-267
32849333-6	2020	When exposed to 100 ppm As, Cd, or Pb, HFD-fed mice accumulated more heavy metals in the liver and kidney along with more severe functional damage than ND-fed mice, indicated by a more dramatic increase of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and urinary total protein (TPU), urinary uric acid (UUA), and urinary creatinine (Ucrea) content.	Arsenic	24-26	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	269-272
32143131-3	2020	The developed method has presented limits of quantification (LOQ) of 0.72, 0.12, and 1.5 mug L-1 for As, Hg, and Se, respectively.	Arsenic	101-103	immunoglobulin kappa variable 1-16	Homo sapiens	93-96
32802886-6	2020	Objective: We will conduct a meta-analysis to illustrate the effects of arsenic on GSH synthesis precursors Glu, Cys, Gly, and rate-limiting enzyme gamma-GCS in mammalian models, as well as the regulation of p38/Nrf2 of gamma-GCS subunit GCLC, and further explore the molecular mechanism of arsenic affecting glutathione synthesis.	Arsenic	291-298	mitogen-activated protein kinase 14	Homo sapiens	208-211
32802886-12	2020	In vivo studies have shown that arsenic exposure can reduce glutamate and cysteine levels and inhibit glutathione synthesis, while in vitro studies have shown that chronic low-dose arsenic exposure can activate the p38/Nrf2 pathway, upregulate GCLC expression, and promote glutathione synthesis.	Arsenic	32-39	mitogen-activated protein kinase 14	Homo sapiens	215-218
32802886-12	2020	In vivo studies have shown that arsenic exposure can reduce glutamate and cysteine levels and inhibit glutathione synthesis, while in vitro studies have shown that chronic low-dose arsenic exposure can activate the p38/Nrf2 pathway, upregulate GCLC expression, and promote glutathione synthesis.	Arsenic	32-39	glutamate-cysteine ligase catalytic subunit	Homo sapiens	244-248
32802886-12	2020	In vivo studies have shown that arsenic exposure can reduce glutamate and cysteine levels and inhibit glutathione synthesis, while in vitro studies have shown that chronic low-dose arsenic exposure can activate the p38/Nrf2 pathway, upregulate GCLC expression, and promote glutathione synthesis.	Arsenic	181-188	mitogen-activated protein kinase 14	Homo sapiens	215-218
32802886-12	2020	In vivo studies have shown that arsenic exposure can reduce glutamate and cysteine levels and inhibit glutathione synthesis, while in vitro studies have shown that chronic low-dose arsenic exposure can activate the p38/Nrf2 pathway, upregulate GCLC expression, and promote glutathione synthesis.	Arsenic	181-188	NFE2 like bZIP transcription factor 2	Homo sapiens	219-223
32802886-12	2020	In vivo studies have shown that arsenic exposure can reduce glutamate and cysteine levels and inhibit glutathione synthesis, while in vitro studies have shown that chronic low-dose arsenic exposure can activate the p38/Nrf2 pathway, upregulate GCLC expression, and promote glutathione synthesis.	Arsenic	181-188	glutamate-cysteine ligase catalytic subunit	Homo sapiens	244-248
32939177-9	2020	Additionally, according to the effect of pH on arsenic trapping, the electrostatic interactions appear as a major factor controlling As(V) adsorption while surface complexation may control As(III) adsorption.	Arsenic	47-54	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	133-138
32143131-4	2020	The precisions of the proposed method expressed as repeatability were 0.92, 2.2, and 3.7% RSD for 2 microg L-1 (n = 10) of As, Hg and Se, respectively.	Arsenic	123-125	immunoglobulin kappa variable 1-16	Homo sapiens	107-110
32143131-6	2020	Concentrations (mug L-1) found in the samples were between <LOQ - 1.3 for As and 3.0-15 for Se.	Arsenic	74-76	immunoglobulin kappa variable 1-16	Homo sapiens	20-23
32304945-4	2020	High Hg and As content in very fine grain-size fractions (up to 100,000 mg/kg of As in metallurgy waste below 10 mum) was significant, as was the predominance of As (III) in metallurgy waste.	Arsenic	12-14	latexin	Homo sapiens	113-116
32802178-0	2020	Deubiquitinase USP7-mediated MCL-1 up-regulation enhances Arsenic and Benzo(a)pyrene co-exposure-induced Cancer Stem Cell-like property and Tumorigenesis.	Arsenic	58-65	ubiquitin specific peptidase 7	Homo sapiens	15-19
32428313-4	2020	Conversion of 2 - 4 with [ t Bu 2 SbP( t Bu)Li(OEt 2 )] 2 leads to the remarkable interpnictogens [( t BuNAs) 2 ( t BuN) 2 ]PnP( t Bu)Sb t Bu 2 (Pn = As ( 5 ), Sb ( 6 ), Bi ( 7 )), whereby 7 is the first example of a molecule containing all five group 15 elements.	Arsenic	106-108	selenium binding protein 1	Homo sapiens	34-37
32802178-0	2020	Deubiquitinase USP7-mediated MCL-1 up-regulation enhances Arsenic and Benzo(a)pyrene co-exposure-induced Cancer Stem Cell-like property and Tumorigenesis.	Arsenic	58-65	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	29-34
32802178-7	2020	Both loss-of-function and gain-of-function approaches were used to validate the role of MCL-1 in arsenic plus BaP co-exposure-enhanced CSC-like property and tumorigenicity.	Arsenic	97-104	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	88-93
32802178-8	2020	Results: Arsenic plus BaP co-exposure-transformed cells express significantly higher protein levels of MCL-1 than the passage-matched control, arsenic or BaP exposure alone-transformed cells.	Arsenic	9-16	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	103-108
32802178-9	2020	Knocking down MCL-1 levels in arsenic plus BaP co-exposure-transformed cells significantly reduced their apoptosis resistance, CSC-like property and tumorigenicity in mice.	Arsenic	30-37	myeloid cell leukemia sequence 1	Mus musculus	14-19
32802178-10	2020	Mechanistic studies revealed that arsenic plus BaP co-exposure up-regulates MCL-1 protein levels by synergistically activating the PI3K/Akt/mTOR pathway to increase the level of a deubiquitinase USP7, which in turn reduces the level of MCL-1 protein ubiquitination and prevents its subsequent proteasome degradation.	Arsenic	34-41	myeloid cell leukemia sequence 1	Mus musculus	76-81
32802178-10	2020	Mechanistic studies revealed that arsenic plus BaP co-exposure up-regulates MCL-1 protein levels by synergistically activating the PI3K/Akt/mTOR pathway to increase the level of a deubiquitinase USP7, which in turn reduces the level of MCL-1 protein ubiquitination and prevents its subsequent proteasome degradation.	Arsenic	34-41	AKT serine/threonine kinase 1	Homo sapiens	136-139
32802178-10	2020	Mechanistic studies revealed that arsenic plus BaP co-exposure up-regulates MCL-1 protein levels by synergistically activating the PI3K/Akt/mTOR pathway to increase the level of a deubiquitinase USP7, which in turn reduces the level of MCL-1 protein ubiquitination and prevents its subsequent proteasome degradation.	Arsenic	34-41	mechanistic target of rapamycin kinase	Homo sapiens	140-144
32802178-10	2020	Mechanistic studies revealed that arsenic plus BaP co-exposure up-regulates MCL-1 protein levels by synergistically activating the PI3K/Akt/mTOR pathway to increase the level of a deubiquitinase USP7, which in turn reduces the level of MCL-1 protein ubiquitination and prevents its subsequent proteasome degradation.	Arsenic	34-41	ubiquitin specific peptidase 7	Homo sapiens	195-199
32802178-10	2020	Mechanistic studies revealed that arsenic plus BaP co-exposure up-regulates MCL-1 protein levels by synergistically activating the PI3K/Akt/mTOR pathway to increase the level of a deubiquitinase USP7, which in turn reduces the level of MCL-1 protein ubiquitination and prevents its subsequent proteasome degradation.	Arsenic	34-41	myeloid cell leukemia sequence 1	Mus musculus	236-241
32802178-11	2020	Conclusions: The deubiquitinase USP7-mediated MCL-1 up-regulation enhances arsenic and BaP co-exposure-induced CSC-like property and tumorigenesis, providing the first evidence demonstrating that USP7 stabilizes MCL-1 protein during the tumorigenic process.	Arsenic	75-82	ubiquitin specific peptidase 7	Homo sapiens	32-36
32802178-11	2020	Conclusions: The deubiquitinase USP7-mediated MCL-1 up-regulation enhances arsenic and BaP co-exposure-induced CSC-like property and tumorigenesis, providing the first evidence demonstrating that USP7 stabilizes MCL-1 protein during the tumorigenic process.	Arsenic	75-82	myeloid cell leukemia sequence 1	Mus musculus	46-51
32802178-11	2020	Conclusions: The deubiquitinase USP7-mediated MCL-1 up-regulation enhances arsenic and BaP co-exposure-induced CSC-like property and tumorigenesis, providing the first evidence demonstrating that USP7 stabilizes MCL-1 protein during the tumorigenic process.	Arsenic	75-82	ubiquitin specific peptidase 7	Homo sapiens	196-200
32802178-11	2020	Conclusions: The deubiquitinase USP7-mediated MCL-1 up-regulation enhances arsenic and BaP co-exposure-induced CSC-like property and tumorigenesis, providing the first evidence demonstrating that USP7 stabilizes MCL-1 protein during the tumorigenic process.	Arsenic	75-82	myeloid cell leukemia sequence 1	Mus musculus	212-217
32650499-0	2020	As3MT and GST Polymorphisms Influencing Arsenic Metabolism in Human Exposure to Drinking Groundwater.	Arsenic	40-47	arsenite methyltransferase	Homo sapiens	0-5
32650499-2	2020	We assessed the influence of polymorphic variants of Arsenic-3-methyl-transferase and Glutathione-S-transferase on urinary arsenic metabolites.	Arsenic	123-130	glutathione S-transferase kappa 1	Homo sapiens	86-111
32650499-9	2020	Univariate analyses among arsenic metabolites and genetic polymorphisms showed MMA concentrations higher in heterozygous and/or homozygous genotypes of As3MT compared to the wild-type genotype.	Arsenic	26-33	arsenite methyltransferase	Homo sapiens	152-157
32650499-13	2020	Interactions between polymorphic variants As3MT*GSTM1 and GSTO2*GSTP1 could be potential modifiers of urinary excretion of arsenic and covariates as age, LADD, and alcohol consumption contribute to largely vary the arsenic individual metabolic capacity in exposed people.	Arsenic	215-222	arsenite methyltransferase	Homo sapiens	42-47
32650499-13	2020	Interactions between polymorphic variants As3MT*GSTM1 and GSTO2*GSTP1 could be potential modifiers of urinary excretion of arsenic and covariates as age, LADD, and alcohol consumption contribute to largely vary the arsenic individual metabolic capacity in exposed people.	Arsenic	123-130	arsenite methyltransferase	Homo sapiens	42-47
32650499-13	2020	Interactions between polymorphic variants As3MT*GSTM1 and GSTO2*GSTP1 could be potential modifiers of urinary excretion of arsenic and covariates as age, LADD, and alcohol consumption contribute to largely vary the arsenic individual metabolic capacity in exposed people.	Arsenic	215-222	glutathione S-transferase mu 1	Homo sapiens	48-53
32650499-13	2020	Interactions between polymorphic variants As3MT*GSTM1 and GSTO2*GSTP1 could be potential modifiers of urinary excretion of arsenic and covariates as age, LADD, and alcohol consumption contribute to largely vary the arsenic individual metabolic capacity in exposed people.	Arsenic	123-130	glutathione S-transferase mu 1	Homo sapiens	48-53
32650499-13	2020	Interactions between polymorphic variants As3MT*GSTM1 and GSTO2*GSTP1 could be potential modifiers of urinary excretion of arsenic and covariates as age, LADD, and alcohol consumption contribute to largely vary the arsenic individual metabolic capacity in exposed people.	Arsenic	123-130	glutathione S-transferase omega 2	Homo sapiens	58-63
32650499-13	2020	Interactions between polymorphic variants As3MT*GSTM1 and GSTO2*GSTP1 could be potential modifiers of urinary excretion of arsenic and covariates as age, LADD, and alcohol consumption contribute to largely vary the arsenic individual metabolic capacity in exposed people.	Arsenic	215-222	glutathione S-transferase omega 2	Homo sapiens	58-63
32650499-13	2020	Interactions between polymorphic variants As3MT*GSTM1 and GSTO2*GSTP1 could be potential modifiers of urinary excretion of arsenic and covariates as age, LADD, and alcohol consumption contribute to largely vary the arsenic individual metabolic capacity in exposed people.	Arsenic	215-222	glutathione S-transferase pi 1	Homo sapiens	64-69
32650499-13	2020	Interactions between polymorphic variants As3MT*GSTM1 and GSTO2*GSTP1 could be potential modifiers of urinary excretion of arsenic and covariates as age, LADD, and alcohol consumption contribute to largely vary the arsenic individual metabolic capacity in exposed people.	Arsenic	123-130	glutathione S-transferase pi 1	Homo sapiens	64-69
32369890-7	2020	Risk modelling, based on pot experimental data, demonstrated soil specific accumulation of As in beef muscle and milk, being furthest reduced (compared to the raw ash addition) by AG 2 in soil A, but increased in soil B by the same treatment.	Arsenic	91-93	anterior gradient 2, protein disulphide isomerase family member	Homo sapiens	180-184
31686395-7	2020	While inorganic arsenic may induce various glucose-related proteins, i.e., GRP78, GRP94 and CHOP, XBP1, and calpains, cadmium upregulates GRP78.	Arsenic	16-23	heat shock protein family A (Hsp70) member 5	Homo sapiens	75-80
32635466-6	2020	We found that both 0.05 and 0.5 ppm As2O3 increased the fasting plasma glucose level; but only 0.5 ppm arsenic exposure significantly decreased muscle mass, muscle endurance, and cross-sectional area of muscle fibers, and increased muscle Atrogin-1 protein expression in the normal mice.	Arsenic	103-110	F-box protein 32	Mus musculus	239-248
31686395-7	2020	While inorganic arsenic may induce various glucose-related proteins, i.e., GRP78, GRP94 and CHOP, XBP1, and calpains, cadmium upregulates GRP78.	Arsenic	16-23	heat shock protein 90 beta family member 1	Homo sapiens	82-87
31686395-7	2020	While inorganic arsenic may induce various glucose-related proteins, i.e., GRP78, GRP94 and CHOP, XBP1, and calpains, cadmium upregulates GRP78.	Arsenic	16-23	DNA damage inducible transcript 3	Homo sapiens	92-96
31686395-7	2020	While inorganic arsenic may induce various glucose-related proteins, i.e., GRP78, GRP94 and CHOP, XBP1, and calpains, cadmium upregulates GRP78.	Arsenic	16-23	X-box binding protein 1	Homo sapiens	98-102
31686395-7	2020	While inorganic arsenic may induce various glucose-related proteins, i.e., GRP78, GRP94 and CHOP, XBP1, and calpains, cadmium upregulates GRP78.	Arsenic	16-23	heat shock protein family A (Hsp70) member 5	Homo sapiens	138-143
32695675-0	2020	HB-EGF Activates the EGFR/HIF-1alpha Pathway to Induce Proliferation of Arsenic-Transformed Cells and Tumor Growth.	Arsenic	72-79	heparin binding EGF like growth factor	Homo sapiens	0-6
32171940-7	2020	In addition, the adsorbed As on schwertmannite is more stable, which led to a minor release of As (0.8%) over a 30-d period, however, the liberated As(V) from CO-Sch accounts for up to 3.2%.	Arsenic	26-28	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	148-153
32315827-9	2020	Our findings suggest that PEDF protects endothelial cells from arsenic-induced VED by increasing NO release and inhibiting apoptosis, where P53 and p38MAPK are its main targets.	Arsenic	63-70	serpin family F member 1	Homo sapiens	26-30
32315827-9	2020	Our findings suggest that PEDF protects endothelial cells from arsenic-induced VED by increasing NO release and inhibiting apoptosis, where P53 and p38MAPK are its main targets.	Arsenic	63-70	tumor protein p53	Homo sapiens	140-143
32159786-0	2020	Arsenic Stimulates Myoblast Mitochondrial EGFR to Impair Myogenesis.	Arsenic	0-7	epidermal growth factor receptor	Mus musculus	42-46
32159786-5	2020	Arsenic prolonged ligand-independent phosphorylation of mitochondrially localized epidermal growth factor receptor (EGFR), a major driver of proliferation.	Arsenic	0-7	epidermal growth factor receptor	Mus musculus	82-114
32159786-5	2020	Arsenic prolonged ligand-independent phosphorylation of mitochondrially localized epidermal growth factor receptor (EGFR), a major driver of proliferation.	Arsenic	0-7	epidermal growth factor receptor	Mus musculus	116-120
32159786-7	2020	AG-1478 decreased arsenic-induced colocalization of pY845EGFR with mitochondrial cytochrome c oxidase subunit II (MTCO2), as well as arsenic-enhanced mitochondrial membrane potential, reactive oxygen species generation, and cell cycling.	Arsenic	18-25	cytochrome c oxidase II, mitochondrial	Mus musculus	81-112
32159786-7	2020	AG-1478 decreased arsenic-induced colocalization of pY845EGFR with mitochondrial cytochrome c oxidase subunit II (MTCO2), as well as arsenic-enhanced mitochondrial membrane potential, reactive oxygen species generation, and cell cycling.	Arsenic	18-25	cytochrome c oxidase II, mitochondrial	Mus musculus	114-119
32159786-9	2020	Thus, arsenic-driven pathogenesis in skeletal muscle requires sustained mitochondrial EGFR activation that promotes progenitor cell cycling and proliferation at the detriment of proper differentiation.	Arsenic	6-13	epidermal growth factor receptor	Mus musculus	86-90
32159786-10	2020	Collectively, these findings suggest that the arsenic-activated mitochondrial EGFR pathway drives pathogenic signaling for impaired myoblast metabolism and function.	Arsenic	46-53	epidermal growth factor receptor	Mus musculus	78-82
32151809-7	2020	The present EC reactor process is able to remove As(III) from groundwater to below 10 mug L-1, which is maximum contaminant level of arsenic in drinking water according to the World Health Organization (WHO).	Arsenic	133-140	immunoglobulin kappa variable 1-16	Homo sapiens	90-93
32315827-0	2020	Pigment epithelium-derived factor (PEDF) ameliorates arsenic-induced vascular endothelial dysfunction in rats and toxicity in endothelial EA.hy926 cells.	Arsenic	53-60	serpin family F member 1	Rattus norvegicus	0-33
32315827-0	2020	Pigment epithelium-derived factor (PEDF) ameliorates arsenic-induced vascular endothelial dysfunction in rats and toxicity in endothelial EA.hy926 cells.	Arsenic	53-60	serpin family F member 1	Rattus norvegicus	35-39
32315827-3	2020	Here, we explored the protective role of PEDF in VED induced by arsenic, and its underlying molecular mechanism, designing an in vivo rat model of arsenic exposure recovery and in vitro endothelial EA.	Arsenic	64-71	serpin family F member 1	Rattus norvegicus	41-45
32695675-0	2020	HB-EGF Activates the EGFR/HIF-1alpha Pathway to Induce Proliferation of Arsenic-Transformed Cells and Tumor Growth.	Arsenic	72-79	epidermal growth factor receptor	Homo sapiens	21-25
32695675-0	2020	HB-EGF Activates the EGFR/HIF-1alpha Pathway to Induce Proliferation of Arsenic-Transformed Cells and Tumor Growth.	Arsenic	72-79	hypoxia inducible factor 1 subunit alpha	Homo sapiens	26-36
32616124-4	2020	Conclusions In the Han population in Hunan Province,the C677T polymorphism of the MTHFR gene is associated with the onset of AS.The T/T mutation at position 677 of the MTHFR gene is an important influencing factor for hyperhcyemia in the AS patients.The T/T mutation at position 677 of the MTHFR gene is associated with genomic DNA hypomethylation.Thus,hypomethylation of DNA may be one of the pathogenic mechanisms of AS.	Arsenic	125-127	methylenetetrahydrofolate reductase	Homo sapiens	82-87
32695675-8	2020	Thus, HB-EGF drives arsenic-induced carcinogenesis, tumor growth, and lung cancer development via the EGFR/PKM2/HIF-1alpha pathway.	Arsenic	20-27	heparin binding EGF like growth factor	Homo sapiens	6-12
32616124-4	2020	Conclusions In the Han population in Hunan Province,the C677T polymorphism of the MTHFR gene is associated with the onset of AS.The T/T mutation at position 677 of the MTHFR gene is an important influencing factor for hyperhcyemia in the AS patients.The T/T mutation at position 677 of the MTHFR gene is associated with genomic DNA hypomethylation.Thus,hypomethylation of DNA may be one of the pathogenic mechanisms of AS.	Arsenic	125-127	methylenetetrahydrofolate reductase	Homo sapiens	168-173
32616124-4	2020	Conclusions In the Han population in Hunan Province,the C677T polymorphism of the MTHFR gene is associated with the onset of AS.The T/T mutation at position 677 of the MTHFR gene is an important influencing factor for hyperhcyemia in the AS patients.The T/T mutation at position 677 of the MTHFR gene is associated with genomic DNA hypomethylation.Thus,hypomethylation of DNA may be one of the pathogenic mechanisms of AS.	Arsenic	125-127	methylenetetrahydrofolate reductase	Homo sapiens	168-173
32695675-8	2020	Thus, HB-EGF drives arsenic-induced carcinogenesis, tumor growth, and lung cancer development via the EGFR/PKM2/HIF-1alpha pathway.	Arsenic	20-27	epidermal growth factor receptor	Homo sapiens	102-106
32695675-8	2020	Thus, HB-EGF drives arsenic-induced carcinogenesis, tumor growth, and lung cancer development via the EGFR/PKM2/HIF-1alpha pathway.	Arsenic	20-27	pyruvate kinase M1/2	Homo sapiens	107-111
32695675-8	2020	Thus, HB-EGF drives arsenic-induced carcinogenesis, tumor growth, and lung cancer development via the EGFR/PKM2/HIF-1alpha pathway.	Arsenic	20-27	hypoxia inducible factor 1 subunit alpha	Homo sapiens	112-122
32307979-5	2020	In cancer cells, the levels of beta-catenin, cyclinD1, c-myc and VEGF in arsenic intervention group were lower than those in control group, while the level of GSK-3beta in arsenic intervention group was higher than that in control group (P<0.05, respectively).	Arsenic	73-80	catenin beta 1	Homo sapiens	31-43
32458955-3	2020	The results showed that the concentrations of Cd in soil, Cd and Pb in wheat, Hg in corn, Cd, Hg, and Pb in vegetables, and Cd and As in PM2.5, PM10, and TSP were all higher than the corresponding limits for heavy metals in China.	Arsenic	131-133	thrombospondin 1	Homo sapiens	154-157
32307979-0	2020	Effects of arsenic on wnt/beta-catenin signaling pathway: A systematic review and meta-analysis.	Arsenic	11-18	Wnt family member 3A	Homo sapiens	22-25
32307979-5	2020	In cancer cells, the levels of beta-catenin, cyclinD1, c-myc and VEGF in arsenic intervention group were lower than those in control group, while the level of GSK-3beta in arsenic intervention group was higher than that in control group (P<0.05, respectively).	Arsenic	73-80	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	55-60
32307979-0	2020	Effects of arsenic on wnt/beta-catenin signaling pathway: A systematic review and meta-analysis.	Arsenic	11-18	catenin beta 1	Homo sapiens	26-38
32307979-5	2020	In cancer cells, the levels of beta-catenin, cyclinD1, c-myc and VEGF in arsenic intervention group were lower than those in control group, while the level of GSK-3beta in arsenic intervention group was higher than that in control group (P<0.05, respectively).	Arsenic	73-80	vascular endothelial growth factor A	Homo sapiens	65-69
32307979-1	2020	We aimed to systematically evaluate the regulatory effect of arsenic on wnt/beta-catenin signaling pathway and to provide theoretical basis for revealing the mechanism of the relationship between arsenic and cell proliferation.	Arsenic	61-68	Wnt family member 3A	Homo sapiens	72-75
32307979-1	2020	We aimed to systematically evaluate the regulatory effect of arsenic on wnt/beta-catenin signaling pathway and to provide theoretical basis for revealing the mechanism of the relationship between arsenic and cell proliferation.	Arsenic	61-68	catenin beta 1	Homo sapiens	76-88
32307979-4	2020	Subgroup analysis showed that for a long time period (>24h), the level of beta-catenin in the arsenic intervention group was higher than that in the control group, and the level of GSK-3beta of the same long-time period (>24h) with low-dose (<=5muM) intervention were lower than those in the control group (P<0.05, respectively).	Arsenic	94-101	catenin beta 1	Homo sapiens	74-86
32307979-5	2020	In cancer cells, the levels of beta-catenin, cyclinD1, c-myc and VEGF in arsenic intervention group were lower than those in control group, while the level of GSK-3beta in arsenic intervention group was higher than that in control group (P<0.05, respectively).	Arsenic	172-179	glycogen synthase kinase 3 alpha	Homo sapiens	159-168
32307979-6	2020	Subgroup analysis showed that the levels of beta-catenin, cyclinD1 and c-myc in the high-dose (>5muM) arsenic intervention group were lower than those in the control group, and the levels of beta-catenin and cyclinD1 in the high-dose (>5muM) arsenic intervention group were lower than those in the low-dose (<=5muM) arsenic intervention group (P<0.05, respectively).	Arsenic	102-109	catenin beta 1	Homo sapiens	44-56
32307979-6	2020	Subgroup analysis showed that the levels of beta-catenin, cyclinD1 and c-myc in the high-dose (>5muM) arsenic intervention group were lower than those in the control group, and the levels of beta-catenin and cyclinD1 in the high-dose (>5muM) arsenic intervention group were lower than those in the low-dose (<=5muM) arsenic intervention group (P<0.05, respectively).	Arsenic	102-109	cyclin D1	Homo sapiens	58-66
32307979-6	2020	Subgroup analysis showed that the levels of beta-catenin, cyclinD1 and c-myc in the high-dose (>5muM) arsenic intervention group were lower than those in the control group, and the levels of beta-catenin and cyclinD1 in the high-dose (>5muM) arsenic intervention group were lower than those in the low-dose (<=5muM) arsenic intervention group (P<0.05, respectively).	Arsenic	102-109	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	71-76
32307979-6	2020	Subgroup analysis showed that the levels of beta-catenin, cyclinD1 and c-myc in the high-dose (>5muM) arsenic intervention group were lower than those in the control group, and the levels of beta-catenin and cyclinD1 in the high-dose (>5muM) arsenic intervention group were lower than those in the low-dose (<=5muM) arsenic intervention group (P<0.05, respectively).	Arsenic	102-109	catenin beta 1	Homo sapiens	191-203
32307979-6	2020	Subgroup analysis showed that the levels of beta-catenin, cyclinD1 and c-myc in the high-dose (>5muM) arsenic intervention group were lower than those in the control group, and the levels of beta-catenin and cyclinD1 in the high-dose (>5muM) arsenic intervention group were lower than those in the low-dose (<=5muM) arsenic intervention group (P<0.05, respectively).	Arsenic	102-109	cyclin D1	Homo sapiens	208-216
32307979-7	2020	In addition, the regulation of arsenic on beta-catenin was dose-dependent in the range of arsenic concentration from 0muM to 7.5muM.	Arsenic	31-38	catenin beta 1	Homo sapiens	42-54
32307979-7	2020	In addition, the regulation of arsenic on beta-catenin was dose-dependent in the range of arsenic concentration from 0muM to 7.5muM.	Arsenic	90-97	catenin beta 1	Homo sapiens	42-54
32307979-8	2020	This study revealed that arsenic could up-regulate wnt/beta-catenin signaling pathway in normal cells and down-regulate it in cancer cells, and its effect was affected by time and dose.	Arsenic	25-32	Wnt family member 3A	Homo sapiens	51-54
32307979-8	2020	This study revealed that arsenic could up-regulate wnt/beta-catenin signaling pathway in normal cells and down-regulate it in cancer cells, and its effect was affected by time and dose.	Arsenic	25-32	catenin beta 1	Homo sapiens	55-67
32475297-6	2022	And in soil B (As 80 mg/kg and Cd 10 mg/kg), the Pd of As were more than 84.68%, the Pds of Cd were about 99%.	Arsenic	55-57	membrane metalloendopeptidase	Homo sapiens	31-36
31571030-0	2020	Oleic Acid Protects from Arsenic-Induced Cardiac Hypertrophy via AMPK/FoxO/NFATc3 Pathway.	Arsenic	25-32	nuclear factor of activated T-cells 3	Rattus norvegicus	75-81
32044640-0	2020	Arsenic induces dysfunctional autophagy via dual regulation of mTOR pathway and Beclin1-Vps34/PI3K complex in MLTC-1 cells.	Arsenic	0-7	mechanistic target of rapamycin kinase	Mus musculus	63-67
32044640-0	2020	Arsenic induces dysfunctional autophagy via dual regulation of mTOR pathway and Beclin1-Vps34/PI3K complex in MLTC-1 cells.	Arsenic	0-7	beclin 1, autophagy related	Mus musculus	80-87
32044640-0	2020	Arsenic induces dysfunctional autophagy via dual regulation of mTOR pathway and Beclin1-Vps34/PI3K complex in MLTC-1 cells.	Arsenic	0-7	phosphatidylinositol 3-kinase catalytic subunit type 3	Mus musculus	88-93
32044640-3	2020	Hence, this study aimed to explore the roles of mTOR and Beclin1-Vps34/PI3K complex during As-induced-toxicity using Rapamycin (mTOR inhibitor), Beclin1 siRNA and 3-methyladenine (3-MA, Vps34/PI3K inhibitor) in testicular stromal cells.	Arsenic	91-93	beclin 1, autophagy related	Mus musculus	57-64
32044640-3	2020	Hence, this study aimed to explore the roles of mTOR and Beclin1-Vps34/PI3K complex during As-induced-toxicity using Rapamycin (mTOR inhibitor), Beclin1 siRNA and 3-methyladenine (3-MA, Vps34/PI3K inhibitor) in testicular stromal cells.	Arsenic	91-93	phosphatidylinositol 3-kinase catalytic subunit type 3	Mus musculus	65-70
32044640-3	2020	Hence, this study aimed to explore the roles of mTOR and Beclin1-Vps34/PI3K complex during As-induced-toxicity using Rapamycin (mTOR inhibitor), Beclin1 siRNA and 3-methyladenine (3-MA, Vps34/PI3K inhibitor) in testicular stromal cells.	Arsenic	91-93	phosphatidylinositol 3-kinase catalytic subunit type 3	Mus musculus	186-191
32044640-6	2020	Meanwhile, arsenic treatment up-regulated autophagic markers including LC3, Atg7, Beclin1 and Vps34 expressions, mTOR downstream autophagy related genes and the Beclin1-Vps34/PI3K complex associated members.	Arsenic	11-18	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	71-74
32044640-6	2020	Meanwhile, arsenic treatment up-regulated autophagic markers including LC3, Atg7, Beclin1 and Vps34 expressions, mTOR downstream autophagy related genes and the Beclin1-Vps34/PI3K complex associated members.	Arsenic	11-18	autophagy related 7	Mus musculus	76-80
32044640-6	2020	Meanwhile, arsenic treatment up-regulated autophagic markers including LC3, Atg7, Beclin1 and Vps34 expressions, mTOR downstream autophagy related genes and the Beclin1-Vps34/PI3K complex associated members.	Arsenic	11-18	beclin 1, autophagy related	Mus musculus	82-89
32044640-6	2020	Meanwhile, arsenic treatment up-regulated autophagic markers including LC3, Atg7, Beclin1 and Vps34 expressions, mTOR downstream autophagy related genes and the Beclin1-Vps34/PI3K complex associated members.	Arsenic	11-18	phosphatidylinositol 3-kinase catalytic subunit type 3	Mus musculus	94-99
32044640-6	2020	Meanwhile, arsenic treatment up-regulated autophagic markers including LC3, Atg7, Beclin1 and Vps34 expressions, mTOR downstream autophagy related genes and the Beclin1-Vps34/PI3K complex associated members.	Arsenic	11-18	mechanistic target of rapamycin kinase	Mus musculus	113-117
32044640-6	2020	Meanwhile, arsenic treatment up-regulated autophagic markers including LC3, Atg7, Beclin1 and Vps34 expressions, mTOR downstream autophagy related genes and the Beclin1-Vps34/PI3K complex associated members.	Arsenic	11-18	beclin 1, autophagy related	Mus musculus	161-168
32044640-6	2020	Meanwhile, arsenic treatment up-regulated autophagic markers including LC3, Atg7, Beclin1 and Vps34 expressions, mTOR downstream autophagy related genes and the Beclin1-Vps34/PI3K complex associated members.	Arsenic	11-18	phosphatidylinositol 3-kinase catalytic subunit type 3	Mus musculus	169-174
32044640-7	2020	Furthermore, silencing of Beclin1, and inhibition of Vps34/PI3K and mTOR altered the arsenic-induced autophagosomes formation.	Arsenic	85-92	beclin 1, autophagy related	Mus musculus	26-33
32044640-7	2020	Furthermore, silencing of Beclin1, and inhibition of Vps34/PI3K and mTOR altered the arsenic-induced autophagosomes formation.	Arsenic	85-92	phosphatidylinositol 3-kinase catalytic subunit type 3	Mus musculus	53-58
32044640-7	2020	Furthermore, silencing of Beclin1, and inhibition of Vps34/PI3K and mTOR altered the arsenic-induced autophagosomes formation.	Arsenic	85-92	mechanistic target of rapamycin kinase	Mus musculus	68-72
32044640-8	2020	However, p62, the substrate protein of autophagy, was also up-regulated by arsenic administration independent on Beclin1-Vps34/PI3K complex.	Arsenic	75-82	nucleoporin 62	Mus musculus	9-12
32044640-8	2020	However, p62, the substrate protein of autophagy, was also up-regulated by arsenic administration independent on Beclin1-Vps34/PI3K complex.	Arsenic	75-82	beclin 1, autophagy related	Mus musculus	113-120
32044640-8	2020	However, p62, the substrate protein of autophagy, was also up-regulated by arsenic administration independent on Beclin1-Vps34/PI3K complex.	Arsenic	75-82	phosphatidylinositol 3-kinase catalytic subunit type 3	Mus musculus	121-126
32044640-9	2020	Altogether, our results revealed that arsenic exposure induced autophagosomes formation via regulation of the Beclin1-Vps34/PI3K complex and mTOR pathway; the blockage of autophagosomes degradation maybe due to impaired function of lysosomes.	Arsenic	38-45	beclin 1, autophagy related	Mus musculus	110-117
32044640-9	2020	Altogether, our results revealed that arsenic exposure induced autophagosomes formation via regulation of the Beclin1-Vps34/PI3K complex and mTOR pathway; the blockage of autophagosomes degradation maybe due to impaired function of lysosomes.	Arsenic	38-45	phosphatidylinositol 3-kinase catalytic subunit type 3	Mus musculus	118-123
32044640-9	2020	Altogether, our results revealed that arsenic exposure induced autophagosomes formation via regulation of the Beclin1-Vps34/PI3K complex and mTOR pathway; the blockage of autophagosomes degradation maybe due to impaired function of lysosomes.	Arsenic	38-45	mechanistic target of rapamycin kinase	Mus musculus	141-145
32503358-1	2020	Modification of a commercial iron oxide ion exchanger (Arsen Xnp) was carried out to enhance the removal of arsenic(V) ions.	Arsenic	108-115	ATRX chromatin remodeler	Homo sapiens	61-64
32503358-10	2020	It is worth noting that the process of removing arsenic on Arsen Xnp-La(III) is fast-equilibrium is reached after about 120 min.	Arsenic	48-55	ATRX chromatin remodeler	Homo sapiens	65-68
32318793-3	2020	The aim of this study was to explore whether polymorphisms of MTHFR and MTR influence arsenic methylation capacity and plasma folate and vitamin B12 levels and if these influences cause developmental delay in preschool children.	Arsenic	86-93	methylenetetrahydrofolate reductase	Homo sapiens	62-67
32318793-10	2020	The MTHFR C677T C/C genotype combined with high total urinary arsenic and poor arsenic methylation capacity indices significantly increased the OR of developmental delay in a dose-response manner.	Arsenic	62-69	methylenetetrahydrofolate reductase	Homo sapiens	4-9
32318793-10	2020	The MTHFR C677T C/C genotype combined with high total urinary arsenic and poor arsenic methylation capacity indices significantly increased the OR of developmental delay in a dose-response manner.	Arsenic	79-86	methylenetetrahydrofolate reductase	Homo sapiens	4-9
31571030-6	2020	Moreover, arsenic results in decreased activity of AMPK and FoxO1 along with increased NFATc3 expression, a known cardiac hypertrophy inducer.	Arsenic	10-17	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	51-55
31571030-6	2020	Moreover, arsenic results in decreased activity of AMPK and FoxO1 along with increased NFATc3 expression, a known cardiac hypertrophy inducer.	Arsenic	10-17	forkhead box O1	Rattus norvegicus	60-65
31571030-6	2020	Moreover, arsenic results in decreased activity of AMPK and FoxO1 along with increased NFATc3 expression, a known cardiac hypertrophy inducer.	Arsenic	10-17	nuclear factor of activated T-cells 3	Rattus norvegicus	87-93
31571030-7	2020	In addition, activation of AMPK and FoxO1 results in reduced NFATc3 expression causing attenuation of arsenic-induced cardiac hypertrophy in H9c2 cells.	Arsenic	102-109	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	27-31
31571030-7	2020	In addition, activation of AMPK and FoxO1 results in reduced NFATc3 expression causing attenuation of arsenic-induced cardiac hypertrophy in H9c2 cells.	Arsenic	102-109	forkhead box O1	Rattus norvegicus	36-41
31571030-7	2020	In addition, activation of AMPK and FoxO1 results in reduced NFATc3 expression causing attenuation of arsenic-induced cardiac hypertrophy in H9c2 cells.	Arsenic	102-109	nuclear factor of activated T-cells 3	Rattus norvegicus	61-67
31571030-9	2020	Our studies on protection from arsenic-induced cardiac hypertrophy by oleic acid in H9c2 cells shows that oleic acid activates AMPK along with increased nuclear FoxO1 localization, thereby reducing NFATc3 expression and attenuating cardiomyocyte hypertrophy.	Arsenic	31-38	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	127-131
31571030-9	2020	Our studies on protection from arsenic-induced cardiac hypertrophy by oleic acid in H9c2 cells shows that oleic acid activates AMPK along with increased nuclear FoxO1 localization, thereby reducing NFATc3 expression and attenuating cardiomyocyte hypertrophy.	Arsenic	31-38	forkhead box O1	Rattus norvegicus	161-166
31571030-9	2020	Our studies on protection from arsenic-induced cardiac hypertrophy by oleic acid in H9c2 cells shows that oleic acid activates AMPK along with increased nuclear FoxO1 localization, thereby reducing NFATc3 expression and attenuating cardiomyocyte hypertrophy.	Arsenic	31-38	nuclear factor of activated T-cells 3	Rattus norvegicus	198-204
32202357-0	2020	ArsH protects Pseudomonas putida from oxidative damage caused by exposure to arsenic.	Arsenic	77-84	arsenical resistance protein ArsH	Pseudomonas putida KT2440	0-4
32066052-8	2020	A concerning result showed that 6.77% of F concentrations larger than 1.5  mg L-1 and 11.46% of As concentrations larger than 10 mug L-1 based on the recommendation by WHO, respectively.	Arsenic	96-98	immunoglobulin kappa variable 1-16	Homo sapiens	133-136
32202357-4	2020	To examine whether the activity of ArsH was linked to a direct action on the arsenic compounds tested, arsH1 and arsH2 genes were expressed in Escherichia coli, which has an endogenous arsRBC operon but lacks an arsH ortholog.	Arsenic	77-84	arsenical resistance protein ArsH	Pseudomonas putida KT2440	35-39
32430121-5	2020	The experimental data also signified that exogenous application of chemical and green synthesized TiNPs conferred tolerance to As-induced oxidative injuries via perking-up the expressions of antioxidant genes and enzyme systems viz; superoxide dismutase and catalase.	Arsenic	127-129	catalase	Vigna radiata	258-266
32066060-0	2020	SFPQ is involved in regulating arsenic-induced oxidative stress by interacting with the miRNA-induced silencing complexes.	Arsenic	31-38	splicing factor proline and glutamine rich	Homo sapiens	0-4
32066060-4	2020	We previously found that the expression of SFPQ, a splicing factor, was positively associated with urinary arsenic concentration in an arsenic-exposed population, suggesting an oxidative stress regulatory role for SFPQ.	Arsenic	107-114	splicing factor proline and glutamine rich	Homo sapiens	43-47
32066060-4	2020	We previously found that the expression of SFPQ, a splicing factor, was positively associated with urinary arsenic concentration in an arsenic-exposed population, suggesting an oxidative stress regulatory role for SFPQ.	Arsenic	135-142	splicing factor proline and glutamine rich	Homo sapiens	43-47
32066060-4	2020	We previously found that the expression of SFPQ, a splicing factor, was positively associated with urinary arsenic concentration in an arsenic-exposed population, suggesting an oxidative stress regulatory role for SFPQ.	Arsenic	135-142	splicing factor proline and glutamine rich	Homo sapiens	214-218
32066060-13	2020	Taken together, we reveal that SFPQ responds to arsenic-induced oxidative stress by interacting with the miRISC.	Arsenic	48-55	splicing factor proline and glutamine rich	Homo sapiens	31-35
32120093-2	2020	Two arsenate reducing genes, arsC and arrA, were both amplified in an indigenous bacterium Bacillus XZM isolated from high arsenic aquifer sediments.	Arsenic	123-130	steroid sulfatase	Homo sapiens	29-33
32120095-0	2020	Fate of oxalic-acid-intervened arsenic during Fe(II)-induced transformation of As(V)-bearing jarosite.	Arsenic	31-38	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	79-84
32460744-8	2020	Our experimental studies using cultured cells with focus on the expression and activity levels of intracellular signal transduction molecules such as c-SRC, c-RET, and oncogenic RET showed risks for malignant transformation and/or progression arose from arsenic and barium.	Arsenic	254-261	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	150-155
32184170-0	2020	Exposure of low-concentration arsenic induces myotube atrophy by inhibiting an Akt signaling pathway.	Arsenic	30-37	AKT serine/threonine kinase 1	Homo sapiens	79-82
32184170-9	2020	These results suggest that arsenic is capable of inducing myotube atrophy by inhibiting an Akt signaling pathway.	Arsenic	27-34	AKT serine/threonine kinase 1	Homo sapiens	91-94
32548482-4	2020	The treatment of ACR included preparing the As-enriched solution via H2SO4 dissolution-neutralization of ACR at pH < 2, As(III) was oxidized by H2O2, and As(V) was immobilized as scorodite.	Arsenic	44-46	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	154-159
32548509-6	2020	Oxidation of As(III) to As(V) occurred on the MSF@BC800 composite surfaces.	Arsenic	13-15	proteoglycan 4	Homo sapiens	46-55
32179354-4	2020	Arsenic concentration range was 1.72-120.5 mug L-1, half of the samples being above the limit of 10 mug L-1 recommended by WHO for drinking water, with the corresponding risks for human health.	Arsenic	0-7	immunoglobulin kappa variable 1-16	Homo sapiens	47-50
32179354-4	2020	Arsenic concentration range was 1.72-120.5 mug L-1, half of the samples being above the limit of 10 mug L-1 recommended by WHO for drinking water, with the corresponding risks for human health.	Arsenic	0-7	immunoglobulin kappa variable 1-16	Homo sapiens	104-107
32179354-5	2020	Pearson correlations were performed, resulting in strong positive correlations for the pairs As/Cl-, As/F-, As/Na and As/V.	Arsenic	93-95	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	118-122
32179354-5	2020	Pearson correlations were performed, resulting in strong positive correlations for the pairs As/Cl-, As/F-, As/Na and As/V.	Arsenic	101-103	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	118-122
32179354-5	2020	Pearson correlations were performed, resulting in strong positive correlations for the pairs As/Cl-, As/F-, As/Na and As/V.	Arsenic	101-103	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	118-122
32460744-8	2020	Our experimental studies using cultured cells with focus on the expression and activity levels of intracellular signal transduction molecules such as c-SRC, c-RET, and oncogenic RET showed risks for malignant transformation and/or progression arose from arsenic and barium.	Arsenic	254-261	ret proto-oncogene	Homo sapiens	159-162
32502790-2	2020	Heavy metals such as Cadmium (Cd), Arsenic (As) and Lead (Pb) are associated with numerous disorders and are considered by some as an aetiological factor for the Chronic Kidney Disease (CKDu1) epidemic in Sri Lanka.	Arsenic	35-42	sorcin	Homo sapiens	205-208
32502790-2	2020	Heavy metals such as Cadmium (Cd), Arsenic (As) and Lead (Pb) are associated with numerous disorders and are considered by some as an aetiological factor for the Chronic Kidney Disease (CKDu1) epidemic in Sri Lanka.	Arsenic	44-46	sorcin	Homo sapiens	205-208
32045263-8	2020	Western blotting confirmed that arsenic significantly decreased TOMM20 in both BAT and WAT, a correlate of mitochondrial abundance; PGC1A, a master regulator of mitochondrial biogenesis; and, CPT1B, the rate limiting step of fatty acid oxidation (FAO).	Arsenic	32-39	translocase of outer mitochondrial membrane 20	Mus musculus	64-70
32499794-9	2020	We also found a significant variation of As and Hg accumulation in the wild-type and cad1-3.	Arsenic	41-43	cinnamyl-alcohol dehydrogenase	Arabidopsis thaliana	85-91
32113565-3	2020	This has led the European Union and other global organizations to reduce the maximum residue limit for the total arsenic up to 10 mug L-1 in water for human consumption.	Arsenic	113-120	immunoglobulin kappa variable 1-16	Homo sapiens	134-137
32113565-14	2020	Five of the analyzed samples had values close to, or superior to the maximum residue limit for the total of arsenic in water intended for human consumption (10 mug L-1).	Arsenic	108-115	immunoglobulin kappa variable 1-16	Homo sapiens	164-167
32113565-15	2020	The validated method CE-ESI(-)-MS for arsenic speciation was applied with success to the analysis of the weakly mineralized water sample (dry residue < 50 mg L-1) of both groundwater and bottled water.	Arsenic	38-45	immunoglobulin kappa variable 1-16	Homo sapiens	158-161
31972529-7	2020	During the sorption process, some ROX molecules were decomposed into inorganic arsenic and organic metabolites by the reactive oxygen species (ROS) generated during the early stages of the reaction.	Arsenic	79-86	MAX network transcriptional repressor	Homo sapiens	34-37
32045263-8	2020	Western blotting confirmed that arsenic significantly decreased TOMM20 in both BAT and WAT, a correlate of mitochondrial abundance; PGC1A, a master regulator of mitochondrial biogenesis; and, CPT1B, the rate limiting step of fatty acid oxidation (FAO).	Arsenic	32-39	carnitine palmitoyltransferase 1b, muscle	Mus musculus	192-197
32045263-8	2020	Western blotting confirmed that arsenic significantly decreased TOMM20 in both BAT and WAT, a correlate of mitochondrial abundance; PGC1A, a master regulator of mitochondrial biogenesis; and, CPT1B, the rate limiting step of fatty acid oxidation (FAO).	Arsenic	32-39	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	132-137
31995775-6	2020	First, the associations among miR-155, NF-AT1 with immunological dysfunction and arsenic-induced skin lesions and carcinogenesis were confirmed using these skin samples.	Arsenic	81-88	microRNA 155	Homo sapiens	30-37
31927375-7	2020	Interestingly, increased trend of inflammatory cytokines (TNF-alpha, IFN-gamma, IL-17) and depleted anti-inflammatory cytokines (IL-10) was observed in As exposed mice.	Arsenic	152-154	tumor necrosis factor	Mus musculus	58-67
31927375-7	2020	Interestingly, increased trend of inflammatory cytokines (TNF-alpha, IFN-gamma, IL-17) and depleted anti-inflammatory cytokines (IL-10) was observed in As exposed mice.	Arsenic	152-154	interferon gamma	Mus musculus	69-78
31927375-7	2020	Interestingly, increased trend of inflammatory cytokines (TNF-alpha, IFN-gamma, IL-17) and depleted anti-inflammatory cytokines (IL-10) was observed in As exposed mice.	Arsenic	152-154	interleukin 17A	Mus musculus	80-85
31927375-7	2020	Interestingly, increased trend of inflammatory cytokines (TNF-alpha, IFN-gamma, IL-17) and depleted anti-inflammatory cytokines (IL-10) was observed in As exposed mice.	Arsenic	152-154	interleukin 10	Mus musculus	129-134
32291614-2	2020	Arsenic (2.90 ng ml-1) and Se (1.41 ng ml-1) in water had the highest concentrations in the return flow drains (Hardy River and Xochimilco Lagoon, respectively).	Arsenic	0-7	interleukin 17F	Homo sapiens	17-21
32096287-2	2020	Settling impoundments containing coal combustion waste (CCW) enriched in trace elements such as arsenic (As), selenium (Se), and mercury (Hg) are often used by free-ranging migratory and resident waterfowl and represent potential sources for contaminant uptake.	Arsenic	96-103	squalene epoxidase	Homo sapiens	0-2
32096287-2	2020	Settling impoundments containing coal combustion waste (CCW) enriched in trace elements such as arsenic (As), selenium (Se), and mercury (Hg) are often used by free-ranging migratory and resident waterfowl and represent potential sources for contaminant uptake.	Arsenic	105-107	squalene epoxidase	Homo sapiens	0-2
32052323-5	2020	Crustal enrichment factors (EFcs) of trace elements (V, Cr, Ni, Zn, As, Se, Rb, Cd, Pb, and Bi) in PM1.1 in that called slight air pollution events were always higher than those in that called severe air pollution events and EFcs of Se were up to 2.5 x 104, while EFcs of Pb, Bi, and Cd were over 100.	Arsenic	68-70	transmembrane protein 11	Homo sapiens	99-102
31995775-7	2020	In the arsenic-exposed group, miR-155-5p, keratin 1(Krt1), keratin 10 (Krt10), and keratin 6c (Krt6c) were significantly increased in the skin (p < 0.05), while NF-AT1, interleukin-2 (IL-2), and interferon-gamma (IFN-gamma) were significantly decreased (p < 0.05).	Arsenic	7-14	keratin 1	Homo sapiens	42-51
31995775-7	2020	In the arsenic-exposed group, miR-155-5p, keratin 1(Krt1), keratin 10 (Krt10), and keratin 6c (Krt6c) were significantly increased in the skin (p < 0.05), while NF-AT1, interleukin-2 (IL-2), and interferon-gamma (IFN-gamma) were significantly decreased (p < 0.05).	Arsenic	7-14	keratin 1	Homo sapiens	52-56
31995775-7	2020	In the arsenic-exposed group, miR-155-5p, keratin 1(Krt1), keratin 10 (Krt10), and keratin 6c (Krt6c) were significantly increased in the skin (p < 0.05), while NF-AT1, interleukin-2 (IL-2), and interferon-gamma (IFN-gamma) were significantly decreased (p < 0.05).	Arsenic	7-14	keratin 10	Homo sapiens	59-69
31995775-7	2020	In the arsenic-exposed group, miR-155-5p, keratin 1(Krt1), keratin 10 (Krt10), and keratin 6c (Krt6c) were significantly increased in the skin (p < 0.05), while NF-AT1, interleukin-2 (IL-2), and interferon-gamma (IFN-gamma) were significantly decreased (p < 0.05).	Arsenic	7-14	keratin 10	Homo sapiens	71-76
31995775-7	2020	In the arsenic-exposed group, miR-155-5p, keratin 1(Krt1), keratin 10 (Krt10), and keratin 6c (Krt6c) were significantly increased in the skin (p < 0.05), while NF-AT1, interleukin-2 (IL-2), and interferon-gamma (IFN-gamma) were significantly decreased (p < 0.05).	Arsenic	7-14	keratin 6C	Homo sapiens	83-93
31995775-7	2020	In the arsenic-exposed group, miR-155-5p, keratin 1(Krt1), keratin 10 (Krt10), and keratin 6c (Krt6c) were significantly increased in the skin (p < 0.05), while NF-AT1, interleukin-2 (IL-2), and interferon-gamma (IFN-gamma) were significantly decreased (p < 0.05).	Arsenic	7-14	keratin 6C	Homo sapiens	95-100
31995775-7	2020	In the arsenic-exposed group, miR-155-5p, keratin 1(Krt1), keratin 10 (Krt10), and keratin 6c (Krt6c) were significantly increased in the skin (p < 0.05), while NF-AT1, interleukin-2 (IL-2), and interferon-gamma (IFN-gamma) were significantly decreased (p < 0.05).	Arsenic	7-14	nuclear factor of activated T cells 2	Homo sapiens	161-167
31995775-7	2020	In the arsenic-exposed group, miR-155-5p, keratin 1(Krt1), keratin 10 (Krt10), and keratin 6c (Krt6c) were significantly increased in the skin (p < 0.05), while NF-AT1, interleukin-2 (IL-2), and interferon-gamma (IFN-gamma) were significantly decreased (p < 0.05).	Arsenic	7-14	interleukin 2	Homo sapiens	169-182
31995775-7	2020	In the arsenic-exposed group, miR-155-5p, keratin 1(Krt1), keratin 10 (Krt10), and keratin 6c (Krt6c) were significantly increased in the skin (p < 0.05), while NF-AT1, interleukin-2 (IL-2), and interferon-gamma (IFN-gamma) were significantly decreased (p < 0.05).	Arsenic	7-14	interleukin 2	Homo sapiens	184-188
31995775-7	2020	In the arsenic-exposed group, miR-155-5p, keratin 1(Krt1), keratin 10 (Krt10), and keratin 6c (Krt6c) were significantly increased in the skin (p < 0.05), while NF-AT1, interleukin-2 (IL-2), and interferon-gamma (IFN-gamma) were significantly decreased (p < 0.05).	Arsenic	7-14	interferon gamma	Homo sapiens	195-211
31995775-7	2020	In the arsenic-exposed group, miR-155-5p, keratin 1(Krt1), keratin 10 (Krt10), and keratin 6c (Krt6c) were significantly increased in the skin (p < 0.05), while NF-AT1, interleukin-2 (IL-2), and interferon-gamma (IFN-gamma) were significantly decreased (p < 0.05).	Arsenic	7-14	interferon gamma	Homo sapiens	213-222
31995775-9	2020	In immortalized human keratinocytes, silencing and overexpression of NF-AT1 could alter the expression and secretion of immunological dysfunction indicators (IL-2 and IFN-gamma) that are induced by arsenic exposure (p < 0.05); however, miR-155-5p levels did not change significantly (p > 0.05).	Arsenic	198-205	nuclear factor of activated T cells 2	Homo sapiens	69-75
31995775-9	2020	In immortalized human keratinocytes, silencing and overexpression of NF-AT1 could alter the expression and secretion of immunological dysfunction indicators (IL-2 and IFN-gamma) that are induced by arsenic exposure (p < 0.05); however, miR-155-5p levels did not change significantly (p > 0.05).	Arsenic	198-205	interleukin 2	Homo sapiens	158-162
31995775-9	2020	In immortalized human keratinocytes, silencing and overexpression of NF-AT1 could alter the expression and secretion of immunological dysfunction indicators (IL-2 and IFN-gamma) that are induced by arsenic exposure (p < 0.05); however, miR-155-5p levels did not change significantly (p > 0.05).	Arsenic	198-205	interferon gamma	Homo sapiens	167-176
31995775-10	2020	The miR-155-5p mimic and inhibitor could regulate the NF-AT1-mediated immunological dysfunction caused by arsenic (p < 0.05).	Arsenic	106-113	microRNA 155	Homo sapiens	4-11
31995775-10	2020	The miR-155-5p mimic and inhibitor could regulate the NF-AT1-mediated immunological dysfunction caused by arsenic (p < 0.05).	Arsenic	106-113	nuclear factor of activated T cells 2	Homo sapiens	54-60
32313131-0	2020	Polymorphism of nucleotide binding domain-like receptor protein 3 (NLRP3) increases susceptibility of total urinary arsenic to renal cell carcinoma.	Arsenic	116-123	NLR family pyrin domain containing 3	Homo sapiens	67-72
34054136-11	2020	High NO3 - in groundwater may at the same time limit concentrations of As in groundwater to levels lower than they could have been by oxidizing both Fe(II) and As(III).	Arsenic	71-73	NBL1, DAN family BMP antagonist	Homo sapiens	5-8
32105321-0	2020	Retraction: "Ethanol Enhances Tumor Angiogenesis In Vitro Induced by Low-Dose Arsenic in Colon Cancer Cells Through Hypoxia-Inducible Factor 1 Alpha Pathway".	Arsenic	78-85	hypoxia inducible factor 1 subunit alpha	Homo sapiens	116-148
31885278-0	2020	The ability of arsenic metabolism affected the expression of lncRNA PANDAR, DNA damage, or DNA methylation in peripheral blood lymphocytes of laborers.	Arsenic	15-22	promoter of CDKN1A antisense DNA damage activated RNA	Homo sapiens	68-74
31885278-4	2020	Here, we investigated whether the ability of arsenic metabolism in individuals affected the expression of PANDAR, DNA damage, and DNA methylation.	Arsenic	45-52	promoter of CDKN1A antisense DNA damage activated RNA	Homo sapiens	106-112
31885278-6	2020	In our study, we demonstrated that arsenic exposure increased PANDAR expression and DNA damage among arsenic smelting plant laborers.	Arsenic	35-42	promoter of CDKN1A antisense DNA damage activated RNA	Homo sapiens	62-68
31885278-11	2020	These findings suggested arsenic metabolism ability and exposure affected the expression of PANDAR, DNA damage, and DNA methylation.	Arsenic	25-32	promoter of CDKN1A antisense DNA damage activated RNA	Homo sapiens	92-98
32201329-12	2020	The interference of RA signaling, and mucin gene expression may be important pathogenic factors in low-dose arsenic induced lung toxicity.	Arsenic	108-115	LOC100508689	Homo sapiens	38-43
32344290-1	2020	CAsE-PE cells are an arsenic-transformed, human prostate epithelial line containing oncogenic mutations in KRAS compared to immortalized, normal KRAS parent cells, RWPE-1.	Arsenic	21-28	KRAS proto-oncogene, GTPase	Homo sapiens	107-111
32200903-5	2020	Furthermore, the linear ranges for arsenic and copper were 0-100 mug L-1 and 0-250 mug L-1 with sensitivities of 0.101 muA (mug L-1)-1 and 0.121 muA (mug L-1)-1, respectively.	Arsenic	35-42	immunoglobulin kappa variable 1-16	Homo sapiens	69-72
32200903-5	2020	Furthermore, the linear ranges for arsenic and copper were 0-100 mug L-1 and 0-250 mug L-1 with sensitivities of 0.101 muA (mug L-1)-1 and 0.121 muA (mug L-1)-1, respectively.	Arsenic	35-42	immunoglobulin kappa variable 1-16	Homo sapiens	87-90
32313131-13	2020	This study is the first to identify the modified effects of NLRP3 risk alleles involved in the association between arsenic and RCC risk in a population with low arsenic exposure.	Arsenic	115-122	NLR family pyrin domain containing 3	Homo sapiens	60-65
32313131-13	2020	This study is the first to identify the modified effects of NLRP3 risk alleles involved in the association between arsenic and RCC risk in a population with low arsenic exposure.	Arsenic	161-168	NLR family pyrin domain containing 3	Homo sapiens	60-65
31831285-2	2020	Inorganic arsenic ions mainly occur in two oxidation states, As(V) and As(III), in the natural environment.	Arsenic	10-17	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	61-66
32068019-6	2020	In utero arsenic exposure produced global DNA hypomethylation and an array of gene-specific DNA methylation changes, including hypomethylation of Cyclin D1 and hypermethylation of Tp53.	Arsenic	9-16	cyclin D1	Mus musculus	146-155
32068019-6	2020	In utero arsenic exposure produced global DNA hypomethylation and an array of gene-specific DNA methylation changes, including hypomethylation of Cyclin D1 and hypermethylation of Tp53.	Arsenic	9-16	transformation related protein 53	Mus musculus	180-184
32112223-1	2020	Polymorphisms in arsenic (+ 3 oxidation state) methyltransferase (AS3MT) have been shown to be related to interindividual variations in arsenic metabolism and to influence adverse health effects in acute promyelocytic leukemia (APL) patients treated with arsenic trioxide (As2O3).	Arsenic	17-24	arsenite methyltransferase	Homo sapiens	66-71
32537408-0	2020	LncRNA UCA1 Antagonizes Arsenic-Induced Cell Cycle Arrest through Destabilizing EZH2 and Facilitating NFATc2 Expression.	Arsenic	24-31	urothelial cancer associated 1	Homo sapiens	7-11
32537408-0	2020	LncRNA UCA1 Antagonizes Arsenic-Induced Cell Cycle Arrest through Destabilizing EZH2 and Facilitating NFATc2 Expression.	Arsenic	24-31	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	80-84
32537408-0	2020	LncRNA UCA1 Antagonizes Arsenic-Induced Cell Cycle Arrest through Destabilizing EZH2 and Facilitating NFATc2 Expression.	Arsenic	24-31	nuclear factor of activated T cells 2	Homo sapiens	102-108
32537408-5	2020	The phosphorylation of EZH2 at the Thr-487 site by cyclin dependent kinase 1 (CDK1) is responsible for As-induced EZH2 protein degradation, and UCA1 enhances this process through increasing the interaction between CDK1 and EZH2.	Arsenic	103-105	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	23-27
32537408-5	2020	The phosphorylation of EZH2 at the Thr-487 site by cyclin dependent kinase 1 (CDK1) is responsible for As-induced EZH2 protein degradation, and UCA1 enhances this process through increasing the interaction between CDK1 and EZH2.	Arsenic	103-105	cyclin dependent kinase 1	Homo sapiens	51-76
32537408-5	2020	The phosphorylation of EZH2 at the Thr-487 site by cyclin dependent kinase 1 (CDK1) is responsible for As-induced EZH2 protein degradation, and UCA1 enhances this process through increasing the interaction between CDK1 and EZH2.	Arsenic	103-105	cyclin dependent kinase 1	Homo sapiens	78-82
32537408-5	2020	The phosphorylation of EZH2 at the Thr-487 site by cyclin dependent kinase 1 (CDK1) is responsible for As-induced EZH2 protein degradation, and UCA1 enhances this process through increasing the interaction between CDK1 and EZH2.	Arsenic	103-105	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	114-118
32537408-5	2020	The phosphorylation of EZH2 at the Thr-487 site by cyclin dependent kinase 1 (CDK1) is responsible for As-induced EZH2 protein degradation, and UCA1 enhances this process through increasing the interaction between CDK1 and EZH2.	Arsenic	103-105	urothelial cancer associated 1	Homo sapiens	144-148
32537408-5	2020	The phosphorylation of EZH2 at the Thr-487 site by cyclin dependent kinase 1 (CDK1) is responsible for As-induced EZH2 protein degradation, and UCA1 enhances this process through increasing the interaction between CDK1 and EZH2.	Arsenic	103-105	cyclin dependent kinase 1	Homo sapiens	214-218
32176848-0	2020	In Vitro Assessment of Arsenic Release and Transformation from As(V)-Sorbed Goethite and Jarosite: The Influence of Human Gut Microbiota.	Arsenic	23-30	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	63-68
32272684-5	2020	Arsenic concentration in urine was associated with all four CNR1 and LEP SNPs, while cadmium concentration in blood was affected by the VDR polymorphism.	Arsenic	0-7	cannabinoid receptor 1	Homo sapiens	60-64
32272684-5	2020	Arsenic concentration in urine was associated with all four CNR1 and LEP SNPs, while cadmium concentration in blood was affected by the VDR polymorphism.	Arsenic	0-7	leptin	Homo sapiens	69-72
32537408-5	2020	The phosphorylation of EZH2 at the Thr-487 site by cyclin dependent kinase 1 (CDK1) is responsible for As-induced EZH2 protein degradation, and UCA1 enhances this process through increasing the interaction between CDK1 and EZH2.	Arsenic	103-105	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	114-118
32537408-7	2020	In conclusion, the findings decipher a novel prosurvival signaling pathway underlying As toxicity from the perspective of epigenetic regulation: UCA1 facilitates the ubiquitination of EZH2 to upregulate NFATc2 and further antagonizes As-induced cell cycle arrest.	Arsenic	86-88	urothelial cancer associated 1	Homo sapiens	145-149
32537408-7	2020	In conclusion, the findings decipher a novel prosurvival signaling pathway underlying As toxicity from the perspective of epigenetic regulation: UCA1 facilitates the ubiquitination of EZH2 to upregulate NFATc2 and further antagonizes As-induced cell cycle arrest.	Arsenic	86-88	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	184-188
32537408-7	2020	In conclusion, the findings decipher a novel prosurvival signaling pathway underlying As toxicity from the perspective of epigenetic regulation: UCA1 facilitates the ubiquitination of EZH2 to upregulate NFATc2 and further antagonizes As-induced cell cycle arrest.	Arsenic	86-88	nuclear factor of activated T cells 2	Homo sapiens	203-209
32537408-7	2020	In conclusion, the findings decipher a novel prosurvival signaling pathway underlying As toxicity from the perspective of epigenetic regulation: UCA1 facilitates the ubiquitination of EZH2 to upregulate NFATc2 and further antagonizes As-induced cell cycle arrest.	Arsenic	234-236	urothelial cancer associated 1	Homo sapiens	145-149
32537408-7	2020	In conclusion, the findings decipher a novel prosurvival signaling pathway underlying As toxicity from the perspective of epigenetic regulation: UCA1 facilitates the ubiquitination of EZH2 to upregulate NFATc2 and further antagonizes As-induced cell cycle arrest.	Arsenic	234-236	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	184-188
32112223-0	2020	Polymorphisms in arsenic (+ 3 oxidation state) methyltransferase (AS3MT) predict the occurrence of hyperleukocytosis and arsenic metabolism in APL patients treated with As2O3.	Arsenic	17-24	arsenite methyltransferase	Homo sapiens	66-71
31119572-5	2020	Multivariate statistical analysis (principle component analysis) identifies two dominant components, PC1: As, Cr, Cu, Pb and Zn, as well as PC2: Ni, Co and total organic carbon.	Arsenic	106-108	polycystin 1, transient receptor potential channel interacting	Homo sapiens	101-104
31983004-3	2020	The initial pH value significantly influenced on the degradation of p-ASA and at the optimal pH (3.0), p-ASA (10 mg L-1) could be completely oxidized to As(V), NH4+, and plentiful phenolic compounds such as phenol and p-hydroquinone via the cleavage of C-N and C-As bonds within 60 min in pure water.	Arsenic	153-155	L1 cell adhesion molecule	Homo sapiens	116-119
32059145-0	2020	Associations of maternal arsenic exposure with adult fasting glucose and insulin resistance in the Strong Heart Study and Strong Heart Family Study.	Arsenic	25-32	insulin	Homo sapiens	73-80
32062438-0	2020	Arsenic and benzo[a]pyrene co-exposure acts synergistically in inducing cancer stem cell-like property and tumorigenesis by epigenetically down-regulating SOCS3 expression.	Arsenic	0-7	suppressor of cytokine signaling 3	Mus musculus	155-160
32062438-17	2020	Mechanistic studies revealed that arsenic and BaP co-exposure does not produce more BPDE-DNA adducts than BaP exposure alone; but acts synergistically in activating aryl hydrocarbon receptor (AhR) to up-regulate the expression of a histone H3 lysine 9 methyltransferase SUV39H1 and increase the level of suppressive H3 lysine 9 dimethylation (H3K9me2), which down-regulates the expression of tumor suppressive SOCS3 leading to enhanced activation of Akt and Erk1/2 to promote cell transformation, CSC-like property and tumorigenesis.	Arsenic	34-41	aryl-hydrocarbon receptor	Mus musculus	165-190
32062438-17	2020	Mechanistic studies revealed that arsenic and BaP co-exposure does not produce more BPDE-DNA adducts than BaP exposure alone; but acts synergistically in activating aryl hydrocarbon receptor (AhR) to up-regulate the expression of a histone H3 lysine 9 methyltransferase SUV39H1 and increase the level of suppressive H3 lysine 9 dimethylation (H3K9me2), which down-regulates the expression of tumor suppressive SOCS3 leading to enhanced activation of Akt and Erk1/2 to promote cell transformation, CSC-like property and tumorigenesis.	Arsenic	34-41	aryl-hydrocarbon receptor	Mus musculus	192-195
32062438-17	2020	Mechanistic studies revealed that arsenic and BaP co-exposure does not produce more BPDE-DNA adducts than BaP exposure alone; but acts synergistically in activating aryl hydrocarbon receptor (AhR) to up-regulate the expression of a histone H3 lysine 9 methyltransferase SUV39H1 and increase the level of suppressive H3 lysine 9 dimethylation (H3K9me2), which down-regulates the expression of tumor suppressive SOCS3 leading to enhanced activation of Akt and Erk1/2 to promote cell transformation, CSC-like property and tumorigenesis.	Arsenic	34-41	suppressor of variegation 3-9 1	Mus musculus	270-277
32062438-17	2020	Mechanistic studies revealed that arsenic and BaP co-exposure does not produce more BPDE-DNA adducts than BaP exposure alone; but acts synergistically in activating aryl hydrocarbon receptor (AhR) to up-regulate the expression of a histone H3 lysine 9 methyltransferase SUV39H1 and increase the level of suppressive H3 lysine 9 dimethylation (H3K9me2), which down-regulates the expression of tumor suppressive SOCS3 leading to enhanced activation of Akt and Erk1/2 to promote cell transformation, CSC-like property and tumorigenesis.	Arsenic	34-41	suppressor of cytokine signaling 3	Mus musculus	410-415
32004920-3	2020	The results showed that the prevalence of methylated hOGG1 and variation genotype (326 Ser/Cys & 326 Cys/Cys) were increased with raised levels of urinary arsenic in arsenicosis subjects.	Arsenic	155-162	8-oxoguanine DNA glycosylase	Homo sapiens	53-58
31983004-5	2020	Furthermore, high-level dissolved organic matters (DOM) (> 2 mg C L-1) exhibited strong interference with both the oxidation of p-ASA and adsorption of arsenic, but the interference could be eliminated by increasing the SiO2-nZVI dosage or adding H2O2.	Arsenic	152-159	adhesion G protein-coupled receptor L1	Homo sapiens	64-69
32062438-17	2020	Mechanistic studies revealed that arsenic and BaP co-exposure does not produce more BPDE-DNA adducts than BaP exposure alone; but acts synergistically in activating aryl hydrocarbon receptor (AhR) to up-regulate the expression of a histone H3 lysine 9 methyltransferase SUV39H1 and increase the level of suppressive H3 lysine 9 dimethylation (H3K9me2), which down-regulates the expression of tumor suppressive SOCS3 leading to enhanced activation of Akt and Erk1/2 to promote cell transformation, CSC-like property and tumorigenesis.	Arsenic	34-41	thymoma viral proto-oncogene 1	Mus musculus	450-453
32062438-17	2020	Mechanistic studies revealed that arsenic and BaP co-exposure does not produce more BPDE-DNA adducts than BaP exposure alone; but acts synergistically in activating aryl hydrocarbon receptor (AhR) to up-regulate the expression of a histone H3 lysine 9 methyltransferase SUV39H1 and increase the level of suppressive H3 lysine 9 dimethylation (H3K9me2), which down-regulates the expression of tumor suppressive SOCS3 leading to enhanced activation of Akt and Erk1/2 to promote cell transformation, CSC-like property and tumorigenesis.	Arsenic	34-41	mitogen-activated protein kinase 3	Mus musculus	458-464
31935557-9	2020	Compared to the expression levels of IRS-1, AKT and GLUT4, GLUT2 might be more vulnerable to arsenic exposure and lead to the abnormalities of glucose metabolism in HepG2 cells.	Arsenic	93-100	solute carrier family 2 member 2	Homo sapiens	59-64
32297149-10	2020	Overall, our findings demonstrate a novel mechanism by which SNHG1 overexpression protects the function of HUVECs, which may delay the progression of AS.	Arsenic	150-152	small nucleolar RNA host gene 1	Homo sapiens	61-66
32215187-9	2020	Recent evidence using in vitro models has shown that mutations in the B2 domain of the PML protein, mediate arsenic resistance.	Arsenic	108-115	PML nuclear body scaffold	Homo sapiens	87-90
32018205-0	2020	Cord blood DNA methylation of DNMT3A mediates the association between in utero arsenic exposure and birth outcomes: Results from a prospective birth cohort in Bangladesh.	Arsenic	79-86	DNA methyltransferase 3 alpha	Homo sapiens	30-36
32018205-7	2020	RESULTS: In an adjusted SEM including birth weight and gestational age, maternal toenail As levels were associated with DNMT3A DNAm (B = 0.40; 95% CI: 0.15, 0.66) and gestational age (B = -0.19 weeks; 95% CI: 0.36, -0.03).	Arsenic	89-91	DNA methyltransferase 3 alpha	Homo sapiens	120-126
32018205-9	2020	There was an indirect effect of As on gestational age mediated through DNMT3A DNAm (B = -0.04; 95% CI: 0.08, -0.01), and there were indirect effects of maternal toenail As levels on birth weight through pathways including gestational age (B = -14.4 g; 95% CI: 29.2, -1.9), DNMT3A DNAm and gestational age (B = -3.1 g; 95% CI: 6.6, -0.8), and maternal weight gain and gestational age (B = -5.1 g; 95% CI: 9.6, -1.5).	Arsenic	32-34	DNA methyltransferase 3 alpha	Homo sapiens	71-77
32018205-12	2020	In utero arsenic exposure was associated with greater methylation of CpGs in DNMT3A which partially mediated associations between prenatal As exposure and birth outcomes.	Arsenic	9-16	DNA methyltransferase 3 alpha	Homo sapiens	77-83
32018205-12	2020	In utero arsenic exposure was associated with greater methylation of CpGs in DNMT3A which partially mediated associations between prenatal As exposure and birth outcomes.	Arsenic	139-141	DNA methyltransferase 3 alpha	Homo sapiens	77-83
31499585-7	2020	We further confirmed that down-expression of the PML (promyelocytic leukemia) protein was sustained for at least 75 days after exposure of bladder cells to As.	Arsenic	156-158	PML nuclear body scaffold	Homo sapiens	49-52
31499585-7	2020	We further confirmed that down-expression of the PML (promyelocytic leukemia) protein was sustained for at least 75 days after exposure of bladder cells to As.	Arsenic	156-158	PML nuclear body scaffold	Homo sapiens	54-76
32188015-0	2020	Overexpression of NRF1-742 or NRF1-772 Reduces Arsenic-Induced Cytotoxicity and Apoptosis in Human HaCaT Keratinocytes.	Arsenic	47-54	nuclear respiratory factor 1	Homo sapiens	18-22
32188015-0	2020	Overexpression of NRF1-742 or NRF1-772 Reduces Arsenic-Induced Cytotoxicity and Apoptosis in Human HaCaT Keratinocytes.	Arsenic	47-54	nuclear respiratory factor 1	Homo sapiens	30-34
32188015-4	2020	We previously demonstrated that the long isoforms of NRF1 (i.e., NRF1-742, NRF1-761 and NRF1-772) are involved in the protection of human keratinocytes from acute arsenic cytotoxicity by enhancing the cellular antioxidant response.	Arsenic	163-170	nuclear respiratory factor 1	Homo sapiens	53-57
32188015-4	2020	We previously demonstrated that the long isoforms of NRF1 (i.e., NRF1-742, NRF1-761 and NRF1-772) are involved in the protection of human keratinocytes from acute arsenic cytotoxicity by enhancing the cellular antioxidant response.	Arsenic	163-170	nuclear respiratory factor 1	Homo sapiens	65-69
32188015-4	2020	We previously demonstrated that the long isoforms of NRF1 (i.e., NRF1-742, NRF1-761 and NRF1-772) are involved in the protection of human keratinocytes from acute arsenic cytotoxicity by enhancing the cellular antioxidant response.	Arsenic	163-170	nuclear respiratory factor 1	Homo sapiens	65-69
32188015-4	2020	We previously demonstrated that the long isoforms of NRF1 (i.e., NRF1-742, NRF1-761 and NRF1-772) are involved in the protection of human keratinocytes from acute arsenic cytotoxicity by enhancing the cellular antioxidant response.	Arsenic	163-170	nuclear respiratory factor 1	Homo sapiens	65-69
32188015-5	2020	The aim of the current study was to investigate the roles of NRF1-742 and NRF1-772 in the arsenic-induced antioxidant response and cytotoxicity.	Arsenic	90-97	nuclear respiratory factor 1	Homo sapiens	61-65
32188015-5	2020	The aim of the current study was to investigate the roles of NRF1-742 and NRF1-772 in the arsenic-induced antioxidant response and cytotoxicity.	Arsenic	90-97	nuclear respiratory factor 1	Homo sapiens	74-78
32188015-6	2020	We found that overexpression of NRF1-742 or NRF1-772 in human HaCaT keratinocytes decreased susceptibility to arsenic-induced apoptosis and cytotoxicity.	Arsenic	110-117	nuclear respiratory factor 1	Homo sapiens	32-36
32188015-6	2020	We found that overexpression of NRF1-742 or NRF1-772 in human HaCaT keratinocytes decreased susceptibility to arsenic-induced apoptosis and cytotoxicity.	Arsenic	110-117	nuclear respiratory factor 1	Homo sapiens	44-48
32188015-11	2020	Overall, overexpression of NRF1-742 and NRF1-772 protected HaCaT cells from arsenic-induced cytotoxicity, mainly through translational modifications and the promotion of antioxidant gene expression.	Arsenic	76-83	nuclear respiratory factor 1	Homo sapiens	27-31
32188015-11	2020	Overall, overexpression of NRF1-742 and NRF1-772 protected HaCaT cells from arsenic-induced cytotoxicity, mainly through translational modifications and the promotion of antioxidant gene expression.	Arsenic	76-83	nuclear respiratory factor 1	Homo sapiens	40-44
32043994-4	2020	The microwave-assisted extraction in the presence of NaCl (10 g L-1) and NaOH (10 g L-1) was used for the isolation of arsenic species from the Lewatit FO 36 resin gel.	Arsenic	119-126	immunoglobulin kappa variable 1-16	Homo sapiens	64-67
32043994-4	2020	The microwave-assisted extraction in the presence of NaCl (10 g L-1) and NaOH (10 g L-1) was used for the isolation of arsenic species from the Lewatit FO 36 resin gel.	Arsenic	119-126	immunoglobulin kappa variable 1-16	Homo sapiens	84-87
31787315-1	2020	In East and Southeast Asia, the health of over 100 million people is threatened by the consumption of groundwater containing high concentrations of arsenic (>10 mug L-1), which is released from sediments through reductive dissolution of arsenic-bearing iron/manganese oxides.	Arsenic	148-155	L1 cell adhesion molecule	Homo sapiens	165-168
32107508-0	2020	Electronic structure, doping effect and topological signature in realistic intermetallics Li3-xNaxM (x = 3, 2, 1, 0; M = N, P, As, Sb, Bi).	Arsenic	127-129	cytochrome P450 family 4 subfamily F member 22	Homo sapiens	90-93
32014540-0	2020	Arsenic induces platelet shape change through altering focal adhesion kinase-mediated actin dynamics, contributing to increased platelet reactivity.	Arsenic	0-7	protein tyrosine kinase 2	Homo sapiens	55-76
32014540-7	2020	Arsenic-induced platelet shape change appeared to increase the sensitivity to thrombin and ADP-induced aggregation.	Arsenic	0-7	coagulation factor II, thrombin	Homo sapiens	78-86
32014540-9	2020	Taken together, we demonstrated that arsenic induces cytoskeletal changes and shape changes of platelets through FAK-mediated alteration of actin dynamics, which renders platelets reactive to activating stimuli, ultimately contributing to increased thrombosis.	Arsenic	37-44	protein tyrosine kinase 2	Homo sapiens	113-116
31058984-9	2020	Hypermethylation of FAM19A4 and/or microRNA124-2 was found in 69 (95%) AS and 19(26%) CS.	Arsenic	71-73	TAFA chemokine like family member 4	Homo sapiens	20-27
31907961-0	2020	Venetoclax and arsenic showed synergistic anti-leukemia activity in vitro and in vivo for acute myeloid leukemia with the NPM1 mutation.	Arsenic	15-22	nucleophosmin 1	Homo sapiens	122-126
32226544-0	2020	Nrf2 and HIF1alpha converge to arsenic-induced metabolic reprogramming and the formation of the cancer stem-like cells.	Arsenic	31-38	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
32226544-0	2020	Nrf2 and HIF1alpha converge to arsenic-induced metabolic reprogramming and the formation of the cancer stem-like cells.	Arsenic	31-38	hypoxia inducible factor 1 subunit alpha	Homo sapiens	9-18
31669990-0	2020	Autophagic-CTSB-inflammasome axis modulates hepatic stellate cells activation in arsenic-induced liver fibrosis.	Arsenic	81-88	cathepsin B	Rattus norvegicus	11-15
31896471-5	2020	Moreover, As or/and Cu treatment significantly increased the MDA content and NOS activity, and simultaneously resulted in reductions in CAT and AHR activities.	Arsenic	10-12	aryl hydrocarbon receptor 1 alpha	Gallus gallus	144-147
31916164-7	2020	The factorial analysis shows that the iNOS, TNOS, and AChE present synergistic effects on Pb, As, and DOP.	Arsenic	94-96	acetylcholinesterase	Mus musculus	54-58
30852732-5	2020	In addition, the concentration of arsenic decreased from 3583 to 49.1 mg L-1.	Arsenic	34-41	immunoglobulin kappa variable 1-16	Homo sapiens	73-76
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Arsenic	103-105	caspase 3	Mus musculus	66-75
31916164-16	2020	PC2 accounted for 23.81% of the total variance with high loadings on B-As, L-As, K-As, and K-SOD, whereas PC3 showed high loadings on B-Pb, L-Pb, and K-Pb and accounted for 19.04% of the total variance.	Arsenic	71-73	minisatellite 6 hypermutable 3	Mus musculus	0-3
31916164-16	2020	PC2 accounted for 23.81% of the total variance with high loadings on B-As, L-As, K-As, and K-SOD, whereas PC3 showed high loadings on B-Pb, L-Pb, and K-Pb and accounted for 19.04% of the total variance.	Arsenic	77-79	minisatellite 6 hypermutable 3	Mus musculus	0-3
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Arsenic	103-105	BCL2-associated X protein	Mus musculus	80-83
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Arsenic	126-128	caspase 3	Mus musculus	66-75
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Arsenic	126-128	BCL2-associated X protein	Mus musculus	80-83
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Arsenic	126-128	caspase 3	Mus musculus	66-75
31916164-10	2020	Compared with that of the control group, the expression levels of caspase-3 and Bax expression in Pb + As, DOP-H, Pb + DOP-H, As + DOP-H, and Pb + As + DOP-H groups were significantly increased in the hippocampus.	Arsenic	126-128	BCL2-associated X protein	Mus musculus	80-83
31518804-1	2020	The oxidation of trivalent arsenic (As(III)) to pentavalent arsenic (As(V)) is a common pretreatment to remove As(III) from the aqueous phase.	Arsenic	27-34	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	69-74
32000108-7	2020	Results showed that Cd and As differently modulate these activities, however, catalase activity was inhibited by both.	Arsenic	27-29	catalase 2	Arabidopsis thaliana	78-86
31892094-10	2020	The content of arsenic in five kinds of natural water samples ranged from 34 ng L-1 to 2.3 mug L-1.	Arsenic	15-22	L1 cell adhesion molecule	Homo sapiens	80-90
32539644-0	2020	Association of arsenic-related AS3MT gene and antioxidant SOD2 gene expression in industrial workers occupationally exposed to arsenic.	Arsenic	15-22	arsenite methyltransferase	Homo sapiens	31-36
32539644-0	2020	Association of arsenic-related AS3MT gene and antioxidant SOD2 gene expression in industrial workers occupationally exposed to arsenic.	Arsenic	127-134	arsenite methyltransferase	Homo sapiens	31-36
32539644-0	2020	Association of arsenic-related AS3MT gene and antioxidant SOD2 gene expression in industrial workers occupationally exposed to arsenic.	Arsenic	127-134	superoxide dismutase 2	Homo sapiens	58-62
32539644-10	2020	This study suggests that decreased AS3MT and SOD2 expression levels may lead to bioaccumulation of As in the body accompanied by increased oxidative stress ultimately inducing DNA damage.	Arsenic	99-101	arsenite methyltransferase	Homo sapiens	35-40
32539644-10	2020	This study suggests that decreased AS3MT and SOD2 expression levels may lead to bioaccumulation of As in the body accompanied by increased oxidative stress ultimately inducing DNA damage.	Arsenic	99-101	superoxide dismutase 2	Homo sapiens	45-49
31927192-8	2020	Alterations in inflammatory biomarkers (CC16, SP-A, MMP-9, and MMP-9/TIMP-1) were significantly associated with As-induced lung function impairment.	Arsenic	112-114	secretoglobin family 1A member 1	Homo sapiens	40-44
31927192-8	2020	Alterations in inflammatory biomarkers (CC16, SP-A, MMP-9, and MMP-9/TIMP-1) were significantly associated with As-induced lung function impairment.	Arsenic	112-114	surfactant protein A1	Homo sapiens	46-50
31927192-8	2020	Alterations in inflammatory biomarkers (CC16, SP-A, MMP-9, and MMP-9/TIMP-1) were significantly associated with As-induced lung function impairment.	Arsenic	112-114	matrix metallopeptidase 9	Homo sapiens	52-57
31927192-8	2020	Alterations in inflammatory biomarkers (CC16, SP-A, MMP-9, and MMP-9/TIMP-1) were significantly associated with As-induced lung function impairment.	Arsenic	112-114	matrix metallopeptidase 9	Homo sapiens	63-68
31927192-8	2020	Alterations in inflammatory biomarkers (CC16, SP-A, MMP-9, and MMP-9/TIMP-1) were significantly associated with As-induced lung function impairment.	Arsenic	112-114	TIMP metallopeptidase inhibitor 1	Homo sapiens	69-75
32025894-0	2020	Estimation of arsenic background concentration in stream sediments in Zia-Abad area (NW Iran).	Arsenic	14-21	hydroxysteroid 17-beta dehydrogenase 10	Homo sapiens	74-78
31518804-1	2020	The oxidation of trivalent arsenic (As(III)) to pentavalent arsenic (As(V)) is a common pretreatment to remove As(III) from the aqueous phase.	Arsenic	60-67	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	69-74
31518804-6	2020	The composite material effectively converted As(III) to As(V) under the light, and the total arsenic concentration decreased in the aqueous phase via the adsorption of As(V).	Arsenic	93-100	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	168-173
31546213-0	2020	Targeting the miR-122/PKM2 autophagy axis relieves arsenic stress.	Arsenic	51-58	microRNA 122	Homo sapiens	14-21
31546213-0	2020	Targeting the miR-122/PKM2 autophagy axis relieves arsenic stress.	Arsenic	51-58	pyruvate kinase M1/2	Homo sapiens	22-26
31546213-6	2020	Under arsenic stress, overexpression of miR-122 significantly induced cell protective autophagy, characterized by lipidation of LC3-II and a corresponding consumption of p62.	Arsenic	6-13	microRNA 122	Homo sapiens	40-47
31786496-4	2020	Obtained results demonstrated that co-exposure of D-pinitol with arsenic increases cell viability, decreases DNA damage and protects PC12 cells from arsenic-induced cytotoxicity by increasing glutathione (GSH) level and glutathione reductase (GR).	Arsenic	65-72	glutathione-disulfide reductase	Rattus norvegicus	220-241
31726603-1	2020	The transport behavior of arsenic (As(V)) loaded by ferric humate (HA-Fe) colloid, denoted as HA-Fe/As(V), moving in a saturated quartz sand column, was tested in the laboratory under varying pH values, ionic strengths, and HA and Fe(III) content.	Arsenic	26-33	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	35-40
31726603-1	2020	The transport behavior of arsenic (As(V)) loaded by ferric humate (HA-Fe) colloid, denoted as HA-Fe/As(V), moving in a saturated quartz sand column, was tested in the laboratory under varying pH values, ionic strengths, and HA and Fe(III) content.	Arsenic	26-33	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	100-105
31372863-0	2020	Serum matrix metalloproteinase-9 in children exposed to arsenic from playground dust at elementary schools in Hermosillo, Sonora, Mexico.	Arsenic	56-63	matrix metallopeptidase 9	Homo sapiens	6-32
31372863-1	2020	Arsenic exposure in adults has been associated with increased serum matrix metalloproteinase-9 (MMP-9), a biomarker which is associated with chronic respiratory disease, lung inflammation, cardiovascular disease and cancer.	Arsenic	0-7	matrix metallopeptidase 9	Homo sapiens	68-94
31372863-1	2020	Arsenic exposure in adults has been associated with increased serum matrix metalloproteinase-9 (MMP-9), a biomarker which is associated with chronic respiratory disease, lung inflammation, cardiovascular disease and cancer.	Arsenic	0-7	matrix metallopeptidase 9	Homo sapiens	96-101
31372863-2	2020	The objective of this study was to evaluate the association between serum MMP-9 levels in children, urinary arsenic, arsenic chronic daily intake (CDI) and arsenic exposure from playground dust.	Arsenic	108-115	matrix metallopeptidase 9	Homo sapiens	74-79
31372863-2	2020	The objective of this study was to evaluate the association between serum MMP-9 levels in children, urinary arsenic, arsenic chronic daily intake (CDI) and arsenic exposure from playground dust.	Arsenic	117-124	matrix metallopeptidase 9	Homo sapiens	74-79
31372863-2	2020	The objective of this study was to evaluate the association between serum MMP-9 levels in children, urinary arsenic, arsenic chronic daily intake (CDI) and arsenic exposure from playground dust.	Arsenic	117-124	matrix metallopeptidase 9	Homo sapiens	74-79
31372863-9	2020	Arsenic concentration in playground dust was positively associated with serum MMP-9 levels in crude analyses and after adjustment (P < 0.01), MMP-9 and CDI were positively associated only after adjustment (P < 0.01), and no association was found between MMP-9 and urinary arsenic.	Arsenic	0-7	matrix metallopeptidase 9	Homo sapiens	78-83
31372863-10	2020	In conclusion, our study showed an association in children between serum MMP-9 levels and playground dust arsenic concentrations.	Arsenic	106-113	matrix metallopeptidase 9	Homo sapiens	73-78
31605998-3	2020	The results showed that the mRNA expression levels of LC3, LC3I, LC3II, Beclin-1, ULK1, Atg13 and Atg14 were significantly increased with a concomitant decrease in mTOR and Bcl-2 up on individual exposure to As and F rather than in combined (As + F) exposure.	Arsenic	208-210	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	54-57
31759742-4	2020	The soluble arsenic in the soils shows significant positive and negative correlations with environmental SO42-/TOC/pH/PO43-, and Fe/Mn, respectively.	Arsenic	12-19	rhomboid 5 homolog 2	Homo sapiens	111-117
31759742-9	2020	Total arsenic, TOC, NO3- and pH are the key environmental factors that indirectly controlled the mobilization and release of arsenic via influencing the structures of the microbial communities in the soils.	Arsenic	125-132	rhomboid 5 homolog 2	Homo sapiens	15-18
31759742-9	2020	Total arsenic, TOC, NO3- and pH are the key environmental factors that indirectly controlled the mobilization and release of arsenic via influencing the structures of the microbial communities in the soils.	Arsenic	125-132	NBL1, DAN family BMP antagonist	Homo sapiens	20-23
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	AKT serine/threonine kinase 1	Rattus norvegicus	235-238
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	AKT serine/threonine kinase 1	Rattus norvegicus	242-245
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	247-252
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	NFE2 like bZIP transcription factor 2	Rattus norvegicus	254-258
31786496-4	2020	Obtained results demonstrated that co-exposure of D-pinitol with arsenic increases cell viability, decreases DNA damage and protects PC12 cells from arsenic-induced cytotoxicity by increasing glutathione (GSH) level and glutathione reductase (GR).	Arsenic	65-72	glutathione-disulfide reductase	Rattus norvegicus	243-245
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	mitogen activated protein kinase 3	Rattus norvegicus	260-264
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	85-92	mechanistic target of rapamycin kinase	Rattus norvegicus	221-225
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	glutathione-disulfide reductase	Rattus norvegicus	266-268
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	Bcl2-like 1	Rattus norvegicus	270-275
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	85-92	mechanistic target of rapamycin kinase	Rattus norvegicus	229-233
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	314-317
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	85-92	AKT serine/threonine kinase 1	Rattus norvegicus	235-238
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	BCL2 associated X, apoptosis regulator	Rattus norvegicus	319-322
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	annexin A3	Rattus norvegicus	338-341
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	85-92	AKT serine/threonine kinase 1	Rattus norvegicus	242-245
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	85-92	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	247-252
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	85-92	NFE2 like bZIP transcription factor 2	Rattus norvegicus	254-258
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	85-92	mitogen activated protein kinase 3	Rattus norvegicus	260-264
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	85-92	glutathione-disulfide reductase	Rattus norvegicus	266-268
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	85-92	Bcl2-like 1	Rattus norvegicus	270-275
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	85-92	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	314-317
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	85-92	BCL2 associated X, apoptosis regulator	Rattus norvegicus	319-322
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	85-92	annexin A3	Rattus norvegicus	338-341
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	mechanistic target of rapamycin kinase	Rattus norvegicus	229-233
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	AKT serine/threonine kinase 1	Rattus norvegicus	235-238
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	AKT serine/threonine kinase 1	Rattus norvegicus	242-245
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	247-252
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	NFE2 like bZIP transcription factor 2	Rattus norvegicus	254-258
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	mitogen activated protein kinase 3	Rattus norvegicus	260-264
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	glutathione-disulfide reductase	Rattus norvegicus	266-268
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	Bcl2-like 1	Rattus norvegicus	270-275
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	314-317
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	BCL2 associated X, apoptosis regulator	Rattus norvegicus	319-322
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	annexin A3	Rattus norvegicus	338-341
31786496-5	2020	Protein expression of western blot analysis showed that co-exposure of D-pinitol and arsenic significantly inhibited arsenic-induced autophagy which further suppressed apoptosis through up-regulation of survival factors; mTOR, p-mTOR, Akt, p-Akt, NF-kB, Nrf2, ERK1, GR, Bcl-x and down-regulation of death factors; p53, Bax, cytochrome c, LC3, although arsenic regulated those factors negatively.	Arsenic	117-124	mechanistic target of rapamycin kinase	Rattus norvegicus	229-233
31450204-7	2020	The release of arsenic was promoted to a different extent with additive chlorine, mainly caused by the AsCl3 (g) formation.	Arsenic	15-22	achaete-scute family bHLH transcription factor 3	Homo sapiens	103-108
31726340-3	2020	This study developed a new class of polyacrylamide-dispersed magnetite (PAM-MAG) nanoparticles and tested the effectiveness for simultaneous control of soil erosion and arsenic leaching from a model soil.	Arsenic	169-176	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	72-75
31710903-9	2020	Availability of As, Cu, Cd and Zn affected dehydrogenase, catalase and urease activities.	Arsenic	16-18	catalase	Homo sapiens	58-66
31466007-0	2020	Arsenic-induced immunomodulatory effects disorient the survival-death interface by stabilizing the Hsp90/Beclin1 interaction.	Arsenic	0-7	heat shock protein 86, pseudogene 1	Mus musculus	99-104
31419065-6	2020	In 22 (23.4%) patients, strong positive AT1R-AA (defined as &gt;40 U/mL) were detected, of whom 16 (72.7%) patients lost their grafts.	Arsenic	57-61	angiotensin II receptor type 1	Homo sapiens	40-44
31712840-8	2020	The mRNA and protein levels of NR1, NR2A and NR2B in the hippocampus of mice were down-regulated by arsenic.	Arsenic	100-107	glutamate receptor, ionotropic, NMDA2A (epsilon 1)	Mus musculus	36-40
31712840-8	2020	The mRNA and protein levels of NR1, NR2A and NR2B in the hippocampus of mice were down-regulated by arsenic.	Arsenic	100-107	glutamate receptor, ionotropic, NMDA2B (epsilon 2)	Mus musculus	45-49
31734849-8	2020	Arsenic induced the phosphorylation of p38 and c-Jun N-terminal kinase (JNK) proteins.	Arsenic	0-7	mitogen-activated protein kinase 14	Homo sapiens	39-42
31734849-8	2020	Arsenic induced the phosphorylation of p38 and c-Jun N-terminal kinase (JNK) proteins.	Arsenic	0-7	mitogen-activated protein kinase 8	Homo sapiens	47-70
31734849-8	2020	Arsenic induced the phosphorylation of p38 and c-Jun N-terminal kinase (JNK) proteins.	Arsenic	0-7	mitogen-activated protein kinase 8	Homo sapiens	72-75
31734849-9	2020	The inhibitors of p38 and JNK significantly reversed the arsenic-induced chondrocyte senescence.	Arsenic	57-64	mitogen-activated protein kinase 14	Homo sapiens	18-21
31734849-9	2020	The inhibitors of p38 and JNK significantly reversed the arsenic-induced chondrocyte senescence.	Arsenic	57-64	mitogen-activated protein kinase 8	Homo sapiens	26-29
31734849-10	2020	Arsenic could also trigger the induction of GATA4-NF-kappaB signaling and senescence-associated secretory phenotype (SASP) by increasing IL-1alpha, IL-1beta, TGF-beta, TNF-alpha, CCL2, PAI-1, and MMP13 mRNA expression.	Arsenic	0-7	GATA binding protein 4	Homo sapiens	44-49
31734849-10	2020	Arsenic could also trigger the induction of GATA4-NF-kappaB signaling and senescence-associated secretory phenotype (SASP) by increasing IL-1alpha, IL-1beta, TGF-beta, TNF-alpha, CCL2, PAI-1, and MMP13 mRNA expression.	Arsenic	0-7	thioredoxin	Homo sapiens	117-121
31734849-10	2020	Arsenic could also trigger the induction of GATA4-NF-kappaB signaling and senescence-associated secretory phenotype (SASP) by increasing IL-1alpha, IL-1beta, TGF-beta, TNF-alpha, CCL2, PAI-1, and MMP13 mRNA expression.	Arsenic	0-7	interleukin 1 alpha	Homo sapiens	137-146
31734849-10	2020	Arsenic could also trigger the induction of GATA4-NF-kappaB signaling and senescence-associated secretory phenotype (SASP) by increasing IL-1alpha, IL-1beta, TGF-beta, TNF-alpha, CCL2, PAI-1, and MMP13 mRNA expression.	Arsenic	0-7	interleukin 1 beta	Homo sapiens	148-156
31734849-10	2020	Arsenic could also trigger the induction of GATA4-NF-kappaB signaling and senescence-associated secretory phenotype (SASP) by increasing IL-1alpha, IL-1beta, TGF-beta, TNF-alpha, CCL2, PAI-1, and MMP13 mRNA expression.	Arsenic	0-7	tumor necrosis factor	Homo sapiens	168-177
31734849-10	2020	Arsenic could also trigger the induction of GATA4-NF-kappaB signaling and senescence-associated secretory phenotype (SASP) by increasing IL-1alpha, IL-1beta, TGF-beta, TNF-alpha, CCL2, PAI-1, and MMP13 mRNA expression.	Arsenic	0-7	C-C motif chemokine ligand 2	Homo sapiens	179-183
31734849-10	2020	Arsenic could also trigger the induction of GATA4-NF-kappaB signaling and senescence-associated secretory phenotype (SASP) by increasing IL-1alpha, IL-1beta, TGF-beta, TNF-alpha, CCL2, PAI-1, and MMP13 mRNA expression.	Arsenic	0-7	serpin family E member 1	Homo sapiens	185-190
31734849-10	2020	Arsenic could also trigger the induction of GATA4-NF-kappaB signaling and senescence-associated secretory phenotype (SASP) by increasing IL-1alpha, IL-1beta, TGF-beta, TNF-alpha, CCL2, PAI-1, and MMP13 mRNA expression.	Arsenic	0-7	matrix metallopeptidase 13	Homo sapiens	196-201
31524614-4	2020	The arsenic concentration of the water spring was 1481.9 mug L-1, and as the distance from the water spring increased, the arsenic concentration in the overlying water, pore-water and surface sediments decreased.	Arsenic	4-11	immunoglobulin kappa variable 1-16	Homo sapiens	61-64
31524615-3	2020	The procedure to remove arsenic was optimized as follows: initial H+ concentration of 5 mol L-1, Cu-to-As molar ratio of 8, Cl-to-As molar ratio of 10, a reaction temperature of 60  C, copper powder particle size of 68-24 mum, and a stirring speed of 300 r min-1.	Arsenic	24-31	CD59 molecule (CD59 blood group)	Homo sapiens	257-262
31466007-0	2020	Arsenic-induced immunomodulatory effects disorient the survival-death interface by stabilizing the Hsp90/Beclin1 interaction.	Arsenic	0-7	beclin 1, autophagy related	Mus musculus	105-112
31466007-5	2020	In addition, pioneering evidences established the ability of arsenic to induce an up regulation of Hsp90, eventually resulting in stabilization of its client protein Beclin-1, an important autophagy-initiating factor.	Arsenic	61-68	heat shock protein 86, pseudogene 1	Mus musculus	99-104
31466007-5	2020	In addition, pioneering evidences established the ability of arsenic to induce an up regulation of Hsp90, eventually resulting in stabilization of its client protein Beclin-1, an important autophagy-initiating factor.	Arsenic	61-68	beclin 1, autophagy related	Mus musculus	166-174
31472347-7	2020	Furthermore, the structure of Chromatoid Body (CB) which presents a typical nebulous shape in round spermatids after spermatogenesis arrested, and the mRNA expression levels of gene TDRD1, TDRD6 and TDRD7 related to CB were changed by arsenic.	Arsenic	235-242	tudor domain containing 1	Mus musculus	182-187
31526998-10	2020	The electrostatic potential of most areas of the PSMP surface was positive, and the H atom on the carboxyl group exhibited a very large positive potential (+56.6 kcal/mol), and thus attracted arsenic oxyanions.	Arsenic	192-199	microseminoprotein, prostate associated	Homo sapiens	49-53
31526998-13	2020	This work provides a clear theoretical basis for the behavior of the PSMP as an arsenic carrier and might aid to improve the environmental toxicity of arsenic.	Arsenic	80-87	microseminoprotein, prostate associated	Homo sapiens	69-73
31526998-13	2020	This work provides a clear theoretical basis for the behavior of the PSMP as an arsenic carrier and might aid to improve the environmental toxicity of arsenic.	Arsenic	151-158	microseminoprotein, prostate associated	Homo sapiens	69-73
31472347-7	2020	Furthermore, the structure of Chromatoid Body (CB) which presents a typical nebulous shape in round spermatids after spermatogenesis arrested, and the mRNA expression levels of gene TDRD1, TDRD6 and TDRD7 related to CB were changed by arsenic.	Arsenic	235-242	tudor domain containing 6	Mus musculus	189-194
31472347-7	2020	Furthermore, the structure of Chromatoid Body (CB) which presents a typical nebulous shape in round spermatids after spermatogenesis arrested, and the mRNA expression levels of gene TDRD1, TDRD6 and TDRD7 related to CB were changed by arsenic.	Arsenic	235-242	tudor domain containing 7	Mus musculus	199-204
31472347-10	2020	H4, HMG2 and PGK2 are regulated by DDX25 which interacts with CRM1 and may play a vital role in spermatogenesis disorder induced by As exposure, which maybe provides one of the underlying mechanisms for As-induced male reproductive toxicity.	Arsenic	132-134	high mobility group box 2	Mus musculus	4-8
31472347-10	2020	H4, HMG2 and PGK2 are regulated by DDX25 which interacts with CRM1 and may play a vital role in spermatogenesis disorder induced by As exposure, which maybe provides one of the underlying mechanisms for As-induced male reproductive toxicity.	Arsenic	132-134	phosphoglycerate kinase 2	Mus musculus	13-17
31472347-10	2020	H4, HMG2 and PGK2 are regulated by DDX25 which interacts with CRM1 and may play a vital role in spermatogenesis disorder induced by As exposure, which maybe provides one of the underlying mechanisms for As-induced male reproductive toxicity.	Arsenic	132-134	DEAD box helicase 25	Mus musculus	35-40
31472347-10	2020	H4, HMG2 and PGK2 are regulated by DDX25 which interacts with CRM1 and may play a vital role in spermatogenesis disorder induced by As exposure, which maybe provides one of the underlying mechanisms for As-induced male reproductive toxicity.	Arsenic	132-134	exportin 1	Mus musculus	62-66
30208742-7	2020	The levels of circulating TNF-alpha, homocysteine (Hcy), uterine-IL-6, and liver metallothionein (MT-1) were significantly elevated in arsenic treated rats.	Arsenic	135-142	tumor necrosis factor	Rattus norvegicus	26-35
30208742-7	2020	The levels of circulating TNF-alpha, homocysteine (Hcy), uterine-IL-6, and liver metallothionein (MT-1) were significantly elevated in arsenic treated rats.	Arsenic	135-142	interleukin 6	Rattus norvegicus	65-69
30208742-7	2020	The levels of circulating TNF-alpha, homocysteine (Hcy), uterine-IL-6, and liver metallothionein (MT-1) were significantly elevated in arsenic treated rats.	Arsenic	135-142	metallothionein 1	Rattus norvegicus	98-102
31845089-8	2019	The arsenic species in (spiked) SCC-7 cell samples were analyzed by the online system with adequate recoveries (89-110%).	Arsenic	4-11	colon tumor susceptibility 7	Mus musculus	32-37
31775542-0	2020	miR-191 is involved in renal dysfunction in arsenic-exposed populations by regulating inflammatory response caused by arsenic from burning arsenic-contaminated coal.	Arsenic	44-51	microRNA 191	Homo sapiens	0-7
31775542-0	2020	miR-191 is involved in renal dysfunction in arsenic-exposed populations by regulating inflammatory response caused by arsenic from burning arsenic-contaminated coal.	Arsenic	118-125	microRNA 191	Homo sapiens	0-7
31775542-0	2020	miR-191 is involved in renal dysfunction in arsenic-exposed populations by regulating inflammatory response caused by arsenic from burning arsenic-contaminated coal.	Arsenic	118-125	microRNA 191	Homo sapiens	0-7
31775542-4	2020	The results clearly show the alteration of miR-191 expression was significantly associated with arsenic-induced renal dysfunction.	Arsenic	96-103	microRNA 191	Homo sapiens	43-50
31775542-6	2020	In other words, miR-191 is involved in renal dysfunction in exposed populations by regulating inflammatory response caused by coal-burning arsenic.	Arsenic	139-146	microRNA 191	Homo sapiens	16-23
33211914-13	2020	In the liver, DAT knockout led to an increase in the content of As, Cd, Co, and Cs and a decrease in Fe; in the kidneys - to an increase in the levels of Pb, As, Cd and Se, in the brain - an increase in the content of most of the studied trace elements, including Pb, As, Cs, Al and Cu.	Arsenic	64-66	solute carrier family 6 member 3	Rattus norvegicus	14-17
33211914-13	2020	In the liver, DAT knockout led to an increase in the content of As, Cd, Co, and Cs and a decrease in Fe; in the kidneys - to an increase in the levels of Pb, As, Cd and Se, in the brain - an increase in the content of most of the studied trace elements, including Pb, As, Cs, Al and Cu.	Arsenic	158-160	solute carrier family 6 member 3	Rattus norvegicus	14-17
33211914-13	2020	In the liver, DAT knockout led to an increase in the content of As, Cd, Co, and Cs and a decrease in Fe; in the kidneys - to an increase in the levels of Pb, As, Cd and Se, in the brain - an increase in the content of most of the studied trace elements, including Pb, As, Cs, Al and Cu.	Arsenic	158-160	solute carrier family 6 member 3	Rattus norvegicus	14-17
31960388-4	2020	Meanwhile, we demonstrate that arsenic stress dedifferentiates CD61+ BEAS-2B cells into CSC-like CD61- cells featured with noncanonical epithelial-mesenchymal transition (EMT), enhanced chemoresistance, and metastasis.	Arsenic	31-38	integrin subunit beta 3	Homo sapiens	63-67
31960388-4	2020	Meanwhile, we demonstrate that arsenic stress dedifferentiates CD61+ BEAS-2B cells into CSC-like CD61- cells featured with noncanonical epithelial-mesenchymal transition (EMT), enhanced chemoresistance, and metastasis.	Arsenic	31-38	integrin subunit beta 3	Homo sapiens	97-101
31960388-5	2020	Finally, we show that oncogene c-Myc expression is associated with arsenic-induced tumor initiation and progression.	Arsenic	67-74	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	31-36
31929802-0	2019	An Exposure Assessment of Arsenic and Other Trace Elements in Ha Nam Province, Northern Vietnam.	Arsenic	26-33	SH3 and cysteine rich domain 3	Homo sapiens	65-68
31542663-5	2019	It is shown that increase of heavy metals concentration (Cd, Pb, Zn, Sb, Co, Ni, Se, Mn) and As in the lakes compared to temporary ponds can be explained by anthropogenic impact including previous human activity in the oasis in late 1970th - early 1990th.	Arsenic	93-95	cAMP responsive element binding protein 3 like 1	Homo sapiens	219-224
31670356-4	2019	In this study, we used APL cell line NB4 or P/R and PML over-expressed 293T cells as well as HeLa cells to reveal the solubility change of P/R and PML by arsenic exposure, and further determined the fate of these insoluble proteins after the removal of arsenic.	Arsenic	154-161	PML nuclear body scaffold	Homo sapiens	147-150
31670356-5	2019	Here, for the first time, we found that arsenic induced P/R or PML protein solubility change is an irreversible process.	Arsenic	40-47	PML nuclear body scaffold	Homo sapiens	63-66
31670356-6	2019	Once arsenic induces a P/R or PML protein solubility change, these insoluble proteins could be degraded by the proteasomal pathway even without continuous arsenic treatment.	Arsenic	5-12	PML nuclear body scaffold	Homo sapiens	30-33
31670356-7	2019	However, PML and P/R proteins can be newly synthesized after the removal of arsenic, suggesting that great caution should be taken in the clinical therapy of APL patients before ending arsenic treatment.	Arsenic	76-83	PML nuclear body scaffold	Homo sapiens	9-12
31670356-7	2019	However, PML and P/R proteins can be newly synthesized after the removal of arsenic, suggesting that great caution should be taken in the clinical therapy of APL patients before ending arsenic treatment.	Arsenic	185-192	PML nuclear body scaffold	Homo sapiens	9-12
31542844-5	2019	Arsenic exposure (0, 50 or 500 ppb exposures) significantly decreased cell proliferation, and increased mRNA levels of genes involved in stress response (Mt1, Mt2, Hmox1) and DNA damage (p53, Ogg1).	Arsenic	0-7	metallothionein 1	Rattus norvegicus	154-157
31542844-5	2019	Arsenic exposure (0, 50 or 500 ppb exposures) significantly decreased cell proliferation, and increased mRNA levels of genes involved in stress response (Mt1, Mt2, Hmox1) and DNA damage (p53, Ogg1).	Arsenic	0-7	metallothionein 2A	Rattus norvegicus	159-162
31542844-5	2019	Arsenic exposure (0, 50 or 500 ppb exposures) significantly decreased cell proliferation, and increased mRNA levels of genes involved in stress response (Mt1, Mt2, Hmox1) and DNA damage (p53, Ogg1).	Arsenic	0-7	heme oxygenase 1	Rattus norvegicus	164-169
31542844-5	2019	Arsenic exposure (0, 50 or 500 ppb exposures) significantly decreased cell proliferation, and increased mRNA levels of genes involved in stress response (Mt1, Mt2, Hmox1) and DNA damage (p53, Ogg1).	Arsenic	0-7	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	187-190
31542844-5	2019	Arsenic exposure (0, 50 or 500 ppb exposures) significantly decreased cell proliferation, and increased mRNA levels of genes involved in stress response (Mt1, Mt2, Hmox1) and DNA damage (p53, Ogg1).	Arsenic	0-7	8-oxoguanine DNA glycosylase	Rattus norvegicus	192-196
31542844-6	2019	When co-exposed to both zinc deficiency and arsenic, zinc deficiency attenuated this response to arsenic, decreasing the expression of Mt1, Hmox1, and Ogg1, and significantly increasing DNA double-strand breaks 2.9-fold.	Arsenic	44-51	metallothionein 1	Rattus norvegicus	135-138
31542844-6	2019	When co-exposed to both zinc deficiency and arsenic, zinc deficiency attenuated this response to arsenic, decreasing the expression of Mt1, Hmox1, and Ogg1, and significantly increasing DNA double-strand breaks 2.9-fold.	Arsenic	44-51	heme oxygenase 1	Rattus norvegicus	140-145
31542844-6	2019	When co-exposed to both zinc deficiency and arsenic, zinc deficiency attenuated this response to arsenic, decreasing the expression of Mt1, Hmox1, and Ogg1, and significantly increasing DNA double-strand breaks 2.9-fold.	Arsenic	44-51	8-oxoguanine DNA glycosylase	Rattus norvegicus	151-155
31142157-5	2019	Emissions of arsenic, lead, and mercury were found to be significantly associated with the incidence of estrogen receptor (ER)-positive breast cancer.	Arsenic	13-20	estrogen receptor 1	Homo sapiens	104-121
31142157-5	2019	Emissions of arsenic, lead, and mercury were found to be significantly associated with the incidence of estrogen receptor (ER)-positive breast cancer.	Arsenic	13-20	estrogen receptor 1	Homo sapiens	123-125
31822296-18	2019	Our results link arsenic compound to the regulation of DNA damage control and RAG1 expression as a mechanism for its cytotoxic effect.	Arsenic	17-24	recombination activating 1	Homo sapiens	78-82
31703545-8	2019	Multivariable linear regression analyses revealed that maternal (p &lt; 0.01) and child (p = 0.02) U-As were positively associated with plasma LL-37 levels.	Arsenic	101-103	cathelicidin antimicrobial peptide	Homo sapiens	143-148
31703545-10	2019	In addition, U-As levels were seen to be negatively associated with PBMC formation of fractalkine and IL-7, and positively associated with that for IL-13, IL-17 and MIP-1alpha.	Arsenic	15-17	interleukin 7	Homo sapiens	102-106
31703545-10	2019	In addition, U-As levels were seen to be negatively associated with PBMC formation of fractalkine and IL-7, and positively associated with that for IL-13, IL-17 and MIP-1alpha.	Arsenic	15-17	interleukin 13	Homo sapiens	148-153
31703545-10	2019	In addition, U-As levels were seen to be negatively associated with PBMC formation of fractalkine and IL-7, and positively associated with that for IL-13, IL-17 and MIP-1alpha.	Arsenic	15-17	interleukin 17A	Homo sapiens	155-160
31703545-10	2019	In addition, U-As levels were seen to be negatively associated with PBMC formation of fractalkine and IL-7, and positively associated with that for IL-13, IL-17 and MIP-1alpha.	Arsenic	15-17	C-C motif chemokine ligand 3	Homo sapiens	165-175
31752878-11	2019	Genes showing the most significant associations with arsenic exposure in females were LEMD1 and UPK3B (fold changes 2.51 and 2.48), and in males, FIBIN and RANBP3L (fold changes 0.14 and 0.15).	Arsenic	53-60	LEM domain containing 1	Homo sapiens	86-91
31209470-11	2019	CONCLUSION: SNP rs75862629, by modulating simultaneously the expression of ERAP1 and ERAP2, provides protection from AS in HLA-B27-positive subjects in Sardinia.	Arsenic	117-119	endoplasmic reticulum aminopeptidase 1	Homo sapiens	75-80
31209470-11	2019	CONCLUSION: SNP rs75862629, by modulating simultaneously the expression of ERAP1 and ERAP2, provides protection from AS in HLA-B27-positive subjects in Sardinia.	Arsenic	117-119	endoplasmic reticulum aminopeptidase 2	Homo sapiens	85-90
31209470-11	2019	CONCLUSION: SNP rs75862629, by modulating simultaneously the expression of ERAP1 and ERAP2, provides protection from AS in HLA-B27-positive subjects in Sardinia.	Arsenic	117-119	major histocompatibility complex, class I, B	Homo sapiens	123-130
31669778-2	2019	Moreover, reformation of PML-NBs in APL by arsenic is considered as one of the important step for APL treatment.	Arsenic	43-50	PML nuclear body scaffold	Homo sapiens	25-28
31758285-5	2019	Rodent offspring exposed to arsenic in utero also showed elevated insulin resistance in the 4 studies evaluating it as well as microRNA changes related to glycemic control in 2 studies.	Arsenic	28-35	insulin	Homo sapiens	66-73
31758285-10	2019	Experimental animal studies and human evidence on the association of in utero arsenic exposure with alterations in gene expression pathways related to diabetes in newborns, support the potential role of early-life arsenic exposure in diabetes development, possibly through increased insulin resistance.	Arsenic	78-85	insulin	Homo sapiens	283-290
31758285-10	2019	Experimental animal studies and human evidence on the association of in utero arsenic exposure with alterations in gene expression pathways related to diabetes in newborns, support the potential role of early-life arsenic exposure in diabetes development, possibly through increased insulin resistance.	Arsenic	214-221	insulin	Homo sapiens	283-290
31540997-2	2019	Differently from the AIRAP worm homologue, aip-1, a gene known to play an important role in preserving animal lifespan and buffering arsenic-induced proteotoxicity, mammals have a second, constitutively expressed, AIRAP-like gene (AIRAPL), recently implicated in myeloid transformation.	Arsenic	133-140	zinc finger AN1-type containing 2A	Homo sapiens	21-26
31540997-2	2019	Differently from the AIRAP worm homologue, aip-1, a gene known to play an important role in preserving animal lifespan and buffering arsenic-induced proteotoxicity, mammals have a second, constitutively expressed, AIRAP-like gene (AIRAPL), recently implicated in myeloid transformation.	Arsenic	133-140	baculoviral IAP repeat containing 3	Homo sapiens	43-48
31772124-1	2019	The yeast stress-activated protein kinase Hog1 is best known for its role in mediating the response to osmotic stress, but it is also activated by various mechanistically distinct environmental stressors, including heat shock, endoplasmic reticulum stress, and arsenic.	Arsenic	261-268	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	42-46
31772124-3	2019	Here, we identified a mode of Hog1 function whereby Hog1 senses arsenic through a direct physical interaction that requires three conserved cysteine residues located adjacent to the catalytic loop.	Arsenic	64-71	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	30-34
31772124-3	2019	Here, we identified a mode of Hog1 function whereby Hog1 senses arsenic through a direct physical interaction that requires three conserved cysteine residues located adjacent to the catalytic loop.	Arsenic	64-71	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	52-56
31772124-4	2019	These residues were essential for Hog1-mediated protection against arsenic, were dispensable for the response to osmotic stress, and promoted the nuclear localization of Hog1 upon exposure of cells to arsenic.	Arsenic	67-74	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	34-38
31772124-4	2019	These residues were essential for Hog1-mediated protection against arsenic, were dispensable for the response to osmotic stress, and promoted the nuclear localization of Hog1 upon exposure of cells to arsenic.	Arsenic	201-208	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	34-38
31772124-4	2019	These residues were essential for Hog1-mediated protection against arsenic, were dispensable for the response to osmotic stress, and promoted the nuclear localization of Hog1 upon exposure of cells to arsenic.	Arsenic	201-208	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	170-174
31772124-5	2019	Hog1 promoted arsenic detoxification by stimulating phosphorylation of the transcription factor Yap8, promoting Yap8 nuclear localization, and stimulating the transcription of the only known Yap8 targets, ARR2 and ARR3, both of which encode proteins that promote arsenic efflux.	Arsenic	14-21	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	0-4
31772124-5	2019	Hog1 promoted arsenic detoxification by stimulating phosphorylation of the transcription factor Yap8, promoting Yap8 nuclear localization, and stimulating the transcription of the only known Yap8 targets, ARR2 and ARR3, both of which encode proteins that promote arsenic efflux.	Arsenic	263-270	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	0-4
31772124-6	2019	The related human kinases ERK1 and ERK2 also bound to arsenic in vitro, suggesting that this may be a conserved feature of some members of the mitogen-activated protein kinase (MAPK) family.	Arsenic	54-61	mitogen-activated protein kinase 3	Homo sapiens	26-30
31772124-6	2019	The related human kinases ERK1 and ERK2 also bound to arsenic in vitro, suggesting that this may be a conserved feature of some members of the mitogen-activated protein kinase (MAPK) family.	Arsenic	54-61	mitogen-activated protein kinase 1	Homo sapiens	35-39
31772124-6	2019	The related human kinases ERK1 and ERK2 also bound to arsenic in vitro, suggesting that this may be a conserved feature of some members of the mitogen-activated protein kinase (MAPK) family.	Arsenic	54-61	mitogen-activated protein kinase 3	Homo sapiens	177-181
31752878-11	2019	Genes showing the most significant associations with arsenic exposure in females were LEMD1 and UPK3B (fold changes 2.51 and 2.48), and in males, FIBIN and RANBP3L (fold changes 0.14 and 0.15).	Arsenic	53-60	uroplakin 3B	Homo sapiens	96-101
31752878-11	2019	Genes showing the most significant associations with arsenic exposure in females were LEMD1 and UPK3B (fold changes 2.51 and 2.48), and in males, FIBIN and RANBP3L (fold changes 0.14 and 0.15).	Arsenic	53-60	fin bud initiation factor homolog	Homo sapiens	146-151
31752878-11	2019	Genes showing the most significant associations with arsenic exposure in females were LEMD1 and UPK3B (fold changes 2.51 and 2.48), and in males, FIBIN and RANBP3L (fold changes 0.14 and 0.15).	Arsenic	53-60	RAN binding protein 3 like	Homo sapiens	156-163
31445708-0	2019	Botrysphin D attenuates arsenic-induced oxidative stress in human lung epithelial cells via activating Nrf2/ARE signaling pathways.	Arsenic	24-31	NFE2 like bZIP transcription factor 2	Homo sapiens	103-107
31729457-0	2019	Retraction Note: Oncogenic transformation of human lung bronchial epithelial cells induced by arsenic involves ROS-dependent activation of STAT3-miR-21-PDCD4 mechanism.	Arsenic	94-101	signal transducer and activator of transcription 3	Homo sapiens	139-144
31729457-0	2019	Retraction Note: Oncogenic transformation of human lung bronchial epithelial cells induced by arsenic involves ROS-dependent activation of STAT3-miR-21-PDCD4 mechanism.	Arsenic	94-101	microRNA 21	Homo sapiens	145-151
31729457-0	2019	Retraction Note: Oncogenic transformation of human lung bronchial epithelial cells induced by arsenic involves ROS-dependent activation of STAT3-miR-21-PDCD4 mechanism.	Arsenic	94-101	programmed cell death 4	Homo sapiens	152-157
31250475-8	2019	In mediobasal hypothalamus, AS or SPS each increased CRH mRNA levels without an additive effect.	Arsenic	28-30	corticotropin releasing hormone	Rattus norvegicus	53-56
31473390-0	2019	Selenium abates reproductive dysfunction via attenuation of biometal accumulation, oxido-inflammatory stress and caspase-3 activation in male rats exposed to arsenic.	Arsenic	158-165	caspase 3	Rattus norvegicus	113-122
31473390-9	2019	Taken together, selenium or DPDS improved reproductive function in arsenic-exposed rats via suppression of inflammation, oxidative stress and caspase-3 activation in rats.	Arsenic	67-74	caspase 3	Rattus norvegicus	142-151
31471020-0	2019	LncRNA PU.1 AS regulates arsenic-induced lipid metabolism through EZH2/Sirt6/SREBP-1c pathway.	Arsenic	25-32	enhancer of zeste 2 polycomb repressive complex 2 subunit	Mus musculus	66-70
31471020-0	2019	LncRNA PU.1 AS regulates arsenic-induced lipid metabolism through EZH2/Sirt6/SREBP-1c pathway.	Arsenic	25-32	sirtuin 6	Mus musculus	71-76
31471020-0	2019	LncRNA PU.1 AS regulates arsenic-induced lipid metabolism through EZH2/Sirt6/SREBP-1c pathway.	Arsenic	25-32	sterol regulatory element binding transcription factor 1	Mus musculus	77-85
31616884-1	2019	Histone H3.3 was identified as an arsenic-binding protein of S-dimethylarsino-glutathione (ZIO-101, darinaparsin ) in leukemia cells by GE-ICP-MS.	Arsenic	34-41	H3.3 histone B	Homo sapiens	0-12
31616884-3	2019	We further validate histone H3.3 as a vital target for ZIO-101, offering new information on the mode of action of arsenic-based anticancer agents.	Arsenic	114-121	H3.3 histone B	Homo sapiens	20-32
31250475-14	2019	This study reveals important effects of AS on the NPY system and demonstrates that intranasal NPY elicits long-lasting reversal of traumatic stress-triggered hyperarousal.	Arsenic	40-42	neuropeptide Y	Rattus norvegicus	94-97
31665930-8	2022	Collectively, these results indicated that orlistat could reverse the suppressive effects induced by As+3 in macrophages through the increased expression of ABCA1, which has the potential to be developed as a therapeutic agent for arsenic-induced immunosuppression.	Arsenic	231-238	ATP binding cassette subfamily A member 1	Homo sapiens	157-162
31781319-0	2019	Enhanced p62-NRF2 Feedback Loop due to Impaired Autophagic Flux Contributes to Arsenic-Induced Malignant Transformation of Human Keratinocytes.	Arsenic	79-86	nucleoporin 62	Homo sapiens	9-12
31781319-0	2019	Enhanced p62-NRF2 Feedback Loop due to Impaired Autophagic Flux Contributes to Arsenic-Induced Malignant Transformation of Human Keratinocytes.	Arsenic	79-86	NFE2 like bZIP transcription factor 2	Homo sapiens	13-17
31066938-9	2019	Higher levels of iron, arsenic, and vanadium were associated with a statistically nonsignificant increased risk of a KRAS wild-type PDAC (OR for higher tertile of arsenic = 3.37, 95% CI 0.98-11.57).	Arsenic	163-170	KRAS proto-oncogene, GTPase	Homo sapiens	117-121
31621443-10	2022	Histological examination of the hepatic and renal tissues revealed marked improvement due to Vit-C supplementation in mice against sadagura and arsenic chronic co-exposure.	Arsenic	144-151	vitrin	Mus musculus	93-96
31621443-12	2022	Chronic Vit-C supplementation study results in mice show its effective remedial potential against combined sadagura and arsenic co-mediated genotoxicity and ultrastructural changes in major organs.	Arsenic	120-127	vitrin	Mus musculus	8-11
31600996-5	2019	Hepatoprotective effects against APAP-induced liver injury (AILI) showed that intragastric pretreatment with AS at 50 mg/kg almost completely prevented mice against APAP-induced increases of serum alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase and ATPase.	Arsenic	109-111	dynein, axonemal, heavy chain 8	Mus musculus	277-283
31401269-2	2019	Therefore, in this work, a novel composite adsorbent consisting of magnetic chitosan (MCS), zinc oxide (ZnO), and sodium alginate (Alg) was prepared to remove arsenic from groundwater.	Arsenic	159-166	Miles-Carpenter X-linked mental retardation syndrome	Homo sapiens	86-89
31407267-5	2019	In order of abundance, the various arsenic species in lichens from the urban site in South Africa were As(V) &gt; As(III) &gt; AsB &gt; dimethylarsinic acid (DMA) &gt; monomethylarsonic acid (MMA), and As(V) &gt; AsB &gt; As(III) &gt; DMA &gt; MMA for the rural site, where MMA was present in extremely low, non-quantifiable concentrations in lichens from both sites.	Arsenic	35-42	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	103-108
31351303-0	2019	Distribution of arsenic and its biotransformation genes in sediments from the East China Sea.	Arsenic	16-23	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	89-92
31352261-0	2019	Dose-dependent relationships between chronic arsenic exposure and cognitive impairment and serum brain-derived neurotrophic factor.	Arsenic	45-52	brain derived neurotrophic factor	Homo sapiens	97-130
31352261-14	2019	A decreased BDNF level may be part of the biochemical basis of chronic arsenic exposure-related cognitive impairment.	Arsenic	71-78	brain derived neurotrophic factor	Homo sapiens	12-16
31396869-10	2019	In addition, a significant (p < 0.05) alteration of biochemical parameters such as ALT, AST, ALP, BChE, and SOD as well as urea and creatinine levels were noted in the As-exposed group compared with the control group and Mn significantly (p < 0.05) attenuated the effects of As in co-exposed mice.	Arsenic	168-170	glutamic pyruvic transaminase, soluble	Mus musculus	83-86
31396869-10	2019	In addition, a significant (p < 0.05) alteration of biochemical parameters such as ALT, AST, ALP, BChE, and SOD as well as urea and creatinine levels were noted in the As-exposed group compared with the control group and Mn significantly (p < 0.05) attenuated the effects of As in co-exposed mice.	Arsenic	168-170	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	88-91
31396869-10	2019	In addition, a significant (p < 0.05) alteration of biochemical parameters such as ALT, AST, ALP, BChE, and SOD as well as urea and creatinine levels were noted in the As-exposed group compared with the control group and Mn significantly (p < 0.05) attenuated the effects of As in co-exposed mice.	Arsenic	168-170	alopecia, recessive	Mus musculus	93-96
31396869-10	2019	In addition, a significant (p < 0.05) alteration of biochemical parameters such as ALT, AST, ALP, BChE, and SOD as well as urea and creatinine levels were noted in the As-exposed group compared with the control group and Mn significantly (p < 0.05) attenuated the effects of As in co-exposed mice.	Arsenic	168-170	butyrylcholinesterase	Mus musculus	98-102
31407267-5	2019	In order of abundance, the various arsenic species in lichens from the urban site in South Africa were As(V) &gt; As(III) &gt; AsB &gt; dimethylarsinic acid (DMA) &gt; monomethylarsonic acid (MMA), and As(V) &gt; AsB &gt; As(III) &gt; DMA &gt; MMA for the rural site, where MMA was present in extremely low, non-quantifiable concentrations in lichens from both sites.	Arsenic	35-42	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	202-207
31233874-5	2019	Comparisons of time-dependent effects (24 h vs 48 h) from low dose arsenic exposed animals showed a significant shift in expression of Myd88 alone, suggesting that the down regulation was sustained for the key genes/signaling pathway.	Arsenic	67-74	myeloid differentiation primary response gene 88	Mus musculus	135-140
31292878-5	2019	The highest HS dose of 2000 mg L-1 resulted in 24.5-, 33.1-, and 12-fold increases of removal for Cd, Ni, and As, respectively.	Arsenic	110-112	immunoglobulin kappa variable 1-16	Homo sapiens	31-34
31611848-8	2019	Among these identified proteins, the ArsA [ATPase from the As(III) efflux pump] was found to be up-regulated in response to both arsenic conditions in the three strains, as well as the Co-enzyme A disulfide reductase (Cdr) in the two more resistant strains.	Arsenic	129-136	arylsulfatase A	Homo sapiens	37-41
31163410-5	2019	When the compressive strain eta becomes as  -2%, the band gap will be further enlarged to 0.045 eV, which is 45% larger than that of the unstrained material.	Arsenic	40-42	endothelin receptor type A	Homo sapiens	28-31
31330140-0	2019	Influence of AS3MT polymorphisms on arsenic metabolism and liver injury in APL patients treated with arsenic trioxide.	Arsenic	36-43	arsenite methyltransferase	Homo sapiens	13-18
31330140-2	2019	We recently demonstrated that AS3MT 14215 (rs3740390) genotypes were associated with urinary arsenic metabolites and hematological and biochemical values.	Arsenic	93-100	arsenite methyltransferase	Homo sapiens	30-35
31532247-1	2019	BACKGROUND: Arsenic-induced liver X receptor/retinoid X receptor (LXR/RXR) signaling inhibition is a potential mechanism underlying the cardiovascular effects caused by arsenic.	Arsenic	12-19	nuclear receptor subfamily 1, group H, member 3	Mus musculus	66-69
31532247-1	2019	BACKGROUND: Arsenic-induced liver X receptor/retinoid X receptor (LXR/RXR) signaling inhibition is a potential mechanism underlying the cardiovascular effects caused by arsenic.	Arsenic	169-176	nuclear receptor subfamily 1, group H, member 3	Mus musculus	66-69
31532247-3	2019	OBJECTIVE: We aimed to explore whether gut microbiota play a role in arsenic-induced LXR/RXR signaling inhibition and the subsequent lipid and cholesterol dysbiosis.	Arsenic	69-76	nuclear receptor subfamily 1, group H, member 3	Mus musculus	85-88
31532247-10	2019	Similarly, under arsenic exposure, the hepatic expression of scavenger receptor class B member 1 (Scarb1), which is involved in reverse cholesterol transport (RCT), was lower in conventional mice, but was higher in AB-treated animals compared with controls.	Arsenic	17-24	scavenger receptor class B, member 1	Mus musculus	61-96
31532247-10	2019	Similarly, under arsenic exposure, the hepatic expression of scavenger receptor class B member 1 (Scarb1), which is involved in reverse cholesterol transport (RCT), was lower in conventional mice, but was higher in AB-treated animals compared with controls.	Arsenic	17-24	scavenger receptor class B, member 1	Mus musculus	98-104
31532247-14	2019	CONCLUSIONS: Our results suggest that in mice, the gut microbiota may be a critical factor regulating arsenic-induced LXR/RXR signaling perturbation, suggesting that modulation of the gut microbiota might be an intervention strategy to reduce the toxic effects of arsenic on lipid and cholesterol homeostasis.	Arsenic	102-109	nuclear receptor subfamily 1, group H, member 3	Mus musculus	118-121
31398423-0	2019	Arsenic impairs GLUT1 trafficking through the inhibition of the calpain system in lymphocytes.	Arsenic	0-7	solute carrier family 2 member 1	Homo sapiens	16-21
31398423-3	2019	We investigated whether arsenic disrupts GLUT1 trafficking and function through calpain inhibition, using lymphocytes as a cell model.	Arsenic	24-31	solute carrier family 2 member 1	Homo sapiens	41-46
31290047-8	2019	Investigating the expression profile of apoptosis pathway genes similarly revealed that caspase-8, as a main upstream contributor to the apoptosis pathway, might play an important role in the induction of apoptosis generated by As and HFD.	Arsenic	228-230	caspase 8	Mus musculus	88-97
31345348-7	2019	Multiple regression analyses revealed that DNA methylation of LINE1, Nrf2, OGG1, and PARP1 was associated with potentially toxic (As, Hg, Mn, Mo, and Pb) and essential (Cu, Se, and Zn) elements, and with their interactions.	Arsenic	130-132	NFE2 like bZIP transcription factor 2	Homo sapiens	69-73
31332900-0	2019	Metformin in contrast to berberine reversed arsenic-induced oxidative stress in mitochondria from rat pancreas probably via Sirt3-dependent pathway.	Arsenic	44-51	MET proto-oncogene, receptor tyrosine kinase	Rattus norvegicus	0-9
31332900-0	2019	Metformin in contrast to berberine reversed arsenic-induced oxidative stress in mitochondria from rat pancreas probably via Sirt3-dependent pathway.	Arsenic	44-51	sirtuin 3	Rattus norvegicus	124-129
31332900-2	2019	In this study berberine (BBR) effects on arsenic-induced sirtuin 3 (Sirt3) modifications in isolated mitochondria from rat pancreas were evaluated and compared with metformin (MET).	Arsenic	41-48	sirtuin 3	Rattus norvegicus	68-73
31345348-7	2019	Multiple regression analyses revealed that DNA methylation of LINE1, Nrf2, OGG1, and PARP1 was associated with potentially toxic (As, Hg, Mn, Mo, and Pb) and essential (Cu, Se, and Zn) elements, and with their interactions.	Arsenic	130-132	8-oxoguanine DNA glycosylase	Homo sapiens	75-79
31345348-7	2019	Multiple regression analyses revealed that DNA methylation of LINE1, Nrf2, OGG1, and PARP1 was associated with potentially toxic (As, Hg, Mn, Mo, and Pb) and essential (Cu, Se, and Zn) elements, and with their interactions.	Arsenic	130-132	poly(ADP-ribose) polymerase 1	Homo sapiens	85-90
31170415-5	2019	In this study, we further showed that subacute or chronic exposure to arsenic diminished miR-199a-5p levels largely due to DNA methylation, which was achieved by increased DNA methyltransferase-1 (DNMT1) activity, mediated by the formation of specific protein 1 (Sp1)/DNMT1 complex.	Arsenic	70-77	DNA methyltransferase 1	Homo sapiens	172-195
31152818-0	2019	Peroxynitrite contributes to arsenic-induced PARP-1 inhibition through ROS/RNS generation.	Arsenic	29-36	poly(ADP-ribose) polymerase 1	Homo sapiens	45-51
31170415-5	2019	In this study, we further showed that subacute or chronic exposure to arsenic diminished miR-199a-5p levels largely due to DNA methylation, which was achieved by increased DNA methyltransferase-1 (DNMT1) activity, mediated by the formation of specific protein 1 (Sp1)/DNMT1 complex.	Arsenic	70-77	DNA methyltransferase 1	Homo sapiens	197-202
31176655-17	2019	These results suggest that overexpression of miR-186 in arsenic exposed tissues likely induces aneuploidy contributing to arsenic-induced carcinogenesis.	Arsenic	56-63	microRNA 186	Homo sapiens	45-52
31176655-0	2019	Overexpression of hsa-miR-186 induces chromosomal instability in arsenic-exposed human keratinocytes.	Arsenic	65-72	microRNA 186	Homo sapiens	22-29
31170415-5	2019	In this study, we further showed that subacute or chronic exposure to arsenic diminished miR-199a-5p levels largely due to DNA methylation, which was achieved by increased DNA methyltransferase-1 (DNMT1) activity, mediated by the formation of specific protein 1 (Sp1)/DNMT1 complex.	Arsenic	70-77	Sp1 transcription factor	Homo sapiens	243-261
31176655-4	2019	hsa-miR-186 overexpression is associated with metastatic cancers as well as arsenic-induced squamous cell carcinoma and is reported to target several mitotic regulators.	Arsenic	76-83	microRNA 186	Homo sapiens	4-11
31176655-17	2019	These results suggest that overexpression of miR-186 in arsenic exposed tissues likely induces aneuploidy contributing to arsenic-induced carcinogenesis.	Arsenic	122-129	microRNA 186	Homo sapiens	45-52
31170415-5	2019	In this study, we further showed that subacute or chronic exposure to arsenic diminished miR-199a-5p levels largely due to DNA methylation, which was achieved by increased DNA methyltransferase-1 (DNMT1) activity, mediated by the formation of specific protein 1 (Sp1)/DNMT1 complex.	Arsenic	70-77	DNA methyltransferase 1	Homo sapiens	268-273
31170415-7	2019	We further identified an association between miR-199a-5p repression and the arsenic-mediated energy metabolic shift, as reflected by mitochondria defects and a switch to glycolysis, in which a glycolytic enzyme pyruvate kinase 2 (PKM2) was a functional target of miR-199a-5p.	Arsenic	76-83	pyruvate kinase M1/2	Homo sapiens	230-234
31170415-8	2019	Taken together, the repression of miR-199a-5p through both Sp1-dependent DNA methylation and Sp1 transcriptional repression promotes an arsenic-mediated metabolic shift from mitochondria respiration to aerobic glycolysis via PKM2.	Arsenic	136-143	pyruvate kinase M1/2	Homo sapiens	225-229
30357758-0	2019	The Variable Regulatory Effect of Arsenic on Nrf2 Signaling Pathway in Mouse: a Systematic Review and Meta-analysis.	Arsenic	34-41	nuclear factor, erythroid derived 2, like 2	Mus musculus	45-49
31663452-3	2019	The animals in the arsenic-treated group were given arsenic orally in drinking water in the form of sodium arsenite at a dose level of 100 mg L-1, and zinc was administered to zinc-treated animals in the form of zinc sulfate orally in drinking water at a dose level of 227 mg L-1.	Arsenic	19-26	ribosomal protein L4	Rattus norvegicus	142-145
31663452-3	2019	The animals in the arsenic-treated group were given arsenic orally in drinking water in the form of sodium arsenite at a dose level of 100 mg L-1, and zinc was administered to zinc-treated animals in the form of zinc sulfate orally in drinking water at a dose level of 227 mg L-1.	Arsenic	19-26	ribosomal protein L4	Rattus norvegicus	276-279
31481945-4	2019	We found that arsC and ereA genes coding for resistance mechanisms to arsenic and to macrolides, respectively, are the most abundant MRG and ARG in the study area.	Arsenic	70-77	steroid sulfatase	Homo sapiens	14-18
31075598-6	2019	Arsenic is found in all water types of the Altiplano-Puna plateau over a wide range of concentrations (0.01 mg L-1 &lt; As in water &gt; 10 mg L-1) which in decreasing order correspond to: AMD, brines, saline waters, hot springs, rivers affected by AMD, rivers and lakes, and groundwater.	Arsenic	0-7	immunoglobulin kappa variable 1-16	Homo sapiens	111-114
31075598-6	2019	Arsenic is found in all water types of the Altiplano-Puna plateau over a wide range of concentrations (0.01 mg L-1 &lt; As in water &gt; 10 mg L-1) which in decreasing order correspond to: AMD, brines, saline waters, hot springs, rivers affected by AMD, rivers and lakes, and groundwater.	Arsenic	0-7	immunoglobulin kappa variable 1-16	Homo sapiens	143-146
32185367-1	2019	Retrospective analysis of 20 water systems from the USEPA"s Arsenic Demonstration Program revealed three patterns of arsenic levels at the tap, after arsenic treatment of the source well water.	Arsenic	117-124	nuclear RNA export factor 1	Homo sapiens	139-142
31195325-2	2019	Both arsenic and fluoride are potent toxicants that are known to induce Nrf2.	Arsenic	5-12	nfe2 like bZIP transcription factor 2a	Danio rerio	72-76
31195325-9	2019	From the results of qRT-PCR it was evident that at each time point co-exposure to arsenic and fluoride seemed to alter the gene expression of Cu/Zn Sod, Mn Sod, Gpx and Nqo1 just like their individual exposure but at a very low magnitude.	Arsenic	82-89	superoxide dismutase 1, soluble	Danio rerio	142-151
31195325-9	2019	From the results of qRT-PCR it was evident that at each time point co-exposure to arsenic and fluoride seemed to alter the gene expression of Cu/Zn Sod, Mn Sod, Gpx and Nqo1 just like their individual exposure but at a very low magnitude.	Arsenic	82-89	superoxide dismutase 2, mitochondrial	Danio rerio	153-159
31195325-9	2019	From the results of qRT-PCR it was evident that at each time point co-exposure to arsenic and fluoride seemed to alter the gene expression of Cu/Zn Sod, Mn Sod, Gpx and Nqo1 just like their individual exposure but at a very low magnitude.	Arsenic	82-89	NAD(P)H dehydrogenase, quinone 1	Danio rerio	169-173
31195325-10	2019	In conclusion, this study demonstrates for the first time the differential expression and activity of Nrf2 and other stress response genes in the zebrafish liver following individual and combined exposure to arsenic and fluoride.	Arsenic	208-215	nfe2 like bZIP transcription factor 2a	Danio rerio	102-106
31085440-6	2019	It was found that the miR-155 has a certain diagnostic value in arsenic-induced skin damage (AUC = 0.83), miR-21 and miR-145 have diagnostic value for liver damage (AUC = 0.80, 0.81) and miR-191 has diagnostic value for kidney damage (AUC = 0.83).	Arsenic	64-71	microRNA 155	Homo sapiens	22-29
31190067-11	2019	These results show that polyamine-dependent release of HMGB1 promotes the expansion of stem cell-like subpopulations in arsenic-transformed keratinocytes while also increasing their invasiveness, suggesting that polyamines may be a potential therapeutic target for the prevention and treatment of arsenic-initiated skin cancers.	Arsenic	120-127	high mobility group box 1	Homo sapiens	55-60
31331165-5	2019	At 1.2 V and an electric energy consumption of 0.06 kWh m-3, the total As concentration can be reduced from 150 to 15 mug L-1 using an electrochemical cell with electrode area of 10 x 8 cm2 and electro-sorption time of 120 min.	Arsenic	71-73	immunoglobulin kappa variable 1-16	Homo sapiens	122-125
30357758-3	2019	Scholars demonstrated that Nrf2 pathway was activated by arsenic.	Arsenic	57-64	nuclear factor, erythroid derived 2, like 2	Mus musculus	27-31
30357758-4	2019	In contrast, other articles established arsenic-induced inhibition of Nrf2 pathway.	Arsenic	40-47	nuclear factor, erythroid derived 2, like 2	Mus musculus	70-74
30357758-5	2019	To resolve the contradiction and elucidate the mechanism of Nrf2 induced by arsenic, 39 publications involving mouse models were identified through exhaustive database retrieval and were analyzed.	Arsenic	76-83	nuclear factor, erythroid derived 2, like 2	Mus musculus	60-64
30357758-6	2019	The pooled results suggested that arsenic obviously elevated transcription and translation levels of Nrf2 and its downstream genes, NAD(P)H dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC), and GST-glutathione-S-transferase1/2 (GSTO1/2).	Arsenic	34-41	nuclear factor, erythroid derived 2, like 2	Mus musculus	101-105
30357758-6	2019	The pooled results suggested that arsenic obviously elevated transcription and translation levels of Nrf2 and its downstream genes, NAD(P)H dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC), and GST-glutathione-S-transferase1/2 (GSTO1/2).	Arsenic	34-41	NAD(P)H dehydrogenase, quinone 1	Mus musculus	157-161
30357758-6	2019	The pooled results suggested that arsenic obviously elevated transcription and translation levels of Nrf2 and its downstream genes, NAD(P)H dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC), and GST-glutathione-S-transferase1/2 (GSTO1/2).	Arsenic	34-41	heme oxygenase 1	Mus musculus	164-180
30357758-6	2019	The pooled results suggested that arsenic obviously elevated transcription and translation levels of Nrf2 and its downstream genes, NAD(P)H dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC), and GST-glutathione-S-transferase1/2 (GSTO1/2).	Arsenic	34-41	heme oxygenase 1	Mus musculus	182-186
30357758-6	2019	The pooled results suggested that arsenic obviously elevated transcription and translation levels of Nrf2 and its downstream genes, NAD(P)H dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC), and GST-glutathione-S-transferase1/2 (GSTO1/2).	Arsenic	34-41	glutamate-cysteine ligase, catalytic subunit	Mus musculus	189-232
30357758-6	2019	The pooled results suggested that arsenic obviously elevated transcription and translation levels of Nrf2 and its downstream genes, NAD(P)H dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC), and GST-glutathione-S-transferase1/2 (GSTO1/2).	Arsenic	34-41	glutamate-cysteine ligase, catalytic subunit	Mus musculus	234-238
30357758-6	2019	The pooled results suggested that arsenic obviously elevated transcription and translation levels of Nrf2 and its downstream genes, NAD(P)H dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC), and GST-glutathione-S-transferase1/2 (GSTO1/2).	Arsenic	34-41	glutathione S-transferase omega 1	Mus musculus	279-286
30357758-8	2019	Subgroup analysis between arsenic and control groups showed that the levels of Nrf2 and its downstream genes are greater in high dose than that in the low dose, higher in short-term exposure than long term, female subjects tolerated better than males, higher in mice than the rats, and greater in other organs than the liver.	Arsenic	26-33	nuclear factor, erythroid derived 2, like 2	Mus musculus	79-83
30357758-9	2019	However, the contents of genes of Nrf2 pathway between the arsenic and control groups were lower in rats than in mice and were less for long-term exposure than the short term (P < 0.05).	Arsenic	59-66	NFE2 like bZIP transcription factor 2	Rattus norvegicus	34-38
30357758-10	2019	Conclusively, a variable regulation of arsenic on Nrf2 pathway is noted.	Arsenic	39-46	nuclear factor, erythroid derived 2, like 2	Mus musculus	50-54
30357758-12	2019	On the other hand, arsenic inhibited Nrf2 pathway for long-term exposure on rats.	Arsenic	19-26	NFE2 like bZIP transcription factor 2	Rattus norvegicus	37-41
30368653-10	2019	In addition, arsenic had a greater correlation (63%) with increased serum S100B biomarker level among other elements.	Arsenic	13-20	S100 calcium binding protein B	Homo sapiens	74-79
30392020-0	2019	Role of Pigment Epithelium-Derived Factor in Arsenic-Induced Vascular Endothelial Dysfunction in a Rat Model.	Arsenic	45-52	serpin family F member 1	Rattus norvegicus	8-41
30392020-7	2019	Regardless of serum or aortic arch endothelium, PEDF levels in the arsenic exposure groups decreased compared to the control group.	Arsenic	67-74	serpin family F member 1	Rattus norvegicus	48-52
30392020-11	2019	Taken together, our study is the first to find that PEDF plays a protective role in arsenic-induced endothelial dysfunction through anti-oxidation and anti-apoptosis, and p38 and P53 may be promising target proteins.	Arsenic	84-91	serpin family F member 1	Rattus norvegicus	52-56
30392020-11	2019	Taken together, our study is the first to find that PEDF plays a protective role in arsenic-induced endothelial dysfunction through anti-oxidation and anti-apoptosis, and p38 and P53 may be promising target proteins.	Arsenic	84-91	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	179-182
31236859-9	2019	Moreover, as  tox increases, it indicates an increase in the concentration of eleven (Ca, P, Co, Cr, Fe, I, Mn, Li, Ni, V, As) and a decrease of two elements in hair (B, Si); for six elements (K, Mg, Na, Cu, Zn, Sn), such a connection was not revealed.	Arsenic	123-125	thymocyte selection associated high mobility group box	Equus caballus	14-17
31228066-5	2019	The high adsorption rate-pseudo-second-order constants in the range 0.509-0.789 g mg-1 min-1 for As(V) and 0.304-0.532 g mg1 min1 for As(III)-justified further application T-Cu(A-C) in a flow system.	Arsenic	97-99	mucin 5B, oligomeric mucus/gel-forming	Homo sapiens	82-92
30667058-5	2019	This review exhibited the effects of arsenic on the metabolism and signaling pathways within adipose tissue (such as sirtuin 3 [SIRT3]- forkhead box O3 [FOXO3a], mitogen-activated protein kinase [MAPK], phosphoinositide-dependant kinase-1 [PDK-1], unfolded protein response, and C/EBP homologous protein [CHOP10]).	Arsenic	37-44	sirtuin 3	Homo sapiens	128-133
31397191-0	2019	Fumaric acids as a novel antagonist of TLR-4 pathway mitigates arsenic-exposed inflammation in human monocyte-derived dendritic cells.	Arsenic	63-70	toll like receptor 4	Homo sapiens	39-44
30667058-5	2019	This review exhibited the effects of arsenic on the metabolism and signaling pathways within adipose tissue (such as sirtuin 3 [SIRT3]- forkhead box O3 [FOXO3a], mitogen-activated protein kinase [MAPK], phosphoinositide-dependant kinase-1 [PDK-1], unfolded protein response, and C/EBP homologous protein [CHOP10]).	Arsenic	37-44	forkhead box O3	Homo sapiens	136-151
30667058-5	2019	This review exhibited the effects of arsenic on the metabolism and signaling pathways within adipose tissue (such as sirtuin 3 [SIRT3]- forkhead box O3 [FOXO3a], mitogen-activated protein kinase [MAPK], phosphoinositide-dependant kinase-1 [PDK-1], unfolded protein response, and C/EBP homologous protein [CHOP10]).	Arsenic	37-44	forkhead box O3	Homo sapiens	153-159
30667058-5	2019	This review exhibited the effects of arsenic on the metabolism and signaling pathways within adipose tissue (such as sirtuin 3 [SIRT3]- forkhead box O3 [FOXO3a], mitogen-activated protein kinase [MAPK], phosphoinositide-dependant kinase-1 [PDK-1], unfolded protein response, and C/EBP homologous protein [CHOP10]).	Arsenic	37-44	pyruvate dehydrogenase kinase 1	Homo sapiens	203-238
30667058-5	2019	This review exhibited the effects of arsenic on the metabolism and signaling pathways within adipose tissue (such as sirtuin 3 [SIRT3]- forkhead box O3 [FOXO3a], mitogen-activated protein kinase [MAPK], phosphoinositide-dependant kinase-1 [PDK-1], unfolded protein response, and C/EBP homologous protein [CHOP10]).	Arsenic	37-44	pyruvate dehydrogenase kinase 1	Homo sapiens	240-245
30667058-5	2019	This review exhibited the effects of arsenic on the metabolism and signaling pathways within adipose tissue (such as sirtuin 3 [SIRT3]- forkhead box O3 [FOXO3a], mitogen-activated protein kinase [MAPK], phosphoinositide-dependant kinase-1 [PDK-1], unfolded protein response, and C/EBP homologous protein [CHOP10]).	Arsenic	37-44	DNA damage inducible transcript 3	Homo sapiens	305-311
30667058-11	2019	Arsenic also elevated cord blood and placental, as well as postnatal serum leptin levels.	Arsenic	0-7	leptin	Homo sapiens	75-81
31141459-7	2019	Finally, we used a biotinylated arsenic probe to establish that Cys306 of yeast Gpd1, a highly conserved residue within the active site, is the key target of MAs(III).	Arsenic	32-39	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	80-84
31039529-5	2019	The significant correlation between As and NO3- indicates that NO3- might be attributed to the use of phosphate fertilizers and a factor responsible for enhancing As in aquifers.	Arsenic	36-38	NBL1, DAN family BMP antagonist	Homo sapiens	43-46
31313788-4	2019	On the other hand, zinc finger motifs in PML protein are considered to be a key target binding site for arsenic-induced PML-RARalpha protein degradation.	Arsenic	104-111	PML nuclear body scaffold	Homo sapiens	120-123
31313788-5	2019	Interestingly, antimony and arsenic lost their ability to degrade PML-RARalpha fusion protein in NB4 cells following pretreatment with phenanthroline (i.e., chelator of zinc ions), indicating that the integrity of zinc finger motifs in PML-RARalpha fusion protein is a fundamental condition for inducing the protein"s degradation by antimony and arsenic.	Arsenic	28-35	PML nuclear body scaffold	Homo sapiens	66-69
31313788-5	2019	Interestingly, antimony and arsenic lost their ability to degrade PML-RARalpha fusion protein in NB4 cells following pretreatment with phenanthroline (i.e., chelator of zinc ions), indicating that the integrity of zinc finger motifs in PML-RARalpha fusion protein is a fundamental condition for inducing the protein"s degradation by antimony and arsenic.	Arsenic	28-35	PML nuclear body scaffold	Homo sapiens	236-239
31313788-5	2019	Interestingly, antimony and arsenic lost their ability to degrade PML-RARalpha fusion protein in NB4 cells following pretreatment with phenanthroline (i.e., chelator of zinc ions), indicating that the integrity of zinc finger motifs in PML-RARalpha fusion protein is a fundamental condition for inducing the protein"s degradation by antimony and arsenic.	Arsenic	346-353	PML nuclear body scaffold	Homo sapiens	66-69
31313790-5	2019	Exposure to As(iii) and As(v) generates an increase in the release of the pro-inflammatory cytokine IL-8 (57-1135%) and an increase in the generation of reactive oxygen and/or nitrogen species (130-340%) in both cell lines.	Arsenic	12-14	C-X-C motif chemokine ligand 8	Homo sapiens	100-104
31346790-9	2019	Likewise, insulin and glutathione concentrations were also significantly decreased (P &lt; 0.001) in arsenic-exposed animals as compared with that of unexposed animals.	Arsenic	101-108	insulin	Homo sapiens	10-17
31346790-10	2019	The alterations in normal values of glucose, insulin, and glutathione exhibited the damaging effects of arsenic exposure in experimental rats.	Arsenic	104-111	insulin	Homo sapiens	45-52
31313788-4	2019	On the other hand, zinc finger motifs in PML protein are considered to be a key target binding site for arsenic-induced PML-RARalpha protein degradation.	Arsenic	104-111	PML nuclear body scaffold	Homo sapiens	41-44
31346790-6	2019	Moreover, urinary arsenic exposure was also associated with higher levels of fasting (P &lt; 0.001) and random blood glucose (P &lt; 0.001), HbA1c (P &lt; 0.001), AST, ALT, MDA, IL-6, CRP, blood urea nitrogen, and creatinine in arsenic-exposed diabetics as compared with that of unexposed diabetics.	Arsenic	18-25	solute carrier family 17 member 5	Homo sapiens	163-166
31346790-6	2019	Moreover, urinary arsenic exposure was also associated with higher levels of fasting (P &lt; 0.001) and random blood glucose (P &lt; 0.001), HbA1c (P &lt; 0.001), AST, ALT, MDA, IL-6, CRP, blood urea nitrogen, and creatinine in arsenic-exposed diabetics as compared with that of unexposed diabetics.	Arsenic	18-25	interleukin 6	Homo sapiens	178-182
31337829-4	2019	Dissolved arsenic was between 5.0 and 15 mug L-1 in Lake Titicaca and reached 78.5 mug L-1 in Lake Uru Uru.	Arsenic	10-17	immunoglobulin kappa variable 1-16	Homo sapiens	45-48
31337829-4	2019	Dissolved arsenic was between 5.0 and 15 mug L-1 in Lake Titicaca and reached 78.5 mug L-1 in Lake Uru Uru.	Arsenic	10-17	immunoglobulin kappa variable 1-16	Homo sapiens	87-90
31077704-6	2019	A review of recent findings that Arsenic causes loss in the cellular levels of Stem Loop Binding Protein (SLBP) resulting in polyadenylation of canonical histones (H3.1) as a default, increasing levels of H3.1 protein outside of S-Phase.	Arsenic	33-40	stem-loop binding protein	Homo sapiens	79-104
31077704-6	2019	A review of recent findings that Arsenic causes loss in the cellular levels of Stem Loop Binding Protein (SLBP) resulting in polyadenylation of canonical histones (H3.1) as a default, increasing levels of H3.1 protein outside of S-Phase.	Arsenic	33-40	stem-loop binding protein	Homo sapiens	106-110
31077704-6	2019	A review of recent findings that Arsenic causes loss in the cellular levels of Stem Loop Binding Protein (SLBP) resulting in polyadenylation of canonical histones (H3.1) as a default, increasing levels of H3.1 protein outside of S-Phase.	Arsenic	33-40	H3 clustered histone 3	Homo sapiens	164-168
31077704-6	2019	A review of recent findings that Arsenic causes loss in the cellular levels of Stem Loop Binding Protein (SLBP) resulting in polyadenylation of canonical histones (H3.1) as a default, increasing levels of H3.1 protein outside of S-Phase.	Arsenic	33-40	H3 clustered histone 3	Homo sapiens	205-209
31039529-5	2019	The significant correlation between As and NO3- indicates that NO3- might be attributed to the use of phosphate fertilizers and a factor responsible for enhancing As in aquifers.	Arsenic	36-38	NBL1, DAN family BMP antagonist	Homo sapiens	63-66
31077704-8	2019	Arsenic induced polyadenylation of H3.1 causes enhanced levels of H3.1 protein displacing H3.3 protein from its cellular binding sites, since the two proteins differ by only 5 amino acids.	Arsenic	0-7	H3 clustered histone 3	Homo sapiens	35-39
31077704-8	2019	Arsenic induced polyadenylation of H3.1 causes enhanced levels of H3.1 protein displacing H3.3 protein from its cellular binding sites, since the two proteins differ by only 5 amino acids.	Arsenic	0-7	H3 clustered histone 3	Homo sapiens	66-70
31947377-5	2019	As our system is held in place with only an elastic strap it offers the same level of comfort as when wearing a normal eye mask.	Arsenic	0-2	serine/threonine kinase receptor associated protein	Homo sapiens	52-57
31336801-5	2019	Several mechanisms that seem to play key roles in As-induced neurotoxicity, including oxidative stress, apoptosis, thiamine deficiency, and decreased acetyl cholinesterase activity, are described.	Arsenic	50-52	butyrylcholinesterase	Homo sapiens	157-171
31355259-10	2019	Taken together, these results prove that PC can promote arsenic methylation metabolism and efflux in L-02 cells, which may be related to the upregulation of GSH, MRP1, and AS3MT levels by PC.	Arsenic	56-63	ATP binding cassette subfamily C member 1	Homo sapiens	162-166
31355259-10	2019	Taken together, these results prove that PC can promote arsenic methylation metabolism and efflux in L-02 cells, which may be related to the upregulation of GSH, MRP1, and AS3MT levels by PC.	Arsenic	56-63	arsenite methyltransferase	Homo sapiens	172-177
30991335-6	2019	The chemical elements As, B, Bi, Cd, Cu, P, Pb, Sb, Sn and Zn (PC2) are strongly spatially associated with soils sampled above high-density urban residential, commercial and industrial sites, and are interpreted to reflect heavy metal contamination from human activities.	Arsenic	22-24	chromobox 4	Homo sapiens	63-66
30456849-11	2019	CONCLUSION: Arsenic was found to enhance UVB-induced production of ROS and to downregulate SOD1 expression, leading to DNA damage and apoptosis in mouse skin cells.	Arsenic	12-19	superoxide dismutase 1, soluble	Mus musculus	91-95
30456849-12	2019	The combination of arsenic and UVB exposure was found to differentially regulate the expression of SOD1 and SOD2.	Arsenic	19-26	superoxide dismutase 1, soluble	Mus musculus	99-103
30456849-12	2019	The combination of arsenic and UVB exposure was found to differentially regulate the expression of SOD1 and SOD2.	Arsenic	19-26	superoxide dismutase 2, mitochondrial	Mus musculus	108-112
30878179-4	2019	In this article we reviewed how biotransformation of ingested arsenic may lead to cancer by modulating the activation of several essential signalling pathways such as EGFR, PI3K/AKT, RTK/Ras/PI3K, JNK/STAT3 and Nrf2-KEAP1; by producing epigenetics modifications and by disrupting normal expression of miRNAs.	Arsenic	62-69	AKT serine/threonine kinase 1	Homo sapiens	178-181
30878179-4	2019	In this article we reviewed how biotransformation of ingested arsenic may lead to cancer by modulating the activation of several essential signalling pathways such as EGFR, PI3K/AKT, RTK/Ras/PI3K, JNK/STAT3 and Nrf2-KEAP1; by producing epigenetics modifications and by disrupting normal expression of miRNAs.	Arsenic	62-69	mitogen-activated protein kinase 8	Homo sapiens	197-200
30878179-4	2019	In this article we reviewed how biotransformation of ingested arsenic may lead to cancer by modulating the activation of several essential signalling pathways such as EGFR, PI3K/AKT, RTK/Ras/PI3K, JNK/STAT3 and Nrf2-KEAP1; by producing epigenetics modifications and by disrupting normal expression of miRNAs.	Arsenic	62-69	signal transducer and activator of transcription 3	Homo sapiens	201-206
30878179-4	2019	In this article we reviewed how biotransformation of ingested arsenic may lead to cancer by modulating the activation of several essential signalling pathways such as EGFR, PI3K/AKT, RTK/Ras/PI3K, JNK/STAT3 and Nrf2-KEAP1; by producing epigenetics modifications and by disrupting normal expression of miRNAs.	Arsenic	62-69	NFE2 like bZIP transcription factor 2	Homo sapiens	211-215
30878179-4	2019	In this article we reviewed how biotransformation of ingested arsenic may lead to cancer by modulating the activation of several essential signalling pathways such as EGFR, PI3K/AKT, RTK/Ras/PI3K, JNK/STAT3 and Nrf2-KEAP1; by producing epigenetics modifications and by disrupting normal expression of miRNAs.	Arsenic	62-69	kelch like ECH associated protein 1	Homo sapiens	216-221
31199764-9	2019	Oral administration of curcumin (20 mg/kg body weight/day) in arsenic-treated rats significantly reinstated these alterations of the antioxidant system followed by an improvement of ovarian steroidogenesis and the circulating level of B12 and folate along with the downregulation of serum homocysteine, metallothionein-1, and cytokines.	Arsenic	62-69	metallothionein 1	Rattus norvegicus	303-320
31199848-12	2019	After adjusting for potential confounders, high blood total arsenic concentration had 2.6-fold increased odds (aOR = 2.603, 95% CI: 1.178, 5.751) of low plasma BDNF level as compared with low blood total arsenic group.	Arsenic	60-67	brain derived neurotrophic factor	Homo sapiens	160-164
31199848-14	2019	CONCLUSIONS: The present findings demonstrate higher blood total arsenic level were more likely to have lower BDNF in early pregnancy.	Arsenic	65-72	brain derived neurotrophic factor	Homo sapiens	110-114
30913429-1	2019	As a problematic element in water systems, arsenic exists as As(III) and As(V).	Arsenic	43-50	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	73-78
30940592-8	2019	The reusability of as-synthesized NST/CS was assessed which due to its high recoverability can be applied as an effective catalyst for degradation of organic substances in water and wastewater especially for degradation of emerging pollutants such pharmaceutical pollutants.	Arsenic	19-21	citrate synthase	Homo sapiens	38-40
30952306-5	2019	The detection limits were obtained at 0.078 for As(III), 0.081 for DMA, 0.078 for MMA and 0.15 mug L-1 for As(V), and 0.016 for Hg(II), 0.027 for MeHg and 0.032 mug L-1 for EtHg, and the reproducibilities (50 mug L-1 for each As-species and 10 mug L-1 for each Hg-species) were all lower than 3.7%.	Arsenic	107-109	immunoglobulin kappa variable 1-16	Homo sapiens	99-102
30952306-5	2019	The detection limits were obtained at 0.078 for As(III), 0.081 for DMA, 0.078 for MMA and 0.15 mug L-1 for As(V), and 0.016 for Hg(II), 0.027 for MeHg and 0.032 mug L-1 for EtHg, and the reproducibilities (50 mug L-1 for each As-species and 10 mug L-1 for each Hg-species) were all lower than 3.7%.	Arsenic	107-109	immunoglobulin kappa variable 1-16	Homo sapiens	99-102
30870814-2	2019	We observe that, for the bulk phase, As1-x Sb x alloy can exhibit not only chemical ordering of As and Sb atoms at x  =  0.5 to form an ordered compound of AsSb stable upon annealing up to [Formula: see text] K, but also a miscibility gap at 475 K [Formula: see text] T [Formula: see text] 550 K in which two disordered solid solutions of As1-x Sb x of different alloy compositions thermodynamically coexist.	Arsenic	37-39	prostaglandin D2 receptor	Homo sapiens	339-342
31120745-0	2019	Arsenic-Induced Neoplastic Transformation Involves Epithelial-Mesenchymal Transition and Activation of the beta-Catenin/c-Myc Pathway in Human Kidney Epithelial Cells.	Arsenic	0-7	catenin beta 1	Homo sapiens	107-119
31120745-0	2019	Arsenic-Induced Neoplastic Transformation Involves Epithelial-Mesenchymal Transition and Activation of the beta-Catenin/c-Myc Pathway in Human Kidney Epithelial Cells.	Arsenic	0-7	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	120-125
31120745-11	2019	In summary, results of this study suggest that chronic exposure to arsenic even at a relatively lower concentration can induce neoplastic transformation through acquisitions of EMT, stemness, and MET phenotypes, which might be related to the beta-catenin/c-Myc signaling pathway.	Arsenic	67-74	SAFB like transcription modulator	Homo sapiens	196-199
31120745-11	2019	In summary, results of this study suggest that chronic exposure to arsenic even at a relatively lower concentration can induce neoplastic transformation through acquisitions of EMT, stemness, and MET phenotypes, which might be related to the beta-catenin/c-Myc signaling pathway.	Arsenic	67-74	catenin beta 1	Homo sapiens	242-254
31120745-11	2019	In summary, results of this study suggest that chronic exposure to arsenic even at a relatively lower concentration can induce neoplastic transformation through acquisitions of EMT, stemness, and MET phenotypes, which might be related to the beta-catenin/c-Myc signaling pathway.	Arsenic	67-74	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	255-260
31199764-7	2019	Blood levels of vitamin B12 and folic acid decreased followed by an increased serum lactate dehydrogenase, homocysteine level, and hepatic metallothionein-1 in arsenic-treated rats.	Arsenic	160-167	metallothionein 1	Rattus norvegicus	139-156
31199764-8	2019	Necrosis of uterine tissue along with the disruption of ovarian steroidogenesis was marked in arsenic-treated rats with an upregulation of uterine NF-kappaB and IL-6 along with a raised level of serum TNF-alpha.	Arsenic	94-101	interleukin 6	Rattus norvegicus	161-165
31199764-8	2019	Necrosis of uterine tissue along with the disruption of ovarian steroidogenesis was marked in arsenic-treated rats with an upregulation of uterine NF-kappaB and IL-6 along with a raised level of serum TNF-alpha.	Arsenic	94-101	tumor necrosis factor	Rattus norvegicus	201-210
30836860-7	2019	To sum up, we report 3 new roles of PFG as, 1. inducer of premature senescence in normal TIG-1 cells, 2. inhibitor of mitosis in cancerous HeLa cells, 3.	Arsenic	40-42	retinoic acid receptor responder 1	Homo sapiens	89-94
31174487-3	2019	METHODS: An assessment was carried out to quantify chronic exposure to cadmium, lead and arsenic through food in people living in an area in Sri Lanka, where prevalence of Chronic Kidney Disease of unknown origin (CKDu) is highest.	Arsenic	89-96	sorcin	Homo sapiens	141-144
30818192-7	2019	With depth, stronger anoxic conditions resulted in the dominance of reductive hydrolysis leading to a co-occurrence scenario of As (max 4.6 mugL-1) with Zn (max 2514 mugL-1) and Pb (max 740 muL-1) with influences of anthropogenic modes of activities like agriculture and dry deposition from a brick kiln.	Arsenic	128-130	mitochondrial E3 ubiquitin protein ligase 1	Homo sapiens	190-195
30890376-0	2019	Silencing GSK3beta instead of DKK1 can inhibit osteogenic differentiation caused by co-exposure to fluoride and arsenic.	Arsenic	112-119	glycogen synthase kinase 3 beta	Homo sapiens	10-18
30890376-13	2019	The results indicate that silencing GSK3beta instead of DKK1 can inhibit osteogenic differentiation caused by co-exposure to fluoride and arsenic.	Arsenic	138-145	glycogen synthase kinase 3 beta	Homo sapiens	36-44
31285125-2	2019	Our lab has obtained the soluble arsenic from realgar named realgar transforming solution or RTS.	Arsenic	33-40	RT1 class Ib, locus EC2	Rattus norvegicus	93-96
30889423-4	2019	We first confirmed that low levels of arsenic induced excess inflammation evidenced by accumulation of macrophages and lymphocytes in bronchoalveolar lavage fluid (BALF), secretion of pro-inflammatory cytokine IL-1beta in BALF and serum, as well as histological analysis.	Arsenic	38-45	interleukin 1 alpha	Mus musculus	210-218
30889423-5	2019	Flow cytometry analysis revealed that arsenic disturbed CD4/CD8 T-cell ratio in isolated pneumonocytes and splenocytes, as well as enhanced IFN-gamma and reduced IL-4 in spleen.	Arsenic	38-45	CD4 antigen	Mus musculus	56-59
30889423-5	2019	Flow cytometry analysis revealed that arsenic disturbed CD4/CD8 T-cell ratio in isolated pneumonocytes and splenocytes, as well as enhanced IFN-gamma and reduced IL-4 in spleen.	Arsenic	38-45	interferon gamma	Mus musculus	140-149
30889423-5	2019	Flow cytometry analysis revealed that arsenic disturbed CD4/CD8 T-cell ratio in isolated pneumonocytes and splenocytes, as well as enhanced IFN-gamma and reduced IL-4 in spleen.	Arsenic	38-45	interleukin 4	Mus musculus	162-166
30889423-7	2019	We further testified that arsenic enhanced the percentages of CD11c+ DCs, and promoted the expressions of antigen presentation molecule MHC II and cytokine IL-12, co-stimulatory molecules (CD86, CD80), and chemokine receptors (CCR7, CCR5) in vivo.	Arsenic	26-33	integrin alpha X	Mus musculus	62-67
30889423-7	2019	We further testified that arsenic enhanced the percentages of CD11c+ DCs, and promoted the expressions of antigen presentation molecule MHC II and cytokine IL-12, co-stimulatory molecules (CD86, CD80), and chemokine receptors (CCR7, CCR5) in vivo.	Arsenic	26-33	chemokine (C-C motif) receptor 7	Mus musculus	227-231
30889423-7	2019	We further testified that arsenic enhanced the percentages of CD11c+ DCs, and promoted the expressions of antigen presentation molecule MHC II and cytokine IL-12, co-stimulatory molecules (CD86, CD80), and chemokine receptors (CCR7, CCR5) in vivo.	Arsenic	26-33	chemokine (C-C motif) receptor 5	Mus musculus	233-237
30903835-5	2019	The column adsorption study revealed that 2-4 times larger water volumes can be treated by GAC-Fe than GAC, reducing the arsenic concentration from 100 mug/L to the WHO guideline of 10 mug/L.	Arsenic	121-128	glutaminase	Homo sapiens	91-97
30903835-5	2019	The column adsorption study revealed that 2-4 times larger water volumes can be treated by GAC-Fe than GAC, reducing the arsenic concentration from 100 mug/L to the WHO guideline of 10 mug/L.	Arsenic	121-128	glutaminase	Homo sapiens	91-94
30903835-7	2019	The study indicates the high potential of GAC-Fe to remove arsenic from contaminated drinking waters in practical column filters.	Arsenic	59-66	glutaminase	Homo sapiens	42-48
31380187-2	2019	In this study, arsenic class of mineral, arsenic trioxide, clinically approved for treating acute promyelocytic leukemia, is demonstrated to reactivate latent provirus in CD4+ T cells from HIV-1 patients and Simian immunodeficiency virus (SIV)-infected macaques, without significant systemic T cell activation and inflammatory responses.	Arsenic	15-22	CD4 molecule	Homo sapiens	171-174
31172012-4	2019	More precisely, Yap1 is activated under oxidative stress, Yap2/Cad1 under cadmium, Yap4/Cin5 and Yap6 under osmotic shock, Yap5 under iron overload and Yap8/Arr1 by arsenic compounds.	Arsenic	165-172	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	16-20
31172012-4	2019	More precisely, Yap1 is activated under oxidative stress, Yap2/Cad1 under cadmium, Yap4/Cin5 and Yap6 under osmotic shock, Yap5 under iron overload and Yap8/Arr1 by arsenic compounds.	Arsenic	165-172	Cad1p	Saccharomyces cerevisiae S288C	58-62
31172012-4	2019	More precisely, Yap1 is activated under oxidative stress, Yap2/Cad1 under cadmium, Yap4/Cin5 and Yap6 under osmotic shock, Yap5 under iron overload and Yap8/Arr1 by arsenic compounds.	Arsenic	165-172	Cad1p	Saccharomyces cerevisiae S288C	63-67
31172012-4	2019	More precisely, Yap1 is activated under oxidative stress, Yap2/Cad1 under cadmium, Yap4/Cin5 and Yap6 under osmotic shock, Yap5 under iron overload and Yap8/Arr1 by arsenic compounds.	Arsenic	165-172	Cin5p	Saccharomyces cerevisiae S288C	83-87
31172012-4	2019	More precisely, Yap1 is activated under oxidative stress, Yap2/Cad1 under cadmium, Yap4/Cin5 and Yap6 under osmotic shock, Yap5 under iron overload and Yap8/Arr1 by arsenic compounds.	Arsenic	165-172	Cin5p	Saccharomyces cerevisiae S288C	88-92
31172012-4	2019	More precisely, Yap1 is activated under oxidative stress, Yap2/Cad1 under cadmium, Yap4/Cin5 and Yap6 under osmotic shock, Yap5 under iron overload and Yap8/Arr1 by arsenic compounds.	Arsenic	165-172	Yap6p	Saccharomyces cerevisiae S288C	97-101
31172012-4	2019	More precisely, Yap1 is activated under oxidative stress, Yap2/Cad1 under cadmium, Yap4/Cin5 and Yap6 under osmotic shock, Yap5 under iron overload and Yap8/Arr1 by arsenic compounds.	Arsenic	165-172	Arr1p	Saccharomyces cerevisiae S288C	152-156
31172012-4	2019	More precisely, Yap1 is activated under oxidative stress, Yap2/Cad1 under cadmium, Yap4/Cin5 and Yap6 under osmotic shock, Yap5 under iron overload and Yap8/Arr1 by arsenic compounds.	Arsenic	165-172	Arr1p	Saccharomyces cerevisiae S288C	157-161
30738161-6	2019	The removal percentages of arsenic with CA-5 and CAP-5 hollow fiber membrane was 34% and 41% with arsenic removal permeability was 44.42 L/m2h bar and 40.11 L/m2h bar respectively.	Arsenic	27-34	carbonic anhydrase 5A	Homo sapiens	40-44
31139082-10	2019	Together, our results provide evidence for the use of Pts to activate the Nrf2 pathway to alleviate arsenic-induced dermal damage.	Arsenic	100-107	NFE2 like bZIP transcription factor 2	Homo sapiens	74-78
31137629-8	2019	PC 2 (As and Cd) is mainly contributed by anthropogenic origins in the basin.	Arsenic	6-8	chromobox 4	Homo sapiens	0-4
31095595-8	2019	Our analyses demonstrated that IL-1b, IL-2, IL-4 and IL-6 were significantly stimulated as a function of urinary arsenic levels in models adjusted for age, body mass index (BMI), smoking status and PAH-DNA adducts.	Arsenic	113-120	interleukin 1 beta	Homo sapiens	31-36
31095595-8	2019	Our analyses demonstrated that IL-1b, IL-2, IL-4 and IL-6 were significantly stimulated as a function of urinary arsenic levels in models adjusted for age, body mass index (BMI), smoking status and PAH-DNA adducts.	Arsenic	113-120	interleukin 2	Homo sapiens	38-42
31095595-8	2019	Our analyses demonstrated that IL-1b, IL-2, IL-4 and IL-6 were significantly stimulated as a function of urinary arsenic levels in models adjusted for age, body mass index (BMI), smoking status and PAH-DNA adducts.	Arsenic	113-120	interleukin 4	Homo sapiens	44-48
31095595-8	2019	Our analyses demonstrated that IL-1b, IL-2, IL-4 and IL-6 were significantly stimulated as a function of urinary arsenic levels in models adjusted for age, body mass index (BMI), smoking status and PAH-DNA adducts.	Arsenic	113-120	interleukin 6	Homo sapiens	53-57
31095595-10	2019	We found a U-shaped dose response relationship between urinary arsenic and IL-1b.	Arsenic	63-70	interleukin 1 beta	Homo sapiens	75-80
31139082-0	2019	Pterostilbene Activates the Nrf2-Dependent Antioxidant Response to Ameliorate Arsenic-Induced Intracellular Damage and Apoptosis in Human Keratinocytes.	Arsenic	78-85	NFE2 like bZIP transcription factor 2	Homo sapiens	28-32
31139082-2	2019	In the current study, we determine whether Pterostilbene (Pts), as a potent activator of Nrf2, has a protective effect on arsenic-induced cytotoxicity and apoptosis in human keratinocytes.	Arsenic	122-129	NFE2 like bZIP transcription factor 2	Homo sapiens	89-93
31139082-7	2019	Furthermore, arsenic-induced decrease of anti-apoptotic factor Bcl-2 and Bcl-xl, and increase of pro-apoptotic factor Bax and Bad, as well as survival signal related factor caspase 3 activation were reversed by Pts treatment.	Arsenic	13-20	BCL2 apoptosis regulator	Homo sapiens	63-68
31139082-7	2019	Furthermore, arsenic-induced decrease of anti-apoptotic factor Bcl-2 and Bcl-xl, and increase of pro-apoptotic factor Bax and Bad, as well as survival signal related factor caspase 3 activation were reversed by Pts treatment.	Arsenic	13-20	BCL2 like 1	Homo sapiens	73-79
31139082-7	2019	Furthermore, arsenic-induced decrease of anti-apoptotic factor Bcl-2 and Bcl-xl, and increase of pro-apoptotic factor Bax and Bad, as well as survival signal related factor caspase 3 activation were reversed by Pts treatment.	Arsenic	13-20	BCL2 associated X, apoptosis regulator	Homo sapiens	118-121
31139082-7	2019	Furthermore, arsenic-induced decrease of anti-apoptotic factor Bcl-2 and Bcl-xl, and increase of pro-apoptotic factor Bax and Bad, as well as survival signal related factor caspase 3 activation were reversed by Pts treatment.	Arsenic	13-20	caspase 3	Homo sapiens	173-182
30635934-6	2019	Inclusion criteria: articles describing or assessing the use of OCT for visualising the AS.	Arsenic	88-90	plexin A2	Homo sapiens	64-67
30109550-0	2019	Chronic Oral Arsenic Exposure and Its Correlation with Serum S100B Concentration.	Arsenic	13-20	S100 protein, beta polypeptide, neural	Mus musculus	61-66
30109550-3	2019	The objective of this study was to determine the impact of chronic arsenic exposure in drinking water and serum S100B correlation.	Arsenic	67-74	S100 protein, beta polypeptide, neural	Mus musculus	112-117
30109550-12	2019	In conclusion, it could be inferred that long-term arsenic exposure via drinking water leads to brain arsenic accumulation with serum S100B elevated concentration as a probable BBB disruption consequence.	Arsenic	51-58	S100 protein, beta polypeptide, neural	Mus musculus	134-139
31135185-13	2019	Among the arsenic-associated CpGs ([Formula: see text]), we observed significant enrichment of genes annotating to the reactive oxygen species pathway, inflammatory response, and tumor necrosis factor [Formula: see text] ([Formula: see text]) signaling via nuclear factor kappa-B ([Formula: see text]) hallmarks ([Formula: see text]).	Arsenic	10-17	tumor necrosis factor	Homo sapiens	179-200
30784751-4	2019	The results showed that 1% (w/v) leonardite (91.86 +- 2.04%) had the highest efficiency in adsorbing initial arsenic concentration of 2 mg L-1, which was higher than bagasse fly ash (16.25 +- 3.97%), rice husk ash (10.36 +- 1.28%), and sawdust fly ash (63.00 +- 5.67%) under the same condition.	Arsenic	109-116	l(1)L1	Drosophila melanogaster	139-142
30708160-10	2019	The bulk adsorbent of PGA/PFe2O3 presents a high column treatment capacity of arsenic-containing groundwater (4750 BV for As(III), 5730 BV for As(V)), producing only 12 BV eluent.	Arsenic	78-85	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	143-148
30716544-3	2019	The adsorption envelopes reveal that the adsorption of TAsIII on alpha-Fe2O3 is significantly less than that of arsenite (AsIII) in the pH range from 7 to 11 with the initial As concentration of 25 mg L-1.	Arsenic	56-58	L1 cell adhesion molecule	Homo sapiens	201-204
30716544-6	2019	Whereas the uptake of As by alpha-Fe2O3 is highly elevated compared with the value predicted by Langmuir model at pH 7 with high As equilibrium concentration (&gt;40 mg L-1), implying the formation of As-bearing (surface) precipitate.	Arsenic	22-24	L1 cell adhesion molecule	Homo sapiens	169-172
30703610-6	2019	A panel of 63 candidate SNPs was selected for genotyping based on their reported associations with arsenic metabolism (including in As3MT, N6AMT1, and GSTO2 genes).	Arsenic	99-106	arsenite methyltransferase	Homo sapiens	132-137
31068908-10	2019	The arsenic induced elevated levels of superoxide dismutase (SOD), catalase (CAT), reduced glutathione, lipid peroxidation (LPO) and DNA fragmentation, and transmembrane mitochondrial potential was alleviated by khambir extract.	Arsenic	4-11	catalase	Homo sapiens	67-75
31068908-10	2019	The arsenic induced elevated levels of superoxide dismutase (SOD), catalase (CAT), reduced glutathione, lipid peroxidation (LPO) and DNA fragmentation, and transmembrane mitochondrial potential was alleviated by khambir extract.	Arsenic	4-11	catalase	Homo sapiens	77-80
30889356-8	2019	The level of 1,4-dioxane degradation was ~30-50% lower for the UV/chloramine AOP than for the UV/H2O2-chloramine AOP when the concentration of residual chloramines in RO permeate was ~50 muM (3.3 mg/L as Cl2).	Arsenic	38-40	endogenous retrovirus group W member 5	Homo sapiens	204-207
30682541-1	2019	In this study we describe the immobilization of arsenic as scorodite (FeAsO4.2H2O) by a thermophilic iron-oxidizing mixed culture from an acidic sulfate medium containing 500 mg L-1 of Fe(II), 500 mg L-1 As(III) and granular activated carbon (GAC) as the main arsenite oxidant.	Arsenic	48-55	L1 cell adhesion molecule	Homo sapiens	178-181
30682541-1	2019	In this study we describe the immobilization of arsenic as scorodite (FeAsO4.2H2O) by a thermophilic iron-oxidizing mixed culture from an acidic sulfate medium containing 500 mg L-1 of Fe(II), 500 mg L-1 As(III) and granular activated carbon (GAC) as the main arsenite oxidant.	Arsenic	48-55	L1 cell adhesion molecule	Homo sapiens	200-203
30958264-1	2019	We find that variation in the dbt-1 gene underlies natural differences in Caenorhabditis elegans responses to the toxin arsenic.	Arsenic	120-127	Lipoamide acyltransferase component of branched-chain alpha-keto acid dehydrogenase complex, mitochondrial	Caenorhabditis elegans	30-35
30958264-3	2019	We causally linked a non-synonymous variant in the conserved lipoyl domain of DBT-1 to differential arsenic responses.	Arsenic	100-107	Lipoamide acyltransferase component of branched-chain alpha-keto acid dehydrogenase complex, mitochondrial	Caenorhabditis elegans	78-83
31232011-10	2019	Our data suggest that dysregulation and cross-talk of Wnt, Shh and BMP signals play great roles in the process of arsenic-induced carcinogenesis, which could be antagonized by arotinoid trometamol.	Arsenic	114-121	sonic hedgehog signaling molecule	Homo sapiens	59-62
31232011-10	2019	Our data suggest that dysregulation and cross-talk of Wnt, Shh and BMP signals play great roles in the process of arsenic-induced carcinogenesis, which could be antagonized by arotinoid trometamol.	Arsenic	114-121	bone morphogenetic protein 1	Homo sapiens	67-70
30557709-4	2019	Our results revealed that arsenic exposure down-regulated the mRNA expressions of all studied steroidogenic genes (Lhr, Star, P450scc, Hsd3b, Cyp17a1, Hsd17b and Arom).	Arsenic	26-33	luteinizing hormone/choriogonadotropin receptor	Rattus norvegicus	115-118
30557709-4	2019	Our results revealed that arsenic exposure down-regulated the mRNA expressions of all studied steroidogenic genes (Lhr, Star, P450scc, Hsd3b, Cyp17a1, Hsd17b and Arom).	Arsenic	26-33	cytochrome P450, family 11, subfamily a, polypeptide 1	Rattus norvegicus	126-133
30557709-4	2019	Our results revealed that arsenic exposure down-regulated the mRNA expressions of all studied steroidogenic genes (Lhr, Star, P450scc, Hsd3b, Cyp17a1, Hsd17b and Arom).	Arsenic	26-33	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 5	Rattus norvegicus	135-140
30557709-4	2019	Our results revealed that arsenic exposure down-regulated the mRNA expressions of all studied steroidogenic genes (Lhr, Star, P450scc, Hsd3b, Cyp17a1, Hsd17b and Arom).	Arsenic	26-33	cytochrome P450, family 17, subfamily a, polypeptide 1	Rattus norvegicus	142-149
30557709-4	2019	Our results revealed that arsenic exposure down-regulated the mRNA expressions of all studied steroidogenic genes (Lhr, Star, P450scc, Hsd3b, Cyp17a1, Hsd17b and Arom).	Arsenic	26-33	PARP1 binding protein	Rattus norvegicus	162-166
30738023-0	2019	Daphnetin activates the Nrf2-dependent antioxidant response to prevent arsenic-induced oxidative insult in human lung epithelial cells.	Arsenic	71-78	NFE2 like bZIP transcription factor 2	Homo sapiens	24-28
30738023-7	2019	Notably, Daph pretreatment reversed the arsenic-induced decrease in anti-apoptotic factor B-cell lymphoma-2 (Bcl-2) and the increase in pro-apoptotic factor Bcl-2-associated X protein (Bax).	Arsenic	40-47	BCL2 apoptosis regulator	Homo sapiens	90-107
30738023-7	2019	Notably, Daph pretreatment reversed the arsenic-induced decrease in anti-apoptotic factor B-cell lymphoma-2 (Bcl-2) and the increase in pro-apoptotic factor Bcl-2-associated X protein (Bax).	Arsenic	40-47	BCL2 apoptosis regulator	Homo sapiens	109-114
30738023-7	2019	Notably, Daph pretreatment reversed the arsenic-induced decrease in anti-apoptotic factor B-cell lymphoma-2 (Bcl-2) and the increase in pro-apoptotic factor Bcl-2-associated X protein (Bax).	Arsenic	40-47	BCL2 associated X, apoptosis regulator	Homo sapiens	157-183
30738023-7	2019	Notably, Daph pretreatment reversed the arsenic-induced decrease in anti-apoptotic factor B-cell lymphoma-2 (Bcl-2) and the increase in pro-apoptotic factor Bcl-2-associated X protein (Bax).	Arsenic	40-47	BCL2 associated X, apoptosis regulator	Homo sapiens	185-188
30738023-8	2019	The effects of Daph on Nrf2 and HO-1 activation, and arsenic-induced cell viability were largely weakened when Nrf2 was depleted in vitro.	Arsenic	53-60	NFE2 like bZIP transcription factor 2	Homo sapiens	111-115
30738023-9	2019	Accordingly, Daph might ameliorate arsenic-induced cytotoxicity and apoptosis, which may be linked to the induction of Nrf2-dependent antioxidant responses as well as stabilization of the anti-apoptotic factor Bcl-2 in human lung epithelial cells.	Arsenic	35-42	NFE2 like bZIP transcription factor 2	Homo sapiens	119-123
30738023-9	2019	Accordingly, Daph might ameliorate arsenic-induced cytotoxicity and apoptosis, which may be linked to the induction of Nrf2-dependent antioxidant responses as well as stabilization of the anti-apoptotic factor Bcl-2 in human lung epithelial cells.	Arsenic	35-42	BCL2 apoptosis regulator	Homo sapiens	210-215
30703610-11	2019	Further, As3MT, GSTO2, and N6AMT1 polymorphisms showed different effect sizes on DMA% conditional on arsenic exposure levels.	Arsenic	101-108	arsenite methyltransferase	Homo sapiens	9-14
30703610-11	2019	Further, As3MT, GSTO2, and N6AMT1 polymorphisms showed different effect sizes on DMA% conditional on arsenic exposure levels.	Arsenic	101-108	glutathione S-transferase omega 2	Homo sapiens	16-21
30703610-11	2019	Further, As3MT, GSTO2, and N6AMT1 polymorphisms showed different effect sizes on DMA% conditional on arsenic exposure levels.	Arsenic	101-108	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	27-33
30769280-0	2019	Circulating miRNA-126, -145 and -155 levels in Mexican women exposed to inorganic arsenic via drinking water.	Arsenic	82-89	microRNA 126	Homo sapiens	12-36
30769280-1	2019	The aim of this research was to investigate circulating expression levels of three miRNAs (miR-126, miR-155, and miR-145) proposed as predictive CVD biomarkers in Mexican women exposed to inorganic arsenic via drinking water.	Arsenic	198-205	microRNA 126	Homo sapiens	91-98
30769280-1	2019	The aim of this research was to investigate circulating expression levels of three miRNAs (miR-126, miR-155, and miR-145) proposed as predictive CVD biomarkers in Mexican women exposed to inorganic arsenic via drinking water.	Arsenic	198-205	microRNA 155	Homo sapiens	100-107
30769280-1	2019	The aim of this research was to investigate circulating expression levels of three miRNAs (miR-126, miR-155, and miR-145) proposed as predictive CVD biomarkers in Mexican women exposed to inorganic arsenic via drinking water.	Arsenic	198-205	microRNA 145	Homo sapiens	113-120
30835071-0	2019	Sulforaphane potentially attenuates arsenic-induced nephrotoxicity via the PI3K/Akt/Nrf2 pathway in albino Wistar rats.	Arsenic	36-43	AKT serine/threonine kinase 1	Rattus norvegicus	80-83
30835071-0	2019	Sulforaphane potentially attenuates arsenic-induced nephrotoxicity via the PI3K/Akt/Nrf2 pathway in albino Wistar rats.	Arsenic	36-43	NFE2 like bZIP transcription factor 2	Rattus norvegicus	84-88
30835071-9	2019	These results show that dietary supplementation with SFN protects against Ar-induced nephrotoxicity via the PI3K/Akt-mediated Nrf2 signaling pathway in the rat kidney.	Arsenic	74-76	AKT serine/threonine kinase 1	Rattus norvegicus	113-116
30835071-9	2019	These results show that dietary supplementation with SFN protects against Ar-induced nephrotoxicity via the PI3K/Akt-mediated Nrf2 signaling pathway in the rat kidney.	Arsenic	74-76	NFE2 like bZIP transcription factor 2	Rattus norvegicus	126-130
30362509-0	2019	Taurine improves low-level inorganic arsenic-induced insulin resistance by activating PPARgamma-mTORC2 signalling and inhibiting hepatic autophagy.	Arsenic	37-44	peroxisome proliferator activated receptor gamma	Mus musculus	86-95
30769048-0	2019	Mangiferin alleviates arsenic induced oxidative lung injury via upregulation of the Nrf2-HO1 axis.	Arsenic	22-29	NFE2 like bZIP transcription factor 2	Homo sapiens	84-88
30769048-0	2019	Mangiferin alleviates arsenic induced oxidative lung injury via upregulation of the Nrf2-HO1 axis.	Arsenic	22-29	heme oxygenase 1	Homo sapiens	89-92
30191986-4	2019	It is in this context that the current study evaluated the effects of long-term arsenic exposure on the cellular response in morphology, and marker genes expression with respect to fibrosis using human kidney 2 (HK-2) epithelial cells.	Arsenic	80-87	hexokinase 2	Homo sapiens	212-216
30191986-5	2019	Results of this study revealed that in addition to increased growth, HK-2 cells underwent phenotypic, biochemical and molecular changes indicative of epithelial-mesenchymal transition (EMT) in response to the exposure to arsenic.	Arsenic	221-228	hexokinase 2	Homo sapiens	69-73
30191986-6	2019	Most importantly, the arsenic-exposed cells acquired the pathogenic features of fibrosis as supported by increased expression of markers for fibrosis, such as Collagen I, Fibronectin, transforming growth factor beta, and alpha-smooth muscle actin.	Arsenic	22-29	fibronectin 1	Homo sapiens	171-182
30191986-6	2019	Most importantly, the arsenic-exposed cells acquired the pathogenic features of fibrosis as supported by increased expression of markers for fibrosis, such as Collagen I, Fibronectin, transforming growth factor beta, and alpha-smooth muscle actin.	Arsenic	22-29	transforming growth factor beta 1	Homo sapiens	184-215
30654099-0	2019	Systematic review of arsenic in fresh seafood from the Mediterranean Sea and European Atlantic coasts: A health risk assessment.	Arsenic	21-28	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	69-72
30256405-0	2019	Nerve growth factor prevents arsenic-induced toxicity in PC12 cells through the AKT/GSK-3beta/NFAT pathway.	Arsenic	29-36	nerve growth factor	Rattus norvegicus	0-19
30256405-0	2019	Nerve growth factor prevents arsenic-induced toxicity in PC12 cells through the AKT/GSK-3beta/NFAT pathway.	Arsenic	29-36	AKT serine/threonine kinase 1	Rattus norvegicus	80-83
30256405-0	2019	Nerve growth factor prevents arsenic-induced toxicity in PC12 cells through the AKT/GSK-3beta/NFAT pathway.	Arsenic	29-36	glycogen synthase kinase 3 beta	Rattus norvegicus	84-93
30256405-0	2019	Nerve growth factor prevents arsenic-induced toxicity in PC12 cells through the AKT/GSK-3beta/NFAT pathway.	Arsenic	29-36	nuclear factor of activated T-cells 5	Rattus norvegicus	94-98
30362509-0	2019	Taurine improves low-level inorganic arsenic-induced insulin resistance by activating PPARgamma-mTORC2 signalling and inhibiting hepatic autophagy.	Arsenic	37-44	CREB regulated transcription coactivator 2	Mus musculus	96-102
30191986-8	2019	Additionally, the expression of epigenetic genes (DNA methyltransferases 3a and 3b; methyl-CpG binding domain 4) was increased in arsenic-exposed cells.	Arsenic	130-137	DNA methyltransferase 3 beta	Homo sapiens	50-82
30684567-0	2019	Arsenic induces gender difference of estrogen receptor in AECII cells from ICR fetal mice.	Arsenic	0-7	estrogen receptor 1 (alpha)	Mus musculus	37-54
30783936-8	2019	The changing levels of As, Zn and Se seems to affect the severity of inflammatory reactions based on IL-6, IL-10 and TNF-alpha levels (r = 0.755, r = 0.679 and r = 0.617, respectively, for all p &lt; 0.01).	Arsenic	23-25	interleukin 6	Homo sapiens	101-105
30783936-8	2019	The changing levels of As, Zn and Se seems to affect the severity of inflammatory reactions based on IL-6, IL-10 and TNF-alpha levels (r = 0.755, r = 0.679 and r = 0.617, respectively, for all p &lt; 0.01).	Arsenic	23-25	interleukin 10	Homo sapiens	107-112
30783936-8	2019	The changing levels of As, Zn and Se seems to affect the severity of inflammatory reactions based on IL-6, IL-10 and TNF-alpha levels (r = 0.755, r = 0.679 and r = 0.617, respectively, for all p &lt; 0.01).	Arsenic	23-25	tumor necrosis factor	Homo sapiens	117-126
30684567-5	2019	Results showed that arsenic increased the expression levels of mRNA and protein of ERbeta, ERK1/2 and NF-kappaB/P65, and ICI182780 inhibited the increase.	Arsenic	20-27	estrogen receptor 2 (beta)	Mus musculus	83-89
30684567-5	2019	Results showed that arsenic increased the expression levels of mRNA and protein of ERbeta, ERK1/2 and NF-kappaB/P65, and ICI182780 inhibited the increase.	Arsenic	20-27	mitogen-activated protein kinase 3	Mus musculus	91-97
30684567-5	2019	Results showed that arsenic increased the expression levels of mRNA and protein of ERbeta, ERK1/2 and NF-kappaB/P65, and ICI182780 inhibited the increase.	Arsenic	20-27	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	102-115
30684567-7	2019	To summarize, the observations here strongly suggested that estrogen receptor and its mediated signal pathway molecules might have critical roles of the gender difference of incidence of lung cancer in arsenic induced.	Arsenic	202-209	estrogen receptor 1 (alpha)	Mus musculus	60-77
30763586-4	2019	ATO acts through a direct arsenic binding to cysteine residues in zinc fingers located in promyelocytic leukemia protein (PML), thus killing the leukemia stem cells (LSCs).	Arsenic	26-33	PML nuclear body scaffold	Homo sapiens	90-120
30674471-8	2019	Critically, the combination of ATRA and arsenic fully rescues therapeutic response in FLT3-ITD APLs, restoring PML/RARA degradation, PML nuclear body reformation, P53 activation, and APL eradication.	Arsenic	40-47	FMS-like tyrosine kinase 3	Mus musculus	86-90
30674471-8	2019	Critically, the combination of ATRA and arsenic fully rescues therapeutic response in FLT3-ITD APLs, restoring PML/RARA degradation, PML nuclear body reformation, P53 activation, and APL eradication.	Arsenic	40-47	promyelocytic leukemia	Mus musculus	111-114
30674471-8	2019	Critically, the combination of ATRA and arsenic fully rescues therapeutic response in FLT3-ITD APLs, restoring PML/RARA degradation, PML nuclear body reformation, P53 activation, and APL eradication.	Arsenic	40-47	retinoic acid receptor, alpha	Mus musculus	115-119
30674471-8	2019	Critically, the combination of ATRA and arsenic fully rescues therapeutic response in FLT3-ITD APLs, restoring PML/RARA degradation, PML nuclear body reformation, P53 activation, and APL eradication.	Arsenic	40-47	promyelocytic leukemia	Mus musculus	133-136
30674471-8	2019	Critically, the combination of ATRA and arsenic fully rescues therapeutic response in FLT3-ITD APLs, restoring PML/RARA degradation, PML nuclear body reformation, P53 activation, and APL eradication.	Arsenic	40-47	transformation related protein 53, pseudogene	Mus musculus	163-166
30674471-9	2019	Moreover, arsenic targeting of normal PML also contributes to APL response in vivo.	Arsenic	10-17	promyelocytic leukemia	Mus musculus	38-41
30674471-10	2019	These unexpected results explain the less favorable outcome of FLT3-ITD APLs with ATRA-based regimens, and stress the key role of PML nuclear bodies in APL eradication by the ATRA/arsenic combination.	Arsenic	180-187	FMS-like tyrosine kinase 3	Mus musculus	63-67
30674471-10	2019	These unexpected results explain the less favorable outcome of FLT3-ITD APLs with ATRA-based regimens, and stress the key role of PML nuclear bodies in APL eradication by the ATRA/arsenic combination.	Arsenic	180-187	promyelocytic leukemia	Mus musculus	130-133
30893314-0	2019	A missense variant in FTCD is associated with arsenic metabolism and toxicity phenotypes in Bangladesh.	Arsenic	46-53	formimidoyltransferase cyclodeaminase	Homo sapiens	22-26
30893314-4	2019	Arsenic metabolism efficiency varies among individuals, in part due to genetic variation near AS3MT (arsenite methyltransferase; 10q24.32).	Arsenic	0-7	arsenite methyltransferase	Homo sapiens	94-99
30893314-10	2019	FTCD is critical for catabolism of histidine, a process that generates one-carbon units that can enter the one-carbon/folate cycle, which provides methyl groups for arsenic metabolism.	Arsenic	165-172	formimidoyltransferase cyclodeaminase	Homo sapiens	0-4
30537579-4	2019	Arsenic exposure was determined as the sum concentration of arsenic metabolites (inorganic arsenic; monomethylarsonic acid, MMA; and dimethylarsinic acid, DMA) in urine (U-As), measured by HPLC-HG-ICP-MS.	Arsenic	0-7	monocyte to macrophage differentiation associated	Homo sapiens	124-127
30537579-6	2019	The women had a wide variation in U-As (range 12-407 mug/L, median 65 mug/L) and a markedly efficient metabolism of arsenic with low %MMA (median 7.7%, range: 2.2-18%) and high %DMA (80%, range: 54-91%) in urine.	Arsenic	116-123	monocyte to macrophage differentiation associated	Homo sapiens	134-137
30677931-6	2019	In particular, after 7 days of P10 application, the highest As concentration in S6, S8 and TR soil solutions reached 2298.4, 829.9 and 153.9 mug/L respectively, with the AsV state accounting for 93%, 97% and 18% of As.	Arsenic	60-62	S100 calcium binding protein A10	Homo sapiens	31-34
30677931-6	2019	In particular, after 7 days of P10 application, the highest As concentration in S6, S8 and TR soil solutions reached 2298.4, 829.9 and 153.9 mug/L respectively, with the AsV state accounting for 93%, 97% and 18% of As.	Arsenic	60-62	ribosomal protein S8	Homo sapiens	84-93
30677931-6	2019	In particular, after 7 days of P10 application, the highest As concentration in S6, S8 and TR soil solutions reached 2298.4, 829.9 and 153.9 mug/L respectively, with the AsV state accounting for 93%, 97% and 18% of As.	Arsenic	170-172	S100 calcium binding protein A10	Homo sapiens	31-34
30763586-4	2019	ATO acts through a direct arsenic binding to cysteine residues in zinc fingers located in promyelocytic leukemia protein (PML), thus killing the leukemia stem cells (LSCs).	Arsenic	26-33	PML nuclear body scaffold	Homo sapiens	122-125
30620428-0	2019	From As-Zincoarsasilene (LZn-As=SiL") to Arsaethynolato (As C-O) and Arsaketenylido (O=C=As) Zinc Complexes.	Arsenic	5-7	STIL centriolar assembly protein	Homo sapiens	32-36
30742845-0	2019	Nrf2 deficiency aggravates the increase in osteoclastogenesis and bone loss induced by inorganic arsenic.	Arsenic	97-104	nuclear factor, erythroid derived 2, like 2	Mus musculus	0-4
30742845-5	2019	Here we tested the hypothesis that loss of Nrf2 will increase arsenic-induced bone loss.	Arsenic	62-69	nuclear factor, erythroid derived 2, like 2	Mus musculus	43-47
30742845-6	2019	We treated 40 week-old Nrf2+/+ and Nrf2-/- mice with 5 ppm arsenic in the drinking water, which produces a blood arsenic level similar to humans living in areas where arsenic exposure is endemic.	Arsenic	59-66	nuclear factor, erythroid derived 2, like 2	Mus musculus	35-39
30742845-7	2019	After 4 months, Micro-CT and dual-energy x-ray analysis revealed a drastic overall decrease in the bone volume with arsenic treatment in mice lacking Nrf2.	Arsenic	116-123	nuclear factor, erythroid derived 2, like 2	Mus musculus	150-154
30742845-8	2019	Deficiency of Nrf2 in RAW 264.7 cells or bone marrow-derived macrophages (BMMs) promoted arsenic-induced osteoclast differentiation.	Arsenic	89-96	nuclear factor, erythroid derived 2, like 2	Mus musculus	14-18
30742845-9	2019	Lack of Nrf2 increases arsenic-induced ROS levels and phosphorylation of p38.	Arsenic	23-30	nuclear factor, erythroid derived 2, like 2	Mus musculus	8-12
30742845-9	2019	Lack of Nrf2 increases arsenic-induced ROS levels and phosphorylation of p38.	Arsenic	23-30	mitogen-activated protein kinase 14	Mus musculus	73-76
30742845-10	2019	N-Acetyl-cysteine and SB203580 pretreatment essentially abolished arsenic-induced phosphorylation of p38 and reversed arsenic-induced increased osteoclast differentiation in Nrf2 deficiency.	Arsenic	66-73	mitogen-activated protein kinase 14	Mus musculus	101-104
30742845-10	2019	N-Acetyl-cysteine and SB203580 pretreatment essentially abolished arsenic-induced phosphorylation of p38 and reversed arsenic-induced increased osteoclast differentiation in Nrf2 deficiency.	Arsenic	66-73	nuclear factor, erythroid derived 2, like 2	Mus musculus	174-178
30742845-10	2019	N-Acetyl-cysteine and SB203580 pretreatment essentially abolished arsenic-induced phosphorylation of p38 and reversed arsenic-induced increased osteoclast differentiation in Nrf2 deficiency.	Arsenic	118-125	nuclear factor, erythroid derived 2, like 2	Mus musculus	174-178
30742845-11	2019	Taken together, our data suggest that loss of Nrf2 causes increased oxidative stress and enhanced susceptibility to arsenic-induced bone loss.	Arsenic	116-123	nuclear factor, erythroid derived 2, like 2	Mus musculus	46-50
30930785-2	2019	Arsenic (As), a toxic metalloid, is known to affect the cultivation of food crops in many regions of the world; however, the changes in chlorophyll, catalase (CAT), and proline in response to As stress and the role of stress relief substances remain largely unknown in mung bean (Vigna radiate L.).	Arsenic	0-7	catalase	Vigna radiata	149-157
30930785-2	2019	Arsenic (As), a toxic metalloid, is known to affect the cultivation of food crops in many regions of the world; however, the changes in chlorophyll, catalase (CAT), and proline in response to As stress and the role of stress relief substances remain largely unknown in mung bean (Vigna radiate L.).	Arsenic	0-7	catalase	Vigna radiata	159-162
30930785-2	2019	Arsenic (As), a toxic metalloid, is known to affect the cultivation of food crops in many regions of the world; however, the changes in chlorophyll, catalase (CAT), and proline in response to As stress and the role of stress relief substances remain largely unknown in mung bean (Vigna radiate L.).	Arsenic	9-11	catalase	Vigna radiata	149-157
30930785-2	2019	Arsenic (As), a toxic metalloid, is known to affect the cultivation of food crops in many regions of the world; however, the changes in chlorophyll, catalase (CAT), and proline in response to As stress and the role of stress relief substances remain largely unknown in mung bean (Vigna radiate L.).	Arsenic	9-11	catalase	Vigna radiata	159-162
30806404-3	2019	Here, by using density functional theory calculations, we predict a series of stable 2D MnX (X = P, As, Sb) monolayers, among which MnP and MnAs monolayers exhibit intrinsic ferromagnetic (FM) ordering and considerably large MAEs of 166 and 281 mueV per Mn atom, respectively.	Arsenic	100-102	keratin 86	Homo sapiens	88-91
30580142-4	2019	Capturing cobalt (Co(II)) from filtered river water doped with competing metals (Cu, As, Ag, Cd, Hg, Tl, and Pb) was most effective from pH 5-8 with binding affinity ranged from IDAA &gt; DE4A &gt; ED3A &gt; Ac-Phos &gt; SH on SAMMS.	Arsenic	85-87	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	18-24
30428081-3	2019	In freshly isolated human platelets in vitro, arsenic potentiated TCPA prompted by diverse cancer cell lines, which was attributable to increased platelet reactivity to TCPA with respect to thrombin generation and P-selectin, GPIIb/IIIa expression.	Arsenic	46-53	coagulation factor II, thrombin	Homo sapiens	190-198
30703382-0	2019	Bi-directional regulation of TGF-beta/Smad pathway by arsenic: A systemic review and meta-analysis of in vivo and in vitro studies.	Arsenic	54-61	transforming growth factor beta 1	Homo sapiens	29-37
30703382-3	2019	However, the mechanism of arsenic-induced fibrosis through TGF-beta/Smad signaling pathway has remained controversial.	Arsenic	26-33	transforming growth factor beta 1	Homo sapiens	59-67
30703382-4	2019	OBJECTIVE: A systematic review and meta-analysis was performed to clarify the relationship between arsenic and TGF-beta/Smad pathway, providing a theoretical basis of fibrosis process caused by arsenic.	Arsenic	99-106	transforming growth factor beta 1	Homo sapiens	111-119
30703382-4	2019	OBJECTIVE: A systematic review and meta-analysis was performed to clarify the relationship between arsenic and TGF-beta/Smad pathway, providing a theoretical basis of fibrosis process caused by arsenic.	Arsenic	194-201	transforming growth factor beta 1	Homo sapiens	111-119
30703382-5	2019	METHODS: A meta-analysis was used to reveal a correlation between arsenic and fibrosis markers of TGF-beta/Smad pathway, including 47 articles of both in vivo and in vitro studies.	Arsenic	66-73	transforming growth factor beta 1	Homo sapiens	98-106
30703382-8	2019	RESULTS: Arsenic exposure up-regulated the expression of TGF-beta1, p-Smad2/3, alpha-SMA, Collagen1/3 and FN.	Arsenic	9-16	transforming growth factor beta 1	Homo sapiens	57-66
30869553-0	2019	Grape seed proanthocyanidin extract alleviates arsenic-induced lung damage through NF-kappaB signaling.	Arsenic	47-54	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	83-92
30664189-0	2019	Arsenic-induced BRCA1 CpG promoter methylation is associated with the downregulation of ERalpha and resistance to tamoxifen in MCF7 breast cancer cells and mouse mammary tumor xenografts.	Arsenic	0-7	BRCA1 DNA repair associated	Homo sapiens	16-21
30664189-0	2019	Arsenic-induced BRCA1 CpG promoter methylation is associated with the downregulation of ERalpha and resistance to tamoxifen in MCF7 breast cancer cells and mouse mammary tumor xenografts.	Arsenic	0-7	estrogen receptor 1	Homo sapiens	88-95
30732868-8	2019	While serum arsenic was negatively associated with Ccr (r = -0.328, p = 0.002) and eGFR (r = -0.248, p  = 0.020).	Arsenic	12-19	epidermal growth factor receptor	Homo sapiens	83-87
30703382-9	2019	The dose-response relationship showed that low dose (&lt;=5 mumol/L) arsenic exposure up-regulated the expression of TGF-beta1, whereas high doses had a tendency to down-regulate that of TGF-beta1.	Arsenic	69-76	transforming growth factor beta 1	Homo sapiens	117-126
30703382-9	2019	The dose-response relationship showed that low dose (&lt;=5 mumol/L) arsenic exposure up-regulated the expression of TGF-beta1, whereas high doses had a tendency to down-regulate that of TGF-beta1.	Arsenic	69-76	transforming growth factor beta 1	Homo sapiens	187-196
30703382-10	2019	Subgroup analysis showed that low or short-term arsenic exposure induced the expression of TGF-beta1 and fibrosis markers.	Arsenic	48-55	transforming growth factor beta 1	Homo sapiens	91-100
30703382-11	2019	CONCLUSION: The results indicated that arsenic activates the TGF-beta/Smad pathway and induced fibrosis.	Arsenic	39-46	transforming growth factor beta 1	Homo sapiens	61-69
28994024-4	2019	Rats that experienced arsenic ingestion showed a significant lessening in the activities of uterine superoxide dismutase (SOD), catalase activities, and the level of non-protein soluble thiol (NPSH) with a concomitant increase in malondialdehyde (MDA) and conjugated dienes (CD).	Arsenic	22-29	catalase	Rattus norvegicus	128-136
30428081-3	2019	In freshly isolated human platelets in vitro, arsenic potentiated TCPA prompted by diverse cancer cell lines, which was attributable to increased platelet reactivity to TCPA with respect to thrombin generation and P-selectin, GPIIb/IIIa expression.	Arsenic	46-53	selectin P	Homo sapiens	214-224
30428081-3	2019	In freshly isolated human platelets in vitro, arsenic potentiated TCPA prompted by diverse cancer cell lines, which was attributable to increased platelet reactivity to TCPA with respect to thrombin generation and P-selectin, GPIIb/IIIa expression.	Arsenic	46-53	integrin subunit alpha 2b	Homo sapiens	226-231
30819207-8	2019	In particular, we identified an inverse relationship between arsenic exposure and expression of the gene encoding the histone methyltransferase, PRDM6 (p &lt; 0.001).	Arsenic	61-68	PR/SET domain 9	Homo sapiens	118-143
30819207-8	2019	In particular, we identified an inverse relationship between arsenic exposure and expression of the gene encoding the histone methyltransferase, PRDM6 (p &lt; 0.001).	Arsenic	61-68	PR/SET domain 6	Homo sapiens	145-150
30677399-5	2019	In human hepatic stellate cell line LX-2 cells, we found that As2O3-induced activation of HSCs was autophagy-dependent, and we found that peroxisome proliferator activated receptors alpha (PPARalpha) played an important role in arsenic-induced HSCs activation.	Arsenic	228-235	peroxisome proliferator activated receptor alpha	Homo sapiens	138-187
30677399-5	2019	In human hepatic stellate cell line LX-2 cells, we found that As2O3-induced activation of HSCs was autophagy-dependent, and we found that peroxisome proliferator activated receptors alpha (PPARalpha) played an important role in arsenic-induced HSCs activation.	Arsenic	228-235	peroxisome proliferator activated receptor alpha	Homo sapiens	189-198
30760301-5	2019	Zip code residential levels of airborne PAHs and metals (arsenic, cadmium, chromium, cobalt, lead, manganese, mercury, nickel, and selenium) were assessed using the 2011 EPA National Air Toxics Assessment.	Arsenic	57-64	death associated protein kinase 3	Homo sapiens	0-3
30317180-10	2019	These results indicate that the prioritization of As and Pb pollution and control of agricultural runoff will play an important role in the ecological protection in the TGR"s riparian ecosystems.	Arsenic	50-52	thioredoxin reductase 3	Homo sapiens	169-172
30813460-4	2019	Immunoblot and RT-qPCR assays showed that arsenic (AS2O3) treatments enhanced the gene expression of MT3.	Arsenic	42-49	metallothionein 3	Homo sapiens	101-104
30813460-7	2019	Moreover, knockdown of MT3 enhanced arsenic-induced apoptosis determined by the Annexin V-FITC apoptosis assay.	Arsenic	36-43	metallothionein 3	Homo sapiens	23-26
30813460-7	2019	Moreover, knockdown of MT3 enhanced arsenic-induced apoptosis determined by the Annexin V-FITC apoptosis assay.	Arsenic	36-43	annexin A5	Homo sapiens	80-89
30813460-9	2019	The experiments indicated that MT3 is an arsenic- and hypoxia-upregulated oncogene that promotes cell growth and invasion of bladder carcinoma cells via downregulation of NDRG1, NDRG2, and MASPIN expressions.	Arsenic	41-48	metallothionein 3	Homo sapiens	31-34
30813460-9	2019	The experiments indicated that MT3 is an arsenic- and hypoxia-upregulated oncogene that promotes cell growth and invasion of bladder carcinoma cells via downregulation of NDRG1, NDRG2, and MASPIN expressions.	Arsenic	41-48	N-myc downstream regulated 1	Homo sapiens	171-176
30813460-9	2019	The experiments indicated that MT3 is an arsenic- and hypoxia-upregulated oncogene that promotes cell growth and invasion of bladder carcinoma cells via downregulation of NDRG1, NDRG2, and MASPIN expressions.	Arsenic	41-48	serpin family B member 5	Homo sapiens	189-195
30439660-0	2019	Ultrafast removal of arsenic using solid solution of aero-gel based Ce1-XTixO2-Y oxide nanoparticles.	Arsenic	21-28	carboxylesterase 1	Homo sapiens	68-71
30523905-0	2019	Density functional theory study of structural and thermodynamical stabilities of ferromagnetic MnX (X = P, As, Sb, Bi) compounds.	Arsenic	107-109	keratin 86	Homo sapiens	95-98
30292115-0	2019	In situ arsenic speciation and the release kinetics in coastal sediments: A case study in Daya Bay, South China Sea.	Arsenic	8-15	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	112-115
30593951-6	2019	Collectively, our results suggest that arsenic may increase host susceptibility to malaria through suppression of B cell proliferation and enhancement of adhesion between iRBC and endothelium by increasing ICAM-1.	Arsenic	39-46	intercellular adhesion molecule 1	Mus musculus	206-212
30593951-5	2019	ICAM-1, an adhesion protein involved in parasite-infected red blood cell (iRBC) binding to endothelium, and HIF-1alpha, a hypoxia marker protein in the descending aorta, were increased in the As-I group compared to the I group.	Arsenic	192-194	intercellular adhesion molecule 1	Mus musculus	0-6
30511220-1	2019	The present work focused on the effects of different reagents on the remediation of arsenic and chromium co-contaminated soil by electrokinetic technology coupled with permeable reactive barrier (EK-PRB).	Arsenic	84-91	RB transcriptional corepressor 1	Homo sapiens	199-202
30511220-7	2019	After EK-PRB, the As and Cr were efficiently captured by CaAl-LDH, resulting in maximal fixed amounts of 126.5 mg/kg (As) and 1507.6 mg/kg (Cr).	Arsenic	18-20	RB transcriptional corepressor 1	Homo sapiens	9-12
30529123-4	2019	MDA-MB-231 cells, when treated with AS concentrations (25-100 mug/mL) resulted in significant reduction of invasion and migration as well as the downregulation of VEGF, uPAR, uPA and MMP-9 (inhibition of PI3K/AKT/NFkappaB pathways).	Arsenic	36-38	vascular endothelial growth factor A	Homo sapiens	163-167
30593951-5	2019	ICAM-1, an adhesion protein involved in parasite-infected red blood cell (iRBC) binding to endothelium, and HIF-1alpha, a hypoxia marker protein in the descending aorta, were increased in the As-I group compared to the I group.	Arsenic	192-194	hypoxia inducible factor 1, alpha subunit	Mus musculus	108-118
30529123-4	2019	MDA-MB-231 cells, when treated with AS concentrations (25-100 mug/mL) resulted in significant reduction of invasion and migration as well as the downregulation of VEGF, uPAR, uPA and MMP-9 (inhibition of PI3K/AKT/NFkappaB pathways).	Arsenic	36-38	plasminogen activator, urokinase receptor	Homo sapiens	169-173
30529123-4	2019	MDA-MB-231 cells, when treated with AS concentrations (25-100 mug/mL) resulted in significant reduction of invasion and migration as well as the downregulation of VEGF, uPAR, uPA and MMP-9 (inhibition of PI3K/AKT/NFkappaB pathways).	Arsenic	36-38	proline rich acidic protein 1	Homo sapiens	169-172
30529123-4	2019	MDA-MB-231 cells, when treated with AS concentrations (25-100 mug/mL) resulted in significant reduction of invasion and migration as well as the downregulation of VEGF, uPAR, uPA and MMP-9 (inhibition of PI3K/AKT/NFkappaB pathways).	Arsenic	36-38	matrix metallopeptidase 9	Homo sapiens	183-188
30529123-4	2019	MDA-MB-231 cells, when treated with AS concentrations (25-100 mug/mL) resulted in significant reduction of invasion and migration as well as the downregulation of VEGF, uPAR, uPA and MMP-9 (inhibition of PI3K/AKT/NFkappaB pathways).	Arsenic	36-38	AKT serine/threonine kinase 1	Homo sapiens	209-212
30529123-4	2019	MDA-MB-231 cells, when treated with AS concentrations (25-100 mug/mL) resulted in significant reduction of invasion and migration as well as the downregulation of VEGF, uPAR, uPA and MMP-9 (inhibition of PI3K/AKT/NFkappaB pathways).	Arsenic	36-38	nuclear factor kappa B subunit 1	Homo sapiens	213-221
30529123-6	2019	Inhibition of Smad3 signaling pathway, downregulation of beta-catenin pathway and upregulation of GSK3beta expression were also observed while, suppression of metastasis and EMT in TGF-beta1-stimulated non-tumorigenic MCF-10A cells was observed when treated with AS.	Arsenic	263-265	SMAD family member 3	Homo sapiens	14-19
30529123-6	2019	Inhibition of Smad3 signaling pathway, downregulation of beta-catenin pathway and upregulation of GSK3beta expression were also observed while, suppression of metastasis and EMT in TGF-beta1-stimulated non-tumorigenic MCF-10A cells was observed when treated with AS.	Arsenic	263-265	transforming growth factor beta 1	Homo sapiens	181-190
30503583-0	2019	Ellagic and ferulic acids protect arsenic-induced male reproductive toxicity via regulating Nfe2l2, Ppargc1a and StAR expressions in testis.	Arsenic	34-41	nuclear factor, erythroid derived 2, like 2	Mus musculus	92-98
30073504-0	2019	Correction to: Sneaky Entry of IFNgamma Through Arsenic-Induced Leaky Blood-Brain Barrier Reduces CD200 Expression by Microglial pro-Inflammatory Cytokine.	Arsenic	48-55	interferon gamma	Homo sapiens	31-39
30385301-0	2019	SirT3 regulates diabetogenic effects caused by arsenic: An implication for mitochondrial complex II modification.	Arsenic	47-54	sirtuin 3	Rattus norvegicus	0-5
30385301-2	2019	Arsenic exposure is a potential risk factor for type 2 diabetes development which, by disrupting mitochondrial respiration and SirT3 enzyme activity, enhances reactive oxygen species (ROS) level and evokes oxidative stress.	Arsenic	0-7	sirtuin 3	Rattus norvegicus	127-132
30385301-3	2019	In this study the impact of arsenic exposure on the mitochondrial function and SirT3 from rat"s liver were examined in the presence or absence of metformin and berberine.	Arsenic	28-35	sirtuin 3	Rattus norvegicus	79-84
29948949-0	2019	Sneaky Entry of IFNgamma Through Arsenic-Induced Leaky Blood-Brain Barrier Reduces CD200 Expression by Microglial pro-Inflammatory Cytokine.	Arsenic	33-40	interferon gamma	Mus musculus	16-24
29948949-0	2019	Sneaky Entry of IFNgamma Through Arsenic-Induced Leaky Blood-Brain Barrier Reduces CD200 Expression by Microglial pro-Inflammatory Cytokine.	Arsenic	33-40	CD200 antigen	Mus musculus	83-88
29948949-2	2019	Previously, we showed that arsenic (0.38 mg/kg body weight) exposure induces microglial activation and consequently IL-6/TNF-alpha secretion.	Arsenic	27-34	interleukin 6	Mus musculus	116-120
29948949-2	2019	Previously, we showed that arsenic (0.38 mg/kg body weight) exposure induces microglial activation and consequently IL-6/TNF-alpha secretion.	Arsenic	27-34	tumor necrosis factor	Mus musculus	121-130
29948949-4	2019	Therefore, the present study was focused on checking arsenic-induced alteration in CD200 expression and revealing the underlying mechanism.	Arsenic	53-60	CD200 antigen	Mus musculus	83-88
29948949-5	2019	Male BALB/c mice were exposed to arsenic (vehicle, 0.038 and 0.38 mg/kg body weight) for 60 days, and the expression level of CD200 was found to be decreased which was rescued by minocycline (33 mg/kg body weight) co-administration.	Arsenic	33-40	CD200 antigen	Mus musculus	126-131
29948949-6	2019	Higher CD68 staining, increased level of IL-6/TNF-alpha, as well as higher level of IFNgamma, were observed in in vivo arsenic-exposed groups.	Arsenic	119-126	CD68 antigen	Mus musculus	7-11
29948949-6	2019	Higher CD68 staining, increased level of IL-6/TNF-alpha, as well as higher level of IFNgamma, were observed in in vivo arsenic-exposed groups.	Arsenic	119-126	interleukin 6	Mus musculus	41-45
29948949-6	2019	Higher CD68 staining, increased level of IL-6/TNF-alpha, as well as higher level of IFNgamma, were observed in in vivo arsenic-exposed groups.	Arsenic	119-126	tumor necrosis factor	Mus musculus	46-55
29948949-6	2019	Higher CD68 staining, increased level of IL-6/TNF-alpha, as well as higher level of IFNgamma, were observed in in vivo arsenic-exposed groups.	Arsenic	119-126	interferon gamma	Mus musculus	84-92
29948949-10	2019	Finally, intracerebral injection of anti-IFNgamma neutralizing antibody in arsenic-exposed brain reduced microglia activation (IL-6 and TNF-alpha and CD68 expression) and subsequently rescued CD200 level.	Arsenic	75-82	interferon gamma	Mus musculus	41-49
29948949-10	2019	Finally, intracerebral injection of anti-IFNgamma neutralizing antibody in arsenic-exposed brain reduced microglia activation (IL-6 and TNF-alpha and CD68 expression) and subsequently rescued CD200 level.	Arsenic	75-82	interleukin 6	Mus musculus	127-131
29948949-10	2019	Finally, intracerebral injection of anti-IFNgamma neutralizing antibody in arsenic-exposed brain reduced microglia activation (IL-6 and TNF-alpha and CD68 expression) and subsequently rescued CD200 level.	Arsenic	75-82	tumor necrosis factor	Mus musculus	136-145
29948949-10	2019	Finally, intracerebral injection of anti-IFNgamma neutralizing antibody in arsenic-exposed brain reduced microglia activation (IL-6 and TNF-alpha and CD68 expression) and subsequently rescued CD200 level.	Arsenic	75-82	CD68 antigen	Mus musculus	150-154
29948949-10	2019	Finally, intracerebral injection of anti-IFNgamma neutralizing antibody in arsenic-exposed brain reduced microglia activation (IL-6 and TNF-alpha and CD68 expression) and subsequently rescued CD200 level.	Arsenic	75-82	CD200 antigen	Mus musculus	192-197
29948949-11	2019	Taken together, the study showed that arsenic-mediated compromised blood-brain barrier is a major driving force to induce microglial IL-6 and TNF-alpha production through serum IFNgamma leading to CD200 downregulation.	Arsenic	38-45	interleukin 6	Mus musculus	133-137
29948949-11	2019	Taken together, the study showed that arsenic-mediated compromised blood-brain barrier is a major driving force to induce microglial IL-6 and TNF-alpha production through serum IFNgamma leading to CD200 downregulation.	Arsenic	38-45	tumor necrosis factor	Mus musculus	142-151
29948949-11	2019	Taken together, the study showed that arsenic-mediated compromised blood-brain barrier is a major driving force to induce microglial IL-6 and TNF-alpha production through serum IFNgamma leading to CD200 downregulation.	Arsenic	38-45	interferon gamma	Mus musculus	177-185
29948949-11	2019	Taken together, the study showed that arsenic-mediated compromised blood-brain barrier is a major driving force to induce microglial IL-6 and TNF-alpha production through serum IFNgamma leading to CD200 downregulation.	Arsenic	38-45	CD200 antigen	Mus musculus	197-202
30503583-0	2019	Ellagic and ferulic acids protect arsenic-induced male reproductive toxicity via regulating Nfe2l2, Ppargc1a and StAR expressions in testis.	Arsenic	34-41	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	100-108
30805085-10	2019	The mRNA and protein expression of Nrf2, HO-1, NQO1, and glutathione-S-transferase increased in the As + GSPE group compared with that in the As group (P &lt; 0.05).	Arsenic	100-102	NFE2 like bZIP transcription factor 2	Homo sapiens	35-39
30805085-10	2019	The mRNA and protein expression of Nrf2, HO-1, NQO1, and glutathione-S-transferase increased in the As + GSPE group compared with that in the As group (P &lt; 0.05).	Arsenic	100-102	heme oxygenase 1	Homo sapiens	41-45
30805085-0	2019	Proanthocyanidins Antagonize Arsenic-Induced Oxidative Damage and Promote Arsenic Methylation through Activation of the Nrf2 Signaling Pathway.	Arsenic	74-81	NFE2 like bZIP transcription factor 2	Homo sapiens	120-124
30805085-10	2019	The mRNA and protein expression of Nrf2, HO-1, NQO1, and glutathione-S-transferase increased in the As + GSPE group compared with that in the As group (P &lt; 0.05).	Arsenic	100-102	NAD(P)H quinone dehydrogenase 1	Homo sapiens	47-51
30805085-10	2019	The mRNA and protein expression of Nrf2, HO-1, NQO1, and glutathione-S-transferase increased in the As + GSPE group compared with that in the As group (P &lt; 0.05).	Arsenic	100-102	glutathione S-transferase kappa 1	Homo sapiens	57-82
30634489-9	2019	Glutamate receptor expression (NMDA and AMPA receptor subunits) showed no significant difference, but gene expressions of serotonin receptor 5B (5-HT 5B) and brain-derived neurotrophic factor (BDNF) were significantly decreased (p &lt; 0.05) in the arsenic-exposed group compared to control group.	Arsenic	249-256	5-hydroxytryptamine (serotonin) receptor 5B	Mus musculus	122-143
30634489-11	2019	Our findings indicate that developmental arsenic exposure might affect social behavior by modulating serotonin receptors and reducing BDNF.	Arsenic	41-48	brain derived neurotrophic factor	Mus musculus	134-138
31468445-0	2019	Taurine Protects Against Arsenic-Induced Apoptosis Via PI3K/Akt Pathway in Primary Cortical Neurons.	Arsenic	25-32	AKT serine/threonine kinase 1	Homo sapiens	60-63
31468453-8	2019	These results indicated that taurine expose protective effect on As-exposed primary cortical neurons and its mechanism maybe involved the regulation of Bax/Bcl-2.	Arsenic	65-67	BCL2-associated X protein	Mus musculus	152-155
29951962-0	2019	ABCA1 Is Coordinated with ABCB1 in the Arsenic-Resistance of Human Cells.	Arsenic	39-46	ATP binding cassette subfamily A member 1	Homo sapiens	0-5
31468453-8	2019	These results indicated that taurine expose protective effect on As-exposed primary cortical neurons and its mechanism maybe involved the regulation of Bax/Bcl-2.	Arsenic	65-67	B cell leukemia/lymphoma 2	Mus musculus	156-161
29951962-0	2019	ABCA1 Is Coordinated with ABCB1 in the Arsenic-Resistance of Human Cells.	Arsenic	39-46	ATP binding cassette subfamily B member 1	Homo sapiens	26-31
29951962-3	2019	The majority of ABC family members (including ABCB1 and ABCC1) are reported to play a role in the development of arsenic and drug resistance in mammals.	Arsenic	113-120	ATP binding cassette subfamily B member 1	Homo sapiens	46-51
29951962-3	2019	The majority of ABC family members (including ABCB1 and ABCC1) are reported to play a role in the development of arsenic and drug resistance in mammals.	Arsenic	113-120	ATP binding cassette subfamily C member 1	Homo sapiens	56-61
29951962-4	2019	Previously, we established a human arsenic-resistant ECV-304 (AsRE) cell line and identified ABCA1 as a novel arsenic resistance gene.	Arsenic	35-42	ATP binding cassette subfamily A member 1	Homo sapiens	93-98
29951962-4	2019	Previously, we established a human arsenic-resistant ECV-304 (AsRE) cell line and identified ABCA1 as a novel arsenic resistance gene.	Arsenic	110-117	ATP binding cassette subfamily A member 1	Homo sapiens	93-98
29951962-6	2019	The arsenic resistance capacity of ABCC1 was the strongest among the three genes, while those of ABCA1 and ABCB1 were similar.	Arsenic	4-11	ATP binding cassette subfamily C member 1	Homo sapiens	35-40
29951962-7	2019	Double or triple gene knockdown of ABCA1, ABCB1, and ABCC1 via RNA interference led to a decrease significant in arsenic resistance when ABCA1/ABCB1 or ABCB1/ABCC1 were simultaneously silenced.	Arsenic	113-120	ATP binding cassette subfamily A member 1	Homo sapiens	35-40
29951962-7	2019	Double or triple gene knockdown of ABCA1, ABCB1, and ABCC1 via RNA interference led to a decrease significant in arsenic resistance when ABCA1/ABCB1 or ABCB1/ABCC1 were simultaneously silenced.	Arsenic	113-120	ATP binding cassette subfamily B member 1	Homo sapiens	42-47
29951962-7	2019	Double or triple gene knockdown of ABCA1, ABCB1, and ABCC1 via RNA interference led to a decrease significant in arsenic resistance when ABCA1/ABCB1 or ABCB1/ABCC1 were simultaneously silenced.	Arsenic	113-120	ATP binding cassette subfamily C member 1	Homo sapiens	53-58
29951962-7	2019	Double or triple gene knockdown of ABCA1, ABCB1, and ABCC1 via RNA interference led to a decrease significant in arsenic resistance when ABCA1/ABCB1 or ABCB1/ABCC1 were simultaneously silenced.	Arsenic	113-120	ATP binding cassette subfamily A member 1	Homo sapiens	137-142
29951962-7	2019	Double or triple gene knockdown of ABCA1, ABCB1, and ABCC1 via RNA interference led to a decrease significant in arsenic resistance when ABCA1/ABCB1 or ABCB1/ABCC1 were simultaneously silenced.	Arsenic	113-120	ATP binding cassette subfamily B member 1	Homo sapiens	143-148
29951962-7	2019	Double or triple gene knockdown of ABCA1, ABCB1, and ABCC1 via RNA interference led to a decrease significant in arsenic resistance when ABCA1/ABCB1 or ABCB1/ABCC1 were simultaneously silenced.	Arsenic	113-120	ATP binding cassette subfamily B member 1	Homo sapiens	143-148
29951962-7	2019	Double or triple gene knockdown of ABCA1, ABCB1, and ABCC1 via RNA interference led to a decrease significant in arsenic resistance when ABCA1/ABCB1 or ABCB1/ABCC1 were simultaneously silenced.	Arsenic	113-120	ATP binding cassette subfamily C member 1	Homo sapiens	158-163
29951962-9	2019	Our findings suggest that ABCA1 and ABCB1 proteins display similar arsenic resistance capabilities and possibly coordinate to promote arsenic resistance in AsRE cells.	Arsenic	67-74	ATP binding cassette subfamily A member 1	Homo sapiens	26-31
29951962-9	2019	Our findings suggest that ABCA1 and ABCB1 proteins display similar arsenic resistance capabilities and possibly coordinate to promote arsenic resistance in AsRE cells.	Arsenic	67-74	ATP binding cassette subfamily B member 1	Homo sapiens	36-41
29951962-9	2019	Our findings suggest that ABCA1 and ABCB1 proteins display similar arsenic resistance capabilities and possibly coordinate to promote arsenic resistance in AsRE cells.	Arsenic	134-141	ATP binding cassette subfamily A member 1	Homo sapiens	26-31
29951962-9	2019	Our findings suggest that ABCA1 and ABCB1 proteins display similar arsenic resistance capabilities and possibly coordinate to promote arsenic resistance in AsRE cells.	Arsenic	134-141	ATP binding cassette subfamily B member 1	Homo sapiens	36-41
31001960-12	2019	CONCLUSION: Moreover, SFN pretreatment shield the liver histoarchitecture observed in Arsenic treated groups suggesting prevention of liver toxicity via PI3K/Akt mediated Nrf2 signaling pathways and could possibly provide a protection against Arsenic induced hepatic burden.	Arsenic	86-93	NFE2 like bZIP transcription factor 2	Rattus norvegicus	171-175
30551535-7	2019	The generation of ROS induced by arsenic could inhibit the expression of PPARgamma.	Arsenic	33-40	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	73-82
30974435-8	2019	This study was descriptive in nature; we calculated the frequency of the IKZF1 gene deletion in a Mexican pediatric population with preB ALL as 20.6%.	Arsenic	12-14	IKAROS family zinc finger 1	Homo sapiens	73-78
30408888-0	2019	Role of pigment epithelium-derived factor (PEDF) on arsenic-induced neuronal apoptosis.	Arsenic	52-59	serpin family F member 1	Rattus norvegicus	8-41
30408888-0	2019	Role of pigment epithelium-derived factor (PEDF) on arsenic-induced neuronal apoptosis.	Arsenic	52-59	serpin family F member 1	Rattus norvegicus	43-47
30408888-6	2019	Our previous study suggested that PEDF might augment arsenic-induced apoptosis in rat brains.	Arsenic	53-60	serpin family F member 1	Rattus norvegicus	34-38
30408888-7	2019	In this study of 151 adults with normal, mild, moderate, and high exposure to arsenic, the measured serum PEDF levels were 15.46 +- 5.87 ng/mL, 17.33 +- 8.22 ng/mL, 19.43 +- 9.51 ng/mL and 21.65 +- 14.46 ng/mL, respectively.	Arsenic	78-85	serpin family F member 1	Rattus norvegicus	106-110
30408888-8	2019	Multiple linear regression analysis revealed an independent positive correlation between serum PEDF levels and arsenic exposure in drinking water.	Arsenic	111-118	serpin family F member 1	Rattus norvegicus	95-99
30408888-9	2019	To study the underlying mechanism of arsenic-induced apoptosis, we exposed PEDF-transfected PC12 cells to NaAsO2.	Arsenic	37-44	serpin family F member 1	Rattus norvegicus	75-79
31001960-3	2019	The current study was designed to evaluate the protective ability of sulforaphane (SFN) against arsenic (As) induced hepatotoxicity by activation of PI3K induced Akt and Nrf2 mediated signaling pathway.	Arsenic	96-103	AKT serine/threonine kinase 1	Rattus norvegicus	162-165
31001960-3	2019	The current study was designed to evaluate the protective ability of sulforaphane (SFN) against arsenic (As) induced hepatotoxicity by activation of PI3K induced Akt and Nrf2 mediated signaling pathway.	Arsenic	96-103	NFE2 like bZIP transcription factor 2	Rattus norvegicus	170-174
31001960-3	2019	The current study was designed to evaluate the protective ability of sulforaphane (SFN) against arsenic (As) induced hepatotoxicity by activation of PI3K induced Akt and Nrf2 mediated signaling pathway.	Arsenic	105-107	AKT serine/threonine kinase 1	Rattus norvegicus	162-165
31001960-3	2019	The current study was designed to evaluate the protective ability of sulforaphane (SFN) against arsenic (As) induced hepatotoxicity by activation of PI3K induced Akt and Nrf2 mediated signaling pathway.	Arsenic	105-107	NFE2 like bZIP transcription factor 2	Rattus norvegicus	170-174
31001960-8	2019	RESULTS: The arsenic-induced oxidative damage was confirmed by a significant (p&lt;0.05) increase in the levels of ALAD, As concentration and depletion in the antioxidant content.	Arsenic	13-20	aminolevulinate dehydratase	Rattus norvegicus	115-119
31001960-9	2019	Furthermore, Arsenics treatments significantly (p&lt;0.05) increased the pro-apoptotic marker (Bax) and DNA damage, with decreased Nrf2 protein responsible for liver protection.	Arsenic	13-21	BCL2 associated X, apoptosis regulator	Rattus norvegicus	95-98
31001960-9	2019	Furthermore, Arsenics treatments significantly (p&lt;0.05) increased the pro-apoptotic marker (Bax) and DNA damage, with decreased Nrf2 protein responsible for liver protection.	Arsenic	13-21	NFE2 like bZIP transcription factor 2	Rattus norvegicus	131-135
31001960-12	2019	CONCLUSION: Moreover, SFN pretreatment shield the liver histoarchitecture observed in Arsenic treated groups suggesting prevention of liver toxicity via PI3K/Akt mediated Nrf2 signaling pathways and could possibly provide a protection against Arsenic induced hepatic burden.	Arsenic	86-93	AKT serine/threonine kinase 1	Rattus norvegicus	158-161
31031465-8	2019	Interactions of AD with the SERT, AQP-4, and TrkA showed the binding energies as -9.93, 8.88, and -7.58 of Kcal/mol, respectively, while for L-DOPA did show -3.93, -5.13, and -6.0 Kcal/mol, respectively.	Arsenic	78-80	solute carrier family 6 member 4	Homo sapiens	28-32
31031465-8	2019	Interactions of AD with the SERT, AQP-4, and TrkA showed the binding energies as -9.93, 8.88, and -7.58 of Kcal/mol, respectively, while for L-DOPA did show -3.93, -5.13, and -6.0 Kcal/mol, respectively.	Arsenic	78-80	neurotrophic receptor tyrosine kinase 1	Homo sapiens	45-49
31708534-2	2019	The present study aims to determine the molecular mechanism of arsenic-induced neurotoxicity and its consequent effect on downstream signaling pathways of mouse N-methyl-D-aspartate receptors (NMDARs) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs).	Arsenic	63-70	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	273-279
30726814-9	2019	Our data suggest an important role of the arsenic-induced suppression of IFN-beta on the disturbances in immunological defense against both bacteria and viruses.	Arsenic	42-49	interferon beta 1, fibroblast	Mus musculus	73-81
30729860-7	2019	Arsenic-exposed fish exhibited significant 1.3- to 1.5-fold reduction in intestinal villus height and 1.4- to 1.6-fold decrease in proliferating cell nuclear antigen (PCNA+) intestinal cells at all weeks examined.	Arsenic	0-7	proliferating cell nuclear antigen	Fundulus heteroclitus	167-172
29889593-6	2019	Both these isolates showed high efficiency in converting As3+ into less toxic concentrations of As5+ respectively from arsenic enriched culture media.	Arsenic	119-126	PDS5 cohesin associated factor B	Homo sapiens	57-60
29889593-8	2019	This study reports the potential As3+-oxidizing bacteria that can play an important role in subsurface arsenic transformation that will aid in designing future bioremediation strategy for the arsenic affected areas.	Arsenic	103-110	PDS5 cohesin associated factor B	Homo sapiens	33-36
29889593-8	2019	This study reports the potential As3+-oxidizing bacteria that can play an important role in subsurface arsenic transformation that will aid in designing future bioremediation strategy for the arsenic affected areas.	Arsenic	192-199	PDS5 cohesin associated factor B	Homo sapiens	33-36
28660791-4	2019	The higher outputs of exoglycosidases were in the AS and ANS groups than in controls at the 1st day (GLU, HEX A) and at the 50th day (GLU, FUC, MAN) of abstinence.	Arsenic	50-52	glucuronidase beta	Homo sapiens	101-104
30805392-12	2019	Ectopic expression of CEBPA-AS was detected in seven of the AML patients.	Arsenic	28-30	CCAAT enhancer binding protein alpha	Homo sapiens	22-27
28660791-4	2019	The higher outputs of exoglycosidases were in the AS and ANS groups than in controls at the 1st day (GLU, HEX A) and at the 50th day (GLU, FUC, MAN) of abstinence.	Arsenic	50-52	hexosaminidase subunit alpha	Homo sapiens	106-111
30575732-5	2018	Mice lacking the primary arsenic detoxification enzyme (As3mt) are hypersensitive to arsenic after antibiotic treatment or when derived germ-free, compared to wild-type and/or conventional counterparts.	Arsenic	25-32	arsenite methyltransferase	Mus musculus	56-61
30588596-6	2018	Positive CEA was defined as &gt;=5 mug/L, CA199 as &gt;=35 U/L; while NLR (neutrophil-to-lymphocyte ratio), MLR (monocyte-to-lymphocyte ratio), PLR (platelet-to-lymphocyte ratio) greater than their cut-off values were defined as positive.	Arsenic	14-16	CEA cell adhesion molecule 3	Homo sapiens	9-12
30575732-5	2018	Mice lacking the primary arsenic detoxification enzyme (As3mt) are hypersensitive to arsenic after antibiotic treatment or when derived germ-free, compared to wild-type and/or conventional counterparts.	Arsenic	85-92	arsenite methyltransferase	Mus musculus	56-61
30575732-6	2018	Human microbiome (stool) transplants protect germ-free As3mt-KO mice from arsenic-induced mortality, but protection depends on microbiome stability and the presence of specific bacteria, including Faecalibacterium.	Arsenic	74-81	arsenite methyltransferase	Mus musculus	55-60
30467571-4	2018	A similar complex [{W6(mu4-O)2(mu3-As)4}(CN)16]10- containing mu3-As3- ligands instead of mu3-CCN3- ones has been synthesized by the reaction between WO3, As and KCN.	Arsenic	35-37	adaptor related protein complex 4 subunit mu 1	Homo sapiens	23-26
30195209-6	2018	Moreover, SO2 and arsenic co-exposure changed the mRNA levels of Bax and Bcl-2, decreased serum testosterone levels, and downregulated the expression of steroidogenic-related genes (LHR, StAR, and ABP) in mice.	Arsenic	18-25	BCL2-associated X protein	Mus musculus	65-68
30195209-6	2018	Moreover, SO2 and arsenic co-exposure changed the mRNA levels of Bax and Bcl-2, decreased serum testosterone levels, and downregulated the expression of steroidogenic-related genes (LHR, StAR, and ABP) in mice.	Arsenic	18-25	B cell leukemia/lymphoma 2	Mus musculus	73-78
30195209-6	2018	Moreover, SO2 and arsenic co-exposure changed the mRNA levels of Bax and Bcl-2, decreased serum testosterone levels, and downregulated the expression of steroidogenic-related genes (LHR, StAR, and ABP) in mice.	Arsenic	18-25	luteinizing hormone/choriogonadotropin receptor	Mus musculus	182-185
30195209-6	2018	Moreover, SO2 and arsenic co-exposure changed the mRNA levels of Bax and Bcl-2, decreased serum testosterone levels, and downregulated the expression of steroidogenic-related genes (LHR, StAR, and ABP) in mice.	Arsenic	18-25	amine oxidase, copper-containing 1	Mus musculus	197-200
30513265-7	2018	LODs for Pb and As were 0.002 and 0.005 microg L-1, respectively.	Arsenic	16-18	immunoglobulin kappa variable 1-16	Homo sapiens	47-50
30286549-10	2018	Urinary inorganic arsenic (%InAs) was associated with GSTP1, LADD, GSTP1*Age, GSTP1*alcohol consumption (r2 = 0.43; likelihood-ratio test, p = 0.000).	Arsenic	18-25	glutathione S-transferase pi 1	Homo sapiens	54-59
30286549-10	2018	Urinary inorganic arsenic (%InAs) was associated with GSTP1, LADD, GSTP1*Age, GSTP1*alcohol consumption (r2 = 0.43; likelihood-ratio test, p = 0.000).	Arsenic	18-25	glutathione S-transferase pi 1	Homo sapiens	67-72
30286549-10	2018	Urinary inorganic arsenic (%InAs) was associated with GSTP1, LADD, GSTP1*Age, GSTP1*alcohol consumption (r2 = 0.43; likelihood-ratio test, p = 0.000).	Arsenic	18-25	glutathione S-transferase pi 1	Homo sapiens	67-72
30543710-9	2018	AS3MT and MiR-548c-3p may regulate arsenic methylation jointly, which when involved in a group of relative mRNAs may play roles in arsenic metabolism and epigenetic changes caused by this metabolism.	Arsenic	35-42	arsenite methyltransferase	Homo sapiens	0-5
30543710-9	2018	AS3MT and MiR-548c-3p may regulate arsenic methylation jointly, which when involved in a group of relative mRNAs may play roles in arsenic metabolism and epigenetic changes caused by this metabolism.	Arsenic	131-138	arsenite methyltransferase	Homo sapiens	0-5
30302732-0	2018	Dysregulation of Sqstm1, mitophagy, and apoptotic genes in chronic exposure to arsenic and high-fat diet (HFD).	Arsenic	79-86	sequestosome 1	Homo sapiens	17-23
30302732-10	2018	Overall, the changes observed in the expression of Sqstm1, BNIP3, and caspase 3 in this study can be related to the level of liver damage caused by exposure to arsenic and HFD and probably, BNIP3 pro-apoptotic protein is associated with an increased cell death due to HFD and As.	Arsenic	160-167	sequestosome 1	Homo sapiens	51-57
30302732-10	2018	Overall, the changes observed in the expression of Sqstm1, BNIP3, and caspase 3 in this study can be related to the level of liver damage caused by exposure to arsenic and HFD and probably, BNIP3 pro-apoptotic protein is associated with an increased cell death due to HFD and As.	Arsenic	160-167	BCL2 interacting protein 3	Homo sapiens	59-64
30302732-10	2018	Overall, the changes observed in the expression of Sqstm1, BNIP3, and caspase 3 in this study can be related to the level of liver damage caused by exposure to arsenic and HFD and probably, BNIP3 pro-apoptotic protein is associated with an increased cell death due to HFD and As.	Arsenic	160-167	caspase 3	Homo sapiens	70-79
30302732-10	2018	Overall, the changes observed in the expression of Sqstm1, BNIP3, and caspase 3 in this study can be related to the level of liver damage caused by exposure to arsenic and HFD and probably, BNIP3 pro-apoptotic protein is associated with an increased cell death due to HFD and As.	Arsenic	160-167	BCL2 interacting protein 3	Homo sapiens	190-195
30262289-6	2018	Our present study provides evidence to reveal that arsenic affects miR-2909 expression in the pancreatic beta-cell and this novel miRNA regulates PDX1 transcriptional expression indirectly through genes coding for c-Jun, MafA, PI3K and directly at the translational level by targeting the PDX1 mRNA.	Arsenic	51-58	pancreatic and duodenal homeobox 1	Mus musculus	146-150
30262289-8	2018	Keeping in view the fact that arsenic is known to cause beta-cell dysfunction and most of the cellular effects of arsenic have been shown to be mediated through miR-2909 RNomics, our study revealed that arsenic employs miR-2909 (at low doses) and c-Jun (at high doses) to down regulate PDX1 in order to cause beta-cell dysfunction leading to diabetic state.	Arsenic	114-121	jun proto-oncogene	Mus musculus	247-252
30262289-8	2018	Keeping in view the fact that arsenic is known to cause beta-cell dysfunction and most of the cellular effects of arsenic have been shown to be mediated through miR-2909 RNomics, our study revealed that arsenic employs miR-2909 (at low doses) and c-Jun (at high doses) to down regulate PDX1 in order to cause beta-cell dysfunction leading to diabetic state.	Arsenic	114-121	pancreatic and duodenal homeobox 1	Mus musculus	286-290
30262289-8	2018	Keeping in view the fact that arsenic is known to cause beta-cell dysfunction and most of the cellular effects of arsenic have been shown to be mediated through miR-2909 RNomics, our study revealed that arsenic employs miR-2909 (at low doses) and c-Jun (at high doses) to down regulate PDX1 in order to cause beta-cell dysfunction leading to diabetic state.	Arsenic	114-121	jun proto-oncogene	Mus musculus	247-252
30262289-8	2018	Keeping in view the fact that arsenic is known to cause beta-cell dysfunction and most of the cellular effects of arsenic have been shown to be mediated through miR-2909 RNomics, our study revealed that arsenic employs miR-2909 (at low doses) and c-Jun (at high doses) to down regulate PDX1 in order to cause beta-cell dysfunction leading to diabetic state.	Arsenic	114-121	pancreatic and duodenal homeobox 1	Mus musculus	286-290
30262289-6	2018	Our present study provides evidence to reveal that arsenic affects miR-2909 expression in the pancreatic beta-cell and this novel miRNA regulates PDX1 transcriptional expression indirectly through genes coding for c-Jun, MafA, PI3K and directly at the translational level by targeting the PDX1 mRNA.	Arsenic	51-58	jun proto-oncogene	Mus musculus	214-219
30262289-6	2018	Our present study provides evidence to reveal that arsenic affects miR-2909 expression in the pancreatic beta-cell and this novel miRNA regulates PDX1 transcriptional expression indirectly through genes coding for c-Jun, MafA, PI3K and directly at the translational level by targeting the PDX1 mRNA.	Arsenic	51-58	v-maf musculoaponeurotic fibrosarcoma oncogene family, protein A (avian)	Mus musculus	221-225
30262289-6	2018	Our present study provides evidence to reveal that arsenic affects miR-2909 expression in the pancreatic beta-cell and this novel miRNA regulates PDX1 transcriptional expression indirectly through genes coding for c-Jun, MafA, PI3K and directly at the translational level by targeting the PDX1 mRNA.	Arsenic	51-58	pancreatic and duodenal homeobox 1	Mus musculus	289-293
30189517-3	2018	Using a US pregnancy cohort, we assessed the impact of receiving well water arsenic test results on subsequent use of arsenic-contaminated tap water.	Arsenic	76-83	nuclear RNA export factor 1	Homo sapiens	139-142
30315444-9	2018	But the increase in the serum E2 level as noted in the ELISA data with impairment in the hepatic estrogen sulfotransferase (SULT1E1) protein expression (immuno-blot data) were noticed with interfered hepatic free-thiols only in ENU and xenograft-E2 group compared to arsenic group.	Arsenic	267-274	sulfotransferase family 1E member 1	Homo sapiens	97-122
30315444-9	2018	But the increase in the serum E2 level as noted in the ELISA data with impairment in the hepatic estrogen sulfotransferase (SULT1E1) protein expression (immuno-blot data) were noticed with interfered hepatic free-thiols only in ENU and xenograft-E2 group compared to arsenic group.	Arsenic	267-274	sulfotransferase family 1E member 1	Homo sapiens	124-131
30189517-3	2018	Using a US pregnancy cohort, we assessed the impact of receiving well water arsenic test results on subsequent use of arsenic-contaminated tap water.	Arsenic	118-125	nuclear RNA export factor 1	Homo sapiens	139-142
30189517-6	2018	Logistic regression was used to estimate the odds of tap water use at one year post-partum in relation to baseline tap water use and arsenic concentration.	Arsenic	133-140	nuclear RNA export factor 1	Homo sapiens	53-56
30189517-8	2018	After adjusting for frequency of prenatal tap water use, mothers were less likely to use tap water for drinking and cooking (OR = 0.34, 95% CI: 0.19, 0.60) and for mixing formula (OR = 0.45, 95% CI: 0.24, 0.86) if the high arsenic concentration (&gt;10 mug/L) was known to them.	Arsenic	223-230	nuclear RNA export factor 1	Homo sapiens	89-92
30130716-0	2018	Flux and source-sink relationship of heavy metals and arsenic in the Bohai Sea, China.	Arsenic	54-61	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	75-78
30026126-3	2018	This study aimed to investigate the role of p63 isoforms in abnormal epidermal proliferation induced by arsenic.	Arsenic	104-111	tumor protein p63	Homo sapiens	44-47
30026126-4	2018	Using arsenic-induced Bowen"s disease (As-BD; an intraepidermal carcinoma) as a disease model, we found that in As-BD, the expression of proliferating basal keratinocytes marker cytokeratin 14 (CK14) and N-terminal truncated p63 isoform (DeltaNp63; proliferation regulator) was increased, however, that of the differentiation marker cytokeratin 10 (CK10) and full-length p63 isoform (TAp63; differentiation regulator) was decreased in squamous cells as compared with healthy subjects.	Arsenic	6-13	keratin 14	Homo sapiens	178-192
30099283-0	2018	Lead, cadmium, arsenic, and mercury combined exposure disrupted synaptic homeostasis through activating the Snk-SPAR pathway.	Arsenic	15-22	polo like kinase 2	Homo sapiens	108-111
30026126-4	2018	Using arsenic-induced Bowen"s disease (As-BD; an intraepidermal carcinoma) as a disease model, we found that in As-BD, the expression of proliferating basal keratinocytes marker cytokeratin 14 (CK14) and N-terminal truncated p63 isoform (DeltaNp63; proliferation regulator) was increased, however, that of the differentiation marker cytokeratin 10 (CK10) and full-length p63 isoform (TAp63; differentiation regulator) was decreased in squamous cells as compared with healthy subjects.	Arsenic	6-13	keratin 14	Homo sapiens	194-198
30026126-4	2018	Using arsenic-induced Bowen"s disease (As-BD; an intraepidermal carcinoma) as a disease model, we found that in As-BD, the expression of proliferating basal keratinocytes marker cytokeratin 14 (CK14) and N-terminal truncated p63 isoform (DeltaNp63; proliferation regulator) was increased, however, that of the differentiation marker cytokeratin 10 (CK10) and full-length p63 isoform (TAp63; differentiation regulator) was decreased in squamous cells as compared with healthy subjects.	Arsenic	6-13	tumor protein p63	Homo sapiens	225-228
30026126-4	2018	Using arsenic-induced Bowen"s disease (As-BD; an intraepidermal carcinoma) as a disease model, we found that in As-BD, the expression of proliferating basal keratinocytes marker cytokeratin 14 (CK14) and N-terminal truncated p63 isoform (DeltaNp63; proliferation regulator) was increased, however, that of the differentiation marker cytokeratin 10 (CK10) and full-length p63 isoform (TAp63; differentiation regulator) was decreased in squamous cells as compared with healthy subjects.	Arsenic	6-13	keratin 10	Homo sapiens	333-347
30026126-4	2018	Using arsenic-induced Bowen"s disease (As-BD; an intraepidermal carcinoma) as a disease model, we found that in As-BD, the expression of proliferating basal keratinocytes marker cytokeratin 14 (CK14) and N-terminal truncated p63 isoform (DeltaNp63; proliferation regulator) was increased, however, that of the differentiation marker cytokeratin 10 (CK10) and full-length p63 isoform (TAp63; differentiation regulator) was decreased in squamous cells as compared with healthy subjects.	Arsenic	6-13	keratin 10	Homo sapiens	349-353
30026126-4	2018	Using arsenic-induced Bowen"s disease (As-BD; an intraepidermal carcinoma) as a disease model, we found that in As-BD, the expression of proliferating basal keratinocytes marker cytokeratin 14 (CK14) and N-terminal truncated p63 isoform (DeltaNp63; proliferation regulator) was increased, however, that of the differentiation marker cytokeratin 10 (CK10) and full-length p63 isoform (TAp63; differentiation regulator) was decreased in squamous cells as compared with healthy subjects.	Arsenic	6-13	tumor protein p63	Homo sapiens	244-247
30026126-7	2018	Treatment of cultured normal human epidermal keratinocytes (HKCs) with arsenic increased CK14 and  Np63 expressions, but decreased TAp63 and CK10 expressions.	Arsenic	71-78	keratin 14	Homo sapiens	89-93
30026126-7	2018	Treatment of cultured normal human epidermal keratinocytes (HKCs) with arsenic increased CK14 and  Np63 expressions, but decreased TAp63 and CK10 expressions.	Arsenic	71-78	keratin 10	Homo sapiens	141-145
30026126-8	2018	Furthermore, knockdown of DeltaNp63 by RNA interference abrogated arsenic-induced CK14 expression and recovered the reduction of TAp63 and CK10 caused by arsenic.	Arsenic	66-73	keratin 14	Homo sapiens	82-86
30026126-8	2018	Furthermore, knockdown of DeltaNp63 by RNA interference abrogated arsenic-induced CK14 expression and recovered the reduction of TAp63 and CK10 caused by arsenic.	Arsenic	154-161	keratin 10	Homo sapiens	139-143
30350630-9	2018	For example, with MICAP-TOFMS, the limit of detection for arsenic is less than 100 ng L-1 even in a 1% NaCl solution; with ICP-MS, 35Cl40Ar+ interferes with 75As+ and arsenic analysis is difficult-to-impossible in chlorine-containing matrices.	Arsenic	58-65	immunoglobulin kappa variable 1-16	Homo sapiens	86-89
30581971-3	2019	Results: ApoE particles from patients genotyped as epsilon4/epsilon4 were 2.2 +- 0.3 times as massive as particles from epsilon3/epsilon3 control subjects and 1.4 +- 0.1 times as massive as particles from epsilon3/epsilon3 AD patients.	Arsenic	48-50	apolipoprotein E	Homo sapiens	9-13
30581971-3	2019	Results: ApoE particles from patients genotyped as epsilon4/epsilon4 were 2.2 +- 0.3 times as massive as particles from epsilon3/epsilon3 control subjects and 1.4 +- 0.1 times as massive as particles from epsilon3/epsilon3 AD patients.	Arsenic	91-93	apolipoprotein E	Homo sapiens	9-13
31565364-5	2019	This compound has high water solubility and causes extensive foaming in a typical flotation chamber and removed 99.4-99.9% of the 5 mg L-1 arsenic present in the contaminated water in a simple, single-stage ion flotation process, using either air or nitrogen gas.	Arsenic	139-146	immunoglobulin kappa variable 1-16	Homo sapiens	135-138
30225639-0	2018	Arsenic induces autophagy in developmental mouse cerebral cortex and hippocampus by inhibiting PI3K/Akt/mTOR signaling pathway: involvement of blood-brain barrier"s tight junction proteins.	Arsenic	0-7	thymoma viral proto-oncogene 1	Mus musculus	100-103
30225639-0	2018	Arsenic induces autophagy in developmental mouse cerebral cortex and hippocampus by inhibiting PI3K/Akt/mTOR signaling pathway: involvement of blood-brain barrier"s tight junction proteins.	Arsenic	0-7	mechanistic target of rapamycin kinase	Mus musculus	104-108
29986226-5	2018	In addition, the depleted activity of catalase and glutathione peroxidase suggested the strong association of copper and arsenic with oxidative stress.	Arsenic	121-128	catalase	Gallus gallus	38-46
30278242-0	2018	Metabolism and disposition of arsenic species from controlled dosing with sodium arsenite in adult female CD-1 mice.	Arsenic	30-37	CD1 antigen complex	Mus musculus	106-110
30153448-1	2018	BACKGROUND: Arsenic methylation efficiency, a susceptibility factor for arsenic toxicity, is in adults partly explained by variation in arsenite methyltransferase (AS3MT) gene.	Arsenic	12-19	arsenite methyltransferase	Homo sapiens	136-162
30144155-10	2018	In childhood, arsenic exposure may reduce peripheral CD4+ cells and interleukin-2 secretion which leads to susceptibility to opportunistic infections.	Arsenic	14-21	CD4 molecule	Homo sapiens	53-56
30144155-10	2018	In childhood, arsenic exposure may reduce peripheral CD4+ cells and interleukin-2 secretion which leads to susceptibility to opportunistic infections.	Arsenic	14-21	interleukin 2	Homo sapiens	68-81
30144155-12	2018	In arsenic-induced Bowen"s disease lesions, a decrease in the number and functions of Langerhans cells and, in parallel, a selective CD4+ cell apoptosis was noticed.	Arsenic	3-10	CD4 molecule	Homo sapiens	133-136
30376133-0	2018	Using the Apolipoprotein E Knock-Out Mouse Model to Define Atherosclerotic Plaque Changes Induced by Low Dose Arsenic.	Arsenic	110-117	apolipoprotein E	Mus musculus	10-26
30145471-4	2018	Concurrent administration arsenic and copper markedly increased levels of NF-kappaB, COX-2, iNOS and PTGEs and pro-inflammatory cytokines in concomitant with a tendency of Th1 bias immune response.	Arsenic	26-33	COX2	Gallus gallus	85-90
30145471-4	2018	Concurrent administration arsenic and copper markedly increased levels of NF-kappaB, COX-2, iNOS and PTGEs and pro-inflammatory cytokines in concomitant with a tendency of Th1 bias immune response.	Arsenic	26-33	nitric oxide synthase 2	Gallus gallus	92-96
30145471-4	2018	Concurrent administration arsenic and copper markedly increased levels of NF-kappaB, COX-2, iNOS and PTGEs and pro-inflammatory cytokines in concomitant with a tendency of Th1 bias immune response.	Arsenic	26-33	prostaglandin E synthase	Gallus gallus	101-106
30145471-9	2018	Heat shock proteins may play protective roles in thymus damage, and HSP60 combines with the IL-17/IL-10 ratio may be potential predictive marker of arsenic and/or copper-subchronic toxicity in chicken thymus.	Arsenic	148-155	heat shock protein family D (Hsp60) member 1	Gallus gallus	68-73
30145471-9	2018	Heat shock proteins may play protective roles in thymus damage, and HSP60 combines with the IL-17/IL-10 ratio may be potential predictive marker of arsenic and/or copper-subchronic toxicity in chicken thymus.	Arsenic	148-155	interleukin 17A	Gallus gallus	92-97
30145471-9	2018	Heat shock proteins may play protective roles in thymus damage, and HSP60 combines with the IL-17/IL-10 ratio may be potential predictive marker of arsenic and/or copper-subchronic toxicity in chicken thymus.	Arsenic	148-155	interleukin 10	Gallus gallus	98-103
30096535-0	2018	Copper or/and arsenic induces autophagy by oxidative stress-related PI3K/AKT/mTOR pathways and cascaded mitochondrial fission in chicken skeletal muscle.	Arsenic	14-21	AKT serine/threonine kinase 1	Homo sapiens	73-76
30096535-0	2018	Copper or/and arsenic induces autophagy by oxidative stress-related PI3K/AKT/mTOR pathways and cascaded mitochondrial fission in chicken skeletal muscle.	Arsenic	14-21	mechanistic target of rapamycin	Gallus gallus	77-81
30267786-6	2018	Arsenic-mediated male reproductive toxicity can be induced by various mechanisms such as inhibition of spermatogenesis, testosterone pathway hinderance, oxidative stress, inflammation, genotoxic effects, activation of heat shock proteins, and activation of a signaling pathway in testes (ERK/AKT/NF-kB signaling pathway), among others.	Arsenic	0-7	mitogen-activated protein kinase 1	Homo sapiens	288-291
30267786-6	2018	Arsenic-mediated male reproductive toxicity can be induced by various mechanisms such as inhibition of spermatogenesis, testosterone pathway hinderance, oxidative stress, inflammation, genotoxic effects, activation of heat shock proteins, and activation of a signaling pathway in testes (ERK/AKT/NF-kB signaling pathway), among others.	Arsenic	0-7	AKT serine/threonine kinase 1	Homo sapiens	292-295
30380796-0	2018	Arsenic and Heavy Metal Accumulation and Risk Assessment in Soils around Mining Areas: The Urad Houqi Area in Arid Northwest China as an Example.	Arsenic	0-7	ureidoimidazoline (2-oxo-4-hydroxy-4-carboxy-5-) decarboxylase	Homo sapiens	91-95
30153448-1	2018	BACKGROUND: Arsenic methylation efficiency, a susceptibility factor for arsenic toxicity, is in adults partly explained by variation in arsenite methyltransferase (AS3MT) gene.	Arsenic	12-19	arsenite methyltransferase	Homo sapiens	164-169
30153448-2	2018	Little is known about the role of AS3MT for children"s arsenic methylation.	Arsenic	55-62	arsenite methyltransferase	Homo sapiens	34-39
30153448-3	2018	OBJECTIVES: Evaluating associations between AS3MT polymorphisms and children"s arsenic methylation efficiency.	Arsenic	79-86	arsenite methyltransferase	Homo sapiens	44-49
30153448-12	2018	CONCLUSIONS: One out of four AS3MT polymorphisms, previously associated with arsenic methylation in adults, was associated with arsenic methylation in children.	Arsenic	77-84	arsenite methyltransferase	Homo sapiens	29-34
30153448-12	2018	CONCLUSIONS: One out of four AS3MT polymorphisms, previously associated with arsenic methylation in adults, was associated with arsenic methylation in children.	Arsenic	128-135	arsenite methyltransferase	Homo sapiens	29-34
30153448-13	2018	Thus, AS3MT variation seems to influence arsenic methylation efficiency in children to a lesser extent than in adults.	Arsenic	41-48	arsenite methyltransferase	Homo sapiens	6-11
30291177-0	2018	Withdrawal: Antioncogenic and oncogenic properties of Nrf2 in arsenic-induced carcinogenesis.	Arsenic	62-69	NFE2 like bZIP transcription factor 2	Homo sapiens	54-58
30189373-0	2018	Reduced testosterone and Ddx3y expression caused by long-term exposure to arsenic and its effect on spermatogenesis in mice.	Arsenic	74-81	DEAD box helicase 3, Y-linked	Mus musculus	25-30
30025855-1	2018	In the eukaryotic model yeast Saccharomyces cerevisiae, arsenic (As) detoxification is regulated by two transcriptional factors, Yap8 and Yap1.	Arsenic	56-63	Arr1p	Saccharomyces cerevisiae S288C	129-133
30025855-1	2018	In the eukaryotic model yeast Saccharomyces cerevisiae, arsenic (As) detoxification is regulated by two transcriptional factors, Yap8 and Yap1.	Arsenic	56-63	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	138-142
30025855-1	2018	In the eukaryotic model yeast Saccharomyces cerevisiae, arsenic (As) detoxification is regulated by two transcriptional factors, Yap8 and Yap1.	Arsenic	65-68	Arr1p	Saccharomyces cerevisiae S288C	129-133
30025855-1	2018	In the eukaryotic model yeast Saccharomyces cerevisiae, arsenic (As) detoxification is regulated by two transcriptional factors, Yap8 and Yap1.	Arsenic	65-68	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	138-142
30025855-2	2018	Yap8 specifically controls As extrusion from the cell, whether Yap1 avoids arsenic-induced oxidative damages.	Arsenic	75-82	Arr1p	Saccharomyces cerevisiae S288C	0-4
30025855-2	2018	Yap8 specifically controls As extrusion from the cell, whether Yap1 avoids arsenic-induced oxidative damages.	Arsenic	75-82	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	63-67
30189373-7	2018	Moreover, arsenic diminished serum testosterone, along with the reduced expression of luteinizing hormone receptor (LHR), steroidogenic acute regulatory protein (StAR) and 17-beta-hydroxysteroid dehydrogenase (17beta-HSD) genes.	Arsenic	10-17	luteinizing hormone/choriogonadotropin receptor	Mus musculus	86-114
30189373-7	2018	Moreover, arsenic diminished serum testosterone, along with the reduced expression of luteinizing hormone receptor (LHR), steroidogenic acute regulatory protein (StAR) and 17-beta-hydroxysteroid dehydrogenase (17beta-HSD) genes.	Arsenic	10-17	luteinizing hormone/choriogonadotropin receptor	Mus musculus	116-119
30189373-7	2018	Moreover, arsenic diminished serum testosterone, along with the reduced expression of luteinizing hormone receptor (LHR), steroidogenic acute regulatory protein (StAR) and 17-beta-hydroxysteroid dehydrogenase (17beta-HSD) genes.	Arsenic	10-17	steroidogenic acute regulatory protein	Mus musculus	122-160
30189373-7	2018	Moreover, arsenic diminished serum testosterone, along with the reduced expression of luteinizing hormone receptor (LHR), steroidogenic acute regulatory protein (StAR) and 17-beta-hydroxysteroid dehydrogenase (17beta-HSD) genes.	Arsenic	10-17	steroidogenic acute regulatory protein	Mus musculus	162-166
28477161-3	2018	On this basis, this paper developed its determination method for inorganic arsenite (As(III)) to further realize the simultaneous and high-resolution measurements of labile inorganic As and S(II) in sediments.	Arsenic	85-87	transcription elongation factor A1	Homo sapiens	190-195
28477161-10	2018	It likely reflected a simultaneous release of As and S(II) in sediments by synchronous reduction of As-hosted oxidized iron and sulfate, respectively.	Arsenic	100-102	transcription elongation factor A1	Homo sapiens	53-58
30246808-6	2018	Results: For any mPAP level, the effect on shunt flow size is much larger for the PS than for AS.	Arsenic	94-96	phospholipid phosphatase 1	Mus musculus	17-21
29859237-4	2018	The aims of this study were to evaluate 1) the association between arsenic methylation capacity and UTUC and/or BC, separately, and 2) the association between polymorphisms of the arsenic metabolism-related genes AS3MT, GSTOs, and PNP against BC and/or UTUC, separately.	Arsenic	180-187	arsenite methyltransferase	Homo sapiens	213-218
30237564-0	2018	Arsenic circumvents the gefitinib resistance by binding to P62 and mediating autophagic degradation of EGFR in non-small cell lung cancer.	Arsenic	0-7	nucleoporin 62	Homo sapiens	59-62
30237564-0	2018	Arsenic circumvents the gefitinib resistance by binding to P62 and mediating autophagic degradation of EGFR in non-small cell lung cancer.	Arsenic	0-7	epidermal growth factor receptor	Homo sapiens	103-107
30189373-7	2018	Moreover, arsenic diminished serum testosterone, along with the reduced expression of luteinizing hormone receptor (LHR), steroidogenic acute regulatory protein (StAR) and 17-beta-hydroxysteroid dehydrogenase (17beta-HSD) genes.	Arsenic	10-17	hydroxysteroid (17-beta) dehydrogenase 1	Mus musculus	172-208
30189373-7	2018	Moreover, arsenic diminished serum testosterone, along with the reduced expression of luteinizing hormone receptor (LHR), steroidogenic acute regulatory protein (StAR) and 17-beta-hydroxysteroid dehydrogenase (17beta-HSD) genes.	Arsenic	10-17	hydroxysteroid (17-beta) dehydrogenase 1	Mus musculus	210-220
30189373-8	2018	Arsenic also down-regulated mRNA levels of ABP and Ddx3y in a dose-dependent manner.	Arsenic	0-7	secretoglobin, family 1B, member 29	Mus musculus	43-46
30189373-8	2018	Arsenic also down-regulated mRNA levels of ABP and Ddx3y in a dose-dependent manner.	Arsenic	0-7	DEAD box helicase 3, Y-linked	Mus musculus	51-56
30189373-9	2018	Meanwhile, the protein levels of StAR, 17beta-HSD and Ddx3y were significantly reduced in arsenic-treated groups.	Arsenic	90-97	steroidogenic acute regulatory protein	Mus musculus	33-37
30189373-9	2018	Meanwhile, the protein levels of StAR, 17beta-HSD and Ddx3y were significantly reduced in arsenic-treated groups.	Arsenic	90-97	hydroxysteroid (17-beta) dehydrogenase 1	Mus musculus	39-49
30189373-9	2018	Meanwhile, the protein levels of StAR, 17beta-HSD and Ddx3y were significantly reduced in arsenic-treated groups.	Arsenic	90-97	DEAD box helicase 3, Y-linked	Mus musculus	54-59
30189373-10	2018	Taken together, these results suggest that the reduced testosterone through inhibition of the expression of multiple genes responsible for the biosynthesis, the damaged androgen homeostasis partially via lessening the expression levels of the ABP gene and the down-regulated expression of Ddx3y, may contribute to spermatogenesis disorders in mice exposed to arsenic.	Arsenic	359-366	secretoglobin, family 1B, member 29	Mus musculus	243-246
30324125-10	2018	Results: Exposure to arsenic caused a significant increase in serum aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine aminotransferase (ALT), and bilirubin, accompanied by a decrease in total protein levels as well as CAT and SOD activities, and GSH.	Arsenic	21-28	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	68-94
30324125-10	2018	Results: Exposure to arsenic caused a significant increase in serum aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine aminotransferase (ALT), and bilirubin, accompanied by a decrease in total protein levels as well as CAT and SOD activities, and GSH.	Arsenic	21-28	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	96-99
29705342-6	2018	In L-02 cells, arsenite, an active form of arsenic, induced up-regulation of miR-145 and down-regulation of ERCC1 and ERCC2, and caused DNA damage.	Arsenic	43-50	microRNA 145	Homo sapiens	77-84
30048668-0	2018	Corrigendum to The polymorphism XRCC1 Arg194Trp and 8-hydroxydeoxyguanosine increased susceptibility to arsenic-related renal cell carcinoma.	Arsenic	104-111	X-ray repair cross complementing 1	Homo sapiens	32-37
30133269-1	2018	The removal of arsenic and metals by sulfide (S(-II)) from acidic wastewater is an efficient method.	Arsenic	15-22	transcription elongation factor A1	Homo sapiens	46-51
30209319-0	2018	Mercury and arsenic attenuate canonical and non-canonical NLRP3 inflammasome activation.	Arsenic	12-19	NLR family, pyrin domain containing 3	Mus musculus	58-63
30209319-4	2018	In this study, we elucidated the effects of four heavy metals, including cadmium (Cd), mercury (Hg), arsenic (As), and lead (Pb), on the activation of NLRP3, NLRC4, and AIM2 inflammasomes.	Arsenic	101-108	NLR family, pyrin domain containing 3	Mus musculus	151-156
30209319-4	2018	In this study, we elucidated the effects of four heavy metals, including cadmium (Cd), mercury (Hg), arsenic (As), and lead (Pb), on the activation of NLRP3, NLRC4, and AIM2 inflammasomes.	Arsenic	101-108	NLR family, CARD domain containing 4	Mus musculus	158-163
30209319-4	2018	In this study, we elucidated the effects of four heavy metals, including cadmium (Cd), mercury (Hg), arsenic (As), and lead (Pb), on the activation of NLRP3, NLRC4, and AIM2 inflammasomes.	Arsenic	101-108	absent in melanoma 2	Mus musculus	169-173
30209319-4	2018	In this study, we elucidated the effects of four heavy metals, including cadmium (Cd), mercury (Hg), arsenic (As), and lead (Pb), on the activation of NLRP3, NLRC4, and AIM2 inflammasomes.	Arsenic	110-112	NLR family, pyrin domain containing 3	Mus musculus	151-156
30209319-4	2018	In this study, we elucidated the effects of four heavy metals, including cadmium (Cd), mercury (Hg), arsenic (As), and lead (Pb), on the activation of NLRP3, NLRC4, and AIM2 inflammasomes.	Arsenic	110-112	NLR family, CARD domain containing 4	Mus musculus	158-163
30209319-5	2018	In our results, mercury and arsenic inhibited interleukin (IL)-1beta and IL-18 secretion resulting from canonical and non-canonical NLRP3 inflammasome activation in macrophages and attenuated elevation of serum IL-1beta in response to LPS treatment in mice.	Arsenic	28-35	interleukin 1 alpha	Mus musculus	46-68
30209319-5	2018	In our results, mercury and arsenic inhibited interleukin (IL)-1beta and IL-18 secretion resulting from canonical and non-canonical NLRP3 inflammasome activation in macrophages and attenuated elevation of serum IL-1beta in response to LPS treatment in mice.	Arsenic	28-35	interleukin 18	Mus musculus	73-78
30209319-5	2018	In our results, mercury and arsenic inhibited interleukin (IL)-1beta and IL-18 secretion resulting from canonical and non-canonical NLRP3 inflammasome activation in macrophages and attenuated elevation of serum IL-1beta in response to LPS treatment in mice.	Arsenic	28-35	NLR family, pyrin domain containing 3	Mus musculus	132-137
30209319-5	2018	In our results, mercury and arsenic inhibited interleukin (IL)-1beta and IL-18 secretion resulting from canonical and non-canonical NLRP3 inflammasome activation in macrophages and attenuated elevation of serum IL-1beta in response to LPS treatment in mice.	Arsenic	28-35	interleukin 1 alpha	Mus musculus	211-219
30209319-7	2018	Both mercury and arsenic inhibited Asc pyroptosome formation and gasdermin D cleavage.	Arsenic	17-24	gasdermin D	Mus musculus	65-76
29864498-3	2018	In this study, we investigated the association between levels of Fas and Bax expression and the three arsenic species (inorganic arsenic (iAs), monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA)) in vivo and vitro.	Arsenic	102-109	BCL2 associated X, apoptosis regulator	Homo sapiens	73-76
30258467-3	2018	This study aimed at exploring the change of arsenic concentration in mice and across MDCK-MDR1 cells and the cytotoxicity on K562 cells when realgar and indigo naturalis were combined.	Arsenic	44-51	ATP binding cassette subfamily B member 1	Canis lupus familiaris	85-94
30258467-6	2018	The apparent permeability coefficients (Papp) of bidirectional transport in MDCK-MDR1 cell permeability experiments showed that arsenic permeability obviously went up when indigo naturalis was incubated together.	Arsenic	128-135	ATP binding cassette subfamily B member 1	Canis lupus familiaris	76-85
30080396-7	2018	Different expression levels of AQP9 and xCT are only partially accountable for the observed differences in arsenic uptake across cell cycle, indicative of the presence of other importers for both ATO and ZIO-101.	Arsenic	107-114	aquaporin 9	Homo sapiens	31-35
30080396-7	2018	Different expression levels of AQP9 and xCT are only partially accountable for the observed differences in arsenic uptake across cell cycle, indicative of the presence of other importers for both ATO and ZIO-101.	Arsenic	107-114	solute carrier family 7 member 11	Homo sapiens	40-43
30369344-0	2018	The Bidirectional Effects of Arsenic on miRNA-21: A Systematic Review and Meta-analysis.	Arsenic	29-36	microRNA 21	Homo sapiens	40-48
30185897-9	2018	Our findings ascertain that miR-301a is an oncogenic miRNA, which targets SMAD4 to establish an essential mechanism for arsenic-induced carcinogenesis, IL-6/STAT3/miR-301a/SMAD4 signaling pathways.	Arsenic	120-127	SMAD family member 4	Homo sapiens	74-79
30185897-9	2018	Our findings ascertain that miR-301a is an oncogenic miRNA, which targets SMAD4 to establish an essential mechanism for arsenic-induced carcinogenesis, IL-6/STAT3/miR-301a/SMAD4 signaling pathways.	Arsenic	120-127	interleukin 6	Homo sapiens	152-156
30185897-9	2018	Our findings ascertain that miR-301a is an oncogenic miRNA, which targets SMAD4 to establish an essential mechanism for arsenic-induced carcinogenesis, IL-6/STAT3/miR-301a/SMAD4 signaling pathways.	Arsenic	120-127	signal transducer and activator of transcription 3	Homo sapiens	157-162
30185897-9	2018	Our findings ascertain that miR-301a is an oncogenic miRNA, which targets SMAD4 to establish an essential mechanism for arsenic-induced carcinogenesis, IL-6/STAT3/miR-301a/SMAD4 signaling pathways.	Arsenic	120-127	SMAD family member 4	Homo sapiens	172-177
29247444-0	2018	Effect of Arsenic Exposure on NRF2-KEAP1 Pathway and Epigenetic Modification.	Arsenic	10-17	NFE2 like bZIP transcription factor 2	Homo sapiens	30-34
29247444-0	2018	Effect of Arsenic Exposure on NRF2-KEAP1 Pathway and Epigenetic Modification.	Arsenic	10-17	kelch like ECH associated protein 1	Homo sapiens	35-40
29247444-14	2018	The findings provide evidence for rather inactivation of NRF2-KEAP1 pathway in response to chronic arsenic exposure.	Arsenic	99-106	NFE2 like bZIP transcription factor 2	Homo sapiens	57-61
29247444-14	2018	The findings provide evidence for rather inactivation of NRF2-KEAP1 pathway in response to chronic arsenic exposure.	Arsenic	99-106	kelch like ECH associated protein 1	Homo sapiens	62-67
30185897-0	2018	Malignant Transformation of Human Bronchial Epithelial Cells Induced by Arsenic through STAT3/miR-301a/SMAD4 Loop.	Arsenic	72-79	signal transducer and activator of transcription 3	Homo sapiens	88-93
30185897-0	2018	Malignant Transformation of Human Bronchial Epithelial Cells Induced by Arsenic through STAT3/miR-301a/SMAD4 Loop.	Arsenic	72-79	microRNA 301a	Homo sapiens	94-102
30185897-0	2018	Malignant Transformation of Human Bronchial Epithelial Cells Induced by Arsenic through STAT3/miR-301a/SMAD4 Loop.	Arsenic	72-79	SMAD family member 4	Homo sapiens	103-108
30185897-1	2018	Arsenic is a well-known of human carcinogen and miR-301a is an oncogenic microRNA, which links to oncogenesis, however, little is understood about its contribution to arsenic-induced cellular transformation and tumorigenesis.	Arsenic	167-174	microRNA 301a	Homo sapiens	48-56
30185897-2	2018	Here, we investigated the role of miR-301a during arsenic-induced cellular transformation and tumor formation.	Arsenic	50-57	microRNA 301a	Homo sapiens	34-42
30185897-3	2018	miR-301a was found to be upregulated during arsenic-induced BEAS-2B transformation and the overexpression of miR-301a was dependent on IL-6/STAT3 signaling.	Arsenic	44-51	microRNA 301a	Homo sapiens	0-8
30185897-3	2018	miR-301a was found to be upregulated during arsenic-induced BEAS-2B transformation and the overexpression of miR-301a was dependent on IL-6/STAT3 signaling.	Arsenic	44-51	interleukin 6	Homo sapiens	135-139
30185897-3	2018	miR-301a was found to be upregulated during arsenic-induced BEAS-2B transformation and the overexpression of miR-301a was dependent on IL-6/STAT3 signaling.	Arsenic	44-51	signal transducer and activator of transcription 3	Homo sapiens	140-145
30185897-9	2018	Our findings ascertain that miR-301a is an oncogenic miRNA, which targets SMAD4 to establish an essential mechanism for arsenic-induced carcinogenesis, IL-6/STAT3/miR-301a/SMAD4 signaling pathways.	Arsenic	120-127	microRNA 301a	Homo sapiens	28-36
30369344-2	2018	miRNA-21 plays a crucial role in arsenic-induced carcinogenesis.	Arsenic	33-40	microRNA 21	Homo sapiens	0-8
30369344-3	2018	We aimed to elucidate the mechanism by which miRNA-21 influences arsenic-induced cancer.	Arsenic	65-72	microRNA 21	Homo sapiens	45-53
30369344-4	2018	METHODS: We used meta-analysis of published studies to determine how arsenic induces cancerous cells through miRNA-21.	Arsenic	69-76	microRNA 21	Homo sapiens	109-117
30369344-5	2018	RESULTS: Low-dose arsenic exposure (  5 mumol/L) can increase miRNA-21 and phosphorylated signal transducter and activator of transcription 3 (pSTAT3) expression, and decrease programmed cell death protein 4 (PDCD4) and protein sprouty homolog 1 (Spry1) expression.	Arsenic	18-25	microRNA 21	Homo sapiens	62-70
30369344-5	2018	RESULTS: Low-dose arsenic exposure (  5 mumol/L) can increase miRNA-21 and phosphorylated signal transducter and activator of transcription 3 (pSTAT3) expression, and decrease programmed cell death protein 4 (PDCD4) and protein sprouty homolog 1 (Spry1) expression.	Arsenic	18-25	programmed cell death 4	Homo sapiens	176-207
30369344-5	2018	RESULTS: Low-dose arsenic exposure (  5 mumol/L) can increase miRNA-21 and phosphorylated signal transducter and activator of transcription 3 (pSTAT3) expression, and decrease programmed cell death protein 4 (PDCD4) and protein sprouty homolog 1 (Spry1) expression.	Arsenic	18-25	programmed cell death 4	Homo sapiens	209-214
30369344-5	2018	RESULTS: Low-dose arsenic exposure (  5 mumol/L) can increase miRNA-21 and phosphorylated signal transducter and activator of transcription 3 (pSTAT3) expression, and decrease programmed cell death protein 4 (PDCD4) and protein sprouty homolog 1 (Spry1) expression.	Arsenic	18-25	sprouty RTK signaling antagonist 1	Homo sapiens	228-245
30369344-5	2018	RESULTS: Low-dose arsenic exposure (  5 mumol/L) can increase miRNA-21 and phosphorylated signal transducter and activator of transcription 3 (pSTAT3) expression, and decrease programmed cell death protein 4 (PDCD4) and protein sprouty homolog 1 (Spry1) expression.	Arsenic	18-25	sprouty RTK signaling antagonist 1	Homo sapiens	247-252
30369344-6	2018	High-dose arsenic exposure (&gt; 5 mumol/L), can increase miRNA-21 expression, and decrease Spry1 and E-cadherin expression.	Arsenic	10-17	microRNA 21	Homo sapiens	58-66
30369344-6	2018	High-dose arsenic exposure (&gt; 5 mumol/L), can increase miRNA-21 expression, and decrease Spry1 and E-cadherin expression.	Arsenic	10-17	sprouty RTK signaling antagonist 1	Homo sapiens	92-97
30369344-6	2018	High-dose arsenic exposure (&gt; 5 mumol/L), can increase miRNA-21 expression, and decrease Spry1 and E-cadherin expression.	Arsenic	10-17	cadherin 1	Homo sapiens	102-112
30369344-7	2018	Short-term arsenic exposure (  24 h) can increase miRNA-21 and pSTAT3 expression, and decrease PDCD4 expression.	Arsenic	11-18	microRNA 21	Homo sapiens	50-58
30369344-7	2018	Short-term arsenic exposure (  24 h) can increase miRNA-21 and pSTAT3 expression, and decrease PDCD4 expression.	Arsenic	11-18	programmed cell death 4	Homo sapiens	95-100
30369344-8	2018	Moreover, long-term arsenic exposure (&gt; 24 h) can increase the miRNA-21, STAT3, and pSTAT3 expression, and decrease PDCD4 expression.	Arsenic	20-27	microRNA 21	Homo sapiens	66-74
30369344-8	2018	Moreover, long-term arsenic exposure (&gt; 24 h) can increase the miRNA-21, STAT3, and pSTAT3 expression, and decrease PDCD4 expression.	Arsenic	20-27	signal transducer and activator of transcription 3	Homo sapiens	76-81
30369344-8	2018	Moreover, long-term arsenic exposure (&gt; 24 h) can increase the miRNA-21, STAT3, and pSTAT3 expression, and decrease PDCD4 expression.	Arsenic	20-27	programmed cell death 4	Homo sapiens	119-124
30369344-9	2018	We found that activation of miRNA-21 and pSTAT3 were most pronounced following long-term arsenic exposure at low doses, and the effects on PDCD4 expression were most pronounced following short-term arsenic exposure at low doses.	Arsenic	89-96	microRNA 21	Homo sapiens	28-36
30369344-9	2018	We found that activation of miRNA-21 and pSTAT3 were most pronounced following long-term arsenic exposure at low doses, and the effects on PDCD4 expression were most pronounced following short-term arsenic exposure at low doses.	Arsenic	198-205	programmed cell death 4	Homo sapiens	139-144
30369344-11	2018	CONCLUSION: Arsenic can cause cancer by activating miRNA-21 and inhibiting the expression of PDCD4, PTEN, and Spry1.	Arsenic	12-19	microRNA 21	Homo sapiens	51-59
30369344-11	2018	CONCLUSION: Arsenic can cause cancer by activating miRNA-21 and inhibiting the expression of PDCD4, PTEN, and Spry1.	Arsenic	12-19	programmed cell death 4	Homo sapiens	93-98
30369344-11	2018	CONCLUSION: Arsenic can cause cancer by activating miRNA-21 and inhibiting the expression of PDCD4, PTEN, and Spry1.	Arsenic	12-19	phosphatase and tensin homolog	Homo sapiens	100-104
30369344-11	2018	CONCLUSION: Arsenic can cause cancer by activating miRNA-21 and inhibiting the expression of PDCD4, PTEN, and Spry1.	Arsenic	12-19	sprouty RTK signaling antagonist 1	Homo sapiens	110-115
29986278-7	2018	Inhibition of the IL-7 signaling pathway was thought to be responsible for the non-genotoxicity induced by low to moderate doses of arsenic.	Arsenic	132-139	interleukin 7	Homo sapiens	18-22
29986281-0	2018	The PKCdelta-Nrf2-ARE signalling pathway may be involved in oxidative stress in arsenic-induced liver damage in rats.	Arsenic	80-87	NFE2 like bZIP transcription factor 2	Rattus norvegicus	13-17
29934829-6	2018	Dissolution of calcite from limestone bedrock and a high concentration of bicarbonate ions in natural river water (about 250 mg L-1) enhanced the neutralization of acidic river water and subsequent chemical precipitation of metals and arsenic.	Arsenic	235-242	immunoglobulin kappa variable 1-16	Homo sapiens	128-131
30064059-10	2018	Moreover, immunohistochemistry revealed that compared to the control group, the groups that were exposed to arsenic exhibited significantly higher levels of DCX expression in the external granular and external pyramidal layers (all Ps&lt;0.001).	Arsenic	108-115	doublecortin	Rattus norvegicus	157-160
29621709-0	2018	Detection of arsenic-binding siderophores in arsenic-tolerating Actinobacteria by a modified CAS assay.	Arsenic	13-20	BCAR1 scaffold protein, Cas family member	Homo sapiens	93-96
30064059-11	2018	Furthermore, the 30 mug/L and 45 mug/L arsenic exposure groups still showed some DCX expression at five weeks after exposure.	Arsenic	39-46	doublecortin	Rattus norvegicus	81-84
30072236-0	2018	In utero exposure to arsenic in tap water and congenital anomalies: A French semi-ecological study.	Arsenic	21-28	nuclear RNA export factor 1	Homo sapiens	32-35
30072236-3	2018	Studies on exposure to arsenic (As) in tap water and the risk of CA have not provided conclusive evidence, particularly when levels of exposure were low (from 10 to 50 mug As/L).	Arsenic	23-30	nuclear RNA export factor 1	Homo sapiens	39-42
30072236-3	2018	Studies on exposure to arsenic (As) in tap water and the risk of CA have not provided conclusive evidence, particularly when levels of exposure were low (from 10 to 50 mug As/L).	Arsenic	32-34	nuclear RNA export factor 1	Homo sapiens	39-42
30072236-10	2018	French guidelines for As in tap water were used to identify the two groups: "&gt;= 10 mug As/L group" and "[0-10) mug As/L group".	Arsenic	22-24	nuclear RNA export factor 1	Homo sapiens	28-31
29940200-0	2018	Hypomethylation of mitochondrial D-loop and ND6 with increased mitochondrial DNA copy number in the arsenic-exposed population.	Arsenic	100-107	mitochondrially encoded NADH dehydrogenase 6	Homo sapiens	44-47
30032600-0	2018	Arsenic-Induced Autophagy in the Developing Mouse Cerebellum: Involvement of the Blood-Brain Barrier"s Tight-Junction Proteins and the PI3K-Akt-mTOR Signaling Pathway.	Arsenic	0-7	thymoma viral proto-oncogene 1	Mus musculus	140-143
30032600-0	2018	Arsenic-Induced Autophagy in the Developing Mouse Cerebellum: Involvement of the Blood-Brain Barrier"s Tight-Junction Proteins and the PI3K-Akt-mTOR Signaling Pathway.	Arsenic	0-7	mechanistic target of rapamycin kinase	Mus musculus	144-148
30032600-1	2018	This study was designed to determine whether the tight-junction (TJ) proteins of the blood-brain barrier (BBB) and the PI3K-Akt-mTOR signaling pathway are involved during arsenic (As)-induced autophagy in developing mouse cerebella after exposure to different As concentrations (0, 0.15, 1.5, and 15 mg/L As(III)) during gestational and lactational periods.	Arsenic	180-182	thymoma viral proto-oncogene 1	Mus musculus	124-127
30032600-1	2018	This study was designed to determine whether the tight-junction (TJ) proteins of the blood-brain barrier (BBB) and the PI3K-Akt-mTOR signaling pathway are involved during arsenic (As)-induced autophagy in developing mouse cerebella after exposure to different As concentrations (0, 0.15, 1.5, and 15 mg/L As(III)) during gestational and lactational periods.	Arsenic	180-182	mechanistic target of rapamycin kinase	Mus musculus	128-132
30032600-8	2018	Finally, we conclude that developmental As exposure significantly alters TJ proteins, resulting an increase in BBB permeability, facilitating the ability of As to cross the BBB and induce autophagy, which might be partly the result of inhibition of the PI3K-Akt-mTOR signaling pathway, in an age-dependent manner (i.e., PND21 mice were found to be more vulnerable to As-induced neurotoxicity), which could be due to the immature BBB allowing As to cross through it.	Arsenic	40-42	thymoma viral proto-oncogene 1	Mus musculus	258-261
30032600-8	2018	Finally, we conclude that developmental As exposure significantly alters TJ proteins, resulting an increase in BBB permeability, facilitating the ability of As to cross the BBB and induce autophagy, which might be partly the result of inhibition of the PI3K-Akt-mTOR signaling pathway, in an age-dependent manner (i.e., PND21 mice were found to be more vulnerable to As-induced neurotoxicity), which could be due to the immature BBB allowing As to cross through it.	Arsenic	40-42	mechanistic target of rapamycin kinase	Mus musculus	262-266
30093655-0	2018	Arsenic targets Pin1 and cooperates with retinoic acid to inhibit cancer-driving pathways and tumor-initiating cells.	Arsenic	0-7	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	16-20
29758887-0	2018	Arsenic-rich shallow groundwater in sandy aquifer systems buffered by rising carbonate waters: A geochemical case study from Mannar Island, Sri Lanka.	Arsenic	0-7	sorcin	Homo sapiens	140-143
29189995-5	2018	Our results point out that arsenic exposure caused oxidative stress in rats" hippocampus, which led to the reactive oxygen species (ROS) generation, mitochondrial swelling, the collapse of the mitochondrial membrane potential, and release of cytochrome c. It also altered Bcl-2/Bax expression ratio and increased caspase-3 and caspase-9 activities.	Arsenic	27-34	BCL2, apoptosis regulator	Rattus norvegicus	272-277
29889218-3	2018	In this study, we first investigated the potential epigenetic mechanisms underlying the phenomenon of NQO1 differential expression in individual subclones of rat arsenic-transformed lung epithelial cells (TLECs).	Arsenic	162-169	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	102-106
29947889-0	2018	Prenatal arsenic exposure is associated with increased plasma IGFBP3 concentrations in 9-year-old children partly via changes in DNA methylation.	Arsenic	9-16	insulin like growth factor binding protein 3	Homo sapiens	62-68
29947889-1	2018	Exposure to inorganic arsenic (As), a carcinogen and epigenetic toxicant, has been associated with lower circulating levels of insulin-like growth factor 1 (IGF1) and impaired growth in children of pre-school age.	Arsenic	31-33	insulin like growth factor 1	Homo sapiens	127-155
29947889-1	2018	Exposure to inorganic arsenic (As), a carcinogen and epigenetic toxicant, has been associated with lower circulating levels of insulin-like growth factor 1 (IGF1) and impaired growth in children of pre-school age.	Arsenic	31-33	insulin like growth factor 1	Homo sapiens	157-161
29947889-2	2018	The aim of this study was to assess the potential impact of exposure to As on IGF1 and insulin-like growth factor-binding protein 3 (IGFBP3) as well as DNA methylation changes in 9-year-old children.	Arsenic	72-74	insulin like growth factor 1	Homo sapiens	78-82
29189995-5	2018	Our results point out that arsenic exposure caused oxidative stress in rats" hippocampus, which led to the reactive oxygen species (ROS) generation, mitochondrial swelling, the collapse of the mitochondrial membrane potential, and release of cytochrome c. It also altered Bcl-2/Bax expression ratio and increased caspase-3 and caspase-9 activities.	Arsenic	27-34	BCL2 associated X, apoptosis regulator	Rattus norvegicus	278-281
29947889-2	2018	The aim of this study was to assess the potential impact of exposure to As on IGF1 and insulin-like growth factor-binding protein 3 (IGFBP3) as well as DNA methylation changes in 9-year-old children.	Arsenic	72-74	insulin like growth factor binding protein 3	Homo sapiens	87-131
29189995-5	2018	Our results point out that arsenic exposure caused oxidative stress in rats" hippocampus, which led to the reactive oxygen species (ROS) generation, mitochondrial swelling, the collapse of the mitochondrial membrane potential, and release of cytochrome c. It also altered Bcl-2/Bax expression ratio and increased caspase-3 and caspase-9 activities.	Arsenic	27-34	caspase 3	Rattus norvegicus	313-322
29947889-10	2018	Mediation analysis suggested that methylation of 12 CpG sites for all children was mediator of effect for the association between prenatal As and IGFBP3.	Arsenic	139-141	insulin like growth factor binding protein 3	Homo sapiens	146-152
29947889-12	2018	In all, our study revealed that prenatal exposure to As was positively associated with IGFBP3 concentrations in children at 9 years, independent of IGF1, and this association may, at least in part, be epigenetically mediated.	Arsenic	53-55	insulin like growth factor binding protein 3	Homo sapiens	87-93
29189995-5	2018	Our results point out that arsenic exposure caused oxidative stress in rats" hippocampus, which led to the reactive oxygen species (ROS) generation, mitochondrial swelling, the collapse of the mitochondrial membrane potential, and release of cytochrome c. It also altered Bcl-2/Bax expression ratio and increased caspase-3 and caspase-9 activities.	Arsenic	27-34	caspase 9	Rattus norvegicus	327-336
29752257-0	2018	Multidrug Resistance Protein 1 (MRP1/ABCC1)-Mediated Cellular Protection and Transport of Methylated Arsenic Metabolites Differs between Human Cell Lines.	Arsenic	101-108	ATP binding cassette subfamily B member 1	Homo sapiens	0-30
29752257-10	2018	Efflux of different arsenic metabolites by MRP1 is likely influenced by multiple factors, including cell and tissue type.	Arsenic	20-27	ATP binding cassette subfamily C member 1	Homo sapiens	43-47
29752257-0	2018	Multidrug Resistance Protein 1 (MRP1/ABCC1)-Mediated Cellular Protection and Transport of Methylated Arsenic Metabolites Differs between Human Cell Lines.	Arsenic	101-108	ATP binding cassette subfamily C member 1	Homo sapiens	32-36
29752257-11	2018	This could have implications for the impact of MRP1 on both tissue-specific susceptibility to arsenic-induced disease and tumor sensitivity to arsenic-based therapeutics.	Arsenic	94-101	ATP binding cassette subfamily C member 1	Homo sapiens	47-51
29752257-0	2018	Multidrug Resistance Protein 1 (MRP1/ABCC1)-Mediated Cellular Protection and Transport of Methylated Arsenic Metabolites Differs between Human Cell Lines.	Arsenic	101-108	ATP binding cassette subfamily C member 1	Homo sapiens	37-42
29752257-1	2018	The ATP-binding cassette (ABC) transporter multidrug resistance protein 1 (MRP1/ABCC1) protects cells from arsenic (a proven human carcinogen) through the cellular efflux of arsenic triglutathione [As(GS)3] and the diglutathione conjugate of monomethylarsonous acid [MMA(GS)2].	Arsenic	107-114	ATP binding cassette subfamily B member 1	Homo sapiens	43-73
29752257-1	2018	The ATP-binding cassette (ABC) transporter multidrug resistance protein 1 (MRP1/ABCC1) protects cells from arsenic (a proven human carcinogen) through the cellular efflux of arsenic triglutathione [As(GS)3] and the diglutathione conjugate of monomethylarsonous acid [MMA(GS)2].	Arsenic	107-114	ATP binding cassette subfamily C member 1	Homo sapiens	75-79
29752257-1	2018	The ATP-binding cassette (ABC) transporter multidrug resistance protein 1 (MRP1/ABCC1) protects cells from arsenic (a proven human carcinogen) through the cellular efflux of arsenic triglutathione [As(GS)3] and the diglutathione conjugate of monomethylarsonous acid [MMA(GS)2].	Arsenic	107-114	ATP binding cassette subfamily C member 1	Homo sapiens	80-85
29752257-4	2018	MRP1 expressed in HEK293 cells reduced the toxicity of the major urinary arsenic metabolite dimethylarsinic acid (DMAV), and HEK-WT-MRP1-enriched vesicles transported DMAV with high apparent affinity and capacity (Km 0.19 microM, Vmax 342 pmol mg-1protein min-1).	Arsenic	73-80	ATP binding cassette subfamily C member 1	Homo sapiens	0-4
29570983-11	2018	CONCLUSIONS: YAS report high satisfaction with the online SCP, as well as a high symptom burden, although the latter were reported less than for AS.	Arsenic	14-16	urocortin 3	Homo sapiens	58-61
29948670-14	2018	Further, reduction in AChE (acetylcholinesterase) and BChE (butyrylcholinesterase) and motor coordination activity were also observed in arsenic-treated groups.	Arsenic	137-144	acetylcholinesterase	Mus musculus	22-26
29948670-14	2018	Further, reduction in AChE (acetylcholinesterase) and BChE (butyrylcholinesterase) and motor coordination activity were also observed in arsenic-treated groups.	Arsenic	137-144	acetylcholinesterase	Mus musculus	28-48
29948670-14	2018	Further, reduction in AChE (acetylcholinesterase) and BChE (butyrylcholinesterase) and motor coordination activity were also observed in arsenic-treated groups.	Arsenic	137-144	butyrylcholinesterase	Mus musculus	54-58
29948670-14	2018	Further, reduction in AChE (acetylcholinesterase) and BChE (butyrylcholinesterase) and motor coordination activity were also observed in arsenic-treated groups.	Arsenic	137-144	butyrylcholinesterase	Mus musculus	60-81
29846136-8	2018	Finally, we show that arsenate [As(V)], a pentavalent form of arsenic, also activates Hog1, but through a pathway that is distinct from that of As(III) and involves activation of the Hog1 MEK Pbs2.	Arsenic	62-69	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	86-90
29944914-0	2018	Arsenic-induced apoptosis in the p53-proficient and p53-deficient cells through differential modulation of NFkB pathway.	Arsenic	0-7	transformation related protein 53	Mus musculus	33-36
29944914-0	2018	Arsenic-induced apoptosis in the p53-proficient and p53-deficient cells through differential modulation of NFkB pathway.	Arsenic	0-7	transformation related protein 53	Mus musculus	52-55
29944914-4	2018	Arsenic reduced cell viability and increased more apoptosis in the p53-/- cells as compared to p53+/+ cells, which was correlated with activation of SAPK/JNK, p38 MAPK, and AKT pathways.	Arsenic	0-7	transformation related protein 53	Mus musculus	67-70
29944914-4	2018	Arsenic reduced cell viability and increased more apoptosis in the p53-/- cells as compared to p53+/+ cells, which was correlated with activation of SAPK/JNK, p38 MAPK, and AKT pathways.	Arsenic	0-7	mitogen-activated protein kinase 14	Mus musculus	159-167
29944914-4	2018	Arsenic reduced cell viability and increased more apoptosis in the p53-/- cells as compared to p53+/+ cells, which was correlated with activation of SAPK/JNK, p38 MAPK, and AKT pathways.	Arsenic	0-7	thymoma viral proto-oncogene 1	Mus musculus	173-176
29944914-5	2018	A transcriptional regulatory network analysis revealed that arsenic activated transcription regulatory elements E2F, Egr1, Trp53, Stat6, Bcl6, Creb2 and ATF4 in the p53+/+ cells, while in the p53-/- cells, arsenic treatment altered transcription factors NFkappaB, Pparg, Creb2, ATF4, and Egr1.	Arsenic	60-67	early growth response 1	Mus musculus	117-121
29944914-5	2018	A transcriptional regulatory network analysis revealed that arsenic activated transcription regulatory elements E2F, Egr1, Trp53, Stat6, Bcl6, Creb2 and ATF4 in the p53+/+ cells, while in the p53-/- cells, arsenic treatment altered transcription factors NFkappaB, Pparg, Creb2, ATF4, and Egr1.	Arsenic	60-67	transformation related protein 53	Mus musculus	123-128
29944914-5	2018	A transcriptional regulatory network analysis revealed that arsenic activated transcription regulatory elements E2F, Egr1, Trp53, Stat6, Bcl6, Creb2 and ATF4 in the p53+/+ cells, while in the p53-/- cells, arsenic treatment altered transcription factors NFkappaB, Pparg, Creb2, ATF4, and Egr1.	Arsenic	60-67	signal transducer and activator of transcription 6	Mus musculus	130-135
29944914-5	2018	A transcriptional regulatory network analysis revealed that arsenic activated transcription regulatory elements E2F, Egr1, Trp53, Stat6, Bcl6, Creb2 and ATF4 in the p53+/+ cells, while in the p53-/- cells, arsenic treatment altered transcription factors NFkappaB, Pparg, Creb2, ATF4, and Egr1.	Arsenic	60-67	B cell leukemia/lymphoma 6	Mus musculus	137-141
29944914-5	2018	A transcriptional regulatory network analysis revealed that arsenic activated transcription regulatory elements E2F, Egr1, Trp53, Stat6, Bcl6, Creb2 and ATF4 in the p53+/+ cells, while in the p53-/- cells, arsenic treatment altered transcription factors NFkappaB, Pparg, Creb2, ATF4, and Egr1.	Arsenic	60-67	activating transcription factor 4	Mus musculus	143-148
29944914-5	2018	A transcriptional regulatory network analysis revealed that arsenic activated transcription regulatory elements E2F, Egr1, Trp53, Stat6, Bcl6, Creb2 and ATF4 in the p53+/+ cells, while in the p53-/- cells, arsenic treatment altered transcription factors NFkappaB, Pparg, Creb2, ATF4, and Egr1.	Arsenic	60-67	activating transcription factor 4	Mus musculus	153-157
29944914-5	2018	A transcriptional regulatory network analysis revealed that arsenic activated transcription regulatory elements E2F, Egr1, Trp53, Stat6, Bcl6, Creb2 and ATF4 in the p53+/+ cells, while in the p53-/- cells, arsenic treatment altered transcription factors NFkappaB, Pparg, Creb2, ATF4, and Egr1.	Arsenic	60-67	transformation related protein 53	Mus musculus	125-128
29944914-5	2018	A transcriptional regulatory network analysis revealed that arsenic activated transcription regulatory elements E2F, Egr1, Trp53, Stat6, Bcl6, Creb2 and ATF4 in the p53+/+ cells, while in the p53-/- cells, arsenic treatment altered transcription factors NFkappaB, Pparg, Creb2, ATF4, and Egr1.	Arsenic	60-67	transformation related protein 53	Mus musculus	165-168
29944914-5	2018	A transcriptional regulatory network analysis revealed that arsenic activated transcription regulatory elements E2F, Egr1, Trp53, Stat6, Bcl6, Creb2 and ATF4 in the p53+/+ cells, while in the p53-/- cells, arsenic treatment altered transcription factors NFkappaB, Pparg, Creb2, ATF4, and Egr1.	Arsenic	60-67	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	254-262
29944914-5	2018	A transcriptional regulatory network analysis revealed that arsenic activated transcription regulatory elements E2F, Egr1, Trp53, Stat6, Bcl6, Creb2 and ATF4 in the p53+/+ cells, while in the p53-/- cells, arsenic treatment altered transcription factors NFkappaB, Pparg, Creb2, ATF4, and Egr1.	Arsenic	60-67	peroxisome proliferator activated receptor gamma	Mus musculus	264-269
29944914-5	2018	A transcriptional regulatory network analysis revealed that arsenic activated transcription regulatory elements E2F, Egr1, Trp53, Stat6, Bcl6, Creb2 and ATF4 in the p53+/+ cells, while in the p53-/- cells, arsenic treatment altered transcription factors NFkappaB, Pparg, Creb2, ATF4, and Egr1.	Arsenic	60-67	activating transcription factor 4	Mus musculus	271-276
29944914-5	2018	A transcriptional regulatory network analysis revealed that arsenic activated transcription regulatory elements E2F, Egr1, Trp53, Stat6, Bcl6, Creb2 and ATF4 in the p53+/+ cells, while in the p53-/- cells, arsenic treatment altered transcription factors NFkappaB, Pparg, Creb2, ATF4, and Egr1.	Arsenic	60-67	activating transcription factor 4	Mus musculus	278-282
29944914-5	2018	A transcriptional regulatory network analysis revealed that arsenic activated transcription regulatory elements E2F, Egr1, Trp53, Stat6, Bcl6, Creb2 and ATF4 in the p53+/+ cells, while in the p53-/- cells, arsenic treatment altered transcription factors NFkappaB, Pparg, Creb2, ATF4, and Egr1.	Arsenic	60-67	early growth response 1	Mus musculus	288-292
29944914-7	2018	Our study confirmed the differential modulation of NFkappaB pathway by arsenic in the p53+/+ or p53-/- cells and this observation of the differential mechanism of cell death between the p53+/+ and p53-/- cells might be linked to the unique ability of arsenic to act as both a carcinogen and a chemotherapeutic agent.	Arsenic	71-78	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	51-59
29944914-7	2018	Our study confirmed the differential modulation of NFkappaB pathway by arsenic in the p53+/+ or p53-/- cells and this observation of the differential mechanism of cell death between the p53+/+ and p53-/- cells might be linked to the unique ability of arsenic to act as both a carcinogen and a chemotherapeutic agent.	Arsenic	71-78	transformation related protein 53	Mus musculus	86-89
29944914-7	2018	Our study confirmed the differential modulation of NFkappaB pathway by arsenic in the p53+/+ or p53-/- cells and this observation of the differential mechanism of cell death between the p53+/+ and p53-/- cells might be linked to the unique ability of arsenic to act as both a carcinogen and a chemotherapeutic agent.	Arsenic	71-78	transformation related protein 53	Mus musculus	96-99
29944914-7	2018	Our study confirmed the differential modulation of NFkappaB pathway by arsenic in the p53+/+ or p53-/- cells and this observation of the differential mechanism of cell death between the p53+/+ and p53-/- cells might be linked to the unique ability of arsenic to act as both a carcinogen and a chemotherapeutic agent.	Arsenic	71-78	transformation related protein 53	Mus musculus	96-99
29944914-7	2018	Our study confirmed the differential modulation of NFkappaB pathway by arsenic in the p53+/+ or p53-/- cells and this observation of the differential mechanism of cell death between the p53+/+ and p53-/- cells might be linked to the unique ability of arsenic to act as both a carcinogen and a chemotherapeutic agent.	Arsenic	71-78	transformation related protein 53	Mus musculus	96-99
29944914-7	2018	Our study confirmed the differential modulation of NFkappaB pathway by arsenic in the p53+/+ or p53-/- cells and this observation of the differential mechanism of cell death between the p53+/+ and p53-/- cells might be linked to the unique ability of arsenic to act as both a carcinogen and a chemotherapeutic agent.	Arsenic	251-258	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	51-59
29846136-8	2018	Finally, we show that arsenate [As(V)], a pentavalent form of arsenic, also activates Hog1, but through a pathway that is distinct from that of As(III) and involves activation of the Hog1 MEK Pbs2.	Arsenic	62-69	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	183-187
29846136-8	2018	Finally, we show that arsenate [As(V)], a pentavalent form of arsenic, also activates Hog1, but through a pathway that is distinct from that of As(III) and involves activation of the Hog1 MEK Pbs2.	Arsenic	62-69	mitogen-activated protein kinase kinase PBS2	Saccharomyces cerevisiae S288C	192-196
29603397-6	2018	Arsenic down-regulated miRNA-31 and the release of this inhibition caused overexpression of special AT-rich sequence-binding protein 2 (SATB2).	Arsenic	0-7	SATB homeobox 2	Homo sapiens	136-141
29603397-7	2018	Arsenic is known to disrupt miRNA expression, and here we report for the first time that arsenic is capable of inhibiting miR-31 expression.	Arsenic	0-7	microRNA 31	Homo sapiens	122-128
29603397-7	2018	Arsenic is known to disrupt miRNA expression, and here we report for the first time that arsenic is capable of inhibiting miR-31 expression.	Arsenic	89-96	microRNA 31	Homo sapiens	122-128
29603397-0	2018	Role of miR-31 and SATB2 in arsenic-induced malignant BEAS-2B cell transformation.	Arsenic	28-35	microRNA 31	Homo sapiens	8-14
29603397-0	2018	Role of miR-31 and SATB2 in arsenic-induced malignant BEAS-2B cell transformation.	Arsenic	28-35	SATB homeobox 2	Homo sapiens	19-24
29603397-6	2018	Arsenic down-regulated miRNA-31 and the release of this inhibition caused overexpression of special AT-rich sequence-binding protein 2 (SATB2).	Arsenic	0-7	SATB homeobox 2	Homo sapiens	92-134
30873793-8	2018	Moreover, 40% of localities with arsenic levels higher than 10 mug/L also present concurrent fluoride exposure higher than 1.5 mgF/L.	Arsenic	33-40	signal transducer and activator of transcription 5A	Homo sapiens	127-130
29603397-9	2018	Results from this study show that arsenic induces the overexpressing SATB2 by inhibiting miR-31 expression, which blocks the translation of SATB2 mRNA, since levels of SATB2 mRNA remain the same but protein levels decrease.	Arsenic	34-41	SATB homeobox 2	Homo sapiens	69-74
29603397-9	2018	Results from this study show that arsenic induces the overexpressing SATB2 by inhibiting miR-31 expression, which blocks the translation of SATB2 mRNA, since levels of SATB2 mRNA remain the same but protein levels decrease.	Arsenic	34-41	microRNA 31	Homo sapiens	89-95
29603397-9	2018	Results from this study show that arsenic induces the overexpressing SATB2 by inhibiting miR-31 expression, which blocks the translation of SATB2 mRNA, since levels of SATB2 mRNA remain the same but protein levels decrease.	Arsenic	34-41	SATB homeobox 2	Homo sapiens	140-145
29603397-9	2018	Results from this study show that arsenic induces the overexpressing SATB2 by inhibiting miR-31 expression, which blocks the translation of SATB2 mRNA, since levels of SATB2 mRNA remain the same but protein levels decrease.	Arsenic	34-41	SATB homeobox 2	Homo sapiens	140-145
30104978-3	2018	We showed previously that C. elegans ABCB6/HMT-1 detoxifies cadmium, copper, and arsenic, and is expressed in liver-like cells, the coelomocytes, head neurons and intestinal cells, which are the cell types that are affected by heavy metal poisoning in humans.	Arsenic	81-88	Heavy metal tolerance factor 1	Caenorhabditis elegans	43-48
29893020-5	2018	Here, a rare chemical form of arsenic, called black-arsenic (b-As), is reported as a cousin of black phosphorus, as an extremely anisotropic layered semiconductor.	Arsenic	30-37	BAS	Homo sapiens	46-65
29894638-2	2018	Arsenic methylation by the enzyme As(III) S-adenosylmethionine (SAM) methyltransferase (ArsM in microbes or AS3MT in animals) detoxifies As(III) in microbes but transforms it into more toxic and potentially more carcinogenic methylated species in humans.	Arsenic	0-7	arsenite methyltransferase	Homo sapiens	108-113
29676841-4	2018	Thermal treatment of 3 leads to the abstraction of one arsenic atom to yield [(L3 Co)2 As3 ] (4).	Arsenic	55-62	PDS5 cohesin associated factor B	Homo sapiens	87-90
29897238-7	2018	Concentrations of heavy metals like As and Ni were greater in CPS milk than those in organic milk ( P &lt; 0.05).	Arsenic	36-38	Weaning weight-maternal milk	Bos taurus	66-70
30031898-0	2018	Interaction of arsenic with gap junction protein connexin 43 alters gap junctional intercellular communication.	Arsenic	15-22	gap junction protein alpha 1	Homo sapiens	49-60
30031898-5	2018	Here we study the dynamic effect of Arsenic on Connexin 43 (Cx43), a protein that forms the gap junctions, whose alteration deeply perturbs the cell-to-cell communication vital for maintaining tissue homeostasis.	Arsenic	36-43	gap junction protein alpha 1	Homo sapiens	47-58
30031898-5	2018	Here we study the dynamic effect of Arsenic on Connexin 43 (Cx43), a protein that forms the gap junctions, whose alteration deeply perturbs the cell-to-cell communication vital for maintaining tissue homeostasis.	Arsenic	36-43	gap junction protein alpha 1	Homo sapiens	60-64
30031898-7	2018	Gap junction communication is severely disrupted by Arsenic due to reduced availability of unaltered Cx43 in the membrane bound form.	Arsenic	52-59	gap junction protein alpha 1	Homo sapiens	101-105
30031898-8	2018	In silico and Inductively Coupled Plasma Mass Spectrometry studies revealed the interaction of Arsenic to the Cx43 preferably occurs through surface exposed cysteines, thereby capping the thiol groups that form disulfide bonds in the tertiary structure.	Arsenic	95-102	gap junction protein alpha 1	Homo sapiens	110-114
29719206-8	2018	The immunoreaction for Sox2 (a specific marker for stem cells), at the same time, was observed in the support and mantle cells, after exposure to arsenic and cadmium, while only in the support cells after exposure to zinc.	Arsenic	146-153	SRY-box transcription factor 2	Danio rerio	23-27
29705899-10	2018	Taken together, we conjectured that, in chicken jejunum, arsenic led to redistribution of trace elements, promoting apoptosis via regulating mitochondrial dynamics, leading to autophagy through PI3K/AKT/mTOR signal pathways.	Arsenic	57-64	mechanistic target of rapamycin	Gallus gallus	203-207
29630858-9	2018	The multilayered pattern of CB +ve cells along with their downregulated expression and low packing density was significantly evident in the arsenic (iAs) alone exposed group as against the controls and AOX supplemented groups.	Arsenic	140-147	acyl-CoA oxidase 1	Rattus norvegicus	202-205
29769245-7	2018	Furthermore, a comprehensive review of current literature reveals an imperative need for future studies to establish and pinpoint the exact conditions for which arsenic can, and through what mechanisms it is able to, differentially regulate the PI3K/AKT/mTOR pathway to maximize the therapeutic and minimize the carcinogenic properties of arsenic.	Arsenic	161-168	AKT serine/threonine kinase 1	Homo sapiens	250-253
29396848-0	2018	Arsenic promotes the COX2/PGE2-SOX2 axis to increase the malignant stemness properties of urothelial cells.	Arsenic	0-7	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	21-25
29396848-0	2018	Arsenic promotes the COX2/PGE2-SOX2 axis to increase the malignant stemness properties of urothelial cells.	Arsenic	0-7	SRY-box transcription factor 2	Homo sapiens	31-35
29396848-3	2018	Using this model, we found that chronic arsenic exposure endows urothelial cells with malignant stemness properties including increased expression of stemness-related factors such as SOX2, sphere formation, self-renewal, invasion and chemoresistance.	Arsenic	40-47	SRY-box transcription factor 2	Homo sapiens	183-187
29396848-5	2018	Following gene set enrichment analyses of arsenic-exposed and arsenic-unexposed cells, we found COX2 as an enriched gene for oncogenic signature.	Arsenic	42-49	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	96-100
29396848-5	2018	Following gene set enrichment analyses of arsenic-exposed and arsenic-unexposed cells, we found COX2 as an enriched gene for oncogenic signature.	Arsenic	62-69	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	96-100
29396848-6	2018	Mechanistically, arsenic-induced COX2/PGE2 increases SOX2 expression that eventually promotes malignant stem cell generation and repopulation.	Arsenic	17-24	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	33-37
29396848-6	2018	Mechanistically, arsenic-induced COX2/PGE2 increases SOX2 expression that eventually promotes malignant stem cell generation and repopulation.	Arsenic	17-24	SRY-box transcription factor 2	Homo sapiens	53-57
29396848-7	2018	In urine samples from 90 subjects exposed to arsenic and 91 control subjects, we found a significant linear correlation between SOX2 and COX2 expression and the potential of SOX2 and COX2 expression as urinary markers to detect subjects exposed to arsenic.	Arsenic	45-52	SRY-box transcription factor 2	Homo sapiens	128-132
29396848-7	2018	In urine samples from 90 subjects exposed to arsenic and 91 control subjects, we found a significant linear correlation between SOX2 and COX2 expression and the potential of SOX2 and COX2 expression as urinary markers to detect subjects exposed to arsenic.	Arsenic	45-52	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	137-141
29396848-7	2018	In urine samples from 90 subjects exposed to arsenic and 91 control subjects, we found a significant linear correlation between SOX2 and COX2 expression and the potential of SOX2 and COX2 expression as urinary markers to detect subjects exposed to arsenic.	Arsenic	45-52	SRY-box transcription factor 2	Homo sapiens	174-178
29396848-7	2018	In urine samples from 90 subjects exposed to arsenic and 91 control subjects, we found a significant linear correlation between SOX2 and COX2 expression and the potential of SOX2 and COX2 expression as urinary markers to detect subjects exposed to arsenic.	Arsenic	45-52	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	183-187
29396848-7	2018	In urine samples from 90 subjects exposed to arsenic and 91 control subjects, we found a significant linear correlation between SOX2 and COX2 expression and the potential of SOX2 and COX2 expression as urinary markers to detect subjects exposed to arsenic.	Arsenic	248-255	SRY-box transcription factor 2	Homo sapiens	128-132
29396848-7	2018	In urine samples from 90 subjects exposed to arsenic and 91 control subjects, we found a significant linear correlation between SOX2 and COX2 expression and the potential of SOX2 and COX2 expression as urinary markers to detect subjects exposed to arsenic.	Arsenic	248-255	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	137-141
29396848-7	2018	In urine samples from 90 subjects exposed to arsenic and 91 control subjects, we found a significant linear correlation between SOX2 and COX2 expression and the potential of SOX2 and COX2 expression as urinary markers to detect subjects exposed to arsenic.	Arsenic	248-255	SRY-box transcription factor 2	Homo sapiens	174-178
29396848-7	2018	In urine samples from 90 subjects exposed to arsenic and 91 control subjects, we found a significant linear correlation between SOX2 and COX2 expression and the potential of SOX2 and COX2 expression as urinary markers to detect subjects exposed to arsenic.	Arsenic	248-255	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	183-187
29396848-10	2018	In conclusion, the COX2/PGE2-SOX2 axis promotes arsenic-induced malignant stem cell transformation.	Arsenic	48-55	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	19-23
29396848-10	2018	In conclusion, the COX2/PGE2-SOX2 axis promotes arsenic-induced malignant stem cell transformation.	Arsenic	48-55	SRY-box transcription factor 2	Homo sapiens	29-33
29769245-7	2018	Furthermore, a comprehensive review of current literature reveals an imperative need for future studies to establish and pinpoint the exact conditions for which arsenic can, and through what mechanisms it is able to, differentially regulate the PI3K/AKT/mTOR pathway to maximize the therapeutic and minimize the carcinogenic properties of arsenic.	Arsenic	161-168	mechanistic target of rapamycin kinase	Homo sapiens	254-258
29674040-4	2018	In environmental waters, arsenic exists predominantly in two chemical forms: As(III) and As(V).	Arsenic	25-32	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	89-94
29361141-0	2018	Vacuolar Transporters for Cadmium and Arsenic in Plants and their Applications in Phytoremediation and Crop Development.	Arsenic	38-45	LUC7 like 3 pre-mRNA splicing factor	Homo sapiens	103-107
29723552-0	2018	PI3K/Akt/GSK3beta induced CREB activation ameliorates arsenic mediated alterations in NMDA receptors and associated signaling in rat hippocampus: Neuroprotective role of curcumin.	Arsenic	54-61	AKT serine/threonine kinase 1	Rattus norvegicus	5-8
29723552-0	2018	PI3K/Akt/GSK3beta induced CREB activation ameliorates arsenic mediated alterations in NMDA receptors and associated signaling in rat hippocampus: Neuroprotective role of curcumin.	Arsenic	54-61	glycogen synthase kinase 3 beta	Rattus norvegicus	9-17
29723552-0	2018	PI3K/Akt/GSK3beta induced CREB activation ameliorates arsenic mediated alterations in NMDA receptors and associated signaling in rat hippocampus: Neuroprotective role of curcumin.	Arsenic	54-61	cAMP responsive element binding protein 1	Rattus norvegicus	26-30
29475479-11	2018	Furthermore, the method can be used for the screening analysis of total arsenic in waters when a cut-off level of 7 ng mL-1 is used.	Arsenic	72-79	L1 cell adhesion molecule	Mus musculus	119-123
29723618-0	2018	Adiponectin gene polymorphisms and obesity increase the susceptibility to arsenic-related renal cell carcinoma.	Arsenic	74-81	adiponectin, C1Q and collagen domain containing	Homo sapiens	0-11
30081983-52	2018	Compared to control group, relative mRNA expressions of Lin28, Bax, Bcl-2 and Fas were all higher in worker who were smelting arsenic( P &lt; 0.	Arsenic	126-133	lin-28 homolog A	Homo sapiens	56-61
30081983-52	2018	Compared to control group, relative mRNA expressions of Lin28, Bax, Bcl-2 and Fas were all higher in worker who were smelting arsenic( P &lt; 0.	Arsenic	126-133	BCL2 associated X, apoptosis regulator	Homo sapiens	63-66
30081983-52	2018	Compared to control group, relative mRNA expressions of Lin28, Bax, Bcl-2 and Fas were all higher in worker who were smelting arsenic( P &lt; 0.	Arsenic	126-133	BCL2 apoptosis regulator	Homo sapiens	68-73
29723618-10	2018	The OR of RCC for the combined effect of high urinary total arsenic levels and obesity, which was dose-dependent, in individuals with the ADIPOQ rs182052 G/A+A/A genotype was 9.33 (3.85-22.62).	Arsenic	60-67	adiponectin, C1Q and collagen domain containing	Homo sapiens	138-144
29723618-11	2018	The present study found significant combined effects of obesity and the ADIPOQ rs182052 G/A+A/A genotype on the arsenic-related risk of RCC in a population with low arsenic exposure.	Arsenic	112-119	adiponectin, C1Q and collagen domain containing	Homo sapiens	72-78
29984327-9	2018	Furthermore, arsenic also elevated hippocampal cytokine levels, TNF-alpha and INF-gamma.	Arsenic	13-20	tumor necrosis factor	Rattus norvegicus	64-73
30046372-6	2018	In conclusion, our study revealed that the PGC-1alpha/TERT pathway might be a possible therapeutic target in AS and catalpol has highly favorable characteristics for the treatment of AS via modulating this pathway.	Arsenic	109-111	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	43-53
30046372-6	2018	In conclusion, our study revealed that the PGC-1alpha/TERT pathway might be a possible therapeutic target in AS and catalpol has highly favorable characteristics for the treatment of AS via modulating this pathway.	Arsenic	109-111	telomerase reverse transcriptase	Mus musculus	54-58
29774349-1	2018	Arsenic (+3 oxidation state) methyltransferase (AS3MT) is a key enzyme responsible for arsenic metabolism in humans, which facilitates conversion of arsenic trioxide (As2O3) to more reactive metabolites such as monomethylarsonous acid (MMAIII) and dimethylarsinous acid (DMAIII).	Arsenic	87-94	arsenite methyltransferase	Homo sapiens	0-46
29774349-1	2018	Arsenic (+3 oxidation state) methyltransferase (AS3MT) is a key enzyme responsible for arsenic metabolism in humans, which facilitates conversion of arsenic trioxide (As2O3) to more reactive metabolites such as monomethylarsonous acid (MMAIII) and dimethylarsinous acid (DMAIII).	Arsenic	87-94	arsenite methyltransferase	Homo sapiens	48-53
29774349-2	2018	However, it is unclear whether the biotransformation of arsenic by AS3MT contributes to the promotion of acute promyelocytic leukemia (APL) therapy.	Arsenic	56-63	arsenite methyltransferase	Homo sapiens	67-72
29569195-6	2018	Meanwhile, the transcription and protein expression levels of Bcl-2-associated X protein (Bax), p53, cytochrome c (Cyt c), and caspase-3, 8, 9 were upregulated and B cell lymphoma-2 (Bcl-2) was downregulated in As, Cu, and As + Cu groups in the liver tissues (P &lt; 0.05, P &lt; 0.01).	Arsenic	211-213	BCL2, apoptosis regulator	Gallus gallus	62-67
29930563-0	2018	Glutathione S-Transferases: Role in Combating Abiotic Stresses Including Arsenic Detoxification in Plants.	Arsenic	73-80	glutathione S-transferase kappa 1	Homo sapiens	0-26
29930563-9	2018	This review provides updated information about the role of GSTs in abiotic and biotic stresses with an emphasis on As uptake, metabolism, and detoxification in plants.	Arsenic	115-117	glutathione S-transferase kappa 1	Homo sapiens	59-63
28497229-5	2018	Compared with similar studies, the cumulative As concentrations released at the 24-h time point were extremely low (range 297 +- 6-3983 +- 396 microg L-1), representing between 0.020 +- 0.002 and 0.036 +- 0.003% of the total As in the PM20.	Arsenic	46-48	immunoglobulin kappa variable 1-16	Homo sapiens	150-153
29043584-1	2018	2,2",3,5",6-Pentachlorobiphenyl (PCB 95) and 2,2",3,4,4",5",6-heptachlorobiphenyl (PCB 183) possess axial chirality and form the aS and aR enantiomers.	Arsenic	129-131	pyruvate carboxylase	Homo sapiens	33-36
29043584-1	2018	2,2",3,5",6-Pentachlorobiphenyl (PCB 95) and 2,2",3,4,4",5",6-heptachlorobiphenyl (PCB 183) possess axial chirality and form the aS and aR enantiomers.	Arsenic	129-131	pyruvate carboxylase	Homo sapiens	83-86
29965645-7	2018	The levels of As, Cd, Cr, Cu, Ni, Pb, and Zn were dominated by human activities and the parent soil material (PC1).	Arsenic	14-16	polycystin 1, transient receptor potential channel interacting	Homo sapiens	110-113
29569195-6	2018	Meanwhile, the transcription and protein expression levels of Bcl-2-associated X protein (Bax), p53, cytochrome c (Cyt c), and caspase-3, 8, 9 were upregulated and B cell lymphoma-2 (Bcl-2) was downregulated in As, Cu, and As + Cu groups in the liver tissues (P &lt; 0.05, P &lt; 0.01).	Arsenic	211-213	BCL2, apoptosis regulator	Gallus gallus	164-181
31815032-0	2018	Deficiency of pyruvate dehydrogenase kinase 4 sensitizes mouse liver to diethylnitrosamine and arsenic toxicity through inducing apoptosis.	Arsenic	95-102	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	14-45
29735091-0	2018	Development of a Cryptosporidium-arsenic multi-risk assessment model for infant formula prepared with tap water in France.	Arsenic	33-40	nuclear RNA export factor 1	Homo sapiens	102-105
29735091-8	2018	Consuming infant formula rehydrated with un-boiled tap water during the first six months of life led to a total of 2250 DALYs per 100,000 infants (90% uncertainty interval [960; 7650]) for Cryptosporidium due to diarrhea, and 1 DALY [0.4; 2] for arsenic due to expected lifetime risk of lung and bladder cancer as a result of early exposure in life.	Arsenic	246-253	nuclear RNA export factor 1	Homo sapiens	51-54
31815032-12	2018	Similarly, chronic arsenic administration induced more severe hepatic apoptosis in Pdk4 -/- mice compared to WT control mice.	Arsenic	19-26	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	83-87
31815032-14	2018	In vitro, Pdk4-deficient primary hepatocytes were more vulnerable to DEN and arsenic challenges and displayed higher caspase activity than wild type cells.	Arsenic	77-84	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	10-14
29795382-1	2018	Retinoic acid (RA) and arsenic target the t(15;17)(q24;q21) PML/RARA driver of acute promyelocytic leukemia (APL), their combination now curing over 95% patients.	Arsenic	23-30	PML nuclear body scaffold	Homo sapiens	60-63
29396895-0	2018	Spin-orbit effects on magnetically induced current densities in the M5- (M = N,P,As,Sb,Bi,Mc) clusters.	Arsenic	81-83	spindlin 1	Homo sapiens	0-4
29882914-1	2018	Magnetohydrodynamics (MHD) is becoming more popular every day among developers of applications based on microfluidics, such as &amp;ldquo;lab on a chip&amp;rdquo; (LOC) and/or &amp;ldquo;micro-total analysis systems&amp;rdquo; (micro-TAS).	Arsenic	96-98	THAS	Homo sapiens	234-237
29621497-8	2018	The corresponding genes GCK and TUSC1 suggest oxidative stress and apoptosis as possible mechanisms for arsenic impacts on beta-cell function.	Arsenic	104-111	glucokinase	Homo sapiens	24-27
29621497-8	2018	The corresponding genes GCK and TUSC1 suggest oxidative stress and apoptosis as possible mechanisms for arsenic impacts on beta-cell function.	Arsenic	104-111	tumor suppressor candidate 1	Homo sapiens	32-37
29795382-1	2018	Retinoic acid (RA) and arsenic target the t(15;17)(q24;q21) PML/RARA driver of acute promyelocytic leukemia (APL), their combination now curing over 95% patients.	Arsenic	23-30	retinoic acid receptor alpha	Homo sapiens	64-68
29795382-6	2018	Accordingly, clonogenic activity of PML/RARA-immortalized progenitors ex vivo is only transiently affected by RA, but selectively abrogated by arsenic.	Arsenic	143-150	PML nuclear body scaffold	Homo sapiens	36-39
29795382-6	2018	Accordingly, clonogenic activity of PML/RARA-immortalized progenitors ex vivo is only transiently affected by RA, but selectively abrogated by arsenic.	Arsenic	143-150	retinoic acid receptor alpha	Homo sapiens	40-44
29783652-14	2018	Arsenic was inversely related with TSH in premenopausal participants with ER- and PR- (beta = -0.305; beta = -0.304, respectively).	Arsenic	0-7	estrogen receptor 1	Homo sapiens	74-76
29783652-14	2018	Arsenic was inversely related with TSH in premenopausal participants with ER- and PR- (beta = -0.305; beta = -0.304, respectively).	Arsenic	0-7	progesterone receptor	Homo sapiens	82-84
29725571-9	2018	Genetic polymorphism of GSTO1 was found to effect individual susceptibility towards arsenic-mediated genotoxicity and was found insignificant when antigenotoxic effect of anethole was considered.	Arsenic	84-91	glutathione S-transferase omega 1	Homo sapiens	24-29
29584948-3	2018	In this work, we demonstrate that black arsenic phosphorus alloy (b-As xP1- x) formed by introducing arsenic into BP can significantly extend the operational wavelength range of photonic devices.	Arsenic	40-47	XPA, DNA damage recognition and repair factor	Homo sapiens	71-74
29507186-0	2018	Increased O-GlcNAcylation of SNAP29 Drives Arsenic-Induced Autophagic Dysfunction.	Arsenic	43-50	synaptosome associated protein 29	Homo sapiens	29-35
29507186-5	2018	Specifically, arsenic disrupts formation of the STX17-SNAP29-VAMP8 SNARE complex, where SNAP29 mediates vesicle fusion through bridging STX17-containing autophagosomes to VAMP8-bearing lysosomes.	Arsenic	14-21	syntaxin 17	Homo sapiens	48-53
29507186-5	2018	Specifically, arsenic disrupts formation of the STX17-SNAP29-VAMP8 SNARE complex, where SNAP29 mediates vesicle fusion through bridging STX17-containing autophagosomes to VAMP8-bearing lysosomes.	Arsenic	14-21	synaptosome associated protein 29	Homo sapiens	54-60
29507186-5	2018	Specifically, arsenic disrupts formation of the STX17-SNAP29-VAMP8 SNARE complex, where SNAP29 mediates vesicle fusion through bridging STX17-containing autophagosomes to VAMP8-bearing lysosomes.	Arsenic	14-21	vesicle associated membrane protein 8	Homo sapiens	61-66
29507186-5	2018	Specifically, arsenic disrupts formation of the STX17-SNAP29-VAMP8 SNARE complex, where SNAP29 mediates vesicle fusion through bridging STX17-containing autophagosomes to VAMP8-bearing lysosomes.	Arsenic	14-21	synaptosome associated protein 29	Homo sapiens	88-94
29507186-5	2018	Specifically, arsenic disrupts formation of the STX17-SNAP29-VAMP8 SNARE complex, where SNAP29 mediates vesicle fusion through bridging STX17-containing autophagosomes to VAMP8-bearing lysosomes.	Arsenic	14-21	syntaxin 17	Homo sapiens	136-141
29507186-5	2018	Specifically, arsenic disrupts formation of the STX17-SNAP29-VAMP8 SNARE complex, where SNAP29 mediates vesicle fusion through bridging STX17-containing autophagosomes to VAMP8-bearing lysosomes.	Arsenic	14-21	vesicle associated membrane protein 8	Homo sapiens	171-176
29507186-6	2018	Mechanistically, arsenic inhibits SNARE complex formation, at least in part, by enhancing O-GlcNAcylation of SNAP29.	Arsenic	17-24	synaptosome associated protein 29	Homo sapiens	109-115
30016266-8	2018	The substrate exhibited a high sensitivity for arsenic detection with a limit of detection down to 1.5 mug L-1, which is much lower than permissible limit (10 mug L-1) set by the WHO.	Arsenic	47-54	L1 cell adhesion molecule	Homo sapiens	107-110
30016266-8	2018	The substrate exhibited a high sensitivity for arsenic detection with a limit of detection down to 1.5 mug L-1, which is much lower than permissible limit (10 mug L-1) set by the WHO.	Arsenic	47-54	L1 cell adhesion molecule	Homo sapiens	163-166
29536422-4	2018	The gradual desorption of As(III) and As(V) in the equilibrium sorption on chitosan is attributed to the different fractions of the dissociated forms of arsenic on the adsorbent surface and in solution and the extent of protonation of chitosan with the changing of solution pH during sorption.	Arsenic	153-160	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	38-43
29499398-7	2018	RESULTS: Arsenic-exposed individuals showed significant promoter hypermethylation (p &lt; 0.0001) of MLH1 and MSH2 compared to those unexposed with consequent down-regulation in their gene expression [MLH1 (p=0.001) and MSH2 (p&lt;0.05)].	Arsenic	9-16	mutL homolog 1	Homo sapiens	101-105
29499398-7	2018	RESULTS: Arsenic-exposed individuals showed significant promoter hypermethylation (p &lt; 0.0001) of MLH1 and MSH2 compared to those unexposed with consequent down-regulation in their gene expression [MLH1 (p=0.001) and MSH2 (p&lt;0.05)].	Arsenic	9-16	mutS homolog 2	Homo sapiens	110-114
29499398-7	2018	RESULTS: Arsenic-exposed individuals showed significant promoter hypermethylation (p &lt; 0.0001) of MLH1 and MSH2 compared to those unexposed with consequent down-regulation in their gene expression [MLH1 (p=0.001) and MSH2 (p&lt;0.05)].	Arsenic	9-16	mutL homolog 1	Homo sapiens	201-205
28825229-3	2018	Al, Pb, Hg, Ni, Cr, and As were detected in 47.8, 29.2, 28.1, 23.6, 12.4, and 9.0% of total milk samples, respectively, and Cd were not detected in all samples.	Arsenic	24-26	Weaning weight-maternal milk	Bos taurus	92-96
29526746-0	2018	Arsenic impairs insulin signaling in differentiated neuroblastoma SH-SY5Y cells.	Arsenic	0-7	insulin	Homo sapiens	16-23
29499398-7	2018	RESULTS: Arsenic-exposed individuals showed significant promoter hypermethylation (p &lt; 0.0001) of MLH1 and MSH2 compared to those unexposed with consequent down-regulation in their gene expression [MLH1 (p=0.001) and MSH2 (p&lt;0.05)].	Arsenic	9-16	mutS homolog 2	Homo sapiens	220-224
29499398-11	2018	DISCUSSION: In summary, the epigenetic repression of DNA damage repair genes due to promoter hypermethylation of MLH1 and MSH2 and inefficient recruitment of MMR complex at the site of DNA damage owing to the reduced level of H3K36me3 impairs the mismatch repair pathway that might render the arsenic-exposed individuals more susceptible towards DNA damage and associated cancer risk.	Arsenic	293-300	mutL homolog 1	Homo sapiens	113-117
29499398-11	2018	DISCUSSION: In summary, the epigenetic repression of DNA damage repair genes due to promoter hypermethylation of MLH1 and MSH2 and inefficient recruitment of MMR complex at the site of DNA damage owing to the reduced level of H3K36me3 impairs the mismatch repair pathway that might render the arsenic-exposed individuals more susceptible towards DNA damage and associated cancer risk.	Arsenic	293-300	mutS homolog 2	Homo sapiens	122-126
29526746-3	2018	Arsenic has been shown to impair insulin signaling in adipocytes and myocytes, however, this impairment has not yet been explored in neurons.	Arsenic	0-7	insulin	Homo sapiens	33-40
30014635-1	2018	OBJECTIVE: To determine the effects of arsenic and estrogen receptor antagonist (ICI182, 780) on the expression of estrogen receptor beta (ERbeta) in alveolar II epithelial cells (AECII) of female and male mice.	Arsenic	39-46	estrogen receptor 2 (beta)	Mus musculus	115-137
29331881-10	2018	The underlying signalling mechanism behind the cytotoxicity of arsenic was investigated and revealed that genistein exhibited neuroprotection significantly by modulating the JNK3 mediated apoptosis, ERK1/2 mediated autophagy and TNFalpha associated inflammatory pathways.	Arsenic	63-70	mitogen-activated protein kinase 10	Mus musculus	174-178
29331881-10	2018	The underlying signalling mechanism behind the cytotoxicity of arsenic was investigated and revealed that genistein exhibited neuroprotection significantly by modulating the JNK3 mediated apoptosis, ERK1/2 mediated autophagy and TNFalpha associated inflammatory pathways.	Arsenic	63-70	mitogen-activated protein kinase 3	Mus musculus	199-205
29331881-10	2018	The underlying signalling mechanism behind the cytotoxicity of arsenic was investigated and revealed that genistein exhibited neuroprotection significantly by modulating the JNK3 mediated apoptosis, ERK1/2 mediated autophagy and TNFalpha associated inflammatory pathways.	Arsenic	63-70	tumor necrosis factor	Mus musculus	229-237
30014635-1	2018	OBJECTIVE: To determine the effects of arsenic and estrogen receptor antagonist (ICI182, 780) on the expression of estrogen receptor beta (ERbeta) in alveolar II epithelial cells (AECII) of female and male mice.	Arsenic	39-46	estrogen receptor 2 (beta)	Mus musculus	139-145
29696383-2	2018	After optimization, the automatic system enabled highly sensitive determinations of As and Se species with detection limits as low as 0.004-0.033 mug L-1 for As and 0.061-0.128 mug L-1 for Se.	Arsenic	84-86	L1 cell adhesion molecule	Homo sapiens	150-153
29331917-8	2018	Using a flow rate of 5mLmin-1 and an initial concentration of As(III) 200microgL-1, gave an oxidation percentage of As(III) of up to 72%, showing a simple and economical alternative to the oxidation step of As(III) to As(V) in the treatment of water contaminated with arsenic.	Arsenic	62-64	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	218-223
29331917-8	2018	Using a flow rate of 5mLmin-1 and an initial concentration of As(III) 200microgL-1, gave an oxidation percentage of As(III) of up to 72%, showing a simple and economical alternative to the oxidation step of As(III) to As(V) in the treatment of water contaminated with arsenic.	Arsenic	268-275	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	218-223
29715297-4	2018	Strains resistant to arsenic concentrations varying from 0.5 to 100 mM arsenite or arsenate were isolated and the presence of genes coding for enzymes involved in arsenic oxidation (aio) or reduction (arsC) investigated.	Arsenic	163-170	steroid sulfatase	Homo sapiens	201-205
29696383-2	2018	After optimization, the automatic system enabled highly sensitive determinations of As and Se species with detection limits as low as 0.004-0.033 mug L-1 for As and 0.061-0.128 mug L-1 for Se.	Arsenic	84-86	L1 cell adhesion molecule	Homo sapiens	181-184
29696383-2	2018	After optimization, the automatic system enabled highly sensitive determinations of As and Se species with detection limits as low as 0.004-0.033 mug L-1 for As and 0.061-0.128 mug L-1 for Se.	Arsenic	158-160	L1 cell adhesion molecule	Homo sapiens	150-153
29324385-10	2018	Finally, these findings imply that selenium is capable to modulate arsenic-induced intrinsic apoptosis pathway via enhancement of mTOR/Akt autophagy signaling pathway through employing antioxidant potentials and through inhibiting the cellular accumulation of arsenic in PC12 cells.	Arsenic	67-74	mechanistic target of rapamycin kinase	Rattus norvegicus	130-134
29674678-3	2018	AioX and its orthologues (ArxX and ArrX) represent the first members of a new sub-family of periplasmic-binding proteins that serve as the first component of a signal transduction system, that"s role is to positively regulate expression of arsenic metabolism enzymes.	Arsenic	240-247	arrestin 3	Homo sapiens	35-39
29278989-4	2018	The concentration of arsenic in 163 collected samples from different locations during four seasons ranged from 0 to 99 mug L-1.	Arsenic	21-28	L1 cell adhesion molecule	Homo sapiens	123-126
29621150-5	2018	The Spearman"s correlation analysis showed a positive relationship between monocyte counts and hair Pb levels, but negative relations between As and IgG and between As and IgE.	Arsenic	165-167	immunoglobulin heavy constant epsilon	Homo sapiens	172-175
29557460-6	2018	When the dosage of Mg7Zn1Fe4-Asp-LDH was 0.8 g L-1, the concentration of As(iii) in the aqueous solution could be reduced from 2 mg L-1 to below 10 mug L-1.When Mg-Zn-Fe-Asp-LDH was applied in practical water samples with a dosage of 0.2 g L-1, the residual concentrations of arsenic in three actual water samples were all lower than 10 mug L-1 after adsorption.	Arsenic	29-31	immunoglobulin kappa variable 1-16	Homo sapiens	47-50
29557460-6	2018	When the dosage of Mg7Zn1Fe4-Asp-LDH was 0.8 g L-1, the concentration of As(iii) in the aqueous solution could be reduced from 2 mg L-1 to below 10 mug L-1.When Mg-Zn-Fe-Asp-LDH was applied in practical water samples with a dosage of 0.2 g L-1, the residual concentrations of arsenic in three actual water samples were all lower than 10 mug L-1 after adsorption.	Arsenic	29-31	immunoglobulin kappa variable 1-16	Homo sapiens	132-135
29557460-6	2018	When the dosage of Mg7Zn1Fe4-Asp-LDH was 0.8 g L-1, the concentration of As(iii) in the aqueous solution could be reduced from 2 mg L-1 to below 10 mug L-1.When Mg-Zn-Fe-Asp-LDH was applied in practical water samples with a dosage of 0.2 g L-1, the residual concentrations of arsenic in three actual water samples were all lower than 10 mug L-1 after adsorption.	Arsenic	29-31	immunoglobulin kappa variable 1-16	Homo sapiens	132-135
29557460-6	2018	When the dosage of Mg7Zn1Fe4-Asp-LDH was 0.8 g L-1, the concentration of As(iii) in the aqueous solution could be reduced from 2 mg L-1 to below 10 mug L-1.When Mg-Zn-Fe-Asp-LDH was applied in practical water samples with a dosage of 0.2 g L-1, the residual concentrations of arsenic in three actual water samples were all lower than 10 mug L-1 after adsorption.	Arsenic	29-31	immunoglobulin kappa variable 1-16	Homo sapiens	132-135
29557460-6	2018	When the dosage of Mg7Zn1Fe4-Asp-LDH was 0.8 g L-1, the concentration of As(iii) in the aqueous solution could be reduced from 2 mg L-1 to below 10 mug L-1.When Mg-Zn-Fe-Asp-LDH was applied in practical water samples with a dosage of 0.2 g L-1, the residual concentrations of arsenic in three actual water samples were all lower than 10 mug L-1 after adsorption.	Arsenic	29-31	immunoglobulin kappa variable 1-16	Homo sapiens	132-135
29557460-6	2018	When the dosage of Mg7Zn1Fe4-Asp-LDH was 0.8 g L-1, the concentration of As(iii) in the aqueous solution could be reduced from 2 mg L-1 to below 10 mug L-1.When Mg-Zn-Fe-Asp-LDH was applied in practical water samples with a dosage of 0.2 g L-1, the residual concentrations of arsenic in three actual water samples were all lower than 10 mug L-1 after adsorption.	Arsenic	276-283	immunoglobulin kappa variable 1-16	Homo sapiens	47-50
29557460-6	2018	When the dosage of Mg7Zn1Fe4-Asp-LDH was 0.8 g L-1, the concentration of As(iii) in the aqueous solution could be reduced from 2 mg L-1 to below 10 mug L-1.When Mg-Zn-Fe-Asp-LDH was applied in practical water samples with a dosage of 0.2 g L-1, the residual concentrations of arsenic in three actual water samples were all lower than 10 mug L-1 after adsorption.	Arsenic	276-283	immunoglobulin kappa variable 1-16	Homo sapiens	132-135
29557460-6	2018	When the dosage of Mg7Zn1Fe4-Asp-LDH was 0.8 g L-1, the concentration of As(iii) in the aqueous solution could be reduced from 2 mg L-1 to below 10 mug L-1.When Mg-Zn-Fe-Asp-LDH was applied in practical water samples with a dosage of 0.2 g L-1, the residual concentrations of arsenic in three actual water samples were all lower than 10 mug L-1 after adsorption.	Arsenic	276-283	immunoglobulin kappa variable 1-16	Homo sapiens	132-135
29557460-6	2018	When the dosage of Mg7Zn1Fe4-Asp-LDH was 0.8 g L-1, the concentration of As(iii) in the aqueous solution could be reduced from 2 mg L-1 to below 10 mug L-1.When Mg-Zn-Fe-Asp-LDH was applied in practical water samples with a dosage of 0.2 g L-1, the residual concentrations of arsenic in three actual water samples were all lower than 10 mug L-1 after adsorption.	Arsenic	276-283	immunoglobulin kappa variable 1-16	Homo sapiens	132-135
29557460-6	2018	When the dosage of Mg7Zn1Fe4-Asp-LDH was 0.8 g L-1, the concentration of As(iii) in the aqueous solution could be reduced from 2 mg L-1 to below 10 mug L-1.When Mg-Zn-Fe-Asp-LDH was applied in practical water samples with a dosage of 0.2 g L-1, the residual concentrations of arsenic in three actual water samples were all lower than 10 mug L-1 after adsorption.	Arsenic	276-283	immunoglobulin kappa variable 1-16	Homo sapiens	132-135
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	47-49	immunoglobulin kappa variable 1-16	Homo sapiens	120-123
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	47-49	immunoglobulin kappa variable 1-16	Homo sapiens	182-185
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	47-49	immunoglobulin kappa variable 1-16	Homo sapiens	182-185
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	47-49	immunoglobulin kappa variable 1-16	Homo sapiens	182-185
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	89-91	immunoglobulin kappa variable 1-16	Homo sapiens	120-123
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	89-91	immunoglobulin kappa variable 1-16	Homo sapiens	182-185
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	89-91	immunoglobulin kappa variable 1-16	Homo sapiens	182-185
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	89-91	immunoglobulin kappa variable 1-16	Homo sapiens	182-185
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	89-91	immunoglobulin kappa variable 1-16	Homo sapiens	120-123
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	89-91	immunoglobulin kappa variable 1-16	Homo sapiens	182-185
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	89-91	immunoglobulin kappa variable 1-16	Homo sapiens	182-185
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	89-91	immunoglobulin kappa variable 1-16	Homo sapiens	182-185
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	89-91	immunoglobulin kappa variable 1-16	Homo sapiens	120-123
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	89-91	immunoglobulin kappa variable 1-16	Homo sapiens	182-185
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	89-91	immunoglobulin kappa variable 1-16	Homo sapiens	182-185
29557460-7	2018	The column test showed that 1.0 g of Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous solution (2 mg L-1) and reduced the concentration of As(iii) to below 10 mug L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1, As(iii) : As(v) = 1 : 1) water, and the effluent concentration was below 10 mug L-1.	Arsenic	89-91	immunoglobulin kappa variable 1-16	Homo sapiens	182-185
29324385-10	2018	Finally, these findings imply that selenium is capable to modulate arsenic-induced intrinsic apoptosis pathway via enhancement of mTOR/Akt autophagy signaling pathway through employing antioxidant potentials and through inhibiting the cellular accumulation of arsenic in PC12 cells.	Arsenic	67-74	AKT serine/threonine kinase 1	Rattus norvegicus	135-138
29751399-10	2018	Polymorphisms in several genes including IL8RA, TXN, NR3C2, COX5A and GCLC showed suggestive differential associations of urine total arsenic with diabetes.	Arsenic	134-141	C-X-C motif chemokine receptor 1	Homo sapiens	41-46
29421402-8	2018	Interactions between SNPs and water As on skin lesion risk were suggestive for three variants: the G allele of MTRR rs1801394 and T allele of FOLR1 rs1540087 were associated with lower odds of skin lesions with lower As (&lt;=50 mug/L), and the T allele of TYMS rs1001761 was associated with higher odds of skin lesions with higher As.	Arsenic	36-38	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	111-115
29421402-8	2018	Interactions between SNPs and water As on skin lesion risk were suggestive for three variants: the G allele of MTRR rs1801394 and T allele of FOLR1 rs1540087 were associated with lower odds of skin lesions with lower As (&lt;=50 mug/L), and the T allele of TYMS rs1001761 was associated with higher odds of skin lesions with higher As.	Arsenic	36-38	folate receptor alpha	Homo sapiens	142-147
29421402-8	2018	Interactions between SNPs and water As on skin lesion risk were suggestive for three variants: the G allele of MTRR rs1801394 and T allele of FOLR1 rs1540087 were associated with lower odds of skin lesions with lower As (&lt;=50 mug/L), and the T allele of TYMS rs1001761 was associated with higher odds of skin lesions with higher As.	Arsenic	36-38	thymidylate synthetase	Homo sapiens	257-261
29751399-10	2018	Polymorphisms in several genes including IL8RA, TXN, NR3C2, COX5A and GCLC showed suggestive differential associations of urine total arsenic with diabetes.	Arsenic	134-141	thioredoxin	Homo sapiens	48-51
29751399-10	2018	Polymorphisms in several genes including IL8RA, TXN, NR3C2, COX5A and GCLC showed suggestive differential associations of urine total arsenic with diabetes.	Arsenic	134-141	nuclear receptor subfamily 3 group C member 2	Homo sapiens	53-58
29751399-10	2018	Polymorphisms in several genes including IL8RA, TXN, NR3C2, COX5A and GCLC showed suggestive differential associations of urine total arsenic with diabetes.	Arsenic	134-141	cytochrome c oxidase subunit 5A	Homo sapiens	60-65
29751399-10	2018	Polymorphisms in several genes including IL8RA, TXN, NR3C2, COX5A and GCLC showed suggestive differential associations of urine total arsenic with diabetes.	Arsenic	134-141	glutamate-cysteine ligase catalytic subunit	Homo sapiens	70-74
29676757-0	2018	Arsenic, cadmium, lead, and chromium in well water, rice, and human urine in Sri Lanka in relation to chronic kidney disease of unknown etiology.	Arsenic	0-7	sorcin	Homo sapiens	77-80
29484434-4	2018	A luciferase reporter assay confirmed that miR-33a-5p targets the 3"-untranslated region of the mechanistic target of rapamycin (mTOR) gene.	Arsenic	47-50	MLX interacting protein	Homo sapiens	43-46
29484434-4	2018	A luciferase reporter assay confirmed that miR-33a-5p targets the 3"-untranslated region of the mechanistic target of rapamycin (mTOR) gene.	Arsenic	47-50	mechanistic target of rapamycin kinase	Homo sapiens	96-127
29484434-4	2018	A luciferase reporter assay confirmed that miR-33a-5p targets the 3"-untranslated region of the mechanistic target of rapamycin (mTOR) gene.	Arsenic	47-50	mechanistic target of rapamycin kinase	Homo sapiens	129-133
29484434-13	2018	In summary, miR-33a-5p inhibited the proliferation of lung adenocarcinoma cells, enhanced the antitumor effect of celastrol, and improved sensitivity to celastrol by targeting mTOR in lung adenocarcinoma in vitro and in vivo.	Arsenic	16-20	MLX interacting protein	Homo sapiens	12-15
29484434-13	2018	In summary, miR-33a-5p inhibited the proliferation of lung adenocarcinoma cells, enhanced the antitumor effect of celastrol, and improved sensitivity to celastrol by targeting mTOR in lung adenocarcinoma in vitro and in vivo.	Arsenic	16-20	mechanistic target of rapamycin kinase	Homo sapiens	176-180
29228391-0	2018	Arsenic Attenuates Heparin-Binding EGF-Like Growth Factor/EGFR Signaling That Promotes Matrix Metalloprotease 9-Dependent Astrocyte Damage in the Developing Rat Brain.	Arsenic	0-7	heparin-binding EGF-like growth factor	Rattus norvegicus	19-57
29101603-5	2018	Associations were found between AS and FKBP5 rs9296158 (p = 0.025) and rs737054 (p = 0.045) in Coloured males.	Arsenic	32-34	FKBP prolyl isomerase 5	Homo sapiens	39-44
29478199-0	2018	Inhibition of miR-219 Alleviates Arsenic-Induced Learning and Memory Impairments and Synaptic Damage Through Up-regulating CaMKII in the Hippocampus.	Arsenic	33-40	calcium/calmodulin-dependent protein kinase II, delta	Mus musculus	123-129
29478199-5	2018	Furthermore, the expression of CaMKII, an experimentally validated target of miR-219, was decreased in the mice exposed to arsenic.	Arsenic	123-130	calcium/calmodulin-dependent protein kinase II, delta	Mus musculus	31-37
29478199-8	2018	Taken together, the results of this study indicate that inhibition of miR-219 regulates arsenic-induced damage in the structure of the hippocampus and impairment of learning and memory, possibly by targeting CaMKII.	Arsenic	88-95	calcium/calmodulin-dependent protein kinase II, delta	Mus musculus	208-214
29319823-0	2018	Differentially Expressed mRNA Targets of Differentially Expressed miRNAs Predict Changes in the TP53 Axis and Carcinogenesis-Related Pathways in Human Keratinocytes Chronically Exposed to Arsenic.	Arsenic	188-195	tumor protein p53	Homo sapiens	96-100
29676757-3	2018	The liver-type fatty acid binding protein (L-FABP) concentration and arsenic, cadmium, lead, and chromium concentrations of the urine samples were analyzed to determine the relation of L-FABP with arsenic, cadmium, lead, and chromium.	Arsenic	197-204	fatty acid binding protein 1	Homo sapiens	185-191
29228391-7	2018	This reduced HB-EGF/EGFR was essentially responsible for arsenic-induced astrocyte damage, obvious from a recombinant-HB-EGF-mediated recovery in GFAP levels and astrocyte morphology and reduction in astrocyte apoptosis, and the reverse by gefitinib.	Arsenic	57-64	heparin-binding EGF-like growth factor	Rattus norvegicus	13-19
29228391-7	2018	This reduced HB-EGF/EGFR was essentially responsible for arsenic-induced astrocyte damage, obvious from a recombinant-HB-EGF-mediated recovery in GFAP levels and astrocyte morphology and reduction in astrocyte apoptosis, and the reverse by gefitinib.	Arsenic	57-64	epidermal growth factor receptor	Rattus norvegicus	20-24
29228391-7	2018	This reduced HB-EGF/EGFR was essentially responsible for arsenic-induced astrocyte damage, obvious from a recombinant-HB-EGF-mediated recovery in GFAP levels and astrocyte morphology and reduction in astrocyte apoptosis, and the reverse by gefitinib.	Arsenic	57-64	heparin-binding EGF-like growth factor	Rattus norvegicus	118-124
29228391-7	2018	This reduced HB-EGF/EGFR was essentially responsible for arsenic-induced astrocyte damage, obvious from a recombinant-HB-EGF-mediated recovery in GFAP levels and astrocyte morphology and reduction in astrocyte apoptosis, and the reverse by gefitinib.	Arsenic	57-64	glial fibrillary acidic protein	Rattus norvegicus	146-150
29228391-8	2018	We found that arsenic also suppressed neuronal HB-EGF levels, which additionally contributed towards astrocyte damage.	Arsenic	14-21	heparin-binding EGF-like growth factor	Rattus norvegicus	47-53
29228391-11	2018	We detected an arsenic-mediated increased BBB permeability, which could be blocked by recombinant-HB-EGF and MMP9 inhibitor, SB-3CT.	Arsenic	15-22	heparin-binding EGF-like growth factor	Rattus norvegicus	98-104
29228391-0	2018	Arsenic Attenuates Heparin-Binding EGF-Like Growth Factor/EGFR Signaling That Promotes Matrix Metalloprotease 9-Dependent Astrocyte Damage in the Developing Rat Brain.	Arsenic	0-7	epidermal growth factor receptor	Rattus norvegicus	58-62
29228391-11	2018	We detected an arsenic-mediated increased BBB permeability, which could be blocked by recombinant-HB-EGF and MMP9 inhibitor, SB-3CT.	Arsenic	15-22	matrix metallopeptidase 9	Rattus norvegicus	109-113
29228391-1	2018	We earlier reported that exposure to arsenic at concentrations in ground water of India attenuated glial fibrillary acidic protein (GFAP) during brain development.	Arsenic	37-44	glial fibrillary acidic protein	Rattus norvegicus	99-130
29228391-12	2018	Thus, our study indicates that via reduced astrocyte and neuronal HB-EGF signaling, arsenic may induce MMP9 levels and GFAP loss in astrocytes, which might adversely affect BBB integrity of the developing rat brain.	Arsenic	84-91	heparin-binding EGF-like growth factor	Rattus norvegicus	66-72
29228391-12	2018	Thus, our study indicates that via reduced astrocyte and neuronal HB-EGF signaling, arsenic may induce MMP9 levels and GFAP loss in astrocytes, which might adversely affect BBB integrity of the developing rat brain.	Arsenic	84-91	matrix metallopeptidase 9	Rattus norvegicus	103-107
29228391-1	2018	We earlier reported that exposure to arsenic at concentrations in ground water of India attenuated glial fibrillary acidic protein (GFAP) during brain development.	Arsenic	37-44	glial fibrillary acidic protein	Rattus norvegicus	132-136
29228391-12	2018	Thus, our study indicates that via reduced astrocyte and neuronal HB-EGF signaling, arsenic may induce MMP9 levels and GFAP loss in astrocytes, which might adversely affect BBB integrity of the developing rat brain.	Arsenic	84-91	glial fibrillary acidic protein	Rattus norvegicus	119-123
29228391-4	2018	We found that arsenic inactivated EGFR, marked by reduced phospho-EGFR in astrocytes.	Arsenic	14-21	epidermal growth factor receptor	Rattus norvegicus	34-38
29228391-4	2018	We found that arsenic inactivated EGFR, marked by reduced phospho-EGFR in astrocytes.	Arsenic	14-21	epidermal growth factor receptor	Rattus norvegicus	66-70
29228391-5	2018	Screening EGFR ligands revealed an arsenic-mediated attenuation in cellular and secreted-Heparin-binding EGF-like growth factor (HB-EGF).	Arsenic	35-42	epidermal growth factor receptor	Rattus norvegicus	10-14
29228391-5	2018	Screening EGFR ligands revealed an arsenic-mediated attenuation in cellular and secreted-Heparin-binding EGF-like growth factor (HB-EGF).	Arsenic	35-42	heparin-binding EGF-like growth factor	Rattus norvegicus	80-127
29228391-5	2018	Screening EGFR ligands revealed an arsenic-mediated attenuation in cellular and secreted-Heparin-binding EGF-like growth factor (HB-EGF).	Arsenic	35-42	heparin-binding EGF-like growth factor	Rattus norvegicus	129-135
29228391-6	2018	Furthermore, we observed that recombinant-HB-EGF cotreatment with arsenic blocked reduction in HB-EGF, secreted-HB-EGF and phospho-EGFR, which could be reversed by EGFR-inhibitor, gefitinib, suggesting that arsenic attenuated an HB-EGF/EGFR loop in astrocytes.	Arsenic	66-73	heparin-binding EGF-like growth factor	Rattus norvegicus	42-48
29228391-6	2018	Furthermore, we observed that recombinant-HB-EGF cotreatment with arsenic blocked reduction in HB-EGF, secreted-HB-EGF and phospho-EGFR, which could be reversed by EGFR-inhibitor, gefitinib, suggesting that arsenic attenuated an HB-EGF/EGFR loop in astrocytes.	Arsenic	66-73	heparin-binding EGF-like growth factor	Rattus norvegicus	95-101
29228391-6	2018	Furthermore, we observed that recombinant-HB-EGF cotreatment with arsenic blocked reduction in HB-EGF, secreted-HB-EGF and phospho-EGFR, which could be reversed by EGFR-inhibitor, gefitinib, suggesting that arsenic attenuated an HB-EGF/EGFR loop in astrocytes.	Arsenic	66-73	heparin-binding EGF-like growth factor	Rattus norvegicus	95-101
29228391-6	2018	Furthermore, we observed that recombinant-HB-EGF cotreatment with arsenic blocked reduction in HB-EGF, secreted-HB-EGF and phospho-EGFR, which could be reversed by EGFR-inhibitor, gefitinib, suggesting that arsenic attenuated an HB-EGF/EGFR loop in astrocytes.	Arsenic	66-73	epidermal growth factor receptor	Rattus norvegicus	131-135
29228391-6	2018	Furthermore, we observed that recombinant-HB-EGF cotreatment with arsenic blocked reduction in HB-EGF, secreted-HB-EGF and phospho-EGFR, which could be reversed by EGFR-inhibitor, gefitinib, suggesting that arsenic attenuated an HB-EGF/EGFR loop in astrocytes.	Arsenic	66-73	epidermal growth factor receptor	Rattus norvegicus	164-168
29228391-6	2018	Furthermore, we observed that recombinant-HB-EGF cotreatment with arsenic blocked reduction in HB-EGF, secreted-HB-EGF and phospho-EGFR, which could be reversed by EGFR-inhibitor, gefitinib, suggesting that arsenic attenuated an HB-EGF/EGFR loop in astrocytes.	Arsenic	66-73	heparin-binding EGF-like growth factor	Rattus norvegicus	95-101
29228391-6	2018	Furthermore, we observed that recombinant-HB-EGF cotreatment with arsenic blocked reduction in HB-EGF, secreted-HB-EGF and phospho-EGFR, which could be reversed by EGFR-inhibitor, gefitinib, suggesting that arsenic attenuated an HB-EGF/EGFR loop in astrocytes.	Arsenic	66-73	epidermal growth factor receptor	Rattus norvegicus	164-168
29228391-6	2018	Furthermore, we observed that recombinant-HB-EGF cotreatment with arsenic blocked reduction in HB-EGF, secreted-HB-EGF and phospho-EGFR, which could be reversed by EGFR-inhibitor, gefitinib, suggesting that arsenic attenuated an HB-EGF/EGFR loop in astrocytes.	Arsenic	207-214	heparin-binding EGF-like growth factor	Rattus norvegicus	42-48
29228391-6	2018	Furthermore, we observed that recombinant-HB-EGF cotreatment with arsenic blocked reduction in HB-EGF, secreted-HB-EGF and phospho-EGFR, which could be reversed by EGFR-inhibitor, gefitinib, suggesting that arsenic attenuated an HB-EGF/EGFR loop in astrocytes.	Arsenic	207-214	epidermal growth factor receptor	Rattus norvegicus	164-168
29228391-6	2018	Furthermore, we observed that recombinant-HB-EGF cotreatment with arsenic blocked reduction in HB-EGF, secreted-HB-EGF and phospho-EGFR, which could be reversed by EGFR-inhibitor, gefitinib, suggesting that arsenic attenuated an HB-EGF/EGFR loop in astrocytes.	Arsenic	207-214	epidermal growth factor receptor	Rattus norvegicus	164-168
29662481-11	2018	Conversely, ST14 draft genomes were enriched with a full-length version of actA gene along with the Listeria Genomic Island 2 (LGI 2) including the ars operon (arsenic resistance) and the cadA4C gene cassette (resistance to 35 mg/l of cadmium chloride).	Arsenic	160-167	suppressor of tumorigenicity 14 protein	Oryctolagus cuniculus	12-16
29602886-2	2018	The SCC lesions began to develop within 12-15 months after beginning the arsenic-containing TM.	Arsenic	73-80	serpin family B member 3	Homo sapiens	4-7
29498700-1	2018	The mining activity in the San Antonio-El Triunfo district, located in a mountainous region at 60 km southeast of La Paz, occured for more than 250 years and left behind severe contamination of soils and riverbed sediments which led to elevated concentrations of arsenic and other trace elements in the surface- and groundwater of the region.	Arsenic	263-270	N-alpha-acetyltransferase 50, NatE catalytic subunit	Homo sapiens	27-30
29248574-0	2018	LncRNA UCA1 attenuates autophagy-dependent cell death through blocking autophagic flux under arsenic stress.	Arsenic	93-100	urothelial cancer associated 1	Homo sapiens	7-11
29278859-7	2018	The arsenic-induced oxidative damage was confirmed by elevation of malondialdehyde (MDA), a lipid peroxidation byproduct, as well as depletion in physiological antioxidant content such as superoxide dismutase (SOD) and catalase (CAT).	Arsenic	4-11	catalase	Rattus norvegicus	219-227
29278859-7	2018	The arsenic-induced oxidative damage was confirmed by elevation of malondialdehyde (MDA), a lipid peroxidation byproduct, as well as depletion in physiological antioxidant content such as superoxide dismutase (SOD) and catalase (CAT).	Arsenic	4-11	catalase	Rattus norvegicus	229-232
29121352-0	2018	Arsenic Induces Members of the mmu-miR-466-669 Cluster Which Reduces NeuroD1 Expression.	Arsenic	0-7	microRNA 466	Mus musculus	31-42
28593471-6	2018	Furthermore, concomitant administration of HFD and arsenic decreased the lipid profile and levels of T4, albumin, total protein, T3, and GSH and increased the levels of TSH, adiponectin, leptin, ROS, MDA, and T4/T3 ratio compared to those in the control LFD or HFD group.	Arsenic	51-58	adiponectin, C1Q and collagen domain containing	Mus musculus	174-185
28593471-6	2018	Furthermore, concomitant administration of HFD and arsenic decreased the lipid profile and levels of T4, albumin, total protein, T3, and GSH and increased the levels of TSH, adiponectin, leptin, ROS, MDA, and T4/T3 ratio compared to those in the control LFD or HFD group.	Arsenic	51-58	leptin	Mus musculus	187-193
29288301-0	2018	Arsenic and/or copper caused inflammatory response via activation of inducible nitric oxide synthase pathway and triggered heat shock protein responses in testis tissues of chicken.	Arsenic	0-7	nitric oxide synthase 2	Gallus gallus	69-100
29276995-6	2018	Mineralogical investigation of leached residue coupled with geochemical modeling confirmed that newly formed Ca, Pb and Ca-Pb arsenates (mimetite, Pb5(AsO4)3Cl) partly control the release of As and other contaminants under circumneutral and alkaline conditions and will be of key importance for the fate of smelter-derived contamination in soils or when stabilization technology is employed.	Arsenic	151-153	capping actin protein of muscle Z-line subunit beta	Homo sapiens	120-125
29413104-7	2018	RESULTS: Caspase-3 was present in rats that were treated with 10 mg/kg of oral atorvastatin and exposed to 0.01 and 0.025 mg/L of arsenic, but no others proteins were present, such as pro Caspase-8, bcl-2, and Fas.	Arsenic	130-137	caspase 3	Rattus norvegicus	9-18
28283887-0	2018	Arsenic, Cadmium, and Lead Like Troglitazone Trigger PPARgamma-Dependent Poly (ADP-Ribose) Polymerase Expression and Subsequent Apoptosis in Rat Brain Astrocytes.	Arsenic	0-7	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	53-62
28283887-0	2018	Arsenic, Cadmium, and Lead Like Troglitazone Trigger PPARgamma-Dependent Poly (ADP-Ribose) Polymerase Expression and Subsequent Apoptosis in Rat Brain Astrocytes.	Arsenic	0-7	poly (ADP-ribose) polymerase 1	Rattus norvegicus	73-101
28283887-14	2018	Overall, our study enlightens a novel PPARgamma-dependent mechanism of As-, Cd-, and Pb-induced astrocyte apoptosis.	Arsenic	71-73	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	38-47
29328451-0	2018	A systematic review and meta-analysis of bidirectional effect of arsenic on ERK signaling pathway.	Arsenic	65-72	mitogen-activated protein kinase 1	Homo sapiens	76-79
29328451-2	2018	ERK is considered a key transcriptional regulator of arsenic-induced apoptosis.	Arsenic	53-60	mitogen-activated protein kinase 1	Homo sapiens	0-3
29328451-3	2018	Due to a few controversial issues about arsenic-mediated extracellular signal-regulated MAP kinases (ERK) signaling, a meta-analysis was performed.	Arsenic	40-47	mitogen-activated protein kinase 1	Homo sapiens	57-99
29328451-3	2018	Due to a few controversial issues about arsenic-mediated extracellular signal-regulated MAP kinases (ERK) signaling, a meta-analysis was performed.	Arsenic	40-47	mitogen-activated protein kinase 1	Homo sapiens	101-104
29328451-4	2018	Subgroup analyses demonstrated that high doses (&gt;=2 micromol/l) of arsenic increased the expression of Ras, ERK, ERK1, ERK2, phosphorylated (p)-ERK, p-ERK1, and p-ERK2, while low doses (&lt;2 micromol/l) decreased the expression of Ras, ERK1, p-ERK, and p-ERK2 when compared to control groups.	Arsenic	70-77	mitogen-activated protein kinase 1	Homo sapiens	111-114
29328451-4	2018	Subgroup analyses demonstrated that high doses (&gt;=2 micromol/l) of arsenic increased the expression of Ras, ERK, ERK1, ERK2, phosphorylated (p)-ERK, p-ERK1, and p-ERK2, while low doses (&lt;2 micromol/l) decreased the expression of Ras, ERK1, p-ERK, and p-ERK2 when compared to control groups.	Arsenic	70-77	mitogen-activated protein kinase 3	Homo sapiens	116-120
29328451-4	2018	Subgroup analyses demonstrated that high doses (&gt;=2 micromol/l) of arsenic increased the expression of Ras, ERK, ERK1, ERK2, phosphorylated (p)-ERK, p-ERK1, and p-ERK2, while low doses (&lt;2 micromol/l) decreased the expression of Ras, ERK1, p-ERK, and p-ERK2 when compared to control groups.	Arsenic	70-77	mitogen-activated protein kinase 1	Homo sapiens	122-126
29328451-4	2018	Subgroup analyses demonstrated that high doses (&gt;=2 micromol/l) of arsenic increased the expression of Ras, ERK, ERK1, ERK2, phosphorylated (p)-ERK, p-ERK1, and p-ERK2, while low doses (&lt;2 micromol/l) decreased the expression of Ras, ERK1, p-ERK, and p-ERK2 when compared to control groups.	Arsenic	70-77	mitogen-activated protein kinase 1	Homo sapiens	116-119
29328451-4	2018	Subgroup analyses demonstrated that high doses (&gt;=2 micromol/l) of arsenic increased the expression of Ras, ERK, ERK1, ERK2, phosphorylated (p)-ERK, p-ERK1, and p-ERK2, while low doses (&lt;2 micromol/l) decreased the expression of Ras, ERK1, p-ERK, and p-ERK2 when compared to control groups.	Arsenic	70-77	mitogen-activated protein kinase 3	Homo sapiens	154-158
29328451-4	2018	Subgroup analyses demonstrated that high doses (&gt;=2 micromol/l) of arsenic increased the expression of Ras, ERK, ERK1, ERK2, phosphorylated (p)-ERK, p-ERK1, and p-ERK2, while low doses (&lt;2 micromol/l) decreased the expression of Ras, ERK1, p-ERK, and p-ERK2 when compared to control groups.	Arsenic	70-77	mitogen-activated protein kinase 1	Homo sapiens	166-170
29328451-4	2018	Subgroup analyses demonstrated that high doses (&gt;=2 micromol/l) of arsenic increased the expression of Ras, ERK, ERK1, ERK2, phosphorylated (p)-ERK, p-ERK1, and p-ERK2, while low doses (&lt;2 micromol/l) decreased the expression of Ras, ERK1, p-ERK, and p-ERK2 when compared to control groups.	Arsenic	70-77	mitogen-activated protein kinase 3	Homo sapiens	154-158
29328451-4	2018	Subgroup analyses demonstrated that high doses (&gt;=2 micromol/l) of arsenic increased the expression of Ras, ERK, ERK1, ERK2, phosphorylated (p)-ERK, p-ERK1, and p-ERK2, while low doses (&lt;2 micromol/l) decreased the expression of Ras, ERK1, p-ERK, and p-ERK2 when compared to control groups.	Arsenic	70-77	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	152-157
29328451-4	2018	Subgroup analyses demonstrated that high doses (&gt;=2 micromol/l) of arsenic increased the expression of Ras, ERK, ERK1, ERK2, phosphorylated (p)-ERK, p-ERK1, and p-ERK2, while low doses (&lt;2 micromol/l) decreased the expression of Ras, ERK1, p-ERK, and p-ERK2 when compared to control groups.	Arsenic	70-77	mitogen-activated protein kinase 1	Homo sapiens	166-170
29328451-5	2018	Long term exposure (&gt;24 h) to arsenic led to inhibition of expression of ERK1, p-ERK1, and p-ERK2, whereas short-term exposure (&lt;=24 h) triggered the expression of ERK1, ERK2, p-ERK, p-ERK1, and p-ERK2.	Arsenic	33-40	mitogen-activated protein kinase 3	Homo sapiens	76-80
29328451-5	2018	Long term exposure (&gt;24 h) to arsenic led to inhibition of expression of ERK1, p-ERK1, and p-ERK2, whereas short-term exposure (&lt;=24 h) triggered the expression of ERK1, ERK2, p-ERK, p-ERK1, and p-ERK2.	Arsenic	33-40	mitogen-activated protein kinase 3	Homo sapiens	84-88
29328451-5	2018	Long term exposure (&gt;24 h) to arsenic led to inhibition of expression of ERK1, p-ERK1, and p-ERK2, whereas short-term exposure (&lt;=24 h) triggered the expression of ERK1, ERK2, p-ERK, p-ERK1, and p-ERK2.	Arsenic	33-40	mitogen-activated protein kinase 1	Homo sapiens	96-100
29328451-5	2018	Long term exposure (&gt;24 h) to arsenic led to inhibition of expression of ERK1, p-ERK1, and p-ERK2, whereas short-term exposure (&lt;=24 h) triggered the expression of ERK1, ERK2, p-ERK, p-ERK1, and p-ERK2.	Arsenic	33-40	mitogen-activated protein kinase 3	Homo sapiens	84-88
29328451-5	2018	Long term exposure (&gt;24 h) to arsenic led to inhibition of expression of ERK1, p-ERK1, and p-ERK2, whereas short-term exposure (&lt;=24 h) triggered the expression of ERK1, ERK2, p-ERK, p-ERK1, and p-ERK2.	Arsenic	33-40	mitogen-activated protein kinase 1	Homo sapiens	176-180
29328451-5	2018	Long term exposure (&gt;24 h) to arsenic led to inhibition of expression of ERK1, p-ERK1, and p-ERK2, whereas short-term exposure (&lt;=24 h) triggered the expression of ERK1, ERK2, p-ERK, p-ERK1, and p-ERK2.	Arsenic	33-40	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	82-87
29328451-5	2018	Long term exposure (&gt;24 h) to arsenic led to inhibition of expression of ERK1, p-ERK1, and p-ERK2, whereas short-term exposure (&lt;=24 h) triggered the expression of ERK1, ERK2, p-ERK, p-ERK1, and p-ERK2.	Arsenic	33-40	mitogen-activated protein kinase 3	Homo sapiens	84-88
29328451-5	2018	Long term exposure (&gt;24 h) to arsenic led to inhibition of expression of ERK1, p-ERK1, and p-ERK2, whereas short-term exposure (&lt;=24 h) triggered the expression of ERK1, ERK2, p-ERK, p-ERK1, and p-ERK2.	Arsenic	33-40	mitogen-activated protein kinase 1	Homo sapiens	176-180
29328451-6	2018	Furthermore, normal cells exposed to arsenic exhibited higher production levels of Ras and p-ERK.	Arsenic	37-44	mitogen-activated protein kinase 1	Homo sapiens	93-96
29328451-7	2018	Conversely, exposure of cancer cells to arsenic showed a lower level of production of Ras and p-ERK as well as higher level of p-ERK1 and p-ERK2 as compared to control group.	Arsenic	40-47	mitogen-activated protein kinase 1	Homo sapiens	96-99
29328451-7	2018	Conversely, exposure of cancer cells to arsenic showed a lower level of production of Ras and p-ERK as well as higher level of p-ERK1 and p-ERK2 as compared to control group.	Arsenic	40-47	mitogen-activated protein kinase 3	Homo sapiens	129-133
29328451-7	2018	Conversely, exposure of cancer cells to arsenic showed a lower level of production of Ras and p-ERK as well as higher level of p-ERK1 and p-ERK2 as compared to control group.	Arsenic	40-47	mitogen-activated protein kinase 1	Homo sapiens	140-144
29328451-8	2018	Short-term exposure of normal cells to high doses of arsenic may promote ERK signaling pathway.	Arsenic	53-60	mitogen-activated protein kinase 1	Homo sapiens	73-76
29328451-9	2018	In contrast, long-term exposure of cancer cells to low doses of arsenic may inhibit ERK signaling pathway.	Arsenic	64-71	mitogen-activated protein kinase 1	Homo sapiens	84-87
29198881-5	2018	With the existing literature, this review exhibits the effect of arsenic on adipose tissue and its signalling events such as SIRT3- FOXO3a signalling pathway, Ras -MAP -AP-1 cascade, PI(3)-K-Akt pathway, endoplasmic reticulum stress protein, C/EBP homologous protein (CHOP10) and GPCR pathway with role of adipokines.	Arsenic	65-72	sirtuin 3	Homo sapiens	125-130
29198881-5	2018	With the existing literature, this review exhibits the effect of arsenic on adipose tissue and its signalling events such as SIRT3- FOXO3a signalling pathway, Ras -MAP -AP-1 cascade, PI(3)-K-Akt pathway, endoplasmic reticulum stress protein, C/EBP homologous protein (CHOP10) and GPCR pathway with role of adipokines.	Arsenic	65-72	forkhead box O3	Homo sapiens	132-138
29198881-5	2018	With the existing literature, this review exhibits the effect of arsenic on adipose tissue and its signalling events such as SIRT3- FOXO3a signalling pathway, Ras -MAP -AP-1 cascade, PI(3)-K-Akt pathway, endoplasmic reticulum stress protein, C/EBP homologous protein (CHOP10) and GPCR pathway with role of adipokines.	Arsenic	65-72	AKT serine/threonine kinase 1	Homo sapiens	191-194
29198881-5	2018	With the existing literature, this review exhibits the effect of arsenic on adipose tissue and its signalling events such as SIRT3- FOXO3a signalling pathway, Ras -MAP -AP-1 cascade, PI(3)-K-Akt pathway, endoplasmic reticulum stress protein, C/EBP homologous protein (CHOP10) and GPCR pathway with role of adipokines.	Arsenic	65-72	DNA damage inducible transcript 3	Homo sapiens	268-274
29121352-0	2018	Arsenic Induces Members of the mmu-miR-466-669 Cluster Which Reduces NeuroD1 Expression.	Arsenic	0-7	neurogenic differentiation 1	Mus musculus	69-76
29121352-6	2018	We found that the expression of several miRNAs important in cellular differentiation, such as miR-9 and miR-199 were decreased by 1.9- and 1.6-fold, respectively, following arsenic exposure, while miR-92a, miR-291a, and miR-709 were increased by 3-, 3.7-, and 1.6-fold, respectively.	Arsenic	173-180	microRNA 291a	Mus musculus	206-214
29121352-6	2018	We found that the expression of several miRNAs important in cellular differentiation, such as miR-9 and miR-199 were decreased by 1.9- and 1.6-fold, respectively, following arsenic exposure, while miR-92a, miR-291a, and miR-709 were increased by 3-, 3.7-, and 1.6-fold, respectively.	Arsenic	173-180	microRNA 709	Mus musculus	220-227
29121352-7	2018	The members of the miR-466-669 cluster and its host gene, Scm-like with 4 Mbt domains 2 (Sfmbt2), were significantly induced by arsenic from 1.5- to 4-fold in a time-dependent manner.	Arsenic	128-135	microRNA 466	Mus musculus	19-26
29121352-7	2018	The members of the miR-466-669 cluster and its host gene, Scm-like with 4 Mbt domains 2 (Sfmbt2), were significantly induced by arsenic from 1.5- to 4-fold in a time-dependent manner.	Arsenic	128-135	Scm-like with four mbt domains 2	Mus musculus	89-95
29121352-9	2018	When consensus anti-miRNAs targeting the miR-466-669 cluster were transfected into P19 cells, arsenic-exposed cells were able to more effectively differentiate.	Arsenic	94-101	microRNA 466	Mus musculus	41-48
29121352-10	2018	The consensus anti-miRNAs appeared to rescue the inhibitory effects of arsenic on cell differentiation due to an increased expression of NeuroD1.	Arsenic	71-78	neurogenic differentiation 1	Mus musculus	137-144
29121352-11	2018	Taken together, we conclude that arsenic induces the miR-466-669 cluster, and that this induction acts to inhibit cellular differentiation in part due to a repression of NeuroD1.	Arsenic	33-40	microRNA 466	Mus musculus	53-60
29121352-11	2018	Taken together, we conclude that arsenic induces the miR-466-669 cluster, and that this induction acts to inhibit cellular differentiation in part due to a repression of NeuroD1.	Arsenic	33-40	neurogenic differentiation 1	Mus musculus	170-177
29248574-6	2018	Functional assessments revealed that UCA1 played a critical role in protecting hepatocytes from As-induced autophagy inhibition.	Arsenic	96-98	urothelial cancer associated 1	Homo sapiens	37-41
29248574-9	2018	Collectively, our study deciphered a lncRNA-dictated molecular mechanism responsible for As toxicity: UCA1 leads a protective role against As-induced cell death through blocking autophagic flux.	Arsenic	89-91	urothelial cancer associated 1	Homo sapiens	102-106
29248574-9	2018	Collectively, our study deciphered a lncRNA-dictated molecular mechanism responsible for As toxicity: UCA1 leads a protective role against As-induced cell death through blocking autophagic flux.	Arsenic	139-141	urothelial cancer associated 1	Homo sapiens	102-106
29425503-5	2018	FUS protein levels in arsenic-induced stress granules were significantly increased in Padi4-/- mouse embryonic fibroblasts (MEFs).	Arsenic	22-29	fused in sarcoma	Mus musculus	0-3
29410996-6	2018	Moreover, inhibition of the Trx system by soft acids, such as mercury-, chromium- and arsenic-containing compounds cause changes in the cellular redox state and contribute to their cell toxicity.	Arsenic	86-93	thioredoxin	Homo sapiens	28-31
29425503-5	2018	FUS protein levels in arsenic-induced stress granules were significantly increased in Padi4-/- mouse embryonic fibroblasts (MEFs).	Arsenic	22-29	peptidyl arginine deiminase, type IV	Mus musculus	86-91
29413340-9	2018	A significantly larger percentage of TSLPR-positive cells was observed after allergen-specific stimulation of basophils from patients with AR compared with subjects with AS.	Arsenic	170-172	cytokine receptor like factor 2	Homo sapiens	37-42
29118024-2	2018	One such pollutant, arsenic, contaminates the drinking water of ~100 million people globally and has been associated with insulin resistance and diabetes in epidemiological studies.	Arsenic	20-27	insulin	Homo sapiens	122-129
29118024-11	2018	Taken together, these data suggest that arsenic exposure impairs glucose tolerance through functional impairments in insulin secretion from beta-cells rather than by augmenting peripheral insulin resistance.	Arsenic	40-47	insulin	Homo sapiens	117-124
29413340-10	2018	Basophil TSLPR expression was as good as or better than CD203c expression in discriminating between patients with AR and subjects with AS, as judged by receiver operating characteristic curves.	Arsenic	135-137	cytokine receptor like factor 2	Homo sapiens	9-14
29169099-0	2018	Exposure to arsenic in tap water and gestational diabetes: A French semi-ecological study.	Arsenic	12-19	nuclear RNA export factor 1	Homo sapiens	23-26
28512695-0	2018	Arsenic Induces Thioredoxin 1 and Apoptosis in Human Liver HHL-5 Cells.	Arsenic	0-7	thioredoxin	Homo sapiens	16-27
28512695-0	2018	Arsenic Induces Thioredoxin 1 and Apoptosis in Human Liver HHL-5 Cells.	Arsenic	0-7	hes family bHLH transcription factor 1	Homo sapiens	59-62
29175755-1	2018	Arsenic (As) is an inhibitor of phosphatase, however, in the complex soil system, the substrate concentration effect and the mechanism of As inhibition of soil alkaline phosphatase (ALP) and its kinetics has not been adequately studied.	Arsenic	0-7	alkaline phosphatase, placental	Homo sapiens	160-180
29175755-1	2018	Arsenic (As) is an inhibitor of phosphatase, however, in the complex soil system, the substrate concentration effect and the mechanism of As inhibition of soil alkaline phosphatase (ALP) and its kinetics has not been adequately studied.	Arsenic	0-7	alkaline phosphatase, placental	Homo sapiens	182-185
29175755-1	2018	Arsenic (As) is an inhibitor of phosphatase, however, in the complex soil system, the substrate concentration effect and the mechanism of As inhibition of soil alkaline phosphatase (ALP) and its kinetics has not been adequately studied.	Arsenic	9-11	alkaline phosphatase, placental	Homo sapiens	160-180
29175755-1	2018	Arsenic (As) is an inhibitor of phosphatase, however, in the complex soil system, the substrate concentration effect and the mechanism of As inhibition of soil alkaline phosphatase (ALP) and its kinetics has not been adequately studied.	Arsenic	9-11	alkaline phosphatase, placental	Homo sapiens	182-185
28512695-1	2018	To further characterize the mechanisms underlying liver toxicity induced by arsenic, we examined in this study the effect of arsenic on thioredoxin (Trx) and the apoptotic signaling pathways in human liver HHL-5 cells.	Arsenic	125-132	thioredoxin	Homo sapiens	136-147
28512695-1	2018	To further characterize the mechanisms underlying liver toxicity induced by arsenic, we examined in this study the effect of arsenic on thioredoxin (Trx) and the apoptotic signaling pathways in human liver HHL-5 cells.	Arsenic	125-132	thioredoxin	Homo sapiens	149-152
28512695-3	2018	A concentration-dependent increase in mRNA and protein levels of Trx1 and TrxR1 was observed in arsenic-treated cells.	Arsenic	96-103	thioredoxin	Homo sapiens	65-69
28512695-3	2018	A concentration-dependent increase in mRNA and protein levels of Trx1 and TrxR1 was observed in arsenic-treated cells.	Arsenic	96-103	thioredoxin reductase 1	Homo sapiens	74-79
28512695-5	2018	In line with this, protein levels of Bax and cytochrome C were increased and Bcl-2 was decreased by arsenic treatments.	Arsenic	100-107	BCL2 associated X, apoptosis regulator	Homo sapiens	37-40
28512695-5	2018	In line with this, protein levels of Bax and cytochrome C were increased and Bcl-2 was decreased by arsenic treatments.	Arsenic	100-107	cytochrome c, somatic	Homo sapiens	45-57
28512695-5	2018	In line with this, protein levels of Bax and cytochrome C were increased and Bcl-2 was decreased by arsenic treatments.	Arsenic	100-107	BCL2 apoptosis regulator	Homo sapiens	77-82
28512695-7	2018	These results indicate that Trx is involved in arsenic-induced liver cell injury, probably through the apoptotic signaling pathway.	Arsenic	47-54	thioredoxin	Homo sapiens	28-31
29107899-8	2018	miR-29a was the most significantly altered, highest expression being in the arsenic exposed group with PN, suggesting its association with the occurrence of PN.	Arsenic	76-83	microRNA 29a	Homo sapiens	0-7
29107899-10	2018	Since this was quite contrary to miRNA regulation, we checked for intermediate players beta-catenin and GSK-3beta upon arsenic exposure which affects PMP22 expression.	Arsenic	119-126	catenin beta 1	Homo sapiens	87-99
29107899-10	2018	Since this was quite contrary to miRNA regulation, we checked for intermediate players beta-catenin and GSK-3beta upon arsenic exposure which affects PMP22 expression.	Arsenic	119-126	glycogen synthase kinase 3 beta	Homo sapiens	104-113
29107899-10	2018	Since this was quite contrary to miRNA regulation, we checked for intermediate players beta-catenin and GSK-3beta upon arsenic exposure which affects PMP22 expression.	Arsenic	119-126	peripheral myelin protein 22	Homo sapiens	150-155
29107899-11	2018	We found that beta-catenin was upregulated in vitro and was also highest in the arsenic exposed group with PN while GSK-3beta followed the reverse pattern.	Arsenic	80-87	catenin beta 1	Homo sapiens	14-26
29107899-12	2018	Our findings suggest that arsenic exposure alters the expression of SA-miRs and the mir-29a/beta catenin/PMP22 axis might be responsible for arsenic induced PN.	Arsenic	26-33	microRNA 29a	Homo sapiens	84-91
29107899-12	2018	Our findings suggest that arsenic exposure alters the expression of SA-miRs and the mir-29a/beta catenin/PMP22 axis might be responsible for arsenic induced PN.	Arsenic	26-33	catenin beta 1	Homo sapiens	92-104
29107899-12	2018	Our findings suggest that arsenic exposure alters the expression of SA-miRs and the mir-29a/beta catenin/PMP22 axis might be responsible for arsenic induced PN.	Arsenic	26-33	peripheral myelin protein 22	Homo sapiens	105-110
29107899-12	2018	Our findings suggest that arsenic exposure alters the expression of SA-miRs and the mir-29a/beta catenin/PMP22 axis might be responsible for arsenic induced PN.	Arsenic	141-148	microRNA 29a	Homo sapiens	84-91
29107899-12	2018	Our findings suggest that arsenic exposure alters the expression of SA-miRs and the mir-29a/beta catenin/PMP22 axis might be responsible for arsenic induced PN.	Arsenic	141-148	catenin beta 1	Homo sapiens	92-104
29107899-12	2018	Our findings suggest that arsenic exposure alters the expression of SA-miRs and the mir-29a/beta catenin/PMP22 axis might be responsible for arsenic induced PN.	Arsenic	141-148	peripheral myelin protein 22	Homo sapiens	105-110
29169099-2	2018	Studies on exposure to arsenic (As) in tap water and the risk of GDM have not provided conclusive evidence, particularly when levels of exposure were low (from 10 to 50microg As/L).	Arsenic	23-30	nuclear RNA export factor 1	Homo sapiens	39-42
29169099-2	2018	Studies on exposure to arsenic (As) in tap water and the risk of GDM have not provided conclusive evidence, particularly when levels of exposure were low (from 10 to 50microg As/L).	Arsenic	32-34	nuclear RNA export factor 1	Homo sapiens	39-42
29169099-7	2018	French guidelines for As in tap water were used to identify groups potentially exposed, designated "As +" (&gt;= 10microg As/L) and "As -" (&lt; 10microg As/L).	Arsenic	22-24	nuclear RNA export factor 1	Homo sapiens	28-31
29155576-0	2018	Chronic Arsenic Exposure Increases Abeta(1-42) Production and Receptor for Advanced Glycation End Products Expression in Rat Brain.	Arsenic	8-15	advanced glycosylation end product-specific receptor	Rattus norvegicus	62-106
29103775-0	2018	Cyclin D1 promoter -56 and -54bp CpG un-methylation predicts invasive progression in arsenic-induced Bowen"s disease.	Arsenic	85-92	cyclin D1	Homo sapiens	0-9
29214690-3	2018	Significant reduction in the activity levels of superoxide dismutase, catalase, and glutathione levels with a concomitant increase in the lipid peroxidation and protein carbonyl content in the testis and the cauda epididymis of arsenic-exposed rats.	Arsenic	228-235	catalase	Rattus norvegicus	70-78
29214690-4	2018	Arsenic intoxication also enhanced the testicular caspase-3 mRNA levels, disorganization of testicular and cauda epididymal architecture as well as increased arsenic content in the testis and the cauda epididymis of rats.	Arsenic	0-7	caspase 3	Rattus norvegicus	50-59
29155576-6	2018	Our results demonstrate that chronic arsenic exposure induces behavioral deficits accompanied of higher levels of soluble and membranal RAGE and the increase of Abeta(1-42) cleaved.	Arsenic	37-44	advanced glycosylation end product-specific receptor	Rattus norvegicus	136-140
29155576-8	2018	These results provide evidence of the effects of arsenic exposure on the production of Abeta(1-42) and cerebral amyloid clearance through RAGE in an in vivo model that displays behavioral alterations.	Arsenic	49-56	advanced glycosylation end product-specific receptor	Rattus norvegicus	138-142
30099960-9	2018	The effect of miRNAs on birthweight varied by gestational age (for miR-1290, miR-195, miR-328) and in utero arsenic exposure (for miR-1290): stronger effect was observed among infants delivered early in gestation or exposed to higher concentrations of arsenic in cord blood.	Arsenic	108-115	microRNA 1290	Homo sapiens	130-138
29152826-4	2018	Ultimately, on treatment of the (mu2 :eta2 ,eta2 -Pn2 ){Ni(IMes)(CO)}2 compounds with carbon monoxide, the Pn2 units can be released, affording P4 in the case of the phosphorus-containing species, and elemental arsenic in the case of (mu2 :eta2 ,eta2 -As2 ){Ni(IMes)(CO)}2 .	Arsenic	211-218	adaptor related protein complex 1 subunit mu 2	Homo sapiens	33-36
29152826-4	2018	Ultimately, on treatment of the (mu2 :eta2 ,eta2 -Pn2 ){Ni(IMes)(CO)}2 compounds with carbon monoxide, the Pn2 units can be released, affording P4 in the case of the phosphorus-containing species, and elemental arsenic in the case of (mu2 :eta2 ,eta2 -As2 ){Ni(IMes)(CO)}2 .	Arsenic	211-218	DNA polymerase iota	Homo sapiens	44-48
29152826-4	2018	Ultimately, on treatment of the (mu2 :eta2 ,eta2 -Pn2 ){Ni(IMes)(CO)}2 compounds with carbon monoxide, the Pn2 units can be released, affording P4 in the case of the phosphorus-containing species, and elemental arsenic in the case of (mu2 :eta2 ,eta2 -As2 ){Ni(IMes)(CO)}2 .	Arsenic	211-218	amyloid beta precursor protein	Homo sapiens	50-53
29152826-4	2018	Ultimately, on treatment of the (mu2 :eta2 ,eta2 -Pn2 ){Ni(IMes)(CO)}2 compounds with carbon monoxide, the Pn2 units can be released, affording P4 in the case of the phosphorus-containing species, and elemental arsenic in the case of (mu2 :eta2 ,eta2 -As2 ){Ni(IMes)(CO)}2 .	Arsenic	211-218	amyloid beta precursor protein	Homo sapiens	107-110
29152826-4	2018	Ultimately, on treatment of the (mu2 :eta2 ,eta2 -Pn2 ){Ni(IMes)(CO)}2 compounds with carbon monoxide, the Pn2 units can be released, affording P4 in the case of the phosphorus-containing species, and elemental arsenic in the case of (mu2 :eta2 ,eta2 -As2 ){Ni(IMes)(CO)}2 .	Arsenic	211-218	DNA polymerase iota	Homo sapiens	44-48
29152826-4	2018	Ultimately, on treatment of the (mu2 :eta2 ,eta2 -Pn2 ){Ni(IMes)(CO)}2 compounds with carbon monoxide, the Pn2 units can be released, affording P4 in the case of the phosphorus-containing species, and elemental arsenic in the case of (mu2 :eta2 ,eta2 -As2 ){Ni(IMes)(CO)}2 .	Arsenic	211-218	DNA polymerase iota	Homo sapiens	44-48
28776197-0	2018	Long-term exposure of immortalized keratinocytes to arsenic induces EMT, impairs differentiation in organotypic skin models and mimics aspects of human skin derangements.	Arsenic	52-59	IL2 inducible T cell kinase	Homo sapiens	68-71
29323258-6	2018	The results showed that the variants of GSTO1, GSTO2 and PNP render the susceptible toward developing arsenic-induced skin lesions in individuals exposed to high-dose inorganic arsenic in northwest China.	Arsenic	102-109	glutathione S-transferase omega 1	Homo sapiens	40-45
29323258-6	2018	The results showed that the variants of GSTO1, GSTO2 and PNP render the susceptible toward developing arsenic-induced skin lesions in individuals exposed to high-dose inorganic arsenic in northwest China.	Arsenic	102-109	glutathione S-transferase omega 2	Homo sapiens	47-52
29323258-6	2018	The results showed that the variants of GSTO1, GSTO2 and PNP render the susceptible toward developing arsenic-induced skin lesions in individuals exposed to high-dose inorganic arsenic in northwest China.	Arsenic	102-109	purine nucleoside phosphorylase	Homo sapiens	57-60
29323258-6	2018	The results showed that the variants of GSTO1, GSTO2 and PNP render the susceptible toward developing arsenic-induced skin lesions in individuals exposed to high-dose inorganic arsenic in northwest China.	Arsenic	177-184	glutathione S-transferase omega 1	Homo sapiens	40-45
29323258-6	2018	The results showed that the variants of GSTO1, GSTO2 and PNP render the susceptible toward developing arsenic-induced skin lesions in individuals exposed to high-dose inorganic arsenic in northwest China.	Arsenic	177-184	glutathione S-transferase omega 2	Homo sapiens	47-52
29323258-6	2018	The results showed that the variants of GSTO1, GSTO2 and PNP render the susceptible toward developing arsenic-induced skin lesions in individuals exposed to high-dose inorganic arsenic in northwest China.	Arsenic	177-184	purine nucleoside phosphorylase	Homo sapiens	57-60
29054558-11	2018	Regression analysis highlighted a significant (p&lt;0.001) association between urinary As and Lp(a), Apo-A1, and Apo-B concentration, and Apo-B/Apo-A1 ratio.	Arsenic	87-89	lipoprotein(a)	Homo sapiens	94-99
29054558-11	2018	Regression analysis highlighted a significant (p&lt;0.001) association between urinary As and Lp(a), Apo-A1, and Apo-B concentration, and Apo-B/Apo-A1 ratio.	Arsenic	87-89	apolipoprotein B	Homo sapiens	113-118
29080535-0	2018	Arsenic biotransformation potential of microbial arsH responses in the biogeochemical cycling of arsenic-contaminated groundwater.	Arsenic	0-7	ArsH	Citrobacter freundii	49-53
29080535-0	2018	Arsenic biotransformation potential of microbial arsH responses in the biogeochemical cycling of arsenic-contaminated groundwater.	Arsenic	97-104	ArsH	Citrobacter freundii	49-53
29080535-3	2018	We found that ArsH gene activity, with arsenite oxidase in the periplasm; it revealed arsenic oxidation potential of the arsH system.	Arsenic	86-93	ArsH	Citrobacter freundii	14-18
29080535-3	2018	We found that ArsH gene activity, with arsenite oxidase in the periplasm; it revealed arsenic oxidation potential of the arsH system.	Arsenic	86-93	ArsH	Citrobacter freundii	121-125
29098576-9	2018	The expression of mtl-1, mtl-2, hsp-6, and hsp-70 were significantly associated with Pb/U, Pb, Sr, and As/Sr/Pb/U, respectively.	Arsenic	103-105	Metallothionein-1	Caenorhabditis elegans	18-23
29098576-9	2018	The expression of mtl-1, mtl-2, hsp-6, and hsp-70 were significantly associated with Pb/U, Pb, Sr, and As/Sr/Pb/U, respectively.	Arsenic	103-105	Metallothionein-2	Caenorhabditis elegans	25-30
29098576-9	2018	The expression of mtl-1, mtl-2, hsp-6, and hsp-70 were significantly associated with Pb/U, Pb, Sr, and As/Sr/Pb/U, respectively.	Arsenic	103-105	Heat shock protein hsp-6	Caenorhabditis elegans	32-37
29098576-9	2018	The expression of mtl-1, mtl-2, hsp-6, and hsp-70 were significantly associated with Pb/U, Pb, Sr, and As/Sr/Pb/U, respectively.	Arsenic	103-105	Heat Shock Protein	Caenorhabditis elegans	43-49
30099960-9	2018	The effect of miRNAs on birthweight varied by gestational age (for miR-1290, miR-195, miR-328) and in utero arsenic exposure (for miR-1290): stronger effect was observed among infants delivered early in gestation or exposed to higher concentrations of arsenic in cord blood.	Arsenic	252-259	microRNA 1290	Homo sapiens	130-138
30175652-10	2018	In an adjusted SEM model, mediation of the association between arsenic and GA by miR124-3 was borderline significant (P = 0.061).	Arsenic	63-70	microRNA 124-3	Homo sapiens	81-89
30175652-12	2018	Specifically, prenatal arsenic exposure was associated with lower methylation of miR124-3 that mediated the exposure-response of arsenic on GA. Future research should evaluate if these epigenetic changes are persistent and associated with disease risk.	Arsenic	23-30	microRNA 124-3	Homo sapiens	81-89
30175652-12	2018	Specifically, prenatal arsenic exposure was associated with lower methylation of miR124-3 that mediated the exposure-response of arsenic on GA. Future research should evaluate if these epigenetic changes are persistent and associated with disease risk.	Arsenic	129-136	microRNA 124-3	Homo sapiens	81-89
29217265-5	2018	The methylation of arsenite by arsenite-3-methyltransferase (As3MT) promotes the clearance of arsenic as pentavalent species, but also generates reactive trivalent intermediates.	Arsenic	94-101	arsenite methyltransferase	Homo sapiens	31-59
29111283-8	2018	Arsenic induced autophagy in pancreatic islets, as evidenced by elevated LC3-II level and depressed P62 level in vivo and in vitro.	Arsenic	0-7	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	100-103
29217265-5	2018	The methylation of arsenite by arsenite-3-methyltransferase (As3MT) promotes the clearance of arsenic as pentavalent species, but also generates reactive trivalent intermediates.	Arsenic	94-101	arsenite methyltransferase	Homo sapiens	61-66
29161537-3	2018	Herein, we identified significant upregulation of H3K79me1, in individuals with arsenic-induced skin lesion (WSL), and H3K79me1 was found to be regulated by the upstream methyltransferase DOT1L.	Arsenic	80-87	DOT1 like histone lysine methyltransferase	Homo sapiens	188-193
29446707-3	2018	The aim of this review is to provide a summary of the most frequently proposed mechanisms underlying hypertension associated with As, Cd, and Hg exposure including: oxidative stress, impaired nitric oxide (NO) signaling, modified vascular response to neurotransmitters and disturbed vascular muscle Ca2+ signaling, renal damage, and interference with the renin-angiotensin system.	Arsenic	130-132	renin	Homo sapiens	355-360
27966075-5	2018	A significant decrease in the expression of DA-D2 receptors associated with alterations in the expression of PKA, pDARPP32 (Thr 34), and PP1 alpha was clearly evident on arsenic exposure.	Arsenic	170-177	protein phosphatase 1 catalytic subunit alpha	Rattus norvegicus	137-146
27966075-6	2018	Expression of BDNF and pGSK3beta in corpus striatum was found decreased in arsenic-exposed rats.	Arsenic	75-82	brain-derived neurotrophic factor	Rattus norvegicus	14-18
27966075-12	2018	The results exhibit that curcumin modulates BDNF/DARPP32/CREB in arsenic-induced alterations in dopaminergic signaling in rat corpus striatum.	Arsenic	65-72	brain-derived neurotrophic factor	Rattus norvegicus	44-48
27966075-12	2018	The results exhibit that curcumin modulates BDNF/DARPP32/CREB in arsenic-induced alterations in dopaminergic signaling in rat corpus striatum.	Arsenic	65-72	protein phosphatase 1, regulatory (inhibitor) subunit 1B	Rattus norvegicus	49-56
27966075-12	2018	The results exhibit that curcumin modulates BDNF/DARPP32/CREB in arsenic-induced alterations in dopaminergic signaling in rat corpus striatum.	Arsenic	65-72	cAMP responsive element binding protein 1	Rattus norvegicus	57-61
27966075-0	2018	Protective Effect of Curcumin by Modulating BDNF/DARPP32/CREB in Arsenic-Induced Alterations in Dopaminergic Signaling in Rat Corpus Striatum.	Arsenic	65-72	brain-derived neurotrophic factor	Rattus norvegicus	44-48
27966075-0	2018	Protective Effect of Curcumin by Modulating BDNF/DARPP32/CREB in Arsenic-Induced Alterations in Dopaminergic Signaling in Rat Corpus Striatum.	Arsenic	65-72	protein phosphatase 1, regulatory (inhibitor) subunit 1B	Rattus norvegicus	49-56
27966075-0	2018	Protective Effect of Curcumin by Modulating BDNF/DARPP32/CREB in Arsenic-Induced Alterations in Dopaminergic Signaling in Rat Corpus Striatum.	Arsenic	65-72	cAMP responsive element binding protein 1	Rattus norvegicus	57-61
29161537-7	2018	Taken together, our findings revealed that H3K79me1 and DOT1L could be a novel epigenetic signature of the arsenic-exposed WSL group.	Arsenic	107-114	DOT1 like histone lysine methyltransferase	Homo sapiens	56-61
29435151-0	2018	Arsenic exposure assists ccm3 genetic polymorphism in elevating blood pressure.	Arsenic	0-7	programmed cell death 10	Homo sapiens	25-29
28857170-6	2018	Mutants of gamma-ECS and PCS1 were hypersensitive to As and had higher root-to-shoot As translocation.	Arsenic	53-55	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	25-29
28857170-9	2018	Arsenic hyperaccumulation can be engineered in A. thaliana by knocking out the HAC1 gene and expressing PvACR3.	Arsenic	0-7	histone acetyltransferase of the CBP family 1	Arabidopsis thaliana	79-83
29049844-11	2018	Chronic and acute exposure to arsenic modulated the expression of transformation-associated genes including Bcl-2A1, IGFL-1, Rab31, and TNC in HaCaT cells.	Arsenic	30-37	BCL2 related protein A1	Homo sapiens	108-115
29049844-11	2018	Chronic and acute exposure to arsenic modulated the expression of transformation-associated genes including Bcl-2A1, IGFL-1, Rab31, and TNC in HaCaT cells.	Arsenic	30-37	IGF like family member 1	Homo sapiens	117-123
29049844-11	2018	Chronic and acute exposure to arsenic modulated the expression of transformation-associated genes including Bcl-2A1, IGFL-1, Rab31, and TNC in HaCaT cells.	Arsenic	30-37	RAB31, member RAS oncogene family	Homo sapiens	125-130
29049844-11	2018	Chronic and acute exposure to arsenic modulated the expression of transformation-associated genes including Bcl-2A1, IGFL-1, Rab31, and TNC in HaCaT cells.	Arsenic	30-37	tenascin C	Homo sapiens	136-139
29390596-8	2017	Urinary fibrinogen and KIM-1 levelscorrelated positively with urinary arsenic levels.	Arsenic	70-77	fibrinogen beta chain	Homo sapiens	8-18
29390596-8	2017	Urinary fibrinogen and KIM-1 levelscorrelated positively with urinary arsenic levels.	Arsenic	70-77	hepatitis A virus cellular receptor 1	Homo sapiens	23-28
29132937-0	2018	Arsenic exposure during embryonic development alters the expression of the long noncoding RNA growth arrest specific-5 (Gas5) in a sex-dependent manner.	Arsenic	0-7	growth arrest specific 5	Mus musculus	94-118
29132937-0	2018	Arsenic exposure during embryonic development alters the expression of the long noncoding RNA growth arrest specific-5 (Gas5) in a sex-dependent manner.	Arsenic	0-7	growth arrest specific 5	Mus musculus	120-124
29132937-1	2018	Our previous studies suggest that prenatal arsenic exposure (50ppb) modifies epigenetic control of the programming of the glucocorticoid receptor (GR) signaling system in the developing mouse brain.	Arsenic	43-50	nuclear receptor subfamily 3, group C, member 1	Mus musculus	122-145
29132937-1	2018	Our previous studies suggest that prenatal arsenic exposure (50ppb) modifies epigenetic control of the programming of the glucocorticoid receptor (GR) signaling system in the developing mouse brain.	Arsenic	43-50	nuclear receptor subfamily 3, group C, member 1	Mus musculus	147-149
29132937-3	2018	To understand the arsenic-induced changes within the GR system, we assessed the impact of in utero arsenic exposure on the levels of the GR and growth arrest-specific-5 (Gas5), a noncoding RNA, across a key gestational period for GR programming (gestational days, GD 14-18) in mice.	Arsenic	18-25	nuclear receptor subfamily 3, group C, member 1	Mus musculus	53-55
29132937-3	2018	To understand the arsenic-induced changes within the GR system, we assessed the impact of in utero arsenic exposure on the levels of the GR and growth arrest-specific-5 (Gas5), a noncoding RNA, across a key gestational period for GR programming (gestational days, GD 14-18) in mice.	Arsenic	99-106	nuclear receptor subfamily 3, group C, member 1	Mus musculus	137-139
29132937-3	2018	To understand the arsenic-induced changes within the GR system, we assessed the impact of in utero arsenic exposure on the levels of the GR and growth arrest-specific-5 (Gas5), a noncoding RNA, across a key gestational period for GR programming (gestational days, GD 14-18) in mice.	Arsenic	99-106	growth arrest specific 5	Mus musculus	144-168
29132937-3	2018	To understand the arsenic-induced changes within the GR system, we assessed the impact of in utero arsenic exposure on the levels of the GR and growth arrest-specific-5 (Gas5), a noncoding RNA, across a key gestational period for GR programming (gestational days, GD 14-18) in mice.	Arsenic	99-106	growth arrest specific 5	Mus musculus	170-174
29132937-3	2018	To understand the arsenic-induced changes within the GR system, we assessed the impact of in utero arsenic exposure on the levels of the GR and growth arrest-specific-5 (Gas5), a noncoding RNA, across a key gestational period for GR programming (gestational days, GD 14-18) in mice.	Arsenic	99-106	nuclear receptor subfamily 3, group C, member 1	Mus musculus	137-139
29132937-5	2018	Prenatal arsenic exposure resulted in sex-dependent and age-dependent shifts in the levels of GR and Gas5 expression in fetal telencephalon.	Arsenic	9-16	nuclear receptor subfamily 3, group C, member 1	Mus musculus	94-96
29132937-5	2018	Prenatal arsenic exposure resulted in sex-dependent and age-dependent shifts in the levels of GR and Gas5 expression in fetal telencephalon.	Arsenic	9-16	growth arrest specific 5	Mus musculus	101-105
29132937-7	2018	Total cellular Gas5 levels were lower in arsenic-exposed males with no changes seen in arsenic-exposed females at GD16 and 18.	Arsenic	41-48	growth arrest specific 5	Mus musculus	15-19
29132937-8	2018	An increase in total cellular Gas-5 along with increased nuclear levels in GD14 arsenic-exposed females, suggests a differential regulation of cellular compartmentalization of Gas5.	Arsenic	80-87	growth arrest specific 5	Mus musculus	176-180
29132937-9	2018	RIP assays revealed reduced Gas5 associated with the GR on GD14 in the nuclear fraction prepared from arsenic-exposed males and females.	Arsenic	102-109	regulation of phenobarbitol-inducible P450	Mus musculus	0-3
29132937-9	2018	RIP assays revealed reduced Gas5 associated with the GR on GD14 in the nuclear fraction prepared from arsenic-exposed males and females.	Arsenic	102-109	growth arrest specific 5	Mus musculus	28-32
29132937-9	2018	RIP assays revealed reduced Gas5 associated with the GR on GD14 in the nuclear fraction prepared from arsenic-exposed males and females.	Arsenic	102-109	nuclear receptor subfamily 3, group C, member 1	Mus musculus	53-55
29132937-11	2018	Thus, nuclear GR signaling potential is decreased in prenatal arsenic-exposed males, while it is increased or maintained at levels approaching normal in prenatal arsenic-exposed females.	Arsenic	62-69	nuclear receptor subfamily 3, group C, member 1	Mus musculus	14-16
29132937-11	2018	Thus, nuclear GR signaling potential is decreased in prenatal arsenic-exposed males, while it is increased or maintained at levels approaching normal in prenatal arsenic-exposed females.	Arsenic	162-169	nuclear receptor subfamily 3, group C, member 1	Mus musculus	14-16
29132937-12	2018	These findings suggest that females, but not males, exposed to arsenic are able to regulate the levels of nuclear free GR by altering Gas5 levels, thereby keeping GR nuclear signaling closer to control (unexposed) levels.	Arsenic	63-70	nuclear receptor subfamily 3, group C, member 1	Mus musculus	119-121
29132937-12	2018	These findings suggest that females, but not males, exposed to arsenic are able to regulate the levels of nuclear free GR by altering Gas5 levels, thereby keeping GR nuclear signaling closer to control (unexposed) levels.	Arsenic	63-70	growth arrest specific 5	Mus musculus	134-138
29132937-12	2018	These findings suggest that females, but not males, exposed to arsenic are able to regulate the levels of nuclear free GR by altering Gas5 levels, thereby keeping GR nuclear signaling closer to control (unexposed) levels.	Arsenic	63-70	nuclear receptor subfamily 3, group C, member 1	Mus musculus	163-165
29924282-0	2018	[Polymorphisms of the Arsenite Methyltransferase (As3MT) gene and urinary efficiency of arsenic metabolism in a population in northern Mexico].	Arsenic	88-95	arsenite methyltransferase	Homo sapiens	22-48
28763940-5	2017	The majority of the wells in two of the aquifer types tap groundwater enriched in aluminum, arsenic, or manganese at levels harmful to human health.	Arsenic	92-99	nuclear RNA export factor 1	Homo sapiens	54-57
29435151-4	2018	Firstly, we found that serum arsenic was positively associated with blood pressure, cholesterol, glucose and C-reactive protein.	Arsenic	29-36	C-reactive protein	Homo sapiens	109-127
29373862-0	2017	Association of Low-Moderate Arsenic Exposure and Arsenic Metabolism with Incident Diabetes and Insulin Resistance in the Strong Heart Family Study.	Arsenic	28-35	insulin	Homo sapiens	95-102
29373862-3	2017	OBJECTIVE: We evaluated the prospective association of arsenic exposure and metabolism with type 2 diabetes and insulin resistance.	Arsenic	55-62	insulin	Homo sapiens	112-119
29211769-9	2017	We then performed quantification by qPCR of two arsenic resistant genes (ArsB, ArsC).	Arsenic	48-55	arylsulfatase B	Homo sapiens	73-77
29373862-16	2017	The association of arsenic metabolism with HOMA2-IR differed by B-vitamin intake and AS3MT genetics variants.	Arsenic	19-26	arsenite methyltransferase	Homo sapiens	85-90
29108910-5	2017	Nuclear factor-E2-related factor 2 (Nrf2), a key regulator in cellular adaptive antioxidant response, is clearly involved in alleviation of arsenic-induced oxidative damage.	Arsenic	140-147	nuclear factor, erythroid derived 2, like 2	Mus musculus	0-34
29108910-5	2017	Nuclear factor-E2-related factor 2 (Nrf2), a key regulator in cellular adaptive antioxidant response, is clearly involved in alleviation of arsenic-induced oxidative damage.	Arsenic	140-147	nuclear factor, erythroid derived 2, like 2	Mus musculus	36-40
29108910-6	2017	Multiple studies demonstrate that Nrf2 deficiency mice are more vulnerable to arsenic-induced intoxication.	Arsenic	78-85	nuclear factor, erythroid derived 2, like 2	Mus musculus	34-38
29108910-7	2017	However, what effect Nrf2 deficiency might have on arsenic metabolism in mice is still unknown.	Arsenic	51-58	nuclear factor, erythroid derived 2, like 2	Mus musculus	21-25
29108910-8	2017	In the present study, we measured the key enzymes involved in arsenic metabolism in Nrf2-WT and Nrf2-KO mice.	Arsenic	62-69	nuclear factor, erythroid derived 2, like 2	Mus musculus	84-88
29108910-8	2017	In the present study, we measured the key enzymes involved in arsenic metabolism in Nrf2-WT and Nrf2-KO mice.	Arsenic	62-69	nuclear factor, erythroid derived 2, like 2	Mus musculus	96-100
29108910-11	2017	Although there were some alterations in arsenic metabolism enzymes between Nrf2-WT and Nrf2-KO mice, the Nrf2 deficiency had no significant effect on arsenic methylation.	Arsenic	40-47	nuclear factor, erythroid derived 2, like 2	Mus musculus	75-79
29108910-11	2017	Although there were some alterations in arsenic metabolism enzymes between Nrf2-WT and Nrf2-KO mice, the Nrf2 deficiency had no significant effect on arsenic methylation.	Arsenic	40-47	nuclear factor, erythroid derived 2, like 2	Mus musculus	87-91
29108910-11	2017	Although there were some alterations in arsenic metabolism enzymes between Nrf2-WT and Nrf2-KO mice, the Nrf2 deficiency had no significant effect on arsenic methylation.	Arsenic	40-47	nuclear factor, erythroid derived 2, like 2	Mus musculus	87-91
29108910-12	2017	These results suggest that the Nrf2-KO mice are more sensitive to arsenic than Nrf2-WT mainly because of differences in adaptive antioxidant detoxification capacity rather than arsenic methylation capacity.	Arsenic	66-73	nuclear factor, erythroid derived 2, like 2	Mus musculus	31-35
28949802-5	2017	Although the arsenic concentrations always fulfilled the requirements of the World Health Organization (WHO) (&lt;=10 mug L-1), the total cancer risk value was higher than the general guidance risk value of 1.00 x 10-6.	Arsenic	13-20	immunoglobulin kappa variable 1-16	Homo sapiens	122-125
29229949-1	2017	We present a Density Functional Theory (DFT) analysis of the optical properties of dilute-As GaN1-xAsx alloys with arsenic (As) content ranging from 0% up to 12.5%.	Arsenic	90-92	gigaxonin	Homo sapiens	93-97
29211769-9	2017	We then performed quantification by qPCR of two arsenic resistant genes (ArsB, ArsC).	Arsenic	48-55	steroid sulfatase	Homo sapiens	79-83
28886535-10	2017	Therefore, the groundwater contamination by Arsenic is detected in the hydrogeological wells (E1 and E2).	Arsenic	44-51	small nucleolar RNA, H/ACA box 73A	Homo sapiens	94-103
28948427-4	2017	The releases of arsenic and Fe(II) increased with increasing AH2/Sc, whereas they decreased as pH increased.	Arsenic	16-23	zinc finger RANBP2-type containing 3	Homo sapiens	61-64
28994022-9	2017	Moreover, the data showed a significant negative association (p &lt; 0.05) between urinary arsenic concentrations and plasma miR-126 levels.	Arsenic	91-98	microRNA 126	Homo sapiens	125-132
29136503-3	2017	Restoration of PML nuclear bodies upon RA- and/or arsenic-initiated PML/RARA degradation is essential, while RA-triggered transcriptional activation is dispensable for APL eradication.	Arsenic	50-57	PML nuclear body scaffold	Homo sapiens	15-18
28942082-16	2017	CONCLUSION: Administration of 3,5,7,3",4"- Pentahydroxy flavone (i.e. Quercetin (QTN)) isolated from MI-ALC showed significant protection against arsenic-induced oxido-nitrosative stress and myocardial injury via modulation of Nrf2, PPAR-gamma, and apoptosis.	Arsenic	146-153	NFE2 like bZIP transcription factor 2	Rattus norvegicus	227-231
28942082-16	2017	CONCLUSION: Administration of 3,5,7,3",4"- Pentahydroxy flavone (i.e. Quercetin (QTN)) isolated from MI-ALC showed significant protection against arsenic-induced oxido-nitrosative stress and myocardial injury via modulation of Nrf2, PPAR-gamma, and apoptosis.	Arsenic	146-153	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	233-243
29017814-4	2017	Remarkably, synaptic changes persist 48h after transient PACAP exposure, featuring a similar increase in FS and an even larger increase in AS.	Arsenic	139-141	adenylate cyclase activating polypeptide 1	Homo sapiens	57-62
28973481-2	2017	Upregulation of systemic and aortic angiotensin II (ANGII) signaling has been proposed to contribute to arsenic-induced vascular dysfunction.	Arsenic	104-111	angiotensinogen	Homo sapiens	36-50
28973481-2	2017	Upregulation of systemic and aortic angiotensin II (ANGII) signaling has been proposed to contribute to arsenic-induced vascular dysfunction.	Arsenic	104-111	angiotensinogen	Homo sapiens	52-57
29136503-3	2017	Restoration of PML nuclear bodies upon RA- and/or arsenic-initiated PML/RARA degradation is essential, while RA-triggered transcriptional activation is dispensable for APL eradication.	Arsenic	50-57	PML nuclear body scaffold	Homo sapiens	68-71
29136503-3	2017	Restoration of PML nuclear bodies upon RA- and/or arsenic-initiated PML/RARA degradation is essential, while RA-triggered transcriptional activation is dispensable for APL eradication.	Arsenic	50-57	retinoic acid receptor alpha	Homo sapiens	72-76
29136503-4	2017	Mutations of the arsenic-binding site of PML/RARA, but also PML, have been detected in therapy-resistant patients, demonstrating the key role of PML in APL cure.	Arsenic	17-24	PML nuclear body scaffold	Homo sapiens	41-44
29136503-4	2017	Mutations of the arsenic-binding site of PML/RARA, but also PML, have been detected in therapy-resistant patients, demonstrating the key role of PML in APL cure.	Arsenic	17-24	retinoic acid receptor alpha	Homo sapiens	45-49
28470405-0	2017	Arsenic-mediated hyperpigmentation in skin via NF-kappa B/endothelin-1 signaling in an originally developed hairless mouse model.	Arsenic	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	47-57
28133775-8	2017	High arsenic level may suppress the sensitivity of gonadotroph cells to GnRH as well as gonadotropin secretion by elevating plasma levels of glucocorticoids.	Arsenic	5-12	gonadotropin releasing hormone 1	Homo sapiens	72-76
28931625-2	2017	Investigating arsenic sensitivity of acute promyelocytic leukemia, we proposed that PML oxidation promotes NB biogenesis.	Arsenic	14-21	PML nuclear body scaffold	Homo sapiens	84-87
28470405-0	2017	Arsenic-mediated hyperpigmentation in skin via NF-kappa B/endothelin-1 signaling in an originally developed hairless mouse model.	Arsenic	0-7	endothelin 1	Mus musculus	58-70
28470405-7	2017	The epidermis of Hr/Hr-mice and human HaCaT skin keratinocytes exposed to arsenic for 2 and 4 months, respectively, showed 5.4-21.5-fold increased levels of endothelin-1 (ET-1) expression via NF-kappa B activation.	Arsenic	74-81	endothelin 1	Homo sapiens	157-169
28470405-7	2017	The epidermis of Hr/Hr-mice and human HaCaT skin keratinocytes exposed to arsenic for 2 and 4 months, respectively, showed 5.4-21.5-fold increased levels of endothelin-1 (ET-1) expression via NF-kappa B activation.	Arsenic	74-81	endothelin 1	Homo sapiens	171-175
28470405-7	2017	The epidermis of Hr/Hr-mice and human HaCaT skin keratinocytes exposed to arsenic for 2 and 4 months, respectively, showed 5.4-21.5-fold increased levels of endothelin-1 (ET-1) expression via NF-kappa B activation.	Arsenic	74-81	nuclear factor kappa B subunit 1	Homo sapiens	192-202
28470405-8	2017	Coexposure of primary normal human epithelial melanocytes to arsenic and ET-1 activated their proliferation and melanin synthesis with increased levels of MITF-M and ET-1 receptor expression.	Arsenic	61-68	endothelin 1	Mus musculus	166-170
28470405-9	2017	Our results suggest that interaction between keratinocytes and melanocytes in the skin through ET-1 and its receptor contributes to arsenic-mediated skin pigmentation, a hallmark of arsenicosis.	Arsenic	132-139	endothelin 1	Mus musculus	95-99
28818758-0	2017	Phytoremediation of arsenic from the contaminated soil using transgenic tobacco plants expressing ACR2 gene of Arabidopsis thaliana.	Arsenic	20-27	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	98-102
28730340-9	2017	In patients that did not receive tamoxifen treatment, increasing CYP2D6 AS, and AS &gt; 0, were associated with superior RFS (each p = 0.0015).	Arsenic	72-74	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	65-71
28843991-7	2017	Furthermore, we affirmed notable disturbance of CD4+ T-cell differentiation in the lung of acute arsenic-exposed mice, as demonstrated by up-regulated mRNA levels of regulator Gata3 and cytokine Il-4 of Th2, enhanced Foxp3 and Il-10 of Treg, down-regulated T-bet and Ifn-gamma of Th1, as well as lessened Ror-gammat and Il-23 of Th17.	Arsenic	97-104	GATA binding protein 3	Mus musculus	176-181
28843991-7	2017	Furthermore, we affirmed notable disturbance of CD4+ T-cell differentiation in the lung of acute arsenic-exposed mice, as demonstrated by up-regulated mRNA levels of regulator Gata3 and cytokine Il-4 of Th2, enhanced Foxp3 and Il-10 of Treg, down-regulated T-bet and Ifn-gamma of Th1, as well as lessened Ror-gammat and Il-23 of Th17.	Arsenic	97-104	interleukin 4	Mus musculus	195-206
28843991-7	2017	Furthermore, we affirmed notable disturbance of CD4+ T-cell differentiation in the lung of acute arsenic-exposed mice, as demonstrated by up-regulated mRNA levels of regulator Gata3 and cytokine Il-4 of Th2, enhanced Foxp3 and Il-10 of Treg, down-regulated T-bet and Ifn-gamma of Th1, as well as lessened Ror-gammat and Il-23 of Th17.	Arsenic	97-104	forkhead box P3	Mus musculus	217-222
28843991-7	2017	Furthermore, we affirmed notable disturbance of CD4+ T-cell differentiation in the lung of acute arsenic-exposed mice, as demonstrated by up-regulated mRNA levels of regulator Gata3 and cytokine Il-4 of Th2, enhanced Foxp3 and Il-10 of Treg, down-regulated T-bet and Ifn-gamma of Th1, as well as lessened Ror-gammat and Il-23 of Th17.	Arsenic	97-104	interleukin 10	Mus musculus	227-232
28843991-7	2017	Furthermore, we affirmed notable disturbance of CD4+ T-cell differentiation in the lung of acute arsenic-exposed mice, as demonstrated by up-regulated mRNA levels of regulator Gata3 and cytokine Il-4 of Th2, enhanced Foxp3 and Il-10 of Treg, down-regulated T-bet and Ifn-gamma of Th1, as well as lessened Ror-gammat and Il-23 of Th17.	Arsenic	97-104	T-box 21	Mus musculus	257-262
28843991-7	2017	Furthermore, we affirmed notable disturbance of CD4+ T-cell differentiation in the lung of acute arsenic-exposed mice, as demonstrated by up-regulated mRNA levels of regulator Gata3 and cytokine Il-4 of Th2, enhanced Foxp3 and Il-10 of Treg, down-regulated T-bet and Ifn-gamma of Th1, as well as lessened Ror-gammat and Il-23 of Th17.	Arsenic	97-104	interferon gamma	Mus musculus	267-276
28843991-7	2017	Furthermore, we affirmed notable disturbance of CD4+ T-cell differentiation in the lung of acute arsenic-exposed mice, as demonstrated by up-regulated mRNA levels of regulator Gata3 and cytokine Il-4 of Th2, enhanced Foxp3 and Il-10 of Treg, down-regulated T-bet and Ifn-gamma of Th1, as well as lessened Ror-gammat and Il-23 of Th17.	Arsenic	97-104	negative elongation factor complex member C/D, Th1l	Mus musculus	280-283
28843991-7	2017	Furthermore, we affirmed notable disturbance of CD4+ T-cell differentiation in the lung of acute arsenic-exposed mice, as demonstrated by up-regulated mRNA levels of regulator Gata3 and cytokine Il-4 of Th2, enhanced Foxp3 and Il-10 of Treg, down-regulated T-bet and Ifn-gamma of Th1, as well as lessened Ror-gammat and Il-23 of Th17.	Arsenic	97-104	interleukin 23, alpha subunit p19	Mus musculus	320-325
28843991-8	2017	However, impressive elevation of cytokine Ifn-gamma and Il-23, as well as moderate enhancement of Il-4 and Il-10 were found in the lung by subchronic arsenic administration.	Arsenic	150-157	interleukin 23, alpha subunit p19	Mus musculus	56-61
28843991-8	2017	However, impressive elevation of cytokine Ifn-gamma and Il-23, as well as moderate enhancement of Il-4 and Il-10 were found in the lung by subchronic arsenic administration.	Arsenic	150-157	interleukin 4	Mus musculus	98-102
28843991-8	2017	However, impressive elevation of cytokine Ifn-gamma and Il-23, as well as moderate enhancement of Il-4 and Il-10 were found in the lung by subchronic arsenic administration.	Arsenic	150-157	interleukin 10	Mus musculus	107-112
28843991-9	2017	Finally, our present study demonstrated that both a single and sustained arsenic exposure prominently increased the expression of immune-related p38, JNK, ERK1/2 and NF-kappaB proteins in the lung tissue.	Arsenic	73-80	mitogen-activated protein kinase 14	Mus musculus	145-148
28843991-9	2017	Finally, our present study demonstrated that both a single and sustained arsenic exposure prominently increased the expression of immune-related p38, JNK, ERK1/2 and NF-kappaB proteins in the lung tissue.	Arsenic	73-80	mitogen-activated protein kinase 8	Mus musculus	150-153
28843991-9	2017	Finally, our present study demonstrated that both a single and sustained arsenic exposure prominently increased the expression of immune-related p38, JNK, ERK1/2 and NF-kappaB proteins in the lung tissue.	Arsenic	73-80	mitogen-activated protein kinase 3	Mus musculus	155-161
28843991-10	2017	While disrupting the pulmonary redox homeostasis by increasing MDA levels, exhausting GSH and impaired enzyme activities of CAT and GSH-Px, antioxidant regulator NRF2 and its downstream targets HO-1 and GSTO1/2 were also up-regulated by both acute and subchronic arsenic treatment.	Arsenic	263-270	nuclear factor, erythroid derived 2, like 2	Mus musculus	162-166
28843991-11	2017	Conclusively, our present study demonstrated both acute and subchronic oral administration of arsenic triggers multiple pulmonary immune responses involving inflammatory molecules and T-cell differentiation, which might be closely associated with the imbalanced redox status and activation of immune-related MAPKs, NF-kappaB and anti-inflammatory NRF2 pathways.	Arsenic	94-101	nuclear factor, erythroid derived 2, like 2	Mus musculus	347-351
28818758-11	2017	We have demonstrated that Arabidopsis thaliana AtACR2 gene is a potential candidate for genetic engineering of plants to develop new crop cultivars that can be grown on arsenic contaminated fields to reduce arsenic content of the soil and can become a source of food containing no arsenic or exhibiting substantially reduced amount of this metalloid.	Arsenic	169-176	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	47-53
28818758-11	2017	We have demonstrated that Arabidopsis thaliana AtACR2 gene is a potential candidate for genetic engineering of plants to develop new crop cultivars that can be grown on arsenic contaminated fields to reduce arsenic content of the soil and can become a source of food containing no arsenic or exhibiting substantially reduced amount of this metalloid.	Arsenic	207-214	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	47-53
28818758-11	2017	We have demonstrated that Arabidopsis thaliana AtACR2 gene is a potential candidate for genetic engineering of plants to develop new crop cultivars that can be grown on arsenic contaminated fields to reduce arsenic content of the soil and can become a source of food containing no arsenic or exhibiting substantially reduced amount of this metalloid.	Arsenic	207-214	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	47-53
29254203-0	2017	Inhibition of STAT3/VEGF/CDK2 axis signaling is critically involved in the antiangiogenic and apoptotic effects of arsenic herbal mixture PROS in non-small lung cancer cells.	Arsenic	115-122	signal transducer and activator of transcription 3	Homo sapiens	14-19
28366046-10	2017	Immunohistochemistry revealed a reduction in the expression of the pro-survival protein-protein kinase B (Akt/PKB) following exposure to arsenic and this was not reversed by withdrawal Discussion: Exposure to arsenic caused cardio-renal toxicity via induction of oxidative stress and down-regulation of Akt/PKB expressions.	Arsenic	137-144	AKT serine/threonine kinase 1	Rattus norvegicus	106-113
28366046-10	2017	Immunohistochemistry revealed a reduction in the expression of the pro-survival protein-protein kinase B (Akt/PKB) following exposure to arsenic and this was not reversed by withdrawal Discussion: Exposure to arsenic caused cardio-renal toxicity via induction of oxidative stress and down-regulation of Akt/PKB expressions.	Arsenic	209-216	AKT serine/threonine kinase 1	Rattus norvegicus	106-113
28366046-10	2017	Immunohistochemistry revealed a reduction in the expression of the pro-survival protein-protein kinase B (Akt/PKB) following exposure to arsenic and this was not reversed by withdrawal Discussion: Exposure to arsenic caused cardio-renal toxicity via induction of oxidative stress and down-regulation of Akt/PKB expressions.	Arsenic	209-216	AKT serine/threonine kinase 1	Rattus norvegicus	303-310
29254203-0	2017	Inhibition of STAT3/VEGF/CDK2 axis signaling is critically involved in the antiangiogenic and apoptotic effects of arsenic herbal mixture PROS in non-small lung cancer cells.	Arsenic	115-122	vascular endothelial growth factor A	Homo sapiens	20-24
29254203-0	2017	Inhibition of STAT3/VEGF/CDK2 axis signaling is critically involved in the antiangiogenic and apoptotic effects of arsenic herbal mixture PROS in non-small lung cancer cells.	Arsenic	115-122	cyclin dependent kinase 2	Homo sapiens	25-29
28823652-0	2017	PKC theta-mediated Ca2+/NF-AT signalling pathway may be involved in T-cell immunosuppression in coal-burning arsenic-poisoned population.	Arsenic	109-116	protein kinase C theta	Homo sapiens	0-9
28798983-2	2017	In addition to its orthodox nutrient substrates, AQP9 also transports multiple neutral and ionic arsenic species including arsenic trioxide, monomethylarsenous acid (MAsIII) and dimethylarsenic acid (DMAV).	Arsenic	97-104	aquaporin 9	Homo sapiens	49-53
28599205-6	2017	It is further proposed that the aberrant regulation of 14 proteins induced by arsenic would disturb cardiac contraction and relaxation, impair heart morphogenesis and development, and induce thrombosis in rats, which is mediated by the Akt/p38 MAPK signaling pathway.	Arsenic	78-85	mitogen activated protein kinase 14	Rattus norvegicus	240-243
28986725-5	2017	The average concentration found was 36.54 mug L-1 and areas with more concentration of As are located in the southern region of the province, in streams that are tributaries of the Atlantic Ocean.	Arsenic	87-89	immunoglobulin kappa variable 1-16	Homo sapiens	46-49
28936873-8	2017	Finally, the products of Rox(III) degradation were identified as As(III) and 2-nitrohydroquinone, demonstrating that ArsI is a dioxygenase that incorporates one oxygen atom from dioxygen into the carbon and the other to the arsenic to catalyze cleavage of the C-As bond.	Arsenic	224-231	MAX network transcriptional repressor	Homo sapiens	25-28
28936873-8	2017	Finally, the products of Rox(III) degradation were identified as As(III) and 2-nitrohydroquinone, demonstrating that ArsI is a dioxygenase that incorporates one oxygen atom from dioxygen into the carbon and the other to the arsenic to catalyze cleavage of the C-As bond.	Arsenic	224-231	arylsulfatase family member I	Homo sapiens	117-121
28655111-3	2017	The results indicate that this method achieved an effluent arsenic concentration of 0.03 mg L-1, which is lower than the arsenic concentration standard for drinking water and irrigation sources in Taiwan, during the charging stage.	Arsenic	59-66	immunoglobulin kappa variable 1-16	Homo sapiens	92-95
28829631-2	2017	In the present work, the effect of lead (Pb), Arsenic (As), and Cadmium (Cd) in primary cultures of Sertoli cells was analyzed by measuring the expression of the genes Cldn11, Ocln, and Gja1 that participate in the tight and gap junctions, which are responsible for maintaining the blood-testis barrier.	Arsenic	55-57	occludin	Rattus norvegicus	176-180
29028684-1	2017	BACKGROUND: Lead (Pb), cadmium (Cd), and arsenic (As) could cause health issues through oxidative stress that is indicated in the elevated tumor necrosis factor-alpha (TNF-alpha).	Arsenic	41-48	tumor necrosis factor	Homo sapiens	139-166
28823652-6	2017	Our analysis demonstrates that the PKC theta-mediated Ca2+/NF-AT signalling pathway may be involved in the T-cell immunosuppression of coal-burning arsenic-poisoned population.	Arsenic	148-155	protein kinase C theta	Homo sapiens	35-44
29028684-1	2017	BACKGROUND: Lead (Pb), cadmium (Cd), and arsenic (As) could cause health issues through oxidative stress that is indicated in the elevated tumor necrosis factor-alpha (TNF-alpha).	Arsenic	41-48	tumor necrosis factor	Homo sapiens	168-177
29028684-1	2017	BACKGROUND: Lead (Pb), cadmium (Cd), and arsenic (As) could cause health issues through oxidative stress that is indicated in the elevated tumor necrosis factor-alpha (TNF-alpha).	Arsenic	50-52	tumor necrosis factor	Homo sapiens	139-166
28960179-8	2017	By contrast, arsenic-exposed mice had significantly reduced plasma TNFalpha in response to systemic lipopolysaccharide challenge, together suggesting that the local airway innate immune response may be relatively preserved from arsenic intoxication.	Arsenic	13-20	tumor necrosis factor	Mus musculus	67-75
29028684-1	2017	BACKGROUND: Lead (Pb), cadmium (Cd), and arsenic (As) could cause health issues through oxidative stress that is indicated in the elevated tumor necrosis factor-alpha (TNF-alpha).	Arsenic	50-52	tumor necrosis factor	Homo sapiens	168-177
29028684-8	2017	RESULTS: Increasing blood Pb, Cd, and As levels were associated with elevated TNF-alpha levels.	Arsenic	38-40	tumor necrosis factor	Homo sapiens	78-87
29028684-12	2017	In the interaction between As and SNPs, workers with AA/AG (-238 G &gt; A) had synergic effect with As and induced higher serum TNF-alpha levels.	Arsenic	27-29	tumor necrosis factor	Homo sapiens	128-137
29028684-13	2017	CONCLUSIONS: Blood Cu and Se were antagonists of toxic metals (Pb, As, and Cd) through lower serum TNF-alpha levels.	Arsenic	67-69	tumor necrosis factor	Homo sapiens	99-108
28524356-0	2017	Association between YAP expression in neoplastic and non-neoplastic breast tissue with arsenic urinary levels.	Arsenic	87-94	Yes1 associated transcriptional regulator	Homo sapiens	20-23
28524356-2	2017	Yes-associated protein (YAP) is an important component of this Hippo pathway because YAP is the nuclear effector of the Hippo tumor suppressor pathway and it is crucial for the response to oxidative stress induced by cellular process and by different xenobiotics, including arsenic.	Arsenic	274-281	Yes1 associated transcriptional regulator	Homo sapiens	0-22
28524356-2	2017	Yes-associated protein (YAP) is an important component of this Hippo pathway because YAP is the nuclear effector of the Hippo tumor suppressor pathway and it is crucial for the response to oxidative stress induced by cellular process and by different xenobiotics, including arsenic.	Arsenic	274-281	Yes1 associated transcriptional regulator	Homo sapiens	24-27
28524356-2	2017	Yes-associated protein (YAP) is an important component of this Hippo pathway because YAP is the nuclear effector of the Hippo tumor suppressor pathway and it is crucial for the response to oxidative stress induced by cellular process and by different xenobiotics, including arsenic.	Arsenic	274-281	Yes1 associated transcriptional regulator	Homo sapiens	85-88
28524356-4	2017	The aim of the study was to assess and compare the expression of YAP in neoplastic and non-neoplastic breast tissue of women chronically exposed to arsenic through drinking water.	Arsenic	148-155	Yes1 associated transcriptional regulator	Homo sapiens	65-68
28733204-0	2017	The polymorphism XRCC1 Arg194Trp and 8-hydroxydeoxyguanosine increased susceptibility to arsenic-related renal cell carcinoma.	Arsenic	89-96	X-ray repair cross complementing 1	Homo sapiens	17-22
28733204-8	2017	The OR of RCC for the combined effect of high urinary 8-OHdG levels and high urinary total arsenic concentration in individuals with a XRCC1(Arg194Trp) Arg/Trp+Trp/Trp genotype was higher than in patients with an Arg/Arg genotype, which was evident in a dose response manner.	Arsenic	91-98	X-ray repair cross complementing 1	Homo sapiens	135-140
28784659-9	2017	Moreover, SUBINs abrogated arsenic-induced degradation of promyelocytic leukemia protein.	Arsenic	27-34	PML nuclear body scaffold	Homo sapiens	58-88
28687885-6	2017	Under optimum chemical vapor generation conditions ([NaBH4] = 1.39%, [HCl] = 2.97 M, total liquid flow = 936 muL min-1), the proposed sample introduction system allowed the determination of arsenic, selenium, and mercury up to 5 mug g-1 with a limit of detection of 25, 140, and 13 mug kg-1, respectively.	Arsenic	190-197	CD59 molecule (CD59 blood group)	Homo sapiens	113-118
29041502-2	2017	The AlAs layer allows greater arsenic incorporation into the LT-GaAs layer, prevents current diffusion into the GaAs substrate, and provides optical back-reflection that enhances below bandgap terahertz generation.	Arsenic	30-37	5'-aminolevulinate synthase 1	Homo sapiens	4-8
28625800-5	2017	We used RNA-seq to define the transcriptional response of HBE cells to Pseudomonas aeruginosa, and investigated how arsenic affected HBE gene networks in the presence and absence of the bacterial challenge.	Arsenic	116-123	hemoglobin subunit epsilon 1	Homo sapiens	133-136
28625800-7	2017	Using pathway analysis, we identified Sox4 and Nrf2-regulated gene networks that are predicted to mediate the arsenic-induced decrease in lysozyme secretion.	Arsenic	110-117	SRY-box transcription factor 4	Homo sapiens	38-42
28625800-7	2017	Using pathway analysis, we identified Sox4 and Nrf2-regulated gene networks that are predicted to mediate the arsenic-induced decrease in lysozyme secretion.	Arsenic	110-117	NFE2 like bZIP transcription factor 2	Homo sapiens	47-51
28712085-0	2017	Long-term spatiotemporal trends and health risk assessment of oyster arsenic levels in coastal waters of northern South China Sea.	Arsenic	69-76	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	126-129
28247524-8	2017	Blood and urinary arsenic levels negatively correlated with HRR1 (r = -.477, p &lt; .001 and r = -.438, p &lt; .001, respectively) and HRR2 (r = -.507, p &lt; .001 and r = -.412, p &lt; .001 respectively).	Arsenic	18-25	nuclear receptor subfamily 1 group H member 4	Homo sapiens	60-64
28190184-0	2017	Changes in Serum Adiponectin in Mice Chronically Exposed to Inorganic Arsenic in Drinking Water.	Arsenic	70-77	adiponectin, C1Q and collagen domain containing	Mus musculus	17-28
28190184-4	2017	We hypothesized that arsenic exposure may increase the risk of cardiovascular disease and diabetes mellitus by affecting the level of adiponectin.	Arsenic	21-28	adiponectin, C1Q and collagen domain containing	Mus musculus	134-145
28190184-8	2017	However, arsenic exposure decreased serum levels of adiponectin, triglyceride, and HDL-cholesterol.	Arsenic	9-16	adiponectin, C1Q and collagen domain containing	Mus musculus	52-63
28190184-9	2017	Further, an inverse relationship was observed between urinary concentrations of total arsenic and serum levels of adiponectin.	Arsenic	86-93	adiponectin, C1Q and collagen domain containing	Mus musculus	114-125
28190184-10	2017	This study suggests that arsenic exposure could disturb the metabolism of lipids and increase the risk of cardiovascular disease by reducing the level of adiponectin.	Arsenic	25-32	adiponectin, C1Q and collagen domain containing	Mus musculus	154-165
28700833-10	2017	The arsB gene seems to be more stable in bestowing bacteria with the capability to respond to the As concentration.	Arsenic	98-100	arylsulfatase B	Homo sapiens	4-8
27804788-7	2017	Elution of As(III) and As(V) from the composite can be done by using small amounts of 0.01 M NaOH solution resulting in preconcentration of arsenic species and possible multiple usage of composite.	Arsenic	140-147	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	23-28
28444938-7	2017	In conclusion, arsenic induced proliferation in human uroepithelial cells after short and long term exposure to arsenite and JAK2/STAT3 signaling pathway might be pivotal in arsenite-induced proliferation by regulating cyclin D1, COX-2, PCNA, and BCL2.	Arsenic	15-22	Janus kinase 2	Homo sapiens	125-129
28444938-7	2017	In conclusion, arsenic induced proliferation in human uroepithelial cells after short and long term exposure to arsenite and JAK2/STAT3 signaling pathway might be pivotal in arsenite-induced proliferation by regulating cyclin D1, COX-2, PCNA, and BCL2.	Arsenic	15-22	signal transducer and activator of transcription 3	Homo sapiens	130-135
28444938-7	2017	In conclusion, arsenic induced proliferation in human uroepithelial cells after short and long term exposure to arsenite and JAK2/STAT3 signaling pathway might be pivotal in arsenite-induced proliferation by regulating cyclin D1, COX-2, PCNA, and BCL2.	Arsenic	15-22	cyclin D1	Homo sapiens	219-228
28444938-7	2017	In conclusion, arsenic induced proliferation in human uroepithelial cells after short and long term exposure to arsenite and JAK2/STAT3 signaling pathway might be pivotal in arsenite-induced proliferation by regulating cyclin D1, COX-2, PCNA, and BCL2.	Arsenic	15-22	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	230-235
28444938-7	2017	In conclusion, arsenic induced proliferation in human uroepithelial cells after short and long term exposure to arsenite and JAK2/STAT3 signaling pathway might be pivotal in arsenite-induced proliferation by regulating cyclin D1, COX-2, PCNA, and BCL2.	Arsenic	15-22	proliferating cell nuclear antigen	Homo sapiens	237-241
28444938-7	2017	In conclusion, arsenic induced proliferation in human uroepithelial cells after short and long term exposure to arsenite and JAK2/STAT3 signaling pathway might be pivotal in arsenite-induced proliferation by regulating cyclin D1, COX-2, PCNA, and BCL2.	Arsenic	15-22	BCL2 apoptosis regulator	Homo sapiens	247-251
28712085-1	2017	Long-term spatiotemporal trends and health risk assessment of oyster arsenic levels in the coastal waters of northern South China Sea were investigated in order to help improve the quality and safety control and sustainable aquaculture for mollusks in China.	Arsenic	69-76	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	130-133
28712085-5	2017	Oyster arsenic levels in the coastal waters of northern South China Sea showed an overall decline from 1989 to 2012, remained relatively low since 2005, and slightly increased after 2007.	Arsenic	7-14	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	68-71
28712085-8	2017	Single-factor index ranged between 0.27 and 0.97, and average health risk coefficient was 3.85 x 10-5, both suggesting that oyster arsenic levels in northern South China Sea are within the safe range for human consumption.	Arsenic	131-138	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	170-173
29100362-6	2017	CDH1 expression was considered positive as &gt;= 30% of the membrane cells staining.	Arsenic	40-44	cadherin 1	Homo sapiens	0-4
28903487-0	2017	From the Cover: Arsenic Induces Hippocampal Neuronal Apoptosis and Cognitive Impairments via an Up-Regulated BMP2/Smad-Dependent Reduced BDNF/TrkB Signaling in Rats.	Arsenic	16-23	bone morphogenetic protein 2	Rattus norvegicus	109-113
28903487-0	2017	From the Cover: Arsenic Induces Hippocampal Neuronal Apoptosis and Cognitive Impairments via an Up-Regulated BMP2/Smad-Dependent Reduced BDNF/TrkB Signaling in Rats.	Arsenic	16-23	brain-derived neurotrophic factor	Rattus norvegicus	137-141
28903487-0	2017	From the Cover: Arsenic Induces Hippocampal Neuronal Apoptosis and Cognitive Impairments via an Up-Regulated BMP2/Smad-Dependent Reduced BDNF/TrkB Signaling in Rats.	Arsenic	16-23	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	142-146
28903487-5	2017	BMP2-silencing and treatment with BMP antagonist, noggin, attenuated the arsenic-induced apoptosis and loss in hippocampal neurons.	Arsenic	73-80	bone morphogenetic protein 2	Rattus norvegicus	0-4
28903487-5	2017	BMP2-silencing and treatment with BMP antagonist, noggin, attenuated the arsenic-induced apoptosis and loss in hippocampal neurons.	Arsenic	73-80	noggin	Rattus norvegicus	50-56
28903487-8	2017	We identified an arsenic-mediated attenuation of BDNF-dependent TrkB signaling, and observed that co-treatment with recombinant-BDNF reinstated BDNF/TrkB and reduced neuronal apoptosis.	Arsenic	17-24	brain-derived neurotrophic factor	Rattus norvegicus	49-53
28903487-8	2017	We identified an arsenic-mediated attenuation of BDNF-dependent TrkB signaling, and observed that co-treatment with recombinant-BDNF reinstated BDNF/TrkB and reduced neuronal apoptosis.	Arsenic	17-24	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	64-68
28903487-8	2017	We identified an arsenic-mediated attenuation of BDNF-dependent TrkB signaling, and observed that co-treatment with recombinant-BDNF reinstated BDNF/TrkB and reduced neuronal apoptosis.	Arsenic	17-24	brain-derived neurotrophic factor	Rattus norvegicus	128-132
28903487-8	2017	We identified an arsenic-mediated attenuation of BDNF-dependent TrkB signaling, and observed that co-treatment with recombinant-BDNF reinstated BDNF/TrkB and reduced neuronal apoptosis.	Arsenic	17-24	brain-derived neurotrophic factor	Rattus norvegicus	128-132
28903487-8	2017	We identified an arsenic-mediated attenuation of BDNF-dependent TrkB signaling, and observed that co-treatment with recombinant-BDNF reinstated BDNF/TrkB and reduced neuronal apoptosis.	Arsenic	17-24	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	149-153
28903487-11	2017	In addition, we found that TrkB-inhibitor, K252a, nullified noggin-induced protection, proving the necessity of a downstream reduced BDNF/TrKB signaling for BMP2/Smad-mediated apoptosis in arsenic-treated neurons.	Arsenic	189-196	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	27-31
28903487-11	2017	In addition, we found that TrkB-inhibitor, K252a, nullified noggin-induced protection, proving the necessity of a downstream reduced BDNF/TrKB signaling for BMP2/Smad-mediated apoptosis in arsenic-treated neurons.	Arsenic	189-196	noggin	Rattus norvegicus	60-66
28903487-11	2017	In addition, we found that TrkB-inhibitor, K252a, nullified noggin-induced protection, proving the necessity of a downstream reduced BDNF/TrKB signaling for BMP2/Smad-mediated apoptosis in arsenic-treated neurons.	Arsenic	189-196	bone morphogenetic protein 2	Rattus norvegicus	157-161
28903487-12	2017	We further related our observations with cognitive performances, and detected noggin-mediated restoration of transfer latency time and learning-memory ability for passive avoidance and Y-Maze tests respectively in arsenic-treated rats.	Arsenic	214-221	noggin	Rattus norvegicus	78-84
28903487-13	2017	Overall, our study proves that arsenic promotes hippocampal neuronal apoptosis through an up-regulated BMP2/Smad-dependent attenuation of BDNF/TrkB pathway, inducing cognitive deficits.	Arsenic	31-38	bone morphogenetic protein 2	Rattus norvegicus	103-107
28903487-13	2017	Overall, our study proves that arsenic promotes hippocampal neuronal apoptosis through an up-regulated BMP2/Smad-dependent attenuation of BDNF/TrkB pathway, inducing cognitive deficits.	Arsenic	31-38	brain-derived neurotrophic factor	Rattus norvegicus	138-142
28903487-13	2017	Overall, our study proves that arsenic promotes hippocampal neuronal apoptosis through an up-regulated BMP2/Smad-dependent attenuation of BDNF/TrkB pathway, inducing cognitive deficits.	Arsenic	31-38	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	143-147
28709971-10	2017	In addition, it is evident that, arsenic can change the components of the epigenome and hence induces diabetes through epigenetic mechanisms, such as alterations in glucose transport and/or metabolism and insulin expression/secretion.	Arsenic	33-40	insulin	Homo sapiens	205-212
28351806-13	2017	In addition, IL-6 was also positively associated with As, Cl and Pe in elderly.	Arsenic	54-56	interleukin 6	Homo sapiens	13-17
28838336-14	2017	Compared with As group, phosphorylation of JNK was lower in the SP600125/As group, phosphorylation of JNK in SP600125/Ms group was lower than the Ms group, and it showed no differences between the SP600125 &amp;amp; As group and the SP600125 &amp;amp; Ms group.	Arsenic	14-16	mitogen-activated protein kinase 8	Rattus norvegicus	43-46
28838336-14	2017	Compared with As group, phosphorylation of JNK was lower in the SP600125/As group, phosphorylation of JNK in SP600125/Ms group was lower than the Ms group, and it showed no differences between the SP600125 &amp;amp; As group and the SP600125 &amp;amp; Ms group.	Arsenic	14-16	mitogen-activated protein kinase 8	Rattus norvegicus	102-105
28838336-14	2017	Compared with As group, phosphorylation of JNK was lower in the SP600125/As group, phosphorylation of JNK in SP600125/Ms group was lower than the Ms group, and it showed no differences between the SP600125 &amp;amp; As group and the SP600125 &amp;amp; Ms group.	Arsenic	73-75	mitogen-activated protein kinase 8	Rattus norvegicus	43-46
28838336-14	2017	Compared with As group, phosphorylation of JNK was lower in the SP600125/As group, phosphorylation of JNK in SP600125/Ms group was lower than the Ms group, and it showed no differences between the SP600125 &amp;amp; As group and the SP600125 &amp;amp; Ms group.	Arsenic	73-75	mitogen-activated protein kinase 8	Rattus norvegicus	102-105
28579250-2	2017	Recently, we reported that arsenic exposure during in utero and early life was associated with impairment in the lung function and abnormal receptor for advanced glycation endproducts (RAGE), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) sputum levels.	Arsenic	27-34	TIMP metallopeptidase inhibitor 1	Homo sapiens	231-277
28549828-8	2017	The up-regulation of arsenic biotransformation genes was due to activated NFE2L2 in Nfe2l1(L)-KD MIN6 cells.	Arsenic	21-28	nuclear factor, erythroid derived 2, like 2	Mus musculus	74-80
28549828-8	2017	The up-regulation of arsenic biotransformation genes was due to activated NFE2L2 in Nfe2l1(L)-KD MIN6 cells.	Arsenic	21-28	nuclear factor, erythroid derived 2,-like 1	Mus musculus	84-90
28549828-10	2017	These results showed that deficiency of L-Nfe2l1 in pancreatic beta-cells increased susceptibility to acute arsenite-induced cytotoxicity by promoting arsenic biotransformation and intracellular MMA levels.	Arsenic	151-158	nuclear factor, erythroid derived 2,-like 1	Mus musculus	40-48
28579250-2	2017	Recently, we reported that arsenic exposure during in utero and early life was associated with impairment in the lung function and abnormal receptor for advanced glycation endproducts (RAGE), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) sputum levels.	Arsenic	27-34	advanced glycosylation end-product specific receptor	Homo sapiens	140-183
28579250-2	2017	Recently, we reported that arsenic exposure during in utero and early life was associated with impairment in the lung function and abnormal receptor for advanced glycation endproducts (RAGE), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) sputum levels.	Arsenic	27-34	advanced glycosylation end-product specific receptor	Homo sapiens	185-189
28579250-2	2017	Recently, we reported that arsenic exposure during in utero and early life was associated with impairment in the lung function and abnormal receptor for advanced glycation endproducts (RAGE), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) sputum levels.	Arsenic	27-34	matrix metallopeptidase 9	Homo sapiens	192-218
28579250-2	2017	Recently, we reported that arsenic exposure during in utero and early life was associated with impairment in the lung function and abnormal receptor for advanced glycation endproducts (RAGE), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) sputum levels.	Arsenic	27-34	matrix metallopeptidase 9	Homo sapiens	220-225
28579250-2	2017	Recently, we reported that arsenic exposure during in utero and early life was associated with impairment in the lung function and abnormal receptor for advanced glycation endproducts (RAGE), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) sputum levels.	Arsenic	27-34	TIMP metallopeptidase inhibitor 1	Homo sapiens	279-285
28579250-3	2017	Based on our results and the reported arsenic impacts on DNA methylation, we designed this study in our cohort of children exposed in utero and early childhood to arsenic with the aim to associate DNA methylation of MMP9, TIMP1 and RAGE genes with its protein sputum levels and with urinary and toenail arsenic levels.	Arsenic	163-170	TIMP metallopeptidase inhibitor 1	Homo sapiens	222-227
28579250-3	2017	Based on our results and the reported arsenic impacts on DNA methylation, we designed this study in our cohort of children exposed in utero and early childhood to arsenic with the aim to associate DNA methylation of MMP9, TIMP1 and RAGE genes with its protein sputum levels and with urinary and toenail arsenic levels.	Arsenic	163-170	advanced glycosylation end-product specific receptor	Homo sapiens	232-236
28579250-3	2017	Based on our results and the reported arsenic impacts on DNA methylation, we designed this study in our cohort of children exposed in utero and early childhood to arsenic with the aim to associate DNA methylation of MMP9, TIMP1 and RAGE genes with its protein sputum levels and with urinary and toenail arsenic levels.	Arsenic	163-170	TIMP metallopeptidase inhibitor 1	Homo sapiens	222-227
28688901-5	2017	Our data demonstrated there were no significantly differences on the contents of cGMP, PKG, MDA and the production of ROS, but the levels of GSH and NO, the activities of SOD, tNOS and iNOS were significantly enhanced in the arsenic-transformed cells.	Arsenic	225-232	nitric oxide synthase 2	Homo sapiens	185-189
28579250-3	2017	Based on our results and the reported arsenic impacts on DNA methylation, we designed this study in our cohort of children exposed in utero and early childhood to arsenic with the aim to associate DNA methylation of MMP9, TIMP1 and RAGE genes with its protein sputum levels and with urinary and toenail arsenic levels.	Arsenic	163-170	advanced glycosylation end-product specific receptor	Homo sapiens	232-236
28579250-4	2017	The results disclosed hypermethylation in MMP9 promotor region in the most exposed children; and an increase in the RAGE sputum levels among children with the mid methylation level; there were also positive associations between MMP9 DNA methylation with arsenic toenail concentrations; RAGE DNA methylation with iAs, and %DMA; and finally between TIMP1 DNA methylation with the first arsenic methylation.	Arsenic	254-261	matrix metallopeptidase 9	Homo sapiens	228-232
28771557-8	2017	Low-moderate arsenic exposure was positively associated with baseline fibrinogen in participants with diabetes and unexpectedly inversely associated with PAI-1.	Arsenic	13-20	fibrinogen beta chain	Homo sapiens	70-80
28737792-9	2017	Cationic disorder increases the d-d electron transition probability between adjacent ionic pairs such as Co2+/Fe3+ and a reduced particle size creates large interfacial polarization in the as-prepared NCF/CB hybrids.	Arsenic	23-25	neutrophil cytosolic factor 4	Homo sapiens	201-204
28771557-8	2017	Low-moderate arsenic exposure was positively associated with baseline fibrinogen in participants with diabetes and unexpectedly inversely associated with PAI-1.	Arsenic	13-20	serpin family E member 1	Homo sapiens	154-159
28551548-15	2017	Compared with the control group, the AS and ATV groups had higher serum levels of TC, TG, LDL, MMP-3, MMP-9 and hs-CRP, and higher AI.	Arsenic	37-39	stromelysin-1	Oryctolagus cuniculus	95-100
28551548-15	2017	Compared with the control group, the AS and ATV groups had higher serum levels of TC, TG, LDL, MMP-3, MMP-9 and hs-CRP, and higher AI.	Arsenic	37-39	matrix metalloproteinase-9	Oryctolagus cuniculus	102-107
28551548-18	2017	The AS and ATV groups showed a positive correlation of EI in the plaque and its ratio in the plaque and arterial lumen with F8 protein expression, MMP-3 and MMP-9.	Arsenic	4-6	stromelysin-1	Oryctolagus cuniculus	147-152
28551548-18	2017	The AS and ATV groups showed a positive correlation of EI in the plaque and its ratio in the plaque and arterial lumen with F8 protein expression, MMP-3 and MMP-9.	Arsenic	4-6	matrix metalloproteinase-9	Oryctolagus cuniculus	157-162
28411545-3	2017	With the increase of P content in water from 0.02 mg L-1 to 0.20 and 2.4 mg L-1, consistent release of As from sediments was observed.	Arsenic	103-105	immunoglobulin kappa variable 1-16	Homo sapiens	76-79
28548590-6	2017	Compared to the lowest exposure tertiles, higher levels of As, Cd, Pb, Mn, and Hg were each associated with increased placental NR3C1 methylation (all P&lt;0.02).	Arsenic	59-61	nuclear receptor subfamily 3 group C member 1	Homo sapiens	128-133
28554006-11	2017	CONCLUSIONS: Urine arsenic was positively associated with CIMT and increased plaque score later in life although the association was small.	Arsenic	19-26	CIMT	Homo sapiens	58-62
28685331-7	2017	The highest are the HQingestion indexes of As and Cr, both for the 3-year-old permanent spa residents (5.74E-02 and 1.71E-02, respectively) and the spa visitors of the same age (7.47E-03 and 2.22E-03, respectively) and the 6-year-old residents (4.31E-02 and 1.28E-02, respectively) and visitors (5.60E-03 and 1.66E-03, respectively).	Arsenic	43-45	surfactant protein A2	Homo sapiens	88-91
28537708-0	2017	Nonsynonymous Polymorphisms in the Human AS3MT Arsenic Methylation Gene: Implications for Arsenic Toxicity.	Arsenic	47-54	arsenite methyltransferase	Homo sapiens	41-46
28685331-14	2017	However, an adverse impact of some sand-contained pollutants that are attributed to the motor traffic (Cu, Zn, Ni, Cr, Co and Pb) and low emissions (mainly As and Cd) has been established in the spa resorts in question.	Arsenic	156-158	surfactant protein A2	Homo sapiens	195-198
28699118-5	2017	It has been estimated that due to the inhalation exposure to carcinogenic elements, i.e., As, Cd, Co, Cr, Ni and Pb, contained in the most mobile fractions (F1 + F2) of PM1, approximately four adults and one child out of one million people living in the vicinity of the coking plants may develop cancer.	Arsenic	90-92	transmembrane protein 11	Homo sapiens	169-172
28720099-8	2017	Some deletions had stronger effect in a specific gender (ZNF658 in males, SGCZ in females) and some had stronger effect in higher arsenic exposure (lincRNA CTD-3179P9.1) suggesting a possible gene-environment interaction.	Arsenic	130-137	zinc finger protein 658	Homo sapiens	57-63
28720099-8	2017	Some deletions had stronger effect in a specific gender (ZNF658 in males, SGCZ in females) and some had stronger effect in higher arsenic exposure (lincRNA CTD-3179P9.1) suggesting a possible gene-environment interaction.	Arsenic	130-137	sarcoglycan zeta	Homo sapiens	74-78
28636814-0	2017	Arsenic Compromises Both p97 and Proteasome Functions.	Arsenic	0-7	melanotransferrin	Homo sapiens	25-28
28636814-8	2017	This loss of both p97 and proteasome functions can explain the catastrophic protein quality control issues observed in acute, high level arsenic exposures.	Arsenic	137-144	melanotransferrin	Homo sapiens	18-21
28537708-0	2017	Nonsynonymous Polymorphisms in the Human AS3MT Arsenic Methylation Gene: Implications for Arsenic Toxicity.	Arsenic	90-97	arsenite methyltransferase	Homo sapiens	41-46
28537708-1	2017	Arsenic methylation, the primary biotransformation in the human body, is catalyzed by the enzyme As(III) S-adenosylmethionine (SAM) methyltransferases (hAS3MT).	Arsenic	0-7	arsenite methyltransferase	Homo sapiens	152-158
28537708-3	2017	However, with long-term low-level exposure, hAS3MT produces intracellular methylarsenite (MAs(III)) and dimethylarsenite (DMAs(III)), which are considerably more toxic than inorganic As(III) and may contribute to arsenic-related diseases.	Arsenic	213-220	arsenite methyltransferase	Homo sapiens	44-50
28537708-10	2017	We propose that amino acid substitutions in hAS3MT with decreased catalytic activity lead to detrimental responses to environmental arsenic and may increase the risk of arsenic-related diseases.	Arsenic	132-139	PDS5 cohesin associated factor B	Homo sapiens	44-48
28537708-10	2017	We propose that amino acid substitutions in hAS3MT with decreased catalytic activity lead to detrimental responses to environmental arsenic and may increase the risk of arsenic-related diseases.	Arsenic	169-176	PDS5 cohesin associated factor B	Homo sapiens	44-48
28544160-5	2017	This assembly-line synthesis provides a flexible approach for the synthesis of agrochemicals and pharmaceuticals, as demonstrated by a four-step, telescoped synthesis of measles therapeutic, AS-136A, in a total residence time of 31.7 min (1.76 g h-1 ).	Arsenic	191-193	H1.5 linker histone, cluster member	Homo sapiens	246-249
28728140-1	2017	BACKGROUND: Arsenic is metabolized through a series of oxidative methylation reactions by arsenic (3) methyltransferase (As3MT) to yield methylated intermediates.	Arsenic	12-19	arsenite methyltransferase	Mus musculus	121-126
29051854-10	2017	As a result of enhanced Nrf 2 activity, neuronal differentiation is accelerated, and the cellular antioxidation responses are also enforced, even under arsenic-induced neurotoxicity.	Arsenic	152-159	NFE2 like bZIP transcription factor 2	Homo sapiens	24-29
28728140-3	2017	OBJECTIVES: Our objective was to define whether methylated arsenic intermediates were proatherogenic and whether arsenic biotransformation by As3MT was required for arsenic-enhanced atherosclerosis.	Arsenic	113-120	arsenite methyltransferase	Mus musculus	142-147
28728140-3	2017	OBJECTIVES: Our objective was to define whether methylated arsenic intermediates were proatherogenic and whether arsenic biotransformation by As3MT was required for arsenic-enhanced atherosclerosis.	Arsenic	113-120	arsenite methyltransferase	Mus musculus	142-147
28728140-7	2017	Finally, bone marrow transplantation studies were performed to define the contribution of As3MT-mediated methylation in different cell types to the development of atherosclerosis after inorganic arsenic exposure.	Arsenic	195-202	arsenite methyltransferase	Mus musculus	90-95
28728140-10	2017	CONCLUSION: Taken together, our findings indicate that As3MT acts to promote cardiovascular toxicity of arsenic and suggest that human AS3MT SNPs that correlate with enzyme function could predict those most at risk to develop atherosclerosis among the millions that are exposed to arsenic.	Arsenic	104-111	arsenite methyltransferase	Homo sapiens	55-60
27685703-4	2017	RESULTS: Hypermethylation of ERCC1 and ERCC2 and suppressed gene expression were found in PBLs and skin lesions of arsenicosis patients and was correlated with the level of arsenic exposure.	Arsenic	115-122	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	29-34
27685703-4	2017	RESULTS: Hypermethylation of ERCC1 and ERCC2 and suppressed gene expression were found in PBLs and skin lesions of arsenicosis patients and was correlated with the level of arsenic exposure.	Arsenic	115-122	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	39-44
27685703-7	2017	CONCLUSION: Hypermethylation of ERCC1 and ERCC2 and concomitant suppression of gene expression might be served as the epigenetic marks associated with arsenic exposure and adverse health effects.	Arsenic	151-158	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	32-37
27685703-7	2017	CONCLUSION: Hypermethylation of ERCC1 and ERCC2 and concomitant suppression of gene expression might be served as the epigenetic marks associated with arsenic exposure and adverse health effects.	Arsenic	151-158	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	42-47
28410520-6	2017	Among mothers, the highest tertile of maternal urinary As during pregnancy was related to a 141.8ng/ml (95% CI 26.1, 257.5; p=0.02) increase maternal plasma VCAM1 levels.	Arsenic	55-57	vascular cell adhesion molecule 1	Homo sapiens	157-162
28374070-7	2017	CONCLUSIONS: A novel interaction between miR-17-5p and VLDLR is revealed and suggests that miR-17-5p may be a potential therapeutic target for AS.	Arsenic	143-145	microRNA 17	Homo sapiens	41-50
28374070-7	2017	CONCLUSIONS: A novel interaction between miR-17-5p and VLDLR is revealed and suggests that miR-17-5p may be a potential therapeutic target for AS.	Arsenic	143-145	very low density lipoprotein receptor	Mus musculus	55-60
28374070-7	2017	CONCLUSIONS: A novel interaction between miR-17-5p and VLDLR is revealed and suggests that miR-17-5p may be a potential therapeutic target for AS.	Arsenic	143-145	microRNA 17	Homo sapiens	91-100
28416223-14	2017	Content of As, Pb, Ba, Cr in solid samples follows the order of ESP + FF ash &gt; bottom ash &gt; gypsum.	Arsenic	11-13	Epidermal stripes and patches	Drosophila melanogaster	64-67
28640505-0	2017	Associations between arsenic (+3 oxidation state) methyltransferase (AS3MT) and N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) polymorphisms, arsenic metabolism, and cancer risk in a chilean population.	Arsenic	21-28	arsenite methyltransferase	Homo sapiens	69-74
28640505-0	2017	Associations between arsenic (+3 oxidation state) methyltransferase (AS3MT) and N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) polymorphisms, arsenic metabolism, and cancer risk in a chilean population.	Arsenic	21-28	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	126-132
28640505-2	2017	Arsenic (+3) methyltransferase (AS3MT) is the primary enzyme involved in arsenic metabolism, and we previously demonstrated in vitro that N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) also methylates the toxic inorganic arsenic (iAs) metabolite, monomethylarsonous acid (MMA), to the less toxic dimethylarsonic acid (DMA).	Arsenic	73-80	arsenite methyltransferase	Homo sapiens	32-37
28640505-2	2017	Arsenic (+3) methyltransferase (AS3MT) is the primary enzyme involved in arsenic metabolism, and we previously demonstrated in vitro that N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) also methylates the toxic inorganic arsenic (iAs) metabolite, monomethylarsonous acid (MMA), to the less toxic dimethylarsonic acid (DMA).	Arsenic	73-80	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	138-182
28640505-2	2017	Arsenic (+3) methyltransferase (AS3MT) is the primary enzyme involved in arsenic metabolism, and we previously demonstrated in vitro that N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) also methylates the toxic inorganic arsenic (iAs) metabolite, monomethylarsonous acid (MMA), to the less toxic dimethylarsonic acid (DMA).	Arsenic	73-80	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	184-190
28640505-2	2017	Arsenic (+3) methyltransferase (AS3MT) is the primary enzyme involved in arsenic metabolism, and we previously demonstrated in vitro that N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) also methylates the toxic inorganic arsenic (iAs) metabolite, monomethylarsonous acid (MMA), to the less toxic dimethylarsonic acid (DMA).	Arsenic	228-235	arsenite methyltransferase	Homo sapiens	32-37
28640505-2	2017	Arsenic (+3) methyltransferase (AS3MT) is the primary enzyme involved in arsenic metabolism, and we previously demonstrated in vitro that N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) also methylates the toxic inorganic arsenic (iAs) metabolite, monomethylarsonous acid (MMA), to the less toxic dimethylarsonic acid (DMA).	Arsenic	228-235	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	138-182
28640505-2	2017	Arsenic (+3) methyltransferase (AS3MT) is the primary enzyme involved in arsenic metabolism, and we previously demonstrated in vitro that N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) also methylates the toxic inorganic arsenic (iAs) metabolite, monomethylarsonous acid (MMA), to the less toxic dimethylarsonic acid (DMA).	Arsenic	228-235	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	184-190
28640505-3	2017	Here, we evaluated whether AS3MT and N6AMT1 gene polymorphisms alter arsenic methylation and impact iAs-related cancer risks.	Arsenic	69-76	arsenite methyltransferase	Homo sapiens	27-32
28414027-6	2017	The results showed that H3K9me2/3 demethylase (JMJD2A) inhibitor, quercetin (Que) significantly attenuated the decrease of H3K9me2/3 and increase of 3beta-HSD expression induced by arsenic.	Arsenic	181-188	lysine (K)-specific demethylase 4A	Mus musculus	47-53
28640505-6	2017	We found several AS3MT polymorphisms associated with both urinary arsenic metabolite profiles and cancer risk.	Arsenic	66-73	arsenite methyltransferase	Homo sapiens	17-22
28640505-10	2017	These results are the first to demonstrate a direct association between AS3MT polymorphisms and arsenic-related internal cancer risk.	Arsenic	96-103	arsenite methyltransferase	Homo sapiens	72-77
28479390-9	2017	Stronger and independent associations were observed with B2 and B6, vitamins previously understudied in relation to arsenic.	Arsenic	116-123	immunoglobulin kappa variable 5-2	Homo sapiens	57-66
28349520-7	2017	High levels of arsenic in the tap water and topsoil supported the occurrence of an epidemic of chronic arsenic poisoning.	Arsenic	15-22	nuclear RNA export factor 1	Homo sapiens	30-33
28432518-4	2017	The aim of the present study is to investigate the correlation of GSTM1 polymorphism in MS patients and the possible association with blood concentration of arsenic (As) and cadmium (Cd) as major heavy metal pollutants.	Arsenic	157-164	glutathione S-transferase mu 1	Homo sapiens	66-71
28432518-4	2017	The aim of the present study is to investigate the correlation of GSTM1 polymorphism in MS patients and the possible association with blood concentration of arsenic (As) and cadmium (Cd) as major heavy metal pollutants.	Arsenic	166-168	glutathione S-transferase mu 1	Homo sapiens	66-71
28414027-7	2017	To further elucidate the mechanism for the activation of 3beta-HSD, we determined the histone H3K9 methylation levels in Hsd3b gene promoter, which also showed significant decrease of H3K9me2/3 in the investigated region after arsenic exposure.	Arsenic	227-234	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase cluster	Mus musculus	121-126
28436716-4	2017	The present study demonstrates significant correlation between severities of skin manifestations with their whole genome DNA methylation status as well as with a particular polymorphism (Ala 140 Asp) status in arsenic metabolizing enzyme Glutathione S-transferase Omega-1 (GSTO1) in arsenic-exposed population of the district of Nadia, West Bengal, India.	Arsenic	210-217	glutathione S-transferase omega 1	Homo sapiens	238-271
28436716-4	2017	The present study demonstrates significant correlation between severities of skin manifestations with their whole genome DNA methylation status as well as with a particular polymorphism (Ala 140 Asp) status in arsenic metabolizing enzyme Glutathione S-transferase Omega-1 (GSTO1) in arsenic-exposed population of the district of Nadia, West Bengal, India.	Arsenic	210-217	glutathione S-transferase omega 1	Homo sapiens	273-278
29029432-3	2017	Oxidative stress induced by arsenic leads to the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) pathway.	Arsenic	28-35	NFE2 like bZIP transcription factor 2	Homo sapiens	63-106
28670501-5	2017	Arsenic treatment diminished the physical association of PTEN with BubR1 and Bub3 but not with Cdc20 and Mad2.	Arsenic	0-7	phosphatase and tensin homolog	Homo sapiens	57-61
28670501-5	2017	Arsenic treatment diminished the physical association of PTEN with BubR1 and Bub3 but not with Cdc20 and Mad2.	Arsenic	0-7	BUB1 mitotic checkpoint serine/threonine kinase B	Homo sapiens	67-72
28670501-5	2017	Arsenic treatment diminished the physical association of PTEN with BubR1 and Bub3 but not with Cdc20 and Mad2.	Arsenic	0-7	BUB3 mitotic checkpoint protein	Homo sapiens	77-81
28640255-1	2017	Aquaporin-9 (AQP9) expression is associated with arsenic sensitivity in leukemia cells.	Arsenic	49-56	aquaporin 9	Homo sapiens	0-11
28640255-1	2017	Aquaporin-9 (AQP9) expression is associated with arsenic sensitivity in leukemia cells.	Arsenic	49-56	aquaporin 9	Homo sapiens	13-17
29029432-3	2017	Oxidative stress induced by arsenic leads to the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) pathway.	Arsenic	28-35	NFE2 like bZIP transcription factor 2	Homo sapiens	108-112
29029432-8	2017	Arsenic decreases the antioxidant enzymes SOD, GPX, and CAT activity and the decrease was inhibited by treatment of EGCG.	Arsenic	0-7	catalase	Homo sapiens	56-59
28471032-1	2017	The activation of yellow arsenic is possible with the silylene [PhC(NtBu)2 SiN(SiMe3 )2 ] (1) and the disilene [(Me3 Si)2 N(eta1 -Me5 C5 )Si=Si(eta1 -Me5 C5 )N(SiMe3 )2 ] (3).	Arsenic	25-32	secreted phosphoprotein 1	Homo sapiens	124-128
28472587-0	2017	Sea Level Rise Induced Arsenic Release from Historically Contaminated Coastal Soils.	Arsenic	23-30	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	0-3
28472587-3	2017	The mechanism by and the extent to which arsenic may be released in contaminated coastal soils due to sea level rise are unknown.	Arsenic	41-48	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	102-105
28472587-4	2017	Here we show a series of data from a coastal arsenic-contaminated soil exposed to sea and river waters in biogeochemical microcosm reactors across field-validated redox conditions.	Arsenic	45-52	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	82-85
28472587-5	2017	We find that reducing conditions lead to arsenic release from historically contaminated coastal soils through reductive dissolution of arsenic-bearing mineral oxides in both sea and river water inundations, with less arsenic release from seawater scenarios than river water due to inhibition of oxide dissolution.	Arsenic	41-48	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	174-177
28472587-5	2017	We find that reducing conditions lead to arsenic release from historically contaminated coastal soils through reductive dissolution of arsenic-bearing mineral oxides in both sea and river water inundations, with less arsenic release from seawater scenarios than river water due to inhibition of oxide dissolution.	Arsenic	135-142	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	174-177
28472587-5	2017	We find that reducing conditions lead to arsenic release from historically contaminated coastal soils through reductive dissolution of arsenic-bearing mineral oxides in both sea and river water inundations, with less arsenic release from seawater scenarios than river water due to inhibition of oxide dissolution.	Arsenic	135-142	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	174-177
28472587-7	2017	Our results demonstrate the threat of sea level rise stands to impact arsenic release from contaminated coastal soils by changing redox conditions.	Arsenic	70-77	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	38-41
28615018-0	2017	The aquaglyceroporin AQP9 contributes to the sex-specific effects of in utero arsenic exposure on placental gene expression.	Arsenic	78-85	aquaporin 9	Homo sapiens	21-25
28615018-8	2017	RESULTS: We found that maternal arsenic exposure was strongly associated with expression of the AQP9 gene, encoding an aquaglyceroporin transporter, in female but not male fetal placenta.	Arsenic	32-39	aquaporin 9	Homo sapiens	96-100
28615018-9	2017	Moreover, AQP9 expression associated with that of a subset of female-specific arsenic-responsive genes.	Arsenic	78-85	aquaporin 9	Homo sapiens	10-14
28615018-10	2017	CONCLUSIONS: Our results suggest that AQP9 is upregulated in response to arsenic exposure in female, but not male, fetal placenta.	Arsenic	73-80	aquaporin 9	Homo sapiens	38-42
28615018-11	2017	Based on these results and prior studies, increased AQP9 expression may lead to increased arsenic transport in the female fetal placenta, which in turn may alter the expression patterns of key developmental genes that we have previously shown to be associated with arsenic exposure.	Arsenic	90-97	aquaporin 9	Homo sapiens	52-56
28615018-11	2017	Based on these results and prior studies, increased AQP9 expression may lead to increased arsenic transport in the female fetal placenta, which in turn may alter the expression patterns of key developmental genes that we have previously shown to be associated with arsenic exposure.	Arsenic	265-272	aquaporin 9	Homo sapiens	52-56
28615018-12	2017	Thus, this study suggests that AQP9 may play a role in the sex-specific effects of in utero arsenic exposure.	Arsenic	92-99	aquaporin 9	Homo sapiens	31-35
28499612-5	2017	Furthermore, down-regulation of the cell-surface expression of the co-stimulatory molecule CD40 after 24h post treatment with arsenic, confirmed arsenic interferers in the phagocytosis process.	Arsenic	126-133	CD40 molecule	Homo sapiens	91-95
28499612-5	2017	Furthermore, down-regulation of the cell-surface expression of the co-stimulatory molecule CD40 after 24h post treatment with arsenic, confirmed arsenic interferers in the phagocytosis process.	Arsenic	145-152	CD40 molecule	Homo sapiens	91-95
28499612-6	2017	Pro inflammatory cytokines, IL1beta and TNFalpha were more expressed in arsenic-treated MDDCs while IL6 transiently was down regulated.	Arsenic	72-79	interleukin 1 beta	Homo sapiens	28-35
28499612-6	2017	Pro inflammatory cytokines, IL1beta and TNFalpha were more expressed in arsenic-treated MDDCs while IL6 transiently was down regulated.	Arsenic	72-79	tumor necrosis factor	Homo sapiens	40-48
28499612-6	2017	Pro inflammatory cytokines, IL1beta and TNFalpha were more expressed in arsenic-treated MDDCs while IL6 transiently was down regulated.	Arsenic	72-79	interleukin 6	Homo sapiens	100-103
28471032-1	2017	The activation of yellow arsenic is possible with the silylene [PhC(NtBu)2 SiN(SiMe3 )2 ] (1) and the disilene [(Me3 Si)2 N(eta1 -Me5 C5 )Si=Si(eta1 -Me5 C5 )N(SiMe3 )2 ] (3).	Arsenic	25-32	secreted phosphoprotein 1	Homo sapiens	144-148
28259079-4	2017	A remarkably high removal efficiency and the maximum adsorption capacity for As(III) were achieved, 96.7% and 94.1 mg/g, respectively, at 298 K. The desorption efficiency of As(III) from the arsenic-saturated Zn2Al-Met-LDHs (&lt;8.7%), far less than that of As(V), promises a specific and reliable uptake of As(III) in sorts of solutions.	Arsenic	191-198	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	258-263
28472268-8	2017	Finally, we find that exposure to low-dose nickel reduces the activity of the MLH1 promoter, but only arsenic leads to long-term MLH1 promoter silencing.	Arsenic	102-109	mutL homolog 1	Homo sapiens	129-133
28259079-4	2017	A remarkably high removal efficiency and the maximum adsorption capacity for As(III) were achieved, 96.7% and 94.1 mg/g, respectively, at 298 K. The desorption efficiency of As(III) from the arsenic-saturated Zn2Al-Met-LDHs (&lt;8.7%), far less than that of As(V), promises a specific and reliable uptake of As(III) in sorts of solutions.	Arsenic	77-79	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	258-263
27149867-0	2017	Arsenic and other trace elements in groundwater and human urine in Ha Nam province, the Northern Vietnam: contamination characteristics and risk assessment.	Arsenic	0-7	SH3 and cysteine rich domain 3	Homo sapiens	70-73
28489362-5	2017	Conversely, the introduction of a methyl group at the methylene hinge connecting the 6-amino-9H-purin-9-yl pendant to the quinazolin-4(3H)-one nucleus of both aS and aR isomers of 1 had a critical effect on the inhibitory activity, indicating that modulation of the conformational space accessible for the two bonds departing from the central methylene considerably affects the binding of compound 1 analogues to PI3Kdelta enzyme.	Arsenic	159-161	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	413-422
28280079-6	2017	These results demonstrate that targeting ALDH1A1- leukemic cells with toxic ALDH1A1 substrates such as arsenic and cyclophosphamide may be a novel targeted therapeutic strategy for this subset of acute myeloid leukemias.	Arsenic	103-110	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	41-48
28280079-6	2017	These results demonstrate that targeting ALDH1A1- leukemic cells with toxic ALDH1A1 substrates such as arsenic and cyclophosphamide may be a novel targeted therapeutic strategy for this subset of acute myeloid leukemias.	Arsenic	103-110	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	76-83
28571865-8	2017	Solid phase extraction showed that arsenate (As(V)) was the main species mobilized by surfactants, accounting for 65.05%-77.68% of the total mobilized arsenic.	Arsenic	151-158	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	45-50
28433805-0	2017	Chronic early childhood exposure to arsenic is associated with a TNF-mediated proteomic signaling response.	Arsenic	36-43	tumor necrosis factor	Homo sapiens	65-68
28238437-4	2017	With the aggravation of PM2.5 pollution, the mass fraction of PM1/PM2.5 increased for (NH4)2SO4 (AS), NH4NO3 (AN) and EC but decreased for organic matter (OM) in summer, and the opposite was found in winter.	Arsenic	97-99	transmembrane protein 11	Homo sapiens	62-65
28475329-2	2017	Examination of the affinity at the human vasopressin receptors revealed that the axial chirality (aS) plays a more important role than the central chirality at C5 in receptor recognition, and the most preferable form was shown to be (E,aS,5S).	Arsenic	98-100	arginine vasopressin	Homo sapiens	41-52
28245978-0	2017	Engineering an FMN-based iLOV protein for the detection of arsenic ions.	Arsenic	59-66	formin 1	Homo sapiens	15-18
29051444-3	2017	The results from both the ICP-MS and ESI-QqTOF-MS/MS investigations indicate that the unexpected arsenic species termed peak 1 was thio-DMA.	Arsenic	97-104	pseudopodium enriched atypical kinase 1	Homo sapiens	120-126
29051444-4	2017	While the unexpected arsenic species termed peak 2 has yet to be identified, this investigation shows that it was not AC, TMAO, DMAA, DMAE, thio-DMA, thio-DMAA or thio-DMAE.	Arsenic	21-28	PEAK1 related, kinase-activating pseudokinase 1	Homo sapiens	44-50
29965087-2	2017	The results showed that the concentration of arsenic in drinking water of major cities in China was very low (0.53 mug L-1), far below the national limit (10 mug L-1) and the total lifetime cancer incidence was 1.76x10-5.	Arsenic	45-52	immunoglobulin kappa variable 1-16	Homo sapiens	119-122
28340714-5	2017	Two compromised HG reaction conditions for simultaneous measurements of As+Bi+Sb (CC1) or As+Sb+Se (CC2) were established.	Arsenic	72-74	C-C motif chemokine ligand 14	Homo sapiens	82-85
29965087-2	2017	The results showed that the concentration of arsenic in drinking water of major cities in China was very low (0.53 mug L-1), far below the national limit (10 mug L-1) and the total lifetime cancer incidence was 1.76x10-5.	Arsenic	45-52	immunoglobulin kappa variable 1-16	Homo sapiens	162-165
28206677-3	2017	Therefore, to solve this conundrum we compared the frequencies of four protective genetic variants of the AS3MT gene associated with efficient arsenic metabolization, between the living populations of Camarones and two other populations historically exposed to lower levels of arsenic.	Arsenic	143-150	arsenite methyltransferase	Homo sapiens	106-111
28206677-3	2017	Therefore, to solve this conundrum we compared the frequencies of four protective genetic variants of the AS3MT gene associated with efficient arsenic metabolization, between the living populations of Camarones and two other populations historically exposed to lower levels of arsenic.	Arsenic	277-284	arsenite methyltransferase	Homo sapiens	106-111
27838757-0	2017	Transcriptomics and methylomics of CD4-positive T cells in arsenic-exposed women.	Arsenic	59-66	CD4 molecule	Homo sapiens	35-38
27838757-5	2017	Key genes regulating the immune system, such as tumor necrosis factor alpha and interferon gamma, as well as genes related to the NF-kappa-beta complex, were significantly downregulated in the high-arsenic group.	Arsenic	198-205	tumor necrosis factor	Homo sapiens	48-75
27838757-5	2017	Key genes regulating the immune system, such as tumor necrosis factor alpha and interferon gamma, as well as genes related to the NF-kappa-beta complex, were significantly downregulated in the high-arsenic group.	Arsenic	198-205	interferon gamma	Homo sapiens	80-96
27838757-7	2017	Differentially methylated regions that were hyper-methylated in the high-arsenic group showed enrichment for immune-related gene ontologies that constitute the basic functions of CD4-positive T cells, such as isotype switching and lymphocyte activation and differentiation.	Arsenic	73-80	CD4 molecule	Homo sapiens	179-182
27838757-8	2017	In conclusion, chronic arsenic exposure from drinking water was related to changes in the transcriptome and methylome of CD4-positive T cells, both genome wide and in specific genes, supporting the hypothesis that arsenic causes immunotoxicity by interfering with gene expression and regulation.	Arsenic	23-30	CD4 molecule	Homo sapiens	121-124
27838757-8	2017	In conclusion, chronic arsenic exposure from drinking water was related to changes in the transcriptome and methylome of CD4-positive T cells, both genome wide and in specific genes, supporting the hypothesis that arsenic causes immunotoxicity by interfering with gene expression and regulation.	Arsenic	214-221	CD4 molecule	Homo sapiens	121-124
28470093-2	2017	This review summarizes four major mechanisms by which arsenic induces diabetes, namely inhibition of insulin-dependent glucose uptake, pancreatic beta-cell damage, pancreatic beta-cell dysfunction and stimulation of liver gluconeogenesis that are supported by both in vivo and in vitro studies.	Arsenic	54-61	insulin	Homo sapiens	101-108
28229933-7	2017	Progerin-expressing human primary HGPS fibroblasts showed lower basal levels of HMOX1 and NQO1 expression; however, in response to arsenic stress both normal and HGPS primary fibroblasts showed Nrf2 nuclear accumulation along with upregulation and phosphorylation of p62/SQSTM1 at Ser351, downregulation of Keap1, and comparable expression of an array of downstream Nrf2-regulated antioxidant genes.	Arsenic	131-138	NFE2 like bZIP transcription factor 2	Homo sapiens	194-198
28229933-7	2017	Progerin-expressing human primary HGPS fibroblasts showed lower basal levels of HMOX1 and NQO1 expression; however, in response to arsenic stress both normal and HGPS primary fibroblasts showed Nrf2 nuclear accumulation along with upregulation and phosphorylation of p62/SQSTM1 at Ser351, downregulation of Keap1, and comparable expression of an array of downstream Nrf2-regulated antioxidant genes.	Arsenic	131-138	sequestosome 1	Homo sapiens	267-270
28229933-7	2017	Progerin-expressing human primary HGPS fibroblasts showed lower basal levels of HMOX1 and NQO1 expression; however, in response to arsenic stress both normal and HGPS primary fibroblasts showed Nrf2 nuclear accumulation along with upregulation and phosphorylation of p62/SQSTM1 at Ser351, downregulation of Keap1, and comparable expression of an array of downstream Nrf2-regulated antioxidant genes.	Arsenic	131-138	sequestosome 1	Homo sapiens	271-277
28229933-7	2017	Progerin-expressing human primary HGPS fibroblasts showed lower basal levels of HMOX1 and NQO1 expression; however, in response to arsenic stress both normal and HGPS primary fibroblasts showed Nrf2 nuclear accumulation along with upregulation and phosphorylation of p62/SQSTM1 at Ser351, downregulation of Keap1, and comparable expression of an array of downstream Nrf2-regulated antioxidant genes.	Arsenic	131-138	kelch like ECH associated protein 1	Homo sapiens	307-312
28229933-7	2017	Progerin-expressing human primary HGPS fibroblasts showed lower basal levels of HMOX1 and NQO1 expression; however, in response to arsenic stress both normal and HGPS primary fibroblasts showed Nrf2 nuclear accumulation along with upregulation and phosphorylation of p62/SQSTM1 at Ser351, downregulation of Keap1, and comparable expression of an array of downstream Nrf2-regulated antioxidant genes.	Arsenic	131-138	NFE2 like bZIP transcription factor 2	Homo sapiens	366-370
28229933-9	2017	These results suggest that the nuclear lamins and progerin have marginal roles in the activation of the antioxidant Nrf2 response to arsenic and cadmium.	Arsenic	133-140	NFE2 like bZIP transcription factor 2	Homo sapiens	116-120
28199894-9	2017	CONCLUSIONS: Adults who had suffered arsenic poisoning during infancy showed decreased height and elevated ALP that suggests abnormalities in bone metabolism possibly induced by arsenic incorporated in the bone matrix.	Arsenic	37-44	alkaline phosphatase, placental	Homo sapiens	107-110
28216136-9	2017	Arsenic in shallow groundwater near a tailings pond exceeded 50 mug L-1 predominantly as As(III) warranting further investigation.	Arsenic	0-7	immunoglobulin kappa variable 1-16	Homo sapiens	68-71
28318385-0	2017	Arsenic-induced sumoylation of Mus81 is involved in regulating genomic stability.	Arsenic	0-7	MUS81 structure-specific endonuclease subunit	Homo sapiens	31-36
28206643-0	2017	In Vivo Exposure to Inorganic Arsenic Alters Differentiation-Specific Gene Expression of Adipose-Derived Mesenchymal Stem/Stromal Cells in C57BL/6J Mouse Model.	Arsenic	30-37	WD and tetratricopeptide repeats 1	Mus musculus	89-96
28426741-0	2017	AS3MT-mediated tolerance to arsenic evolved by multiple independent horizontal gene transfers from bacteria to eukaryotes.	Arsenic	28-35	arsenite methyltransferase	Homo sapiens	0-5
28426741-4	2017	In humans, arsenite methyltransferase (AS3MT) appears to be the main metabolic enzyme that methylates arsenic.	Arsenic	102-109	arsenite methyltransferase	Homo sapiens	39-44
28426741-7	2017	These findings are supported by the observation that genetic variation in AS3MT correlates with the capacity to methylate arsenic.	Arsenic	122-129	arsenite methyltransferase	Homo sapiens	74-79
28420331-0	2017	Arsenic treatment increase Aurora-A overexpression through E2F1 activation in bladder cells.	Arsenic	0-7	aurora kinase A S homeolog	Xenopus laevis	27-35
28420331-0	2017	Arsenic treatment increase Aurora-A overexpression through E2F1 activation in bladder cells.	Arsenic	0-7	E2F transcription factor 1 L homeolog	Xenopus laevis	59-63
28420331-6	2017	We have reported that low concentration ( 1 muM) of arsenic treatment increases Aurora-A expression in immortalized bladder urothelial E7 cells.	Arsenic	52-59	aurora kinase A	Mus musculus	80-88
28420331-7	2017	However, how arsenic induces carcinogenesis through Aurora-A activation remaining unclear.	Arsenic	13-20	aurora kinase A	Mus musculus	52-60
28420331-12	2017	Mouse model was utilized to confirm the relationship between arsenic and Aurora-A.	Arsenic	61-68	aurora kinase A	Mus musculus	73-81
28318385-5	2017	Sumoylated proteins from arsenic-treated cells constitutively expressing His6-SUMO2 were pulled down by Ni-IDA resin under denaturing conditions.	Arsenic	25-32	small ubiquitin like modifier 2	Homo sapiens	78-83
28420331-14	2017	We also detected increased Aurora-A expression at mRNA and protein levels in immortalized bladder urothelial E7 cells exposed to low doses of arsenic.	Arsenic	142-149	aurora kinase A	Mus musculus	27-35
28420331-15	2017	Arsenic-treated cells displayed increased multiple centrosome which is resulted from overexpressed Aurora-A.	Arsenic	0-7	aurora kinase A	Mus musculus	99-107
28420331-17	2017	We further disclosed that Aurora-A expression and cell proliferation were increased in bladder and uterus tissues of the BALB/c mice after long-term arsenic (1 mg/L) exposure for 2 months.	Arsenic	149-156	aurora kinase A	Mus musculus	26-34
28235556-2	2017	The present study was designed to explore whether polymorphisms and haplotypes of arsenic methyltransferase (AS3MT), glutathione-S-transferase omegas (GSTOs), and purine nucleoside phosphorylase (PNP) affect arsenic methylation capacity and developmental delay.	Arsenic	82-89	arsenite methyltransferase	Homo sapiens	109-114
28420331-18	2017	CONCLUSION: We reveal that low dose of arsenic induced cell proliferation is through Aurora-A overexpression, which is transcriptionally regulated by E2F1 both in vitro and in vivo.	Arsenic	39-46	aurora kinase A	Mus musculus	85-93
28420331-18	2017	CONCLUSION: We reveal that low dose of arsenic induced cell proliferation is through Aurora-A overexpression, which is transcriptionally regulated by E2F1 both in vitro and in vivo.	Arsenic	39-46	E2F transcription factor 1	Mus musculus	150-154
28420331-19	2017	Our findings disclose a new possibility that arsenic at low concentration activates Aurora-A to induce carcinogenesis.	Arsenic	45-52	aurora kinase A	Mus musculus	84-92
28185734-3	2017	In this study, we examined the effects of different biogeochemical processes (e.g. NO3- and SO42- reduction) on arsenic, by investigating the chemical characteristics and bacterial community structure of groundwater in the Datong Basin, northern China.	Arsenic	112-119	NBL1, DAN family BMP antagonist	Homo sapiens	83-86
28185734-11	2017	Moreover, NO3- reduction process can significantly restrain the release of arsenic, but the process of SO42- reduction is insignificant for arsenic concentration decline in natural groundwater.	Arsenic	75-82	NBL1, DAN family BMP antagonist	Homo sapiens	10-13
28235556-13	2017	Our data provide evidence that AS3MT genes are related to developmental delay and may partially influence arsenic methylation capacity.	Arsenic	106-113	arsenite methyltransferase	Homo sapiens	31-36
28442938-0	2017	Environmental arsenic exposure and risk of diabetes type 2 in Ron Phibun subdistrict, Nakhon Si Thammarat Province, Thailand: unmatched and matched case-control studies.	Arsenic	14-21	macrophage stimulating 1 receptor	Homo sapiens	62-65
28399171-0	2017	Association between arsenic exposure and soluble thrombomodulin: A cross sectional study in Bangladesh.	Arsenic	20-27	thrombomodulin	Homo sapiens	49-63
28442938-2	2017	In Ron Phibun subdistrict, Nakhon Si Thammarat Province, Thailand, a low level of arsenic exposure among population was observed and increased diabetes mellitus (DM) rate was identified.	Arsenic	82-89	macrophage stimulating 1 receptor	Homo sapiens	3-6
28108741-3	2017	In fact, the enzymatic conversion of inorganic arsenic by Arsenic (+3 oxidation state) methyltransferase (AS3MT) to mono- and dimethylated arsenic species has long been considered as a major route for detoxification.	Arsenic	58-65	arsenite methyltransferase	Homo sapiens	106-111
28108741-3	2017	In fact, the enzymatic conversion of inorganic arsenic by Arsenic (+3 oxidation state) methyltransferase (AS3MT) to mono- and dimethylated arsenic species has long been considered as a major route for detoxification.	Arsenic	47-54	arsenite methyltransferase	Homo sapiens	106-111
28130978-0	2017	Novel ion exchange chromatography method for nca arsenic separation.	Arsenic	49-56	CEA cell adhesion molecule 4	Homo sapiens	45-48
28188921-1	2017	Response to arsenic stress in Saccharomyces cerevisiae is orchestrated by the regulatory protein Yap8, which mediates transcriptional activation of ACR2 and ACR3.	Arsenic	12-19	Arr1p	Saccharomyces cerevisiae S288C	97-101
28255683-7	2017	NR2A genes were significantly upregulated by 90 and 74%, respectively, on exposure to Pb + As and Pb + Cd.	Arsenic	91-93	glutamate receptor, ionotropic, NMDA2A (epsilon 1)	Mus musculus	0-4
28255683-8	2017	NR2B genes were upregulated by 85.3, 68.6, 62.7, and 62.7% on exposure to As, Pb + Hg, Pb + As, and Pb + Cd, respectively.	Arsenic	74-76	glutamate receptor, ionotropic, NMDA2B (epsilon 2)	Mus musculus	0-4
28255683-8	2017	NR2B genes were upregulated by 85.3, 68.6, 62.7, and 62.7% on exposure to As, Pb + Hg, Pb + As, and Pb + Cd, respectively.	Arsenic	92-94	glutamate receptor, ionotropic, NMDA2B (epsilon 2)	Mus musculus	0-4
28255683-9	2017	Exposure to As, Pb + Cd, and Pb + Hg + As significantly upregulated Bcl-2 genes by 2.01-, 1.84-, and 1.80-fold, respectively.	Arsenic	12-14	BCL2 apoptosis regulator a	Danio rerio	68-73
28255683-9	2017	Exposure to As, Pb + Cd, and Pb + Hg + As significantly upregulated Bcl-2 genes by 2.01-, 1.84-, and 1.80-fold, respectively.	Arsenic	39-41	BCL2 apoptosis regulator a	Danio rerio	68-73
28255683-13	2017	These data suggest that altered expression of NMDA receptor subunits and Bcl-2 genes may explain toxicity of low concentration individual and mixtures of Pb, Hg, As, and Cd.	Arsenic	162-164	BCL2 apoptosis regulator a	Danio rerio	73-78
28188921-1	2017	Response to arsenic stress in Saccharomyces cerevisiae is orchestrated by the regulatory protein Yap8, which mediates transcriptional activation of ACR2 and ACR3.	Arsenic	12-19	Arr2p	Saccharomyces cerevisiae S288C	148-152
28188921-1	2017	Response to arsenic stress in Saccharomyces cerevisiae is orchestrated by the regulatory protein Yap8, which mediates transcriptional activation of ACR2 and ACR3.	Arsenic	12-19	Arr3p	Saccharomyces cerevisiae S288C	157-161
28061371-7	2017	Multivariable Cox-proportional hazards regression with Efron approximation was employed to evaluate TTP as a function of drinking water arsenic concentrations among planned pregnancies, adjusted for covariates.	Arsenic	136-143	ZFP36 ring finger protein	Homo sapiens	100-103
28224177-0	2017	Joint Toxicity of Arsenic, Copper and Glyphosate on Behavior, Reproduction and Heat Shock Protein Response in Caenorhabditis elegans.	Arsenic	18-25	Heat shock protein 110	Caenorhabditis elegans	79-97
26886836-5	2017	There were a rise in lipid peroxidation and a decline in reduced glutathione, glutathione peroxidase, glutathione-S-transferase, superoxide dismutase and catalase in heart tissue of arsenic-administered rats.	Arsenic	182-189	hematopoietic prostaglandin D synthase	Rattus norvegicus	102-127
26886836-5	2017	There were a rise in lipid peroxidation and a decline in reduced glutathione, glutathione peroxidase, glutathione-S-transferase, superoxide dismutase and catalase in heart tissue of arsenic-administered rats.	Arsenic	182-189	catalase	Rattus norvegicus	154-162
28237621-10	2017	Finally, treatment of IMR-90 cells with MG-132 abrogated the reduction in XPC protein, suggesting an involvement of the proteasome in the reduction of XPC protein produced by treatment of cells with arsenic.	Arsenic	199-206	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	74-77
28237621-10	2017	Finally, treatment of IMR-90 cells with MG-132 abrogated the reduction in XPC protein, suggesting an involvement of the proteasome in the reduction of XPC protein produced by treatment of cells with arsenic.	Arsenic	199-206	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	151-154
28157645-6	2017	Arsenic in tap water at each cohort members address from 1973 to 2012 was estimated for all cohort members.	Arsenic	0-7	nuclear RNA export factor 1	Homo sapiens	11-14
28157645-10	2017	However, in the Aarhus area, fourth arsenic quartile (2.21-25.34mug/L) was associated with an IRR of 1.48 (95% confidence interval (CI): 1.19-1.83) when compared with first quartile (0.05-1.83mug/L).	Arsenic	36-43	insulin receptor related receptor	Homo sapiens	94-97
28157645-11	2017	An IRR of 1.26 (95% CI: 0.89-1.79) was found for ever (versus never) having lived at an address with 10mug/L or more arsenic in the drinking water.	Arsenic	117-124	insulin receptor related receptor	Homo sapiens	3-6
27943011-8	2017	In contrast, the phosphorylated Akt concentration in macrophages treated with endotoxin plus vasopressin was significantly higher than that in macrophages treated with endotoxin or in macrophages treated with endotoxin plus vasopressin plus LY294002, TGX-221, IC-87114, or AS-252424, but not PIK-75.	Arsenic	273-275	thymoma viral proto-oncogene 1	Mus musculus	32-35
28150588-13	2017	Arsenic exposure in rat lowered GSH concentration but potentiated inflammation and oxidative stress evidenced in the raised levels of MPO, NO and MDA.	Arsenic	0-7	myeloperoxidase	Rattus norvegicus	134-137
28189647-2	2017	Arsenic is capable of modulating the expression of aryl hydrocarbon receptor (AhR)-regulated genes, nevertheless, whether its trivalent organic metabolites have similar effects or not need to be investigated.	Arsenic	0-7	aryl hydrocarbon receptor	Homo sapiens	51-76
28140452-11	2017	On multivariate analysis adjusted for multiple potential confounders, the odds of prevalent frailty were 2.5 times as great with B2M levels of 1.9 to 2.1 mg/L as with levels less than 1.6 mg/L and 2.0 times as great with B2M levels of 2.2 mg/L or more.	Arsenic	115-117	beta-2-microglobulin	Homo sapiens	129-132
28265077-6	2017	These results demonstrate that MTHFD1 and SHMT1, which are key enzymes providing one-carbon units for dTMP biosynthesis in the form of 5,10-methylenetetrahydrofolate, are direct targets of As2O3-induced proteolytic degradation, providing a mechanism for arsenic in the etiology of cancer and developmental anomalies.	Arsenic	254-261	methylenetetrahydrofolate dehydrogenase, cyclohydrolase and formyltetrahydrofolate synthetase 1	Homo sapiens	31-37
28265077-6	2017	These results demonstrate that MTHFD1 and SHMT1, which are key enzymes providing one-carbon units for dTMP biosynthesis in the form of 5,10-methylenetetrahydrofolate, are direct targets of As2O3-induced proteolytic degradation, providing a mechanism for arsenic in the etiology of cancer and developmental anomalies.	Arsenic	254-261	serine hydroxymethyltransferase 1	Homo sapiens	42-47
28115242-0	2017	Arsenic downregulates tight junction claudin proteins through p38 and NF-kappaB in intestinal epithelial cell line, HT-29.	Arsenic	0-7	mitogen-activated protein kinase 14	Homo sapiens	62-65
28115242-0	2017	Arsenic downregulates tight junction claudin proteins through p38 and NF-kappaB in intestinal epithelial cell line, HT-29.	Arsenic	0-7	nuclear factor kappa B subunit 1	Homo sapiens	70-79
28115242-8	2017	Arsenic decreased expression of TJ proteins (i.e., claudin-1 and claudin-5) and transepithelial electrical resistance (TEER) whereas pretreatment of NAC (5-10mM, 1h) attenuated the observed claudins downregulation and TEER.	Arsenic	0-7	claudin 1	Homo sapiens	51-60
28115242-8	2017	Arsenic decreased expression of TJ proteins (i.e., claudin-1 and claudin-5) and transepithelial electrical resistance (TEER) whereas pretreatment of NAC (5-10mM, 1h) attenuated the observed claudins downregulation and TEER.	Arsenic	0-7	claudin 5	Homo sapiens	65-74
28115242-10	2017	Arsenic increased phosphorylation of p38 and nuclear translocation of nuclear factor-kappa B (NF-kappaB) p65, while NAC attenuated these intracellular events.	Arsenic	0-7	mitogen-activated protein kinase 14	Homo sapiens	37-40
28115242-10	2017	Arsenic increased phosphorylation of p38 and nuclear translocation of nuclear factor-kappa B (NF-kappaB) p65, while NAC attenuated these intracellular events.	Arsenic	0-7	nuclear factor kappa B subunit 1	Homo sapiens	70-92
28115242-10	2017	Arsenic increased phosphorylation of p38 and nuclear translocation of nuclear factor-kappa B (NF-kappaB) p65, while NAC attenuated these intracellular events.	Arsenic	0-7	nuclear factor kappa B subunit 1	Homo sapiens	94-103
28115242-10	2017	Arsenic increased phosphorylation of p38 and nuclear translocation of nuclear factor-kappa B (NF-kappaB) p65, while NAC attenuated these intracellular events.	Arsenic	0-7	RELA proto-oncogene, NF-kB subunit	Homo sapiens	105-108
28115242-11	2017	Results demonstrated that arsenic can damage intestinal epithelial cells by proinflammatory process (oxidative stress, p38 and NF-kappaB) which resulted in the downregulation of claudins and NAC can protect intestinal TJs from arsenic toxicity.	Arsenic	26-33	mitogen-activated protein kinase 14	Homo sapiens	119-122
28115242-11	2017	Results demonstrated that arsenic can damage intestinal epithelial cells by proinflammatory process (oxidative stress, p38 and NF-kappaB) which resulted in the downregulation of claudins and NAC can protect intestinal TJs from arsenic toxicity.	Arsenic	26-33	nuclear factor kappa B subunit 1	Homo sapiens	127-136
29515638-0	2017	The HER-2 as a Target Gene of Curcumin to Protect Hepatocytes Against the Arsenic-induced Carcinoma in Mice.	Arsenic	74-81	erb-b2 receptor tyrosine kinase 2	Mus musculus	4-9
28296918-3	2017	We identified CPK31 as an interacting protein of a nodulin 26-like intrinsic protein (NIP1;1), an aquaporin involved in As(III) uptake.	Arsenic	120-122	calcium-dependent protein kinase 31	Arabidopsis thaliana	14-19
28296918-3	2017	We identified CPK31 as an interacting protein of a nodulin 26-like intrinsic protein (NIP1;1), an aquaporin involved in As(III) uptake.	Arsenic	120-122	NEP-interacting protein 1	Arabidopsis thaliana	86-90
28189647-2	2017	Arsenic is capable of modulating the expression of aryl hydrocarbon receptor (AhR)-regulated genes, nevertheless, whether its trivalent organic metabolites have similar effects or not need to be investigated.	Arsenic	0-7	aryl hydrocarbon receptor	Homo sapiens	78-81
28189647-13	2017	This modulation of CYP1A1 proves that trivalent metabolites of arsenic are highly reactive and could participate in arsenic toxicity.	Arsenic	63-70	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	19-25
28191970-0	2017	Various Arsenic Network Structures in 112-Type Ca1-xLaxFe1-yPdyAs2 Revealed by Synchrotron X-ray Diffraction Experiments.	Arsenic	8-15	carbonic anhydrase 1	Homo sapiens	47-50
28191970-2	2017	Whereas in-plane arsenic zigzag chains were found in the 112-type superconducting iron arsenide Ca1-xLaxFeAs2 with maximum Tc = 34 K, deformed arsenic network structures appeared in other 112-type materials, such as longitudinal arsenic zigzag chains in CaFe1-yPdyAs2 (y ~ 0.51) and arsenic square sheets constructed via hypervalent bonding in Ca1-xLaxFe1-yPdyAs2 (x ~ 0.31, y ~ 0.30).	Arsenic	17-24	carbonic anhydrase 1	Homo sapiens	96-99
27255443-0	2017	RKIP expression of liver and kidney after arsenic exposure.	Arsenic	42-49	phosphatidylethanolamine binding protein 1	Mus musculus	0-4
27920122-6	2017	Increased expression of miR-33a was associated with improving hemodynamic parameters.	Arsenic	28-31	microRNA 615	Mus musculus	24-27
27550154-7	2017	Toxic and potential toxic elements Cr, As, Cd, Tl, Pb in water and Al, Cr, As, Hg, Tl in feed were significantly correlated with those in milk (p &lt; 0.05).	Arsenic	39-41	Weaning weight-maternal milk	Bos taurus	138-142
27550154-7	2017	Toxic and potential toxic elements Cr, As, Cd, Tl, Pb in water and Al, Cr, As, Hg, Tl in feed were significantly correlated with those in milk (p &lt; 0.05).	Arsenic	75-77	Weaning weight-maternal milk	Bos taurus	138-142
27498811-4	2017	Our meta-analysis showed that arsenic exposure generally suppressed measured levels of the antioxidants, SOD, CAT, GSH, GPx, GST, and GR, but increased levels of the oxidants, GSSG, MDA, and ROS.	Arsenic	30-37	catalase	Mus musculus	110-113
27498811-4	2017	Our meta-analysis showed that arsenic exposure generally suppressed measured levels of the antioxidants, SOD, CAT, GSH, GPx, GST, and GR, but increased levels of the oxidants, GSSG, MDA, and ROS.	Arsenic	30-37	hematopoietic prostaglandin D synthase	Mus musculus	125-128
27498811-4	2017	Our meta-analysis showed that arsenic exposure generally suppressed measured levels of the antioxidants, SOD, CAT, GSH, GPx, GST, and GR, but increased levels of the oxidants, GSSG, MDA, and ROS.	Arsenic	30-37	glutathione reductase	Mus musculus	134-136
27943565-10	2017	CONCLUSION: Continuous long-term DPP-4 inhibitor use (defined as &gt;4.0-8.5 years of DPP-4 inhibitor use for any fracture, &gt;3.0-8.5 years for osteoporotic fracture and &gt;2.0-8.5 years for hip fracture was not associated with risk of any, osteoporotic or hip fracture.	Arsenic	62-64	dipeptidyl peptidase 4	Homo sapiens	33-38
27943565-10	2017	CONCLUSION: Continuous long-term DPP-4 inhibitor use (defined as &gt;4.0-8.5 years of DPP-4 inhibitor use for any fracture, &gt;3.0-8.5 years for osteoporotic fracture and &gt;2.0-8.5 years for hip fracture was not associated with risk of any, osteoporotic or hip fracture.	Arsenic	62-64	dipeptidyl peptidase 4	Homo sapiens	86-91
27255443-3	2017	In order to investigate the effect of arsenic to RKIP of liver and kidney, the expression of RKIP of liver and kidney with As (III) was explored in this study.	Arsenic	38-45	phosphatidylethanolamine binding protein 1	Mus musculus	49-53
28099871-10	2017	Compared with controls, ERK and p-ERK levels decreased in the hippocampus and cerebral cortex in pups exposed to combined fluoride and arsenic.	Arsenic	135-142	Eph receptor B1	Rattus norvegicus	24-27
27930956-1	2017	Mg-Al layered double hydroxide intercalated with NO3- and Mg-Al oxide were found to remove hazardous materials such as B and As, as well as Cl- and SO42-, from artificial and real hot spring wastewater.	Arsenic	125-127	NBL1, DAN family BMP antagonist	Homo sapiens	49-52
28003426-8	2017	Interestingly, the induced cyclin E1 and cyclin A2 caused by Pdk4 deficiency was repressed by arsenic treatment in mouse liver and in HCC cells.	Arsenic	94-101	cyclin E1	Mus musculus	27-36
28003426-8	2017	Interestingly, the induced cyclin E1 and cyclin A2 caused by Pdk4 deficiency was repressed by arsenic treatment in mouse liver and in HCC cells.	Arsenic	94-101	cyclin A2	Mus musculus	41-50
28003426-8	2017	Interestingly, the induced cyclin E1 and cyclin A2 caused by Pdk4 deficiency was repressed by arsenic treatment in mouse liver and in HCC cells.	Arsenic	94-101	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	61-65
28099871-0	2017	Fluoride and arsenic exposure affects spatial memory and activates the ERK/CREB signaling pathway in offspring rats.	Arsenic	13-20	Eph receptor B1	Rattus norvegicus	71-74
28099871-0	2017	Fluoride and arsenic exposure affects spatial memory and activates the ERK/CREB signaling pathway in offspring rats.	Arsenic	13-20	cAMP responsive element binding protein 1	Rattus norvegicus	75-79
28099871-3	2017	This study explored the effects of fluoride and arsenic exposure in drinking water on spatial learning, memory and key protein expression in the ERK/CREB signaling pathway in hippocampal and cerebral cortex tissue in rat offspring.	Arsenic	48-55	Eph receptor B1	Rattus norvegicus	145-148
28099871-10	2017	Compared with controls, ERK and p-ERK levels decreased in the hippocampus and cerebral cortex in pups exposed to combined fluoride and arsenic.	Arsenic	135-142	Eph receptor B1	Rattus norvegicus	34-37
28099871-3	2017	This study explored the effects of fluoride and arsenic exposure in drinking water on spatial learning, memory and key protein expression in the ERK/CREB signaling pathway in hippocampal and cerebral cortex tissue in rat offspring.	Arsenic	48-55	cAMP responsive element binding protein 1	Rattus norvegicus	149-153
28099871-11	2017	CREB protein expression in the cerebral cortex decreased in pups exposed to fluoride, arsenic, and the fluoride and arsenic combination.	Arsenic	86-93	cAMP responsive element binding protein 1	Rattus norvegicus	0-4
28099871-11	2017	CREB protein expression in the cerebral cortex decreased in pups exposed to fluoride, arsenic, and the fluoride and arsenic combination.	Arsenic	116-123	cAMP responsive element binding protein 1	Rattus norvegicus	0-4
28099871-12	2017	p-CREB protein expression in both the hippocampus and cerebral cortex was decreased in pups exposed to fluoride and arsenic in combination compared to the control group.	Arsenic	116-123	cAMP responsive element binding protein 1	Rattus norvegicus	2-6
28099871-14	2017	These data indicate that exposure to fluoride and arsenic in early life stage changes ERK, p-ERK, CREB and p-CREB protein expression in the hippocampus and cerebral cortex of rat offspring at PND21 and PND 42, which may contribute to impaired neurodevelopment following exposure.	Arsenic	50-57	Eph receptor B1	Rattus norvegicus	86-89
28099871-14	2017	These data indicate that exposure to fluoride and arsenic in early life stage changes ERK, p-ERK, CREB and p-CREB protein expression in the hippocampus and cerebral cortex of rat offspring at PND21 and PND 42, which may contribute to impaired neurodevelopment following exposure.	Arsenic	50-57	Eph receptor B1	Rattus norvegicus	93-96
28099871-14	2017	These data indicate that exposure to fluoride and arsenic in early life stage changes ERK, p-ERK, CREB and p-CREB protein expression in the hippocampus and cerebral cortex of rat offspring at PND21 and PND 42, which may contribute to impaired neurodevelopment following exposure.	Arsenic	50-57	cAMP responsive element binding protein 1	Rattus norvegicus	98-102
28099871-14	2017	These data indicate that exposure to fluoride and arsenic in early life stage changes ERK, p-ERK, CREB and p-CREB protein expression in the hippocampus and cerebral cortex of rat offspring at PND21 and PND 42, which may contribute to impaired neurodevelopment following exposure.	Arsenic	50-57	cAMP responsive element binding protein 1	Rattus norvegicus	109-113
28000977-9	2017	Our analysis revealed arsenic-induced overexpression of aldo-keto reductase family 1 member C2 (AKR1C2), aldo-keto reductase family 1 member C3 (AKR1C3), glutamate-cysteine ligase catalytic subunit (GCLC), and NAD(P)H dehydrogenase [quinone] 1 (NQO1) among others.	Arsenic	22-29	aldo-keto reductase family 1 member C2	Homo sapiens	56-94
28000977-9	2017	Our analysis revealed arsenic-induced overexpression of aldo-keto reductase family 1 member C2 (AKR1C2), aldo-keto reductase family 1 member C3 (AKR1C3), glutamate-cysteine ligase catalytic subunit (GCLC), and NAD(P)H dehydrogenase [quinone] 1 (NQO1) among others.	Arsenic	22-29	aldo-keto reductase family 1 member C2	Homo sapiens	96-102
28000977-9	2017	Our analysis revealed arsenic-induced overexpression of aldo-keto reductase family 1 member C2 (AKR1C2), aldo-keto reductase family 1 member C3 (AKR1C3), glutamate-cysteine ligase catalytic subunit (GCLC), and NAD(P)H dehydrogenase [quinone] 1 (NQO1) among others.	Arsenic	22-29	aldo-keto reductase family 1 member C3	Homo sapiens	105-143
28000977-9	2017	Our analysis revealed arsenic-induced overexpression of aldo-keto reductase family 1 member C2 (AKR1C2), aldo-keto reductase family 1 member C3 (AKR1C3), glutamate-cysteine ligase catalytic subunit (GCLC), and NAD(P)H dehydrogenase [quinone] 1 (NQO1) among others.	Arsenic	22-29	aldo-keto reductase family 1 member C3	Homo sapiens	145-151
28000977-9	2017	Our analysis revealed arsenic-induced overexpression of aldo-keto reductase family 1 member C2 (AKR1C2), aldo-keto reductase family 1 member C3 (AKR1C3), glutamate-cysteine ligase catalytic subunit (GCLC), and NAD(P)H dehydrogenase [quinone] 1 (NQO1) among others.	Arsenic	22-29	glutamate-cysteine ligase catalytic subunit	Homo sapiens	154-197
28000977-9	2017	Our analysis revealed arsenic-induced overexpression of aldo-keto reductase family 1 member C2 (AKR1C2), aldo-keto reductase family 1 member C3 (AKR1C3), glutamate-cysteine ligase catalytic subunit (GCLC), and NAD(P)H dehydrogenase [quinone] 1 (NQO1) among others.	Arsenic	22-29	glutamate-cysteine ligase catalytic subunit	Homo sapiens	199-203
28000977-9	2017	Our analysis revealed arsenic-induced overexpression of aldo-keto reductase family 1 member C2 (AKR1C2), aldo-keto reductase family 1 member C3 (AKR1C3), glutamate-cysteine ligase catalytic subunit (GCLC), and NAD(P)H dehydrogenase [quinone] 1 (NQO1) among others.	Arsenic	22-29	NAD(P)H quinone dehydrogenase 1	Homo sapiens	210-243
28000977-9	2017	Our analysis revealed arsenic-induced overexpression of aldo-keto reductase family 1 member C2 (AKR1C2), aldo-keto reductase family 1 member C3 (AKR1C3), glutamate-cysteine ligase catalytic subunit (GCLC), and NAD(P)H dehydrogenase [quinone] 1 (NQO1) among others.	Arsenic	22-29	NAD(P)H quinone dehydrogenase 1	Homo sapiens	245-249
28025110-0	2017	Hypomethylation of inflammatory genes (COX2, EGR1, and SOCS3) and increased urinary 8-nitroguanine in arsenic-exposed newborns and children.	Arsenic	102-109	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	39-43
28192915-7	2017	The instrument is applicable for multielement analysis, and the LODs ranged from 0.16 to 11.65 mug L-1 for Zn, Pb, Ag, Cd, Au, Cu, Mn, Fe, Cr, and As.	Arsenic	147-149	immunoglobulin kappa variable 1-16	Homo sapiens	99-102
28069514-11	2017	This study for the first time shows that miR21 plays an important role in contributing to arsenic induced dermatological and non-dermatological health outcomes in an exposed population.	Arsenic	90-97	microRNA 21	Homo sapiens	41-46
28337271-12	2017	Long term low- or high-dose arsenic induces epithelial-mesenchymal transition, likely via downregulation of E-cadherin, activates p53, and differently affects cell proliferation/growth.	Arsenic	28-35	cadherin 1	Homo sapiens	108-118
28337271-12	2017	Long term low- or high-dose arsenic induces epithelial-mesenchymal transition, likely via downregulation of E-cadherin, activates p53, and differently affects cell proliferation/growth.	Arsenic	28-35	tumor protein p53	Homo sapiens	130-133
28150704-0	2017	Genome-wide DNA methylation reprogramming in response to inorganic arsenic links inhibition of CTCF binding, DNMT expression and cellular transformation.	Arsenic	67-74	CCCTC-binding factor	Homo sapiens	95-99
28150704-0	2017	Genome-wide DNA methylation reprogramming in response to inorganic arsenic links inhibition of CTCF binding, DNMT expression and cellular transformation.	Arsenic	67-74	DNA methyltransferase 1	Homo sapiens	109-113
28130831-0	2017	Identification of amino acid residues important for the arsenic resistance function of Arabidopsis ABCC1.	Arsenic	56-63	multidrug resistance-associated protein 1	Arabidopsis thaliana	99-104
28130831-1	2017	The Arabidopsis ATP-Binding Cassette (ABC) transporter ABCC1 sequesters arsenic (As)-phytochelatin conjugates into the vacuole, thereby conferring As resistance.	Arsenic	72-84	multidrug resistance-associated protein 1	Arabidopsis thaliana	55-60
28626252-8	2017	In addition, SLE abrogated arsenic-mediated elevation of serum alkaline phosphatase (ALP), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), uric acid and glucose.	Arsenic	27-34	glutamic pyruvic transaminase, soluble	Mus musculus	91-115
28626252-8	2017	In addition, SLE abrogated arsenic-mediated elevation of serum alkaline phosphatase (ALP), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), uric acid and glucose.	Arsenic	27-34	glutamic pyruvic transaminase, soluble	Mus musculus	117-120
27863446-6	2017	In summary, GSTP1-1 can detoxify arsenic-based drugs by sequestration at the active site and at the dimer interface, in situations where there is a plentiful supply of GSH, and at the reactive cysteines in conditions of low GSH.	Arsenic	33-40	glutathione S-transferase pi 1	Homo sapiens	12-19
27890409-0	2017	Geochemistry of arsenic in low sulfide-high carbonate coal waste rock, Elk Valley, British Columbia, Canada.	Arsenic	16-23	potassium voltage-gated channel subfamily H member 8	Homo sapiens	71-74
28025110-0	2017	Hypomethylation of inflammatory genes (COX2, EGR1, and SOCS3) and increased urinary 8-nitroguanine in arsenic-exposed newborns and children.	Arsenic	102-109	early growth response 1	Homo sapiens	45-49
28025110-0	2017	Hypomethylation of inflammatory genes (COX2, EGR1, and SOCS3) and increased urinary 8-nitroguanine in arsenic-exposed newborns and children.	Arsenic	102-109	suppressor of cytokine signaling 3	Homo sapiens	55-60
28025110-3	2017	Our previous study reported that prenatal arsenic exposure leads to increased mRNA expression of several genes related to inflammation, including COX2, EGR1, and SOCS3.	Arsenic	42-49	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	146-150
28025110-3	2017	Our previous study reported that prenatal arsenic exposure leads to increased mRNA expression of several genes related to inflammation, including COX2, EGR1, and SOCS3.	Arsenic	42-49	early growth response 1	Homo sapiens	152-156
28025110-3	2017	Our previous study reported that prenatal arsenic exposure leads to increased mRNA expression of several genes related to inflammation, including COX2, EGR1, and SOCS3.	Arsenic	42-49	suppressor of cytokine signaling 3	Homo sapiens	162-167
28025110-4	2017	This study aimed to investigate the effects of arsenic exposure on promoter DNA methylation and mRNA expression of these inflammatory genes (COX2, EGR1, and SOCS3), as well as the generation of 8-nitroguanine, which is a mutagenic DNA lesion involved in inflammation-related carcinogenesis.	Arsenic	47-54	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	141-145
28025110-4	2017	This study aimed to investigate the effects of arsenic exposure on promoter DNA methylation and mRNA expression of these inflammatory genes (COX2, EGR1, and SOCS3), as well as the generation of 8-nitroguanine, which is a mutagenic DNA lesion involved in inflammation-related carcinogenesis.	Arsenic	47-54	early growth response 1	Homo sapiens	147-151
28025110-4	2017	This study aimed to investigate the effects of arsenic exposure on promoter DNA methylation and mRNA expression of these inflammatory genes (COX2, EGR1, and SOCS3), as well as the generation of 8-nitroguanine, which is a mutagenic DNA lesion involved in inflammation-related carcinogenesis.	Arsenic	47-54	suppressor of cytokine signaling 3	Homo sapiens	157-162
28025110-5	2017	Prenatally arsenic-exposed newborns had promoter hypomethylation of COX2, EGR1, and SOCS3 in cord blood lymphocytes (p&lt;0.01).	Arsenic	11-18	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	68-72
28025110-5	2017	Prenatally arsenic-exposed newborns had promoter hypomethylation of COX2, EGR1, and SOCS3 in cord blood lymphocytes (p&lt;0.01).	Arsenic	11-18	early growth response 1	Homo sapiens	74-78
28025110-5	2017	Prenatally arsenic-exposed newborns had promoter hypomethylation of COX2, EGR1, and SOCS3 in cord blood lymphocytes (p&lt;0.01).	Arsenic	11-18	suppressor of cytokine signaling 3	Homo sapiens	84-89
28025110-10	2017	These results indicated that early-life exposure to arsenic causes hypomethylation of COX2, EGR1, and SOCS3, increases mRNA expression of these genes, and increases 8-nitroguanine formation.	Arsenic	52-59	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	86-90
28025110-10	2017	These results indicated that early-life exposure to arsenic causes hypomethylation of COX2, EGR1, and SOCS3, increases mRNA expression of these genes, and increases 8-nitroguanine formation.	Arsenic	52-59	early growth response 1	Homo sapiens	92-96
28025110-10	2017	These results indicated that early-life exposure to arsenic causes hypomethylation of COX2, EGR1, and SOCS3, increases mRNA expression of these genes, and increases 8-nitroguanine formation.	Arsenic	52-59	suppressor of cytokine signaling 3	Homo sapiens	102-107
28125038-0	2017	Arsenic Induces p62 Expression to Form a Positive Feedback Loop with Nrf2 in Human Epidermal Keratinocytes: Implications for Preventing Arsenic-Induced Skin Cancer.	Arsenic	0-7	nucleoporin 62	Homo sapiens	16-19
28125064-3	2017	In the present study, we for the first time establish whether organic arsenic species phenylarsine oxide (PAO) could induce the mutant PML-IV (A216V) protein solubility changes and degradation.	Arsenic	70-77	PML nuclear body scaffold	Homo sapiens	135-138
28125038-0	2017	Arsenic Induces p62 Expression to Form a Positive Feedback Loop with Nrf2 in Human Epidermal Keratinocytes: Implications for Preventing Arsenic-Induced Skin Cancer.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	69-73
28125038-0	2017	Arsenic Induces p62 Expression to Form a Positive Feedback Loop with Nrf2 in Human Epidermal Keratinocytes: Implications for Preventing Arsenic-Induced Skin Cancer.	Arsenic	136-143	nucleoporin 62	Homo sapiens	16-19
28125038-4	2017	Here, we have shown that arsenic induces p62 expression in an autophagy-independent manner in human HaCaT keratinocytes.	Arsenic	25-32	nucleoporin 62	Homo sapiens	41-44
28125038-5	2017	In mouse skin, chronic arsenic exposure through drinking water increases p62 protein levels in the epidermis.	Arsenic	23-30	nucleoporin 62	Mus musculus	73-76
28125038-6	2017	Nrf2 is required for basal and arsenic-induced p62 up-regulation.	Arsenic	31-38	nuclear factor, erythroid derived 2, like 2	Mus musculus	0-4
28125038-6	2017	Nrf2 is required for basal and arsenic-induced p62 up-regulation.	Arsenic	31-38	nucleoporin 62	Mus musculus	47-50
28125038-7	2017	p62 knockdown reduces arsenic-induced Nrf2 activity, and induces sustained p21 up-regulation.	Arsenic	22-29	nucleoporin 62	Mus musculus	0-3
28125038-7	2017	p62 knockdown reduces arsenic-induced Nrf2 activity, and induces sustained p21 up-regulation.	Arsenic	22-29	nuclear factor, erythroid derived 2, like 2	Mus musculus	38-42
28125038-10	2017	Our findings indicate that arsenic induces p62 expression to regulate the Nrf2 pathway in human keratinocytes and suggest that targeting p62 may help prevent arsenic-induced skin cancer.	Arsenic	27-34	nucleoporin 62	Homo sapiens	43-46
28125038-10	2017	Our findings indicate that arsenic induces p62 expression to regulate the Nrf2 pathway in human keratinocytes and suggest that targeting p62 may help prevent arsenic-induced skin cancer.	Arsenic	27-34	NFE2 like bZIP transcription factor 2	Homo sapiens	74-78
28125038-10	2017	Our findings indicate that arsenic induces p62 expression to regulate the Nrf2 pathway in human keratinocytes and suggest that targeting p62 may help prevent arsenic-induced skin cancer.	Arsenic	27-34	nucleoporin 62	Homo sapiens	137-140
28125038-10	2017	Our findings indicate that arsenic induces p62 expression to regulate the Nrf2 pathway in human keratinocytes and suggest that targeting p62 may help prevent arsenic-induced skin cancer.	Arsenic	158-165	nucleoporin 62	Homo sapiens	137-140
32263664-3	2017	0.57 mug L-1) and showed high selectivity towards arsenic ions over other metal ions.	Arsenic	50-57	L1 cell adhesion molecule	Homo sapiens	9-12
27736677-11	2017	Among the mitochondrial genes, expression of Cox1 was significantly high only after 90 days in liver, while in kidney it enhanced at 7, 30 and 60 days of arsenic exposure.	Arsenic	154-161	cytochrome c oxidase I, mitochondrial	Danio rerio	45-49
27480915-4	2017	The objective of this study was to compare the adsorption kinetics and isotherm of arsenite (As(III)) and arsenate (As(V)) on bare hematite nanoparticles and aggregates and how this affects the fate of arsenic in the environment.	Arsenic	202-209	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	116-121
29202485-0	2017	Selenite restores Pax6 expression in neuronal cells of chronically arsenic-exposed Golden Syrian hamsters.	Arsenic	67-74	paired box protein Pax-6	Mesocricetus auratus	18-22
29202485-4	2017	One such target of arsenic is the Pax6 gene that encodes a transcription factor in neuronal cells.	Arsenic	19-26	paired box protein Pax-6	Mesocricetus auratus	34-38
29202485-5	2017	The aim of this study was to evaluate the effect of two antioxidants, alpha-tocopheryl succinate (alpha-TOS) and sodium selenite, on Pax6 gene expression levels in the forebrain and cerebellum of Golden Syrian hamsters chronically exposed to arsenic in drinking water.	Arsenic	242-249	paired box protein Pax-6	Mesocricetus auratus	133-137
29202485-7	2017	Using quantitative real-time reverse transcriptase (RT)-PCR analysis, we confirmed that arsenic downregulates Pax6 expression in nervous tissues by 53 +- 21% and 32 +- 7% in the forebrain and cerebellum, respectively.	Arsenic	88-95	paired box protein Pax-6	Mesocricetus auratus	110-114
29202485-8	2017	In the presence of arsenic, treatment with alpha-TOS did not modify Pax6 expression in nervous tissues; however, sodium selenite completely restored Pax6 expression in the arsenic-exposed hamster forebrain, but not the cerebellum.	Arsenic	172-179	paired box protein Pax-6	Mesocricetus auratus	149-153
28849505-0	2017	Taurine Protects Mouse Liver Against Arsenic-Induced Apoptosis Through JNK Pathway.	Arsenic	37-44	mitogen-activated protein kinase 8	Mus musculus	71-74
28365685-5	2017	RESULTS: The results showed that arsenic treatment significantly increased oxidative stress levels (as indicated by catalase, malonyldialdehyde, superoxide dismutase, glutathione and reactive oxygen species), increased levels of inflammatory cytokines and promoted apoptosis.	Arsenic	33-40	catalase	Mus musculus	116-124
28365685-7	2017	Arsenic exposure also significantly decreased the frequency of T(CD3) (from 32.5% to 19.2%) and B(CD19) cells (from 55.1 to 32.5%).	Arsenic	0-7	CD19 antigen	Mus musculus	98-102
27958705-8	2017	Instead, the As concentration in the groundwater of up to 1 muM is due to equilibrium-controlled desorption of arsenic, adsorbed to the sediment before river water started to infiltrate due to municipal pumping.	Arsenic	111-118	latexin	Homo sapiens	60-63
27856639-6	2017	Follow-up studies demonstrated that hYVH1 co-localizes with YB-1 and fragile X mental retardation protein on stress granules in response to arsenic treatment.	Arsenic	140-147	dual specificity phosphatase 12	Homo sapiens	36-41
27856639-6	2017	Follow-up studies demonstrated that hYVH1 co-localizes with YB-1 and fragile X mental retardation protein on stress granules in response to arsenic treatment.	Arsenic	140-147	Y-box binding protein 1	Homo sapiens	60-64
27884605-0	2017	Arsenic-Induced Activation of the Homeodomain-Interacting Protein Kinase 2 (HIPK2) to cAMP-Response Element Binding Protein (CREB) Axis.	Arsenic	0-7	homeodomain interacting protein kinase 2	Homo sapiens	34-74
27884605-0	2017	Arsenic-Induced Activation of the Homeodomain-Interacting Protein Kinase 2 (HIPK2) to cAMP-Response Element Binding Protein (CREB) Axis.	Arsenic	0-7	homeodomain interacting protein kinase 2	Homo sapiens	76-81
27884605-0	2017	Arsenic-Induced Activation of the Homeodomain-Interacting Protein Kinase 2 (HIPK2) to cAMP-Response Element Binding Protein (CREB) Axis.	Arsenic	0-7	cAMP responsive element binding protein 1	Homo sapiens	125-129
27884605-9	2017	These results suggest that the HIPK2-phospho-Ser271 CREB axis is a new arsenic-responsive CREB activation mechanism in parallel with the PKA-phospho-Ser133 CREB axis.	Arsenic	71-78	homeodomain interacting protein kinase 2	Homo sapiens	31-36
27884605-9	2017	These results suggest that the HIPK2-phospho-Ser271 CREB axis is a new arsenic-responsive CREB activation mechanism in parallel with the PKA-phospho-Ser133 CREB axis.	Arsenic	71-78	cAMP responsive element binding protein 1	Homo sapiens	52-56
27884605-9	2017	These results suggest that the HIPK2-phospho-Ser271 CREB axis is a new arsenic-responsive CREB activation mechanism in parallel with the PKA-phospho-Ser133 CREB axis.	Arsenic	71-78	cAMP responsive element binding protein 1	Homo sapiens	90-94
27884605-9	2017	These results suggest that the HIPK2-phospho-Ser271 CREB axis is a new arsenic-responsive CREB activation mechanism in parallel with the PKA-phospho-Ser133 CREB axis.	Arsenic	71-78	cAMP responsive element binding protein 1	Homo sapiens	90-94
27932253-0	2017	Regulation of cyclin D1 by arsenic and microRNA inhibits adipogenesis.	Arsenic	27-34	cyclin D1	Homo sapiens	14-23
27932253-5	2017	Arsenic increased the expression of miR-29b in white adipose tissue, as well as human mesenchymal stem cells (hMSCs) isolated from adipose tissue.	Arsenic	0-7	microRNA 29b-1	Homo sapiens	36-43
27932253-6	2017	Exposing hMSCs to arsenic increased abundance of miR-29b and cyclin D1 to promote proliferation over differentiation.	Arsenic	18-25	microRNA 29b-1	Homo sapiens	49-56
27932253-6	2017	Exposing hMSCs to arsenic increased abundance of miR-29b and cyclin D1 to promote proliferation over differentiation.	Arsenic	18-25	cyclin D1	Homo sapiens	61-70
27932253-7	2017	Paradoxically, inhibition of miR-29b enhanced the inhibitory effect of arsenic on differentiation.	Arsenic	71-78	microRNA 29b-1	Homo sapiens	29-36
27932253-9	2017	Temporal regulation of cyclin D1 is critical for adipogenic differentiation, and the data suggest a paradigm where arsenic disruption of miR-29b regulatory pathways impairs adipogenic differentiation and ultimately adipose metabolic homeostasis.	Arsenic	115-122	cyclin D1	Homo sapiens	23-32
27932253-9	2017	Temporal regulation of cyclin D1 is critical for adipogenic differentiation, and the data suggest a paradigm where arsenic disruption of miR-29b regulatory pathways impairs adipogenic differentiation and ultimately adipose metabolic homeostasis.	Arsenic	115-122	microRNA 29b-1	Homo sapiens	137-144
28880708-4	2017	E2F1 expression and activity is inhibited by inorganic arsenic (iAs) that has a dual role as a cancer therapeutic and as a toxin that leads to diseases including cancer.	Arsenic	55-62	E2F transcription factor 1 L homeolog	Xenopus laevis	0-4
27352405-12	2017	Among the candidate arsenic variant associations, functional SNPs in AS3MT and 10q24 were most significant (p &lt; 9.33 x 10-5).	Arsenic	20-27	arsenite methyltransferase	Homo sapiens	69-74
27352405-13	2017	CONCLUSIONS: This hypothesis-driven association study supports the role of common variants in arsenic metabolism, particularly AS3MT and 10q24.	Arsenic	94-101	arsenite methyltransferase	Homo sapiens	127-132
28013473-12	2017	Across all the soil data in the five regions, the total Cu, Zn, Pb, Cd, Cr, and As level was negatively correlated with urease activity, alkaline phosphatase activity, and invertase activity, but the relationship was not significant.	Arsenic	80-82	alkaline phosphatase, placental	Homo sapiens	137-157
28553665-5	2017	The median of the main arsenic species found in the 4-year-old children was 9.71 mug/l (arsenobetaine-AsB), 3.97 mug/l (dimethylarsinic acid-DMA), 0.44 mug/l (monomethylarsonic acid-MMA) and 0.35 mug/l (i-As).	Arsenic	23-30	arylsulfatase B	Homo sapiens	102-105
27815852-8	2017	The presence of Ca2+ or Cd2+ significantly increased arsenic removal at higher pH.	Arsenic	53-60	CD2 molecule	Homo sapiens	24-27
27978490-0	2017	Acute arsenic exposure induces inflammatory responses and CD4+ T cell subpopulations differentiation in spleen and thymus with the involvement of MAPK, NF-kB, and Nrf2.	Arsenic	6-13	CD4 antigen	Mus musculus	58-61
28286610-8	2017	Due to genetic polymorphisms can contribute to the variability in AS3MT activity; they may contribute to interindividual as well as intra-ethnic differences in response to the detoxification of arsenic.	Arsenic	194-201	arsenite methyltransferase	Homo sapiens	66-71
27592797-5	2017	Using this SE model, we showed that arsenic initiated SUV39H2-mediated epigenetic modification of E2F1, which induced centrosome amplification in keratinocytes in 2 days; this, however, led to caspase-8-mediated apoptosis in 10 days.	Arsenic	36-43	SUV39H2 histone lysine methyltransferase	Homo sapiens	54-61
27592797-5	2017	Using this SE model, we showed that arsenic initiated SUV39H2-mediated epigenetic modification of E2F1, which induced centrosome amplification in keratinocytes in 2 days; this, however, led to caspase-8-mediated apoptosis in 10 days.	Arsenic	36-43	E2F transcription factor 1	Homo sapiens	98-102
27592797-5	2017	Using this SE model, we showed that arsenic initiated SUV39H2-mediated epigenetic modification of E2F1, which induced centrosome amplification in keratinocytes in 2 days; this, however, led to caspase-8-mediated apoptosis in 10 days.	Arsenic	36-43	caspase 8	Homo sapiens	193-202
27592797-6	2017	In parallel, arsenic stimulated tumor necrosis factor-alpha release mainly from peripheral blood mononuclear cells.	Arsenic	13-20	tumor necrosis factor	Homo sapiens	32-59
27592797-7	2017	Tumor necrosis factor-alpha triggered anti-apoptotic signals via FLIP-associated caspase-8 inactivation in arsenic-treated keratinocytes, which in turn contributed to cell survival and aneuploidy.	Arsenic	107-114	tumor necrosis factor	Homo sapiens	0-27
27592797-7	2017	Tumor necrosis factor-alpha triggered anti-apoptotic signals via FLIP-associated caspase-8 inactivation in arsenic-treated keratinocytes, which in turn contributed to cell survival and aneuploidy.	Arsenic	107-114	caspase 8	Homo sapiens	81-90
28273963-11	2017	RESULTS: Treatment with arsenic decreased the levels of BG, liver glycogen and PA, tissue protein and G6Pase activity, GOT activity in liver and muscle, and increased free amino acid content in kidney and muscle, GPT activity in liver and kidney.	Arsenic	24-31	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	102-108
28273963-11	2017	RESULTS: Treatment with arsenic decreased the levels of BG, liver glycogen and PA, tissue protein and G6Pase activity, GOT activity in liver and muscle, and increased free amino acid content in kidney and muscle, GPT activity in liver and kidney.	Arsenic	24-31	glutamic--pyruvic transaminase	Rattus norvegicus	213-216
28948046-5	2017	Changes in the high-intensity volume ratio were of high intensity, and parameters influencing the ratio were analyzed using 3D AS-OCT.	Arsenic	127-129	plexin A2	Homo sapiens	130-133
28088268-2	2017	The aim of this study was to investigate p63, E-cadherin, and beta-catenin proteins in urothelial carcinoma (UC) in both arsenic contaminated areas [so-called blackfoot disease (BFD) area] and non-BFD areas.	Arsenic	121-128	tumor protein p63	Homo sapiens	41-44
28088268-2	2017	The aim of this study was to investigate p63, E-cadherin, and beta-catenin proteins in urothelial carcinoma (UC) in both arsenic contaminated areas [so-called blackfoot disease (BFD) area] and non-BFD areas.	Arsenic	121-128	catenin beta 1	Homo sapiens	62-74
27978490-0	2017	Acute arsenic exposure induces inflammatory responses and CD4+ T cell subpopulations differentiation in spleen and thymus with the involvement of MAPK, NF-kB, and Nrf2.	Arsenic	6-13	nuclear factor, erythroid derived 2, like 2	Mus musculus	163-167
27978490-4	2017	We found that arsenic significantly decreased the spleen and thymus weights and indices, and flow cytometry revealed that arsenic decreased the relative frequency of CD4+ T cell subpopulation and the ratios of CD4/CD8 in spleen.	Arsenic	122-129	CD4 antigen	Mus musculus	166-169
27978490-4	2017	We found that arsenic significantly decreased the spleen and thymus weights and indices, and flow cytometry revealed that arsenic decreased the relative frequency of CD4+ T cell subpopulation and the ratios of CD4/CD8 in spleen.	Arsenic	122-129	CD4 antigen	Mus musculus	210-213
27978490-7	2017	Moreover, arsenic enhanced oxidative stress and induced the activation of extracellular-signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK) and p38 and their downstream transcription factors nuclear factor kappa B (NF-kB) and nuclear factor E2-related factor 2 (Nrf2), which comprise important mechanistic pathways involved in immune-inflammatory manifestations.	Arsenic	10-17	mitogen-activated protein kinase 3	Mus musculus	74-116
27978490-7	2017	Moreover, arsenic enhanced oxidative stress and induced the activation of extracellular-signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK) and p38 and their downstream transcription factors nuclear factor kappa B (NF-kB) and nuclear factor E2-related factor 2 (Nrf2), which comprise important mechanistic pathways involved in immune-inflammatory manifestations.	Arsenic	10-17	mitogen-activated protein kinase 3	Mus musculus	118-124
27978490-7	2017	Moreover, arsenic enhanced oxidative stress and induced the activation of extracellular-signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK) and p38 and their downstream transcription factors nuclear factor kappa B (NF-kB) and nuclear factor E2-related factor 2 (Nrf2), which comprise important mechanistic pathways involved in immune-inflammatory manifestations.	Arsenic	10-17	jun proto-oncogene	Mus musculus	127-132
27978490-7	2017	Moreover, arsenic enhanced oxidative stress and induced the activation of extracellular-signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK) and p38 and their downstream transcription factors nuclear factor kappa B (NF-kB) and nuclear factor E2-related factor 2 (Nrf2), which comprise important mechanistic pathways involved in immune-inflammatory manifestations.	Arsenic	10-17	mitogen-activated protein kinase 14	Mus musculus	162-165
27978490-7	2017	Moreover, arsenic enhanced oxidative stress and induced the activation of extracellular-signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK) and p38 and their downstream transcription factors nuclear factor kappa B (NF-kB) and nuclear factor E2-related factor 2 (Nrf2), which comprise important mechanistic pathways involved in immune-inflammatory manifestations.	Arsenic	10-17	nuclear factor, erythroid derived 2, like 2	Mus musculus	280-284
27751817-0	2017	Prenatal arsenic exposure alters REST/NRSF and microRNA regulators of embryonic neural stem cell fate in a sex-dependent manner.	Arsenic	9-16	RE1-silencing transcription factor	Mus musculus	38-42
27751817-8	2017	The female response to arsenic was limited to increased expression of CoREST and Ptbp2, an RNA binding protein that allows for appropriate splicing of genes involved in the progression of neurogenesis.	Arsenic	23-30	REST corepressor 2	Mus musculus	70-76
27751817-8	2017	The female response to arsenic was limited to increased expression of CoREST and Ptbp2, an RNA binding protein that allows for appropriate splicing of genes involved in the progression of neurogenesis.	Arsenic	23-30	polypyrimidine tract binding protein 2	Mus musculus	81-86
27751817-13	2017	Arsenic-induced dysregulation of the regulatory loop formed by REST/NRSF, its target microRNAs, miR-9 and miR-124, and RNA splicing proteins, PTBP1 and 2, leads to aberrant programming of NSC function that is perhaps perpetuated into adulthood inducing deficits in differentiation we have previously observed.	Arsenic	0-7	RE1-silencing transcription factor	Mus musculus	68-72
27751817-13	2017	Arsenic-induced dysregulation of the regulatory loop formed by REST/NRSF, its target microRNAs, miR-9 and miR-124, and RNA splicing proteins, PTBP1 and 2, leads to aberrant programming of NSC function that is perhaps perpetuated into adulthood inducing deficits in differentiation we have previously observed.	Arsenic	0-7	polypyrimidine tract binding protein 1	Mus musculus	142-153
27889505-0	2016	Candesartan ameliorates arsenic-induced hypertensive vascular remodeling by regularizing angiotensin II and TGF-beta signaling in rats.	Arsenic	24-31	angiotensinogen	Rattus norvegicus	89-103
27829122-7	2017	OXT was measured higher in AS and CHS group, but not in CHeS-loaded rats, whereas AVP significantly increased in rats exposed to AS and CHeS.	Arsenic	27-29	oxytocin/neurophysin I prepropeptide	Rattus norvegicus	0-3
27648529-10	2017	The occurrence of boreholes with high dissolved arsenic as As(V) and oxidizing conditions is attributed to extensive sulfide oxidation and alkaline desorption.	Arsenic	48-55	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	59-64
27637898-0	2017	Interactive Influence of N6AMT1 and As3MT Genetic Variations on Arsenic Metabolism in the Population of Inner Mongolia, China.	Arsenic	64-71	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	25-31
27637898-0	2017	Interactive Influence of N6AMT1 and As3MT Genetic Variations on Arsenic Metabolism in the Population of Inner Mongolia, China.	Arsenic	64-71	arsenite methyltransferase	Homo sapiens	36-41
27637898-2	2017	In humans, inorganic arsenic (iAs) is metabolized to monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) mainly mediated by arsenic (+3 oxidation state) methyltransferase (As3MT).	Arsenic	21-28	arsenite methyltransferase	Homo sapiens	180-185
27637898-6	2017	Overall, we showed that N6AMT1 genetic polymorphisms were associated with arsenic biomethylation in the Chinese population, and its interaction with As3MT was observed in specific haplotype combinations.	Arsenic	74-81	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	24-30
27637898-6	2017	Overall, we showed that N6AMT1 genetic polymorphisms were associated with arsenic biomethylation in the Chinese population, and its interaction with As3MT was observed in specific haplotype combinations.	Arsenic	74-81	arsenite methyltransferase	Homo sapiens	149-154
29081891-0	2017	NRF2 Is a Potential Modulator of Hyperresistance to Arsenic Toxicity in Stem-Like Keratinocytes.	Arsenic	52-59	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
27494459-6	2017	Finally, comparing serum and plasma samples of 12 male never smokers (NS) and 29 male active smokers (AS) we observed a significant increase in microparticle-associated TF activity (MP-TF) as well as BDNF in AS, while in serum, BDNF behaved oppositely.	Arsenic	102-104	brain derived neurotrophic factor	Homo sapiens	200-204
27494459-6	2017	Finally, comparing serum and plasma samples of 12 male never smokers (NS) and 29 male active smokers (AS) we observed a significant increase in microparticle-associated TF activity (MP-TF) as well as BDNF in AS, while in serum, BDNF behaved oppositely.	Arsenic	102-104	brain derived neurotrophic factor	Homo sapiens	228-232
27851896-0	2017	Corrigendum to "Low doses of arsenic, via perturbing p53, promotes tumorigenesis" [Toxicol.	Arsenic	29-36	tumor protein p53	Homo sapiens	53-56
29903164-0	2017	[Improving the expression of TP53INP1 in A549 cells enhances the sensitivity of cells to arsenic treatment].	Arsenic	89-96	tumor protein p53 inducible nuclear protein 1	Homo sapiens	29-37
29903164-1	2017	OBJECTIVE: To explore if improving the expression of TP53INP1 could enhance the sensitivity of A549 cells to arsenic.	Arsenic	109-116	tumor protein p53 inducible nuclear protein 1	Homo sapiens	53-61
29903164-12	2017	CONCLUSION: Enhancement of TP53INP1 can significantly improve apoptosis response and enhance sensitivity of A549 cells to arsenic.	Arsenic	122-129	tumor protein p53 inducible nuclear protein 1	Homo sapiens	27-35
29903164-13	2017	It is suggested that TP53INP1 could be used as a new target in arsenic-based cancer treatment.	Arsenic	63-70	tumor protein p53 inducible nuclear protein 1	Homo sapiens	21-29
27889505-0	2016	Candesartan ameliorates arsenic-induced hypertensive vascular remodeling by regularizing angiotensin II and TGF-beta signaling in rats.	Arsenic	24-31	transforming growth factor, beta 1	Rattus norvegicus	108-116
27889505-2	2016	Earlier, we reported that arsenic-mediated enhancement of angiotensin II (AngII) signaling can impair vascular physiology.	Arsenic	26-33	angiotensinogen	Rattus norvegicus	58-72
27889505-2	2016	Earlier, we reported that arsenic-mediated enhancement of angiotensin II (AngII) signaling can impair vascular physiology.	Arsenic	26-33	angiotensinogen	Rattus norvegicus	74-79
27889505-10	2016	Further, AngII caused concentration-dependent incremental change in mean arterial pressure in the arsenic-exposed rats.	Arsenic	98-105	angiotensinogen	Rattus norvegicus	9-14
27889505-11	2016	Arsenic upregulated AT1 and TbetaRII receptor proteins; elevated the levels of PTK, ERK-1/2, TGF-beta and CTGF, decreased RasGAP level and augmented the immunoreactivities of Smad3, Smad4 and collagen III.	Arsenic	0-7	angiotensin II receptor, type 1a	Rattus norvegicus	20-23
27889505-11	2016	Arsenic upregulated AT1 and TbetaRII receptor proteins; elevated the levels of PTK, ERK-1/2, TGF-beta and CTGF, decreased RasGAP level and augmented the immunoreactivities of Smad3, Smad4 and collagen III.	Arsenic	0-7	mitogen activated protein kinase 3	Rattus norvegicus	84-91
27889505-11	2016	Arsenic upregulated AT1 and TbetaRII receptor proteins; elevated the levels of PTK, ERK-1/2, TGF-beta and CTGF, decreased RasGAP level and augmented the immunoreactivities of Smad3, Smad4 and collagen III.	Arsenic	0-7	transforming growth factor, beta 1	Rattus norvegicus	93-101
27889505-11	2016	Arsenic upregulated AT1 and TbetaRII receptor proteins; elevated the levels of PTK, ERK-1/2, TGF-beta and CTGF, decreased RasGAP level and augmented the immunoreactivities of Smad3, Smad4 and collagen III.	Arsenic	0-7	cellular communication network factor 2	Rattus norvegicus	106-110
27889505-11	2016	Arsenic upregulated AT1 and TbetaRII receptor proteins; elevated the levels of PTK, ERK-1/2, TGF-beta and CTGF, decreased RasGAP level and augmented the immunoreactivities of Smad3, Smad4 and collagen III.	Arsenic	0-7	RAS p21 protein activator 1	Rattus norvegicus	122-128
27889505-11	2016	Arsenic upregulated AT1 and TbetaRII receptor proteins; elevated the levels of PTK, ERK-1/2, TGF-beta and CTGF, decreased RasGAP level and augmented the immunoreactivities of Smad3, Smad4 and collagen III.	Arsenic	0-7	SMAD family member 3	Rattus norvegicus	175-180
27889505-11	2016	Arsenic upregulated AT1 and TbetaRII receptor proteins; elevated the levels of PTK, ERK-1/2, TGF-beta and CTGF, decreased RasGAP level and augmented the immunoreactivities of Smad3, Smad4 and collagen III.	Arsenic	0-7	SMAD family member 4	Rattus norvegicus	182-187
27889505-14	2016	Our results demonstrate that candesartan can ameliorate the arsenic-mediated systemic hypertension and vascular remodeling in rats by regularizing the signaling pathways of AngII and TGF-beta.	Arsenic	60-67	angiotensinogen	Rattus norvegicus	173-178
27889505-14	2016	Our results demonstrate that candesartan can ameliorate the arsenic-mediated systemic hypertension and vascular remodeling in rats by regularizing the signaling pathways of AngII and TGF-beta.	Arsenic	60-67	transforming growth factor, beta 1	Rattus norvegicus	183-191
26721309-0	2016	Mitigation of arsenic-induced acquired cancer phenotype in prostate cancer stem cells by miR-143 restoration.	Arsenic	14-21	microRNA 143	Homo sapiens	89-96
26992476-6	2016	In the arsenic group rats, we determined deterioration in the structure of seminiferous tubules, a decrease in the number of spermatogenic cells, an increase in the number of apoptotic cells, a decrease in the number of PCNA-positive cells, a decrease in SOD, CAT and GSH-Px activities, and an increase in the MDA level in testicular tissue.	Arsenic	7-14	catalase	Rattus norvegicus	260-263
27741521-4	2016	However, the mechanism underlying RNS-mediated PARP inhibition by arsenic remains unknown.	Arsenic	66-73	poly(ADP-ribose) polymerase 1	Homo sapiens	47-51
27591999-1	2016	Arsenic (+3 oxidation state) methyltransferase is the key enzyme in the methylation pathway for inorganic arsenic.	Arsenic	106-113	arsenite methyltransferase	Mus musculus	0-46
26721309-5	2016	In prior work, miR-143 was markedly downregulated in As-CSCs, suggesting a role in arsenic-induced malignant transformation.	Arsenic	83-90	microRNA 143	Homo sapiens	15-22
26721309-6	2016	In the present study, we investigated whether loss of miR-143 expression is important in arsenic-induced transformation of prostate SCs.	Arsenic	89-96	microRNA 143	Homo sapiens	54-61
26721309-9	2016	Secreted matrix metalloproteinase (MMP) activity was increased by arsenic-induced malignant transformation, but miR-143 restoration decreased secreted MMP-2 and MMP-9 enzyme activities compared with scramble controls.	Arsenic	66-73	matrix metallopeptidase 2	Homo sapiens	35-38
26721309-14	2016	These findings clearly show that miR-143 restoration mitigated multiple cancer characteristics in the As-CSCs, suggesting a potential role in arsenic-induced transformation of prostate SCs.	Arsenic	142-149	microRNA 143	Homo sapiens	33-40
26721309-15	2016	Thus, miR-143 is a potential biomarker and therapeutic target for arsenic-induced prostate cancer.	Arsenic	66-73	microRNA 143	Homo sapiens	6-13
27659809-0	2016	Polymorphic variants of MRP4/ABCC4 differentially modulate the transport of methylated arsenic metabolites and physiological organic anions.	Arsenic	87-94	ATP binding cassette subfamily C member 4	Homo sapiens	24-28
27764696-5	2016	The retention of As and Se also decreased along the column, suggesting the uptake of As(V) and Se(VI) was highly dependent upon the ZVI corrosion evolution.	Arsenic	17-19	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	85-90
27764696-10	2016	In addition, the evolution of different oxidation states of As and Se retained in the column were identified by XPS, further demonstrating the comprehensive mechanisms of As(V)/Se(VI) removal involving reduction and adsorption in the ZVI/H2O2 column.	Arsenic	60-62	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	171-176
27876813-0	2016	Oncogenic transformation of human lung bronchial epithelial cells induced by arsenic involves ROS-dependent activation of STAT3-miR-21-PDCD4 mechanism.	Arsenic	77-84	signal transducer and activator of transcription 3	Homo sapiens	122-127
27876813-0	2016	Oncogenic transformation of human lung bronchial epithelial cells induced by arsenic involves ROS-dependent activation of STAT3-miR-21-PDCD4 mechanism.	Arsenic	77-84	microRNA 21	Homo sapiens	128-134
27876813-0	2016	Oncogenic transformation of human lung bronchial epithelial cells induced by arsenic involves ROS-dependent activation of STAT3-miR-21-PDCD4 mechanism.	Arsenic	77-84	programmed cell death 4	Homo sapiens	135-140
27876813-2	2016	The present study explored the role of the onco-miR, miR-21 and its target protein, programmed cell death 4 (PDCD4) in arsenic induced malignant cell transformation and tumorigenesis.	Arsenic	119-126	membrane associated ring-CH-type finger 8	Homo sapiens	48-51
27876813-2	2016	The present study explored the role of the onco-miR, miR-21 and its target protein, programmed cell death 4 (PDCD4) in arsenic induced malignant cell transformation and tumorigenesis.	Arsenic	119-126	microRNA 21	Homo sapiens	53-59
27876813-2	2016	The present study explored the role of the onco-miR, miR-21 and its target protein, programmed cell death 4 (PDCD4) in arsenic induced malignant cell transformation and tumorigenesis.	Arsenic	119-126	programmed cell death 4	Homo sapiens	84-107
27876813-2	2016	The present study explored the role of the onco-miR, miR-21 and its target protein, programmed cell death 4 (PDCD4) in arsenic induced malignant cell transformation and tumorigenesis.	Arsenic	119-126	programmed cell death 4	Homo sapiens	109-114
27876813-3	2016	Our results showed that treatment of human bronchial epithelial (BEAS-2B) cells with arsenic induces ROS through p47phox, one of the NOX subunits that is the key source of arsenic-induced ROS.	Arsenic	85-92	neutrophil cytosolic factor 1	Homo sapiens	113-120
27876813-3	2016	Our results showed that treatment of human bronchial epithelial (BEAS-2B) cells with arsenic induces ROS through p47phox, one of the NOX subunits that is the key source of arsenic-induced ROS.	Arsenic	172-179	neutrophil cytosolic factor 1	Homo sapiens	113-120
27876813-4	2016	Arsenic exposure induced an upregulation of miR-21 expression associated with inhibition of PDCD4, and caused malignant cell transformation and tumorigenesis of BEAS-2B cells.	Arsenic	0-7	microRNA 21	Homo sapiens	44-50
27876813-4	2016	Arsenic exposure induced an upregulation of miR-21 expression associated with inhibition of PDCD4, and caused malignant cell transformation and tumorigenesis of BEAS-2B cells.	Arsenic	0-7	programmed cell death 4	Homo sapiens	92-97
27876813-5	2016	Indispensably, STAT3 transcriptional activation by IL-6 is crucial for the arsenic induced miR-21 increase.	Arsenic	75-82	signal transducer and activator of transcription 3	Homo sapiens	15-20
27876813-5	2016	Indispensably, STAT3 transcriptional activation by IL-6 is crucial for the arsenic induced miR-21 increase.	Arsenic	75-82	interleukin 6	Homo sapiens	51-55
27876813-5	2016	Indispensably, STAT3 transcriptional activation by IL-6 is crucial for the arsenic induced miR-21 increase.	Arsenic	75-82	microRNA 21	Homo sapiens	91-97
27876813-6	2016	Upregulated miR-21 levels and suppressed PDCD4 expression was also observed in xenograft tumors generated with chronic arsenic exposed BEAS-2B cells.	Arsenic	119-126	microRNA 21	Homo sapiens	12-18
27876813-6	2016	Upregulated miR-21 levels and suppressed PDCD4 expression was also observed in xenograft tumors generated with chronic arsenic exposed BEAS-2B cells.	Arsenic	119-126	programmed cell death 4	Homo sapiens	41-46
27876813-7	2016	Stable shut down of miR-21, p47phox or STAT3 and overexpression of PDCD4 or catalase in BEAS-2B cells markedly inhibited the arsenic induced malignant transformation and tumorigenesis.	Arsenic	125-132	microRNA 21	Homo sapiens	20-26
27876813-7	2016	Stable shut down of miR-21, p47phox or STAT3 and overexpression of PDCD4 or catalase in BEAS-2B cells markedly inhibited the arsenic induced malignant transformation and tumorigenesis.	Arsenic	125-132	neutrophil cytosolic factor 1	Homo sapiens	28-35
27876813-7	2016	Stable shut down of miR-21, p47phox or STAT3 and overexpression of PDCD4 or catalase in BEAS-2B cells markedly inhibited the arsenic induced malignant transformation and tumorigenesis.	Arsenic	125-132	signal transducer and activator of transcription 3	Homo sapiens	39-44
27876813-7	2016	Stable shut down of miR-21, p47phox or STAT3 and overexpression of PDCD4 or catalase in BEAS-2B cells markedly inhibited the arsenic induced malignant transformation and tumorigenesis.	Arsenic	125-132	programmed cell death 4	Homo sapiens	67-72
27876813-7	2016	Stable shut down of miR-21, p47phox or STAT3 and overexpression of PDCD4 or catalase in BEAS-2B cells markedly inhibited the arsenic induced malignant transformation and tumorigenesis.	Arsenic	125-132	catalase	Homo sapiens	76-84
27876813-9	2016	Furthermore, arsenic suppressed the downstream protein E-cadherin expression and induced beta-catenin/TCF-dependent transcription of uPAR and c-Myc.	Arsenic	13-20	cadherin 1	Homo sapiens	55-65
27876813-9	2016	Furthermore, arsenic suppressed the downstream protein E-cadherin expression and induced beta-catenin/TCF-dependent transcription of uPAR and c-Myc.	Arsenic	13-20	catenin beta 1	Homo sapiens	89-101
27876813-9	2016	Furthermore, arsenic suppressed the downstream protein E-cadherin expression and induced beta-catenin/TCF-dependent transcription of uPAR and c-Myc.	Arsenic	13-20	hepatocyte nuclear factor 4 alpha	Homo sapiens	102-105
27876813-9	2016	Furthermore, arsenic suppressed the downstream protein E-cadherin expression and induced beta-catenin/TCF-dependent transcription of uPAR and c-Myc.	Arsenic	13-20	plasminogen activator, urokinase receptor	Homo sapiens	133-137
27876813-9	2016	Furthermore, arsenic suppressed the downstream protein E-cadherin expression and induced beta-catenin/TCF-dependent transcription of uPAR and c-Myc.	Arsenic	13-20	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	142-147
27876813-10	2016	These results indicate that the ROS-STAT3-miR-21-PDCD4 signaling axis plays an important role in arsenic -induced carcinogenesis.	Arsenic	97-104	signal transducer and activator of transcription 3	Homo sapiens	36-41
27876813-10	2016	These results indicate that the ROS-STAT3-miR-21-PDCD4 signaling axis plays an important role in arsenic -induced carcinogenesis.	Arsenic	97-104	microRNA 21	Homo sapiens	42-48
27876813-10	2016	These results indicate that the ROS-STAT3-miR-21-PDCD4 signaling axis plays an important role in arsenic -induced carcinogenesis.	Arsenic	97-104	programmed cell death 4	Homo sapiens	49-54
27728822-3	2016	Arsenic in the mine precipitate was present as As(V) and schwertmannite was the main Fe mineral.	Arsenic	0-7	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	47-52
27659809-0	2016	Polymorphic variants of MRP4/ABCC4 differentially modulate the transport of methylated arsenic metabolites and physiological organic anions.	Arsenic	87-94	ATP binding cassette subfamily C member 4	Homo sapiens	29-34
27659809-2	2016	We recently identified human multidrug resistance protein 4 (MRP4/ABCC4) as a novel pathway for the cellular export of dimethylarsinic acid (DMAV), the major urinary arsenic metabolite in humans, and the diglutathione conjugate of the highly toxic monomethylarsonous acid [MMA(GS)2].	Arsenic	166-173	ATP binding cassette subfamily C member 4	Homo sapiens	61-65
27659809-2	2016	We recently identified human multidrug resistance protein 4 (MRP4/ABCC4) as a novel pathway for the cellular export of dimethylarsinic acid (DMAV), the major urinary arsenic metabolite in humans, and the diglutathione conjugate of the highly toxic monomethylarsonous acid [MMA(GS)2].	Arsenic	166-173	ATP binding cassette subfamily C member 4	Homo sapiens	66-71
27659809-3	2016	These findings, together with the basolateral and apical membrane localization of MRP4 in hepatocytes and renal proximal tubule cells, respectively, suggest a role for MRP4 in the urinary elimination of hepatic arsenic metabolites.	Arsenic	211-218	ATP binding cassette subfamily C member 4	Homo sapiens	82-86
27659809-3	2016	These findings, together with the basolateral and apical membrane localization of MRP4 in hepatocytes and renal proximal tubule cells, respectively, suggest a role for MRP4 in the urinary elimination of hepatic arsenic metabolites.	Arsenic	211-218	ATP binding cassette subfamily C member 4	Homo sapiens	168-172
27659809-8	2016	Thus, MRP4 variants have differing abilities to transport arsenic and endogenous metabolites through both altered function and membrane localization.	Arsenic	58-65	ATP binding cassette subfamily C member 4	Homo sapiens	6-10
27659809-9	2016	Further investigation is warranted to determine if genetic variations in ABCC4 contribute to inter-individual differences in susceptibility to arsenic-induced (and potentially other) diseases.	Arsenic	143-150	ATP binding cassette subfamily C member 4	Homo sapiens	73-78
27428365-10	2016	Results showed that AtMRP1 is important for vacuolar accumulation of antifolates as well as tolerance against arsenic, both of which involved phosphorylation in the serine triads at the C terminal NBD of AtMRP1.	Arsenic	110-117	multidrug resistance-associated protein 1	Arabidopsis thaliana	20-26
27262276-2	2016	Organic arsenic compounds and their degradation products, arsenate (As(V)) and arsenite (As(III)), exist in the effluent from anaerobic reactors treating animal manure contaminated by ROX or ASA with ammonium (NH4(+)-N) and phosphate (PO4(3-)-P) together.	Arsenic	8-15	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	68-73
27262276-8	2016	In addition, the arsenic content of As(V) in the struvite was higher than that of As(III), ASA and ROX.	Arsenic	17-24	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	36-41
27549238-3	2016	Average concentrations of total As in colostrum and cord serum were 18.51 +- 7.00 and 19.83 +- 10.50 mug L-1.	Arsenic	32-34	immunoglobulin kappa variable 1-16	Homo sapiens	105-108
27018130-12	2016	Phospho-Syk and phospho-p85 phosphoinositide 3-kinase enzyme-linked immunosorbent assays data show that arsenic inhibits early phosphorylation events.	Arsenic	104-111	spleen associated tyrosine kinase	Rattus norvegicus	8-11
27736728-5	2016	We compared the arsenic sensitivity, and the expression and responses to arsenic of the arsenic-related transporters, MRP1, MRP2, and ASNA1, in paired parent/arsenic-resistant HL-60/RS/HL-60 and arsenic-sensitive/parental K562/ADM/K562 cells.	Arsenic	73-80	ATP binding cassette subfamily C member 1	Homo sapiens	118-122
27736728-5	2016	We compared the arsenic sensitivity, and the expression and responses to arsenic of the arsenic-related transporters, MRP1, MRP2, and ASNA1, in paired parent/arsenic-resistant HL-60/RS/HL-60 and arsenic-sensitive/parental K562/ADM/K562 cells.	Arsenic	73-80	ATP binding cassette subfamily C member 1	Homo sapiens	118-122
27736728-5	2016	We compared the arsenic sensitivity, and the expression and responses to arsenic of the arsenic-related transporters, MRP1, MRP2, and ASNA1, in paired parent/arsenic-resistant HL-60/RS/HL-60 and arsenic-sensitive/parental K562/ADM/K562 cells.	Arsenic	73-80	ATP binding cassette subfamily C member 1	Homo sapiens	118-122
27736728-8	2016	In conclusion, the cross-resistance of conventional chemotherapeutics-resistant leukemic cells to arsenic trioxide is determined by both levels of MRP1, MRP2, and ASNA1, and also by the responses of these transporters to arsenic stress.	Arsenic	98-105	ATP binding cassette subfamily C member 1	Homo sapiens	147-151
27736728-8	2016	In conclusion, the cross-resistance of conventional chemotherapeutics-resistant leukemic cells to arsenic trioxide is determined by both levels of MRP1, MRP2, and ASNA1, and also by the responses of these transporters to arsenic stress.	Arsenic	98-105	synaptonemal complex central element protein 1 like	Homo sapiens	153-157
27736728-8	2016	In conclusion, the cross-resistance of conventional chemotherapeutics-resistant leukemic cells to arsenic trioxide is determined by both levels of MRP1, MRP2, and ASNA1, and also by the responses of these transporters to arsenic stress.	Arsenic	98-105	guided entry of tail-anchored proteins factor 3, ATPase	Homo sapiens	163-168
27721063-1	2016	We previously reported that two splicing variants of human AS3MT mRNA, exon-3 skipping form (Delta3) and exons-4 and -5 skipping form (Delta4,5), were detected in HepG2 cells and that both variants lacked arsenic methylation activity (Sumi et al., 2011).	Arsenic	205-212	arsenite methyltransferase	Homo sapiens	59-64
27638049-2	2016	Here, we show that arsenic induction of the UPR triggers ATF4, which is involved in regulating this ER-mitochondrial crosstalk that is important for the molecular pathogenesis of arsenic toxicity.	Arsenic	19-26	activating transcription factor 4	Homo sapiens	57-61
27526673-1	2016	Arsenic, a metalloid with cytotoxic and carcinogenic effects related to the disruption of glutathione homeostasis, induces the expression of ATF4, a central transcription factor in the cellular stress response.	Arsenic	0-7	activating transcription factor 4	Mus musculus	141-145
27512893-1	2016	This study examines arsenic, copper, lead and manganese drinking water contamination at the domestic consumer"s kitchen tap in homes of New South Wales, Australia.	Arsenic	20-27	nuclear RNA export factor 1	Homo sapiens	120-123
27428365-10	2016	Results showed that AtMRP1 is important for vacuolar accumulation of antifolates as well as tolerance against arsenic, both of which involved phosphorylation in the serine triads at the C terminal NBD of AtMRP1.	Arsenic	110-117	multidrug resistance-associated protein 1	Arabidopsis thaliana	204-210
28149117-9	2016	RESULTS: In rats with liver damage due to arsenic exposure, melatonin administration significantly decreased the levels of IL-6, macrophage migration inhibitory factor, and monocyte chemotactic protein-1 (p&lt;0.001, p=0.02 and p=0.04, respectively).	Arsenic	42-49	interleukin 6	Rattus norvegicus	123-127
28149117-9	2016	RESULTS: In rats with liver damage due to arsenic exposure, melatonin administration significantly decreased the levels of IL-6, macrophage migration inhibitory factor, and monocyte chemotactic protein-1 (p&lt;0.001, p=0.02 and p=0.04, respectively).	Arsenic	42-49	macrophage migration inhibitory factor	Rattus norvegicus	129-167
28149117-9	2016	RESULTS: In rats with liver damage due to arsenic exposure, melatonin administration significantly decreased the levels of IL-6, macrophage migration inhibitory factor, and monocyte chemotactic protein-1 (p&lt;0.001, p=0.02 and p=0.04, respectively).	Arsenic	42-49	C-C motif chemokine ligand 2	Rattus norvegicus	173-203
27799742-8	2016	Arsenic toxicity caused significant rise in serum aspartate aminotransferase, alanine aminotransferase and total bilirubin, and a significant decrease in total protein (TP) and albumin levels after 3 weeks of experimental period.	Arsenic	0-7	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	50-76
27622732-10	2016	CETP protein levels of HepG2 cells were significantly elevated under arsenic exposure.	Arsenic	69-76	cholesteryl ester transfer protein	Homo sapiens	0-4
27622732-12	2016	In conclusion, arsenic not only inhibits LXR-beta and SREBP-1c mRNA and protein levels but also independently increases CETP protein levels in HepG2 cells.	Arsenic	15-22	nuclear receptor subfamily 1 group H member 2	Homo sapiens	41-49
27622732-12	2016	In conclusion, arsenic not only inhibits LXR-beta and SREBP-1c mRNA and protein levels but also independently increases CETP protein levels in HepG2 cells.	Arsenic	15-22	sterol regulatory element binding transcription factor 1	Homo sapiens	54-62
27622732-12	2016	In conclusion, arsenic not only inhibits LXR-beta and SREBP-1c mRNA and protein levels but also independently increases CETP protein levels in HepG2 cells.	Arsenic	15-22	cholesteryl ester transfer protein	Homo sapiens	120-124
27113276-0	2016	Assessing multimedia/multipathway exposures to inorganic arsenic at population and individual level using MERLIN-Expo.	Arsenic	57-64	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	106-112
27785370-8	2016	Core apoptosis related and glutathione metabolism genes in 1 and 10 muM of arsenic-treated HepG2 cells were analyzed after 12 h of incubation.	Arsenic	75-82	latexin	Homo sapiens	68-71
27785370-9	2016	An arsenic treatment of 1 muM exhibits no cell death at 12 h, whereas 10 muM arsenic treatment reveals around 50% cell death at 12 h. Results depict 28 and 44 affected genes in 1 and 10 muM arsenic-treated cells, respectively.	Arsenic	3-10	latexin	Homo sapiens	26-29
27785370-9	2016	An arsenic treatment of 1 muM exhibits no cell death at 12 h, whereas 10 muM arsenic treatment reveals around 50% cell death at 12 h. Results depict 28 and 44 affected genes in 1 and 10 muM arsenic-treated cells, respectively.	Arsenic	77-84	latexin	Homo sapiens	73-76
27785370-9	2016	An arsenic treatment of 1 muM exhibits no cell death at 12 h, whereas 10 muM arsenic treatment reveals around 50% cell death at 12 h. Results depict 28 and 44 affected genes in 1 and 10 muM arsenic-treated cells, respectively.	Arsenic	77-84	latexin	Homo sapiens	73-76
27785370-9	2016	An arsenic treatment of 1 muM exhibits no cell death at 12 h, whereas 10 muM arsenic treatment reveals around 50% cell death at 12 h. Results depict 28 and 44 affected genes in 1 and 10 muM arsenic-treated cells, respectively.	Arsenic	77-84	latexin	Homo sapiens	73-76
27785370-9	2016	An arsenic treatment of 1 muM exhibits no cell death at 12 h, whereas 10 muM arsenic treatment reveals around 50% cell death at 12 h. Results depict 28 and 44 affected genes in 1 and 10 muM arsenic-treated cells, respectively.	Arsenic	77-84	latexin	Homo sapiens	73-76
27113276-1	2016	In this study, we report on model simulations performed using the newly developed exposure tool, MERLIN-Expo, in order to assess inorganic arsenic (iAs) exposure to adults resulting from past emissions by non-ferrous smelters in Belgium (Northern Campine area).	Arsenic	139-146	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	97-103
27782044-2	2016	Association of Children"s Urinary CC16 Levels with Arsenic Concentrations in Multiple Environmental Media.	Arsenic	51-58	secretoglobin family 1A member 1	Homo sapiens	34-38
27711833-5	2016	In this experiment, aqueous arsenic in released pore water ranged from 17.5 to 21.3 mug L-1 and the accumulated content of the released arsenic was 17.576 mug during the compaction.	Arsenic	28-35	immunoglobulin kappa variable 1-16	Homo sapiens	88-91
27782045-2	2016	Association of Children"s Urinary CC16 Levels with Arsenic Concentrations in Multiple Environmental Media.	Arsenic	51-58	secretoglobin family 1A member 1	Homo sapiens	34-38
27431456-0	2016	Environmental exposure to arsenic and chromium in children is associated with kidney injury molecule-1.	Arsenic	26-33	hepatitis A virus cellular receptor 1	Homo sapiens	78-102
27427777-2	2016	Here, we report the first three isolates of anaerobic As(V)-reducing bacterial strains (strains JQ, DJ-3 and DJ-4) from a soil sample containing 48.7% of total As in the form of As(III) collected in Chifeng, Inner Mongolia, China.	Arsenic	54-56	DnaJ heat shock protein family (Hsp40) member A2	Homo sapiens	100-104
27427777-2	2016	Here, we report the first three isolates of anaerobic As(V)-reducing bacterial strains (strains JQ, DJ-3 and DJ-4) from a soil sample containing 48.7% of total As in the form of As(III) collected in Chifeng, Inner Mongolia, China.	Arsenic	54-56	DnaJ heat shock protein family (Hsp40) member B6	Homo sapiens	109-113
27427777-7	2016	Strain DJ-3 not only possesses the strongest resistance to As(V) but could also reduce 53% of the As(V) to As(III) in the treatment of 60 mM As(V) in 5 d. All three strains could release As from goethite; strain DJ-4 has the highest ability to promote the release of As (90.5%) from goethite.	Arsenic	59-61	DnaJ heat shock protein family (Hsp40) member A2	Homo sapiens	7-11
27427777-8	2016	These results suggested that strains JQ, DJ-3 and DJ-4 may play an important role in the mobilization and transformation of As in soil.	Arsenic	124-126	DnaJ heat shock protein family (Hsp40) member A2	Homo sapiens	41-45
27427777-8	2016	These results suggested that strains JQ, DJ-3 and DJ-4 may play an important role in the mobilization and transformation of As in soil.	Arsenic	124-126	DnaJ heat shock protein family (Hsp40) member B6	Homo sapiens	50-54
27908234-8	2016	Alterations in complex I, a main site for reactive oxygen species (ROS) production as well as increased expression of ROS-producing NOX4 in arsenic-transformed cells suggested a role of oxidative stress in tumorigenic transformation of prostate epithelial cells.	Arsenic	140-147	NADPH oxidase 4	Homo sapiens	132-136
27372261-6	2016	In the presence of 48.6 mg L(-1) Cu(II), the sorption capacity of As(V) increased from 1.5 to 3.8 mg g(-1) after 240 h. The sorption data for As(III)/As(V) and Cu(II) conformed the Freundlich and Langmuir isotherm models, respectively.	Arsenic	66-68	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	150-155
27448814-11	2016	Our findings also suggested that GSTT1 and hOGG1 gene polymorphisms might play an important role in the individual risk of As-induced carotid atherosclerosis.	Arsenic	123-125	glutathione S-transferase theta 1	Homo sapiens	33-38
27448814-11	2016	Our findings also suggested that GSTT1 and hOGG1 gene polymorphisms might play an important role in the individual risk of As-induced carotid atherosclerosis.	Arsenic	123-125	8-oxoguanine DNA glycosylase	Homo sapiens	43-48
27431456-6	2016	Almost all tap and well water samples had levels of arsenic (81.5%) and fluoride (100%) above the permissible levels recommended by the World Health Organization.	Arsenic	52-59	nuclear RNA export factor 1	Homo sapiens	11-14
27431456-10	2016	Arsenic upper tertile was also associated with higher urinary KIM-1 (372pg/mL).	Arsenic	0-7	hepatitis A virus cellular receptor 1	Homo sapiens	62-67
27413109-0	2016	From the Cover: Arsenic Induces Accumulation of alpha-Synuclein: Implications for Synucleinopathies and Neurodegeneration.	Arsenic	16-23	synuclein alpha	Homo sapiens	48-63
27692299-2	2016	In a Genome Wide Association Study (GWAS) on Bangladesh population, a significant association of asingle nucleotide polymorphism (SNP) in the C10orf32 region (rs 9527; G&gt;A) with urinary metabolites and arsenic induced skin lesions was reported.	Arsenic	205-212	BLOC-1 related complex subunit 7	Homo sapiens	142-150
27692299-3	2016	This study aims to evaluate the association of the C10orf32 G to A polymorphism (rs9527), concerned with As3MT read-through transcription, with the development of arsenic induced skin lesions in the arsenic exposed individuals of West Bengal, India.	Arsenic	163-170	BLOC-1 related complex subunit 7	Homo sapiens	51-59
27692299-3	2016	This study aims to evaluate the association of the C10orf32 G to A polymorphism (rs9527), concerned with As3MT read-through transcription, with the development of arsenic induced skin lesions in the arsenic exposed individuals of West Bengal, India.	Arsenic	163-170	arsenite methyltransferase	Homo sapiens	105-110
27692299-7	2016	Hence, it can be concluded that G&gt;A change in the C10orf32 region plays an important role in arsenic induced toxicity and susceptibility.	Arsenic	96-103	BLOC-1 related complex subunit 7	Homo sapiens	53-61
27427241-7	2016	The most potent metals, Cd(2+), Zn(2+) and As(3+) induced highest levels of oxidative activity, and ROS appeared to be central in their CXCL8 and IL-6 responses.	Arsenic	43-45	C-X-C motif chemokine ligand 8	Homo sapiens	136-141
27427241-7	2016	The most potent metals, Cd(2+), Zn(2+) and As(3+) induced highest levels of oxidative activity, and ROS appeared to be central in their CXCL8 and IL-6 responses.	Arsenic	43-45	interleukin 6	Homo sapiens	146-150
27397144-8	2016	Taken together, our findings show that As-I stimulates osteoblast differentiation through the Wnt/beta-catenin signaling pathway, which also activates the BMP pathway and RANK pathway, thus highlighting the As-I for pharmaceutical and medicinal applications such as treating bone disease.	Arsenic	39-41	catenin (cadherin associated protein), beta 1	Mus musculus	98-110
27397144-8	2016	Taken together, our findings show that As-I stimulates osteoblast differentiation through the Wnt/beta-catenin signaling pathway, which also activates the BMP pathway and RANK pathway, thus highlighting the As-I for pharmaceutical and medicinal applications such as treating bone disease.	Arsenic	39-41	bone morphogenetic protein 2	Mus musculus	155-158
27517564-5	2016	Incomplete rescue of Oct4 expression in arsenic-treated cells ectopically expressing an siRNA-resistant PML transcript suggested that OCT4 regulation in liver CSCs involves other factors in addition to PML.	Arsenic	40-47	POU class 5 homeobox 1	Homo sapiens	21-25
27517564-5	2016	Incomplete rescue of Oct4 expression in arsenic-treated cells ectopically expressing an siRNA-resistant PML transcript suggested that OCT4 regulation in liver CSCs involves other factors in addition to PML.	Arsenic	40-47	PML nuclear body scaffold	Homo sapiens	104-107
27517564-5	2016	Incomplete rescue of Oct4 expression in arsenic-treated cells ectopically expressing an siRNA-resistant PML transcript suggested that OCT4 regulation in liver CSCs involves other factors in addition to PML.	Arsenic	40-47	POU class 5 homeobox 1	Homo sapiens	134-138
27413109-5	2016	We therefore examined the role of As in the oligomerization of SYN, and the consequences thereof.	Arsenic	34-36	synemin, intermediate filament protein	Mus musculus	63-66
27413109-8	2016	Mice exposed to As (100 ppb) for 1 month, exhibited elevated SYN accumulation in the cortex and striatum, and elevations in protein ubiquitination and LC3-I and II levels.	Arsenic	16-18	synemin, intermediate filament protein	Mus musculus	61-64
27413109-8	2016	Mice exposed to As (100 ppb) for 1 month, exhibited elevated SYN accumulation in the cortex and striatum, and elevations in protein ubiquitination and LC3-I and II levels.	Arsenic	16-18	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	151-154
27461142-13	2016	These studies identify a novel role for ATF4 in underlying pathogenesis of macrophage dysregulation and immuno-toxicity of arsenic.	Arsenic	123-130	activating transcription factor 4	Mus musculus	40-44
27613243-12	2016	Hsa-miR-33a modulated 28 genes, such as C1S.	Arsenic	7-11	complement C1s	Homo sapiens	40-43
27018134-9	2016	On inhibiting Akt (by PI3K inhibitor, LY294002) and ERK1/2 (by ERK1/2 inhibitor, PD98059) specifically, caspase 3 got activated abolishing mangiferin"s protective role on As-induced hepatotoxicity.	Arsenic	171-173	AKT serine/threonine kinase 1	Homo sapiens	14-17
27018134-9	2016	On inhibiting Akt (by PI3K inhibitor, LY294002) and ERK1/2 (by ERK1/2 inhibitor, PD98059) specifically, caspase 3 got activated abolishing mangiferin"s protective role on As-induced hepatotoxicity.	Arsenic	171-173	mitogen-activated protein kinase 3	Homo sapiens	52-58
27018134-9	2016	On inhibiting Akt (by PI3K inhibitor, LY294002) and ERK1/2 (by ERK1/2 inhibitor, PD98059) specifically, caspase 3 got activated abolishing mangiferin"s protective role on As-induced hepatotoxicity.	Arsenic	171-173	caspase 3	Homo sapiens	104-113
26767369-3	2016	There was a decrease in mitochondrial superoxide dismutase (MnSOD) activity in arsenic-treated rats that might be responsible for increased protein and lipid oxidation as observed in our study.	Arsenic	79-86	superoxide dismutase 2	Rattus norvegicus	24-58
27492940-1	2016	The arsenic(III) and antimony(III) cyanides M(CN)3 (M=As, Sb) have been prepared in quantitative yields from the corresponding trifluorides through fluoride-cyanide exchange with Me3 SiCN in acetonitrile.	Arsenic	4-11	malic enzyme 3	Homo sapiens	179-182
27585557-7	2016	It is further proposed that arsenic mainly impaired spermatogenesis and fertilization via aberrant modulation of these male reproduction-related proteins and metabolites, which may be mediated by the ERK/AKT/NF-kappaB-dependent signaling pathway.	Arsenic	28-35	Eph receptor B1	Rattus norvegicus	200-203
27585557-7	2016	It is further proposed that arsenic mainly impaired spermatogenesis and fertilization via aberrant modulation of these male reproduction-related proteins and metabolites, which may be mediated by the ERK/AKT/NF-kappaB-dependent signaling pathway.	Arsenic	28-35	AKT serine/threonine kinase 1	Rattus norvegicus	204-207
26404762-7	2016	TMP inhibited arsenic-induced activations of JNK, p38 MAPK, ERK, AP-1 and Nrf2 and block HO-1 protein expression.	Arsenic	14-21	mitogen-activated protein kinase 8	Homo sapiens	45-48
26404762-7	2016	TMP inhibited arsenic-induced activations of JNK, p38 MAPK, ERK, AP-1 and Nrf2 and block HO-1 protein expression.	Arsenic	14-21	mitogen-activated protein kinase 14	Homo sapiens	50-53
26404762-7	2016	TMP inhibited arsenic-induced activations of JNK, p38 MAPK, ERK, AP-1 and Nrf2 and block HO-1 protein expression.	Arsenic	14-21	mitogen-activated protein kinase 1	Homo sapiens	54-58
26404762-7	2016	TMP inhibited arsenic-induced activations of JNK, p38 MAPK, ERK, AP-1 and Nrf2 and block HO-1 protein expression.	Arsenic	14-21	mitogen-activated protein kinase 1	Homo sapiens	60-63
26404762-7	2016	TMP inhibited arsenic-induced activations of JNK, p38 MAPK, ERK, AP-1 and Nrf2 and block HO-1 protein expression.	Arsenic	14-21	FosB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	65-69
26404762-7	2016	TMP inhibited arsenic-induced activations of JNK, p38 MAPK, ERK, AP-1 and Nrf2 and block HO-1 protein expression.	Arsenic	14-21	NFE2 like bZIP transcription factor 2	Homo sapiens	74-78
26404762-7	2016	TMP inhibited arsenic-induced activations of JNK, p38 MAPK, ERK, AP-1 and Nrf2 and block HO-1 protein expression.	Arsenic	14-21	heme oxygenase 1	Homo sapiens	89-93
26404762-0	2016	2,3,5,6-Tetramethylpyrazine (TMP) down-regulated arsenic-induced heme oxygenase-1 and ARS2 expression by inhibiting Nrf2, NF-kappaB, AP-1 and MAPK pathways in human proximal tubular cells.	Arsenic	49-56	heme oxygenase 1	Homo sapiens	65-81
26404762-0	2016	2,3,5,6-Tetramethylpyrazine (TMP) down-regulated arsenic-induced heme oxygenase-1 and ARS2 expression by inhibiting Nrf2, NF-kappaB, AP-1 and MAPK pathways in human proximal tubular cells.	Arsenic	49-56	serrate, RNA effector molecule	Homo sapiens	86-90
26404762-0	2016	2,3,5,6-Tetramethylpyrazine (TMP) down-regulated arsenic-induced heme oxygenase-1 and ARS2 expression by inhibiting Nrf2, NF-kappaB, AP-1 and MAPK pathways in human proximal tubular cells.	Arsenic	49-56	NFE2 like bZIP transcription factor 2	Homo sapiens	116-120
26404762-0	2016	2,3,5,6-Tetramethylpyrazine (TMP) down-regulated arsenic-induced heme oxygenase-1 and ARS2 expression by inhibiting Nrf2, NF-kappaB, AP-1 and MAPK pathways in human proximal tubular cells.	Arsenic	49-56	nuclear factor kappa B subunit 1	Homo sapiens	122-131
26404762-0	2016	2,3,5,6-Tetramethylpyrazine (TMP) down-regulated arsenic-induced heme oxygenase-1 and ARS2 expression by inhibiting Nrf2, NF-kappaB, AP-1 and MAPK pathways in human proximal tubular cells.	Arsenic	49-56	FosB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	133-137
26404762-0	2016	2,3,5,6-Tetramethylpyrazine (TMP) down-regulated arsenic-induced heme oxygenase-1 and ARS2 expression by inhibiting Nrf2, NF-kappaB, AP-1 and MAPK pathways in human proximal tubular cells.	Arsenic	49-56	mitogen-activated protein kinase 1	Homo sapiens	142-146
26404762-2	2016	The present study demonstrated that arsenic exposure resulted in protein and enzymatic induction of heme oxygenase-1 (HO-1) in dose- and time-dependent manners in HK-2 cells.	Arsenic	36-43	heme oxygenase 1	Homo sapiens	100-116
26404762-2	2016	The present study demonstrated that arsenic exposure resulted in protein and enzymatic induction of heme oxygenase-1 (HO-1) in dose- and time-dependent manners in HK-2 cells.	Arsenic	36-43	heme oxygenase 1	Homo sapiens	118-122
26404762-3	2016	Blocking HO-1 enzymatic activity by zinc protoporphyrin (ZnPP) augmented arsenic-induced apoptosis, ROS production and mitochondrial dysfunction, suggesting a critical role for HO-1 as a renal protectant in this procession.	Arsenic	73-80	heme oxygenase 1	Homo sapiens	9-13
26404762-3	2016	Blocking HO-1 enzymatic activity by zinc protoporphyrin (ZnPP) augmented arsenic-induced apoptosis, ROS production and mitochondrial dysfunction, suggesting a critical role for HO-1 as a renal protectant in this procession.	Arsenic	73-80	heme oxygenase 1	Homo sapiens	177-181
26404762-8	2016	The present study, furthermore, demonstrated arsenic-induced expression of arsenic response protein 2 (ARS2) that was regulated by p38 MAPK, ERK and NF-kappaB.	Arsenic	45-52	serrate, RNA effector molecule	Homo sapiens	75-101
26404762-8	2016	The present study, furthermore, demonstrated arsenic-induced expression of arsenic response protein 2 (ARS2) that was regulated by p38 MAPK, ERK and NF-kappaB.	Arsenic	45-52	serrate, RNA effector molecule	Homo sapiens	103-107
26404762-8	2016	The present study, furthermore, demonstrated arsenic-induced expression of arsenic response protein 2 (ARS2) that was regulated by p38 MAPK, ERK and NF-kappaB.	Arsenic	45-52	mitogen-activated protein kinase 14	Homo sapiens	131-134
26404762-8	2016	The present study, furthermore, demonstrated arsenic-induced expression of arsenic response protein 2 (ARS2) that was regulated by p38 MAPK, ERK and NF-kappaB.	Arsenic	45-52	mitogen-activated protein kinase 1	Homo sapiens	141-144
26404762-8	2016	The present study, furthermore, demonstrated arsenic-induced expression of arsenic response protein 2 (ARS2) that was regulated by p38 MAPK, ERK and NF-kappaB.	Arsenic	45-52	nuclear factor kappa B subunit 1	Homo sapiens	149-158
26404762-9	2016	To our knowledge, this is the first report showing that ARS2 involved in arsenic-induced nephrotoxicity, while TMP pretreatment prevented such an up-regulation of ARS2 in HK-2 cells.	Arsenic	73-80	serrate, RNA effector molecule	Homo sapiens	56-60
26404762-11	2016	In summary, our study highlighted a role of HO-1 in the protection against arsenic-induced cytotoxicity downstream from the primary targets of TMP and further indicated that TMP may be used as a potential therapeutic agent in the treatment of arsenic-induced nephrotoxicity.	Arsenic	75-82	heme oxygenase 1	Homo sapiens	44-48
26404762-11	2016	In summary, our study highlighted a role of HO-1 in the protection against arsenic-induced cytotoxicity downstream from the primary targets of TMP and further indicated that TMP may be used as a potential therapeutic agent in the treatment of arsenic-induced nephrotoxicity.	Arsenic	243-250	heme oxygenase 1	Homo sapiens	44-48
26767369-3	2016	There was a decrease in mitochondrial superoxide dismutase (MnSOD) activity in arsenic-treated rats that might be responsible for increased protein and lipid oxidation as observed in our study.	Arsenic	79-86	superoxide dismutase 2	Rattus norvegicus	60-65
26404762-4	2016	On the other hand, TMP, upstream of HO-1, inhibited arsenic-induced ROS production and ROS-dependent HO-1 expression.	Arsenic	52-59	heme oxygenase 1	Homo sapiens	36-40
26767369-5	2016	The protein and mRNA expression of MnSOD was reduced suggesting increased mitochondrial oxidative damage after arsenic treatment.	Arsenic	111-118	superoxide dismutase 2	Rattus norvegicus	35-40
26404762-6	2016	Our results revealed that the regulation of arsenic-induced HO-1 expression was performed through multiple ROS-dependent signal pathways and the corresponding transcription factors, including p38 MAPK and JNK (but not ERK), AP-1, Nrf2 and NF-kappaB.	Arsenic	44-51	heme oxygenase 1	Homo sapiens	60-64
26404762-6	2016	Our results revealed that the regulation of arsenic-induced HO-1 expression was performed through multiple ROS-dependent signal pathways and the corresponding transcription factors, including p38 MAPK and JNK (but not ERK), AP-1, Nrf2 and NF-kappaB.	Arsenic	44-51	mitogen-activated protein kinase 14	Homo sapiens	192-195
25605447-8	2016	Exposure to iAs from food and water combined, in areas where tap water As concentration is &lt;=10 mug/l, may contribute to As-induced changes in a biomarker associated with toxicity.	Arsenic	13-15	nuclear RNA export factor 1	Homo sapiens	61-64
26404762-6	2016	Our results revealed that the regulation of arsenic-induced HO-1 expression was performed through multiple ROS-dependent signal pathways and the corresponding transcription factors, including p38 MAPK and JNK (but not ERK), AP-1, Nrf2 and NF-kappaB.	Arsenic	44-51	mitogen-activated protein kinase 1	Homo sapiens	196-200
26404762-6	2016	Our results revealed that the regulation of arsenic-induced HO-1 expression was performed through multiple ROS-dependent signal pathways and the corresponding transcription factors, including p38 MAPK and JNK (but not ERK), AP-1, Nrf2 and NF-kappaB.	Arsenic	44-51	mitogen-activated protein kinase 8	Homo sapiens	205-208
26404762-6	2016	Our results revealed that the regulation of arsenic-induced HO-1 expression was performed through multiple ROS-dependent signal pathways and the corresponding transcription factors, including p38 MAPK and JNK (but not ERK), AP-1, Nrf2 and NF-kappaB.	Arsenic	44-51	mitogen-activated protein kinase 1	Homo sapiens	218-221
26404762-6	2016	Our results revealed that the regulation of arsenic-induced HO-1 expression was performed through multiple ROS-dependent signal pathways and the corresponding transcription factors, including p38 MAPK and JNK (but not ERK), AP-1, Nrf2 and NF-kappaB.	Arsenic	44-51	FosB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	224-228
26404762-6	2016	Our results revealed that the regulation of arsenic-induced HO-1 expression was performed through multiple ROS-dependent signal pathways and the corresponding transcription factors, including p38 MAPK and JNK (but not ERK), AP-1, Nrf2 and NF-kappaB.	Arsenic	44-51	NFE2 like bZIP transcription factor 2	Homo sapiens	230-234
26404762-6	2016	Our results revealed that the regulation of arsenic-induced HO-1 expression was performed through multiple ROS-dependent signal pathways and the corresponding transcription factors, including p38 MAPK and JNK (but not ERK), AP-1, Nrf2 and NF-kappaB.	Arsenic	44-51	nuclear factor kappa B subunit 1	Homo sapiens	239-248
27307033-4	2016	Median and 95th percentiles of concentrations in tap water were in mug/L: Al: &lt;10, 48.3, As: 0.2, 2.1; B: &lt;100, 100; Ba: 30.7, 149.4; Ca: 85,000, 121,700; Cd: &lt;0.5, &lt;0.5; Ce: &lt;0.5, &lt;0.5; Co: &lt;0.5, 0.8; Cr: &lt;5, &lt;5; Cu: 70, 720; K: 2210, 6740; Fe: &lt;20, 46; Mn: &lt;5, &lt;5; Mo: &lt;0.5, 1.5; Na: 14,500, 66,800; Ni: &lt;2, 10.2; Mg: 6500, 21,200; Pb: &lt;1, 5.4; Sb: &lt;0.5, &lt;0.5; Se: &lt;1, 6.7; Sr: 256.9, 1004; Tl: &lt;0.5, &lt;0.5; U: &lt;0.5, 2.4; V: &lt;1, 1; Zn: 53, 208.	Arsenic	92-94	nuclear RNA export factor 1	Homo sapiens	49-52
26663816-0	2016	Arsenic exposure is associated with diminished insulin sensitivity in non-diabetic Amish adults.	Arsenic	0-7	insulin	Homo sapiens	47-54
26663816-3	2016	However, only a few epidemiologic studies have examined measures of insulin resistance and beta-cell function in relation to arsenic exposure, and no studies have tested for associations with the oral glucose tolerance test (OGTT).	Arsenic	125-132	insulin	Homo sapiens	68-75
26663816-11	2016	CONCLUSIONS: This preliminary study found that urinary total arsenic was associated with insulin sensitivity but not beta-cell function measures, suggesting that low-level arsenic exposure may influence diabetes risk through impairing insulin sensitivity.	Arsenic	61-68	insulin	Homo sapiens	89-96
26663816-11	2016	CONCLUSIONS: This preliminary study found that urinary total arsenic was associated with insulin sensitivity but not beta-cell function measures, suggesting that low-level arsenic exposure may influence diabetes risk through impairing insulin sensitivity.	Arsenic	61-68	insulin	Homo sapiens	235-242
26663816-11	2016	CONCLUSIONS: This preliminary study found that urinary total arsenic was associated with insulin sensitivity but not beta-cell function measures, suggesting that low-level arsenic exposure may influence diabetes risk through impairing insulin sensitivity.	Arsenic	172-179	insulin	Homo sapiens	89-96
26663816-11	2016	CONCLUSIONS: This preliminary study found that urinary total arsenic was associated with insulin sensitivity but not beta-cell function measures, suggesting that low-level arsenic exposure may influence diabetes risk through impairing insulin sensitivity.	Arsenic	172-179	insulin	Homo sapiens	235-242
25605447-0	2016	Relation of dietary inorganic arsenic to serum matrix metalloproteinase-9 (MMP-9) at different threshold concentrations of tap water arsenic.	Arsenic	30-37	matrix metallopeptidase 9	Homo sapiens	47-73
25605447-0	2016	Relation of dietary inorganic arsenic to serum matrix metalloproteinase-9 (MMP-9) at different threshold concentrations of tap water arsenic.	Arsenic	30-37	matrix metallopeptidase 9	Homo sapiens	75-80
26531802-5	2016	At all three time points, exclusively formula-fed infants had GM arsenic exposures ~8 times higher than exclusively breastfed infants owing to arsenic in both tap water and formula powder.	Arsenic	143-150	nuclear RNA export factor 1	Homo sapiens	159-162
26531802-6	2016	Estimated maximum exposures reached 9 mug/kg/day among exclusively formula-fed infants in households with high tap water arsenic (80 mug/l).	Arsenic	121-128	nuclear RNA export factor 1	Homo sapiens	111-114
26531802-7	2016	Overall, modeled arsenic exposures via breast milk and formula were low throughout the first year of life, unless formula was prepared with arsenic-contaminated tap water.	Arsenic	140-147	nuclear RNA export factor 1	Homo sapiens	161-164
27604641-0	2016	Erratum to: Arsenic Promotes NF-Kappab-Mediated Fibroblast Dysfunction and Matrix Remodeling to Impair Muscle Stem Cell Function.	Arsenic	12-19	nuclear factor kappa B subunit 1	Homo sapiens	29-38
27084675-12	2016	An interaction between XRCC1 Arg399Gln and arsenic exposure was also observed (all P interaction = 0.04).	Arsenic	43-50	X-ray repair cross complementing 1	Homo sapiens	23-28
27425645-0	2016	Arsenic-induced mitochondrial oxidative damage is mediated by decreased PGC-1alpha expression and its downstream targets in rat brain.	Arsenic	0-7	PPARG coactivator 1 alpha	Rattus norvegicus	72-82
27370415-0	2016	Association Between Variants in Arsenic (+3 Oxidation State) Methyltranserase (AS3MT) and Urinary Metabolites of Inorganic Arsenic: Role of Exposure Level.	Arsenic	32-39	arsenite methyltransferase	Homo sapiens	79-84
27370415-0	2016	Association Between Variants in Arsenic (+3 Oxidation State) Methyltranserase (AS3MT) and Urinary Metabolites of Inorganic Arsenic: Role of Exposure Level.	Arsenic	123-130	arsenite methyltransferase	Homo sapiens	79-84
27370415-1	2016	Variants in AS3MT, the gene encoding arsenic (+3 oxidation state) methyltranserase, have been shown to influence patterns of inorganic arsenic (iAs) metabolism.	Arsenic	37-44	arsenite methyltransferase	Homo sapiens	12-17
27370415-1	2016	Variants in AS3MT, the gene encoding arsenic (+3 oxidation state) methyltranserase, have been shown to influence patterns of inorganic arsenic (iAs) metabolism.	Arsenic	135-142	arsenite methyltransferase	Homo sapiens	12-17
27425828-0	2016	Low doses of arsenic, via perturbing p53, promotes tumorigenesis.	Arsenic	13-20	tumor protein p53	Homo sapiens	37-40
27425828-3	2016	In this study, we demonstrate that low doses of arsenic exposure mitigate or mask p53 function and further perturb intracellular redox state, which triggers persistent endoplasmic reticulum (ER) stress and activates UPR (unfolded protein response), leading to transformation or tumorigenesis.	Arsenic	48-55	tumor protein p53	Homo sapiens	82-85
27425828-4	2016	Thus, the results suggest that low doses of arsenic exposure, through attenuating p53-regulated tumor suppressive function, change the state of intracellular redox and create a microenvironment for tumorigenesis.	Arsenic	44-51	tumor protein p53	Homo sapiens	82-85
27425645-3	2016	The expression of mitochondrial biogenesis regulator PGC-1alpha, and its downstream targets NRF-1, NRF-2 and Tfam were decreased significantly both at mRNA and protein levels suggesting impaired biogenesis following chronic arsenic-exposure.	Arsenic	224-231	PPARG coactivator 1 alpha	Rattus norvegicus	53-63
27425645-3	2016	The expression of mitochondrial biogenesis regulator PGC-1alpha, and its downstream targets NRF-1, NRF-2 and Tfam were decreased significantly both at mRNA and protein levels suggesting impaired biogenesis following chronic arsenic-exposure.	Arsenic	224-231	nuclear respiratory factor 1	Rattus norvegicus	92-97
27425645-3	2016	The expression of mitochondrial biogenesis regulator PGC-1alpha, and its downstream targets NRF-1, NRF-2 and Tfam were decreased significantly both at mRNA and protein levels suggesting impaired biogenesis following chronic arsenic-exposure.	Arsenic	224-231	NFE2 like bZIP transcription factor 2	Rattus norvegicus	99-104
27425645-3	2016	The expression of mitochondrial biogenesis regulator PGC-1alpha, and its downstream targets NRF-1, NRF-2 and Tfam were decreased significantly both at mRNA and protein levels suggesting impaired biogenesis following chronic arsenic-exposure.	Arsenic	224-231	transcription factor A, mitochondrial	Rattus norvegicus	109-113
27425645-6	2016	The immunohistochemical studies showed both nuclear and cytosolic localization of NRF-1 and NRF-2 in arsenic-exposed rat brain further suggesting regulatory role of these transcription factors under arsenic neurotoxicity.	Arsenic	101-108	nuclear respiratory factor 1	Rattus norvegicus	82-87
27425645-6	2016	The immunohistochemical studies showed both nuclear and cytosolic localization of NRF-1 and NRF-2 in arsenic-exposed rat brain further suggesting regulatory role of these transcription factors under arsenic neurotoxicity.	Arsenic	101-108	NFE2 like bZIP transcription factor 2	Rattus norvegicus	92-97
27292127-10	2016	Participants with the high-risk genotype of DNMT1 rs8101626 and DNMT3A rs34048824 with concurrently high urinary total arsenic levels had even higher OR of ccRCC in a dose-response manner.	Arsenic	119-126	DNA methyltransferase 1	Homo sapiens	44-49
27292127-10	2016	Participants with the high-risk genotype of DNMT1 rs8101626 and DNMT3A rs34048824 with concurrently high urinary total arsenic levels had even higher OR of ccRCC in a dose-response manner.	Arsenic	119-126	DNA methyltransferase 3 alpha	Homo sapiens	64-70
27292127-11	2016	This is the first study to evaluate variant DNMT1 rs8101626 and DNMT3A rs34048824 genotypes that modify the arsenic-related ccRCC risk in a geographic area without significant arsenic exposure in Taiwan.	Arsenic	108-115	DNA methyltransferase 1	Homo sapiens	44-49
27317373-0	2016	Nrf2 activation ameliorates cytotoxic effects of arsenic trioxide in acute promyelocytic leukemia cells through increased glutathione levels and arsenic efflux from cells.	Arsenic	49-56	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
27317373-7	2016	Therefore, Nrf2-associated activation of the GSH biosynthetic pathway, followed by increased levels of intracellular GSH, are key mechanisms underlying accelerated arsenic efflux and attenuation of the cytotoxic effects of ATO.	Arsenic	164-171	NFE2 like bZIP transcription factor 2	Homo sapiens	11-15
27292127-11	2016	This is the first study to evaluate variant DNMT1 rs8101626 and DNMT3A rs34048824 genotypes that modify the arsenic-related ccRCC risk in a geographic area without significant arsenic exposure in Taiwan.	Arsenic	108-115	DNA methyltransferase 3 alpha	Homo sapiens	64-70
27306194-5	2016	To understand the molecular basis of the Nrf2-dependent protection, we analyzed the gene expression profiles after arsenite exposure, and found that the genes involved in the antioxidative function (prdx1 and gclc), arsenic metabolism (gstp1) and xenobiotic elimination (abcc2) were induced in an Nrf2-dependent manner.	Arsenic	216-223	nfe2 like bZIP transcription factor 2a	Danio rerio	41-45
27306194-6	2016	Furthermore, pre-treatment with sulforaphane, a well-known Nrf2 activator improved the survival of zebrafish larvae after arsenic exposure.	Arsenic	122-129	nfe2 like bZIP transcription factor 2a	Danio rerio	59-63
29964747-6	2016	The maximum amount of adsorption of arsenic was 96.5 mg kg-1 and 249.1 mg kg-1 when the arsenic concentration was 0.10 mg L-1 and 1.00 mg L-1, respectively.	Arsenic	36-43	immunoglobulin kappa variable 1-16	Homo sapiens	122-131
27519253-12	2016	CONCLUSIONS: The revised 2014 AMSA scorecard, with its more stringent criteria for evaluating COI policies, assigned fewer As and more Bs and Cs than in years past.	Arsenic	123-125	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	94-97
27507651-0	2016	Comment on "SUMO deconjugation is required for arsenic-triggered ubiquitylation of PML".	Arsenic	47-54	PML nuclear body scaffold	Homo sapiens	83-87
27507651-1	2016	Fasci et al proposed that a SENP1-mediated switch from SUMO2 to SUMO1 conjugation on Lys(65) in promyelocytic leukemia protein (PML) is required for arsenic-induced PML degradation, the basis for the antileukemic activity of arsenic.	Arsenic	149-156	SUMO specific peptidase 1	Homo sapiens	28-33
27507651-1	2016	Fasci et al proposed that a SENP1-mediated switch from SUMO2 to SUMO1 conjugation on Lys(65) in promyelocytic leukemia protein (PML) is required for arsenic-induced PML degradation, the basis for the antileukemic activity of arsenic.	Arsenic	149-156	small ubiquitin like modifier 2	Homo sapiens	55-60
27507651-1	2016	Fasci et al proposed that a SENP1-mediated switch from SUMO2 to SUMO1 conjugation on Lys(65) in promyelocytic leukemia protein (PML) is required for arsenic-induced PML degradation, the basis for the antileukemic activity of arsenic.	Arsenic	149-156	small ubiquitin like modifier 1	Homo sapiens	64-69
27507651-1	2016	Fasci et al proposed that a SENP1-mediated switch from SUMO2 to SUMO1 conjugation on Lys(65) in promyelocytic leukemia protein (PML) is required for arsenic-induced PML degradation, the basis for the antileukemic activity of arsenic.	Arsenic	149-156	PML nuclear body scaffold	Homo sapiens	96-126
27507651-1	2016	Fasci et al proposed that a SENP1-mediated switch from SUMO2 to SUMO1 conjugation on Lys(65) in promyelocytic leukemia protein (PML) is required for arsenic-induced PML degradation, the basis for the antileukemic activity of arsenic.	Arsenic	149-156	PML nuclear body scaffold	Homo sapiens	128-131
27507651-1	2016	Fasci et al proposed that a SENP1-mediated switch from SUMO2 to SUMO1 conjugation on Lys(65) in promyelocytic leukemia protein (PML) is required for arsenic-induced PML degradation, the basis for the antileukemic activity of arsenic.	Arsenic	149-156	PML nuclear body scaffold	Homo sapiens	165-168
29964747-6	2016	The maximum amount of adsorption of arsenic was 96.5 mg kg-1 and 249.1 mg kg-1 when the arsenic concentration was 0.10 mg L-1 and 1.00 mg L-1, respectively.	Arsenic	36-43	immunoglobulin kappa variable 1-16	Homo sapiens	122-125
27507651-1	2016	Fasci et al proposed that a SENP1-mediated switch from SUMO2 to SUMO1 conjugation on Lys(65) in promyelocytic leukemia protein (PML) is required for arsenic-induced PML degradation, the basis for the antileukemic activity of arsenic.	Arsenic	225-232	SUMO specific peptidase 1	Homo sapiens	28-33
27507651-1	2016	Fasci et al proposed that a SENP1-mediated switch from SUMO2 to SUMO1 conjugation on Lys(65) in promyelocytic leukemia protein (PML) is required for arsenic-induced PML degradation, the basis for the antileukemic activity of arsenic.	Arsenic	225-232	small ubiquitin like modifier 2	Homo sapiens	55-60
29964747-6	2016	The maximum amount of adsorption of arsenic was 96.5 mg kg-1 and 249.1 mg kg-1 when the arsenic concentration was 0.10 mg L-1 and 1.00 mg L-1, respectively.	Arsenic	88-95	immunoglobulin kappa variable 1-16	Homo sapiens	122-131
27507651-1	2016	Fasci et al proposed that a SENP1-mediated switch from SUMO2 to SUMO1 conjugation on Lys(65) in promyelocytic leukemia protein (PML) is required for arsenic-induced PML degradation, the basis for the antileukemic activity of arsenic.	Arsenic	225-232	small ubiquitin like modifier 1	Homo sapiens	64-69
29964747-6	2016	The maximum amount of adsorption of arsenic was 96.5 mg kg-1 and 249.1 mg kg-1 when the arsenic concentration was 0.10 mg L-1 and 1.00 mg L-1, respectively.	Arsenic	88-95	immunoglobulin kappa variable 1-16	Homo sapiens	122-125
27507651-1	2016	Fasci et al proposed that a SENP1-mediated switch from SUMO2 to SUMO1 conjugation on Lys(65) in promyelocytic leukemia protein (PML) is required for arsenic-induced PML degradation, the basis for the antileukemic activity of arsenic.	Arsenic	225-232	PML nuclear body scaffold	Homo sapiens	96-126
27507651-1	2016	Fasci et al proposed that a SENP1-mediated switch from SUMO2 to SUMO1 conjugation on Lys(65) in promyelocytic leukemia protein (PML) is required for arsenic-induced PML degradation, the basis for the antileukemic activity of arsenic.	Arsenic	225-232	PML nuclear body scaffold	Homo sapiens	128-131
27444184-0	2016	Preliminary human health risk assessment of arsenic and fluoride in tap water from Zacatecas, Mexico.	Arsenic	44-51	nuclear RNA export factor 1	Homo sapiens	68-71
27507651-1	2016	Fasci et al proposed that a SENP1-mediated switch from SUMO2 to SUMO1 conjugation on Lys(65) in promyelocytic leukemia protein (PML) is required for arsenic-induced PML degradation, the basis for the antileukemic activity of arsenic.	Arsenic	225-232	PML nuclear body scaffold	Homo sapiens	165-168
27507652-0	2016	Response to Comment on "SUMO deconjugation is required for arsenic-triggered ubiquitylation of PML".	Arsenic	59-66	protein PML	Mandrillus leucophaeus	95-99
26438402-8	2016	Thus, Ogg1 genetic background and arsenic-induced 8-OH-dG proved relevant for arsenic-mediated carcinogenic effects.	Arsenic	78-85	8-oxoguanine DNA glycosylase	Homo sapiens	6-10
26359225-0	2016	Polymorphisms of human 8-oxoguanine DNA glycosylase 1 and 8-hydroxydeoxyguanosine increase susceptibility to arsenic methylation capacity-related urothelial carcinoma.	Arsenic	109-116	8-oxoguanine DNA glycosylase	Homo sapiens	23-51
26438402-2	2016	Our previous work demonstrated that environmentally relevant arsenic exposures generate an accelerated accumulation of pre-carcinogen 8-OH-dG DNA lesions under Ogg1-deficient backgrounds, but it remains unproved whether this observed arsenic-induced oxidative DNA damage (ODD) is certainly important in terms of cancer.	Arsenic	61-68	8-oxoguanine DNA glycosylase	Homo sapiens	160-164
26438402-2	2016	Our previous work demonstrated that environmentally relevant arsenic exposures generate an accelerated accumulation of pre-carcinogen 8-OH-dG DNA lesions under Ogg1-deficient backgrounds, but it remains unproved whether this observed arsenic-induced oxidative DNA damage (ODD) is certainly important in terms of cancer.	Arsenic	234-241	8-oxoguanine DNA glycosylase	Homo sapiens	160-164
27179243-3	2016	The sequential extraction procedure and further speciation analysis of heavy metals demonstrated that the primary components of arsenic and cadmium in the soil were residual As (O-As) and exchangeable fraction, which accounted for 60% and 70% of total arsenic and cadmium, respectively.	Arsenic	128-135	SPARC related modular calcium binding 1	Homo sapiens	178-182
27217333-9	2016	Furthermore, arsenic decreased hepatic PDK4 expression as well as diminished the induction of PDK4 by BRD in mouse liver and hepatocytes.	Arsenic	13-20	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	39-43
27217333-0	2016	Arsenic silences hepatic PDK4 expression through activation of histone H3K9 methylatransferase G9a.	Arsenic	0-7	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	25-29
27217333-3	2016	However, the epigenetic mechanisms mediated by arsenic to control PDK4 expression remain elusive.	Arsenic	47-54	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	66-70
27165195-5	2016	In vitro studies of inorganic arsenic-treated T lymphocytes (Jurkat and CCRF-CEM, 0.1, 1, and 100 mug/L) showed arsenic-related modifications of H3K9Ac and changes in the levels of the histone deacetylating enzyme HDAC2 at very low arsenic concentrations.	Arsenic	30-37	histone deacetylase 2	Homo sapiens	214-219
27165195-5	2016	In vitro studies of inorganic arsenic-treated T lymphocytes (Jurkat and CCRF-CEM, 0.1, 1, and 100 mug/L) showed arsenic-related modifications of H3K9Ac and changes in the levels of the histone deacetylating enzyme HDAC2 at very low arsenic concentrations.	Arsenic	112-119	histone deacetylase 2	Homo sapiens	214-219
27165195-5	2016	In vitro studies of inorganic arsenic-treated T lymphocytes (Jurkat and CCRF-CEM, 0.1, 1, and 100 mug/L) showed arsenic-related modifications of H3K9Ac and changes in the levels of the histone deacetylating enzyme HDAC2 at very low arsenic concentrations.	Arsenic	112-119	histone deacetylase 2	Homo sapiens	214-219
27165195-6	2016	Further, in vitro exposure of kidney HEK293 cells to arsenic (1 and 5 muM) altered the protein levels of PCNA and DNMT1, parts of a gene expression repressor complex, as well as MAML1.	Arsenic	53-60	latexin	Homo sapiens	70-73
27165195-6	2016	Further, in vitro exposure of kidney HEK293 cells to arsenic (1 and 5 muM) altered the protein levels of PCNA and DNMT1, parts of a gene expression repressor complex, as well as MAML1.	Arsenic	53-60	proliferating cell nuclear antigen	Homo sapiens	105-109
27165195-6	2016	Further, in vitro exposure of kidney HEK293 cells to arsenic (1 and 5 muM) altered the protein levels of PCNA and DNMT1, parts of a gene expression repressor complex, as well as MAML1.	Arsenic	53-60	DNA methyltransferase 1	Homo sapiens	114-119
27165195-6	2016	Further, in vitro exposure of kidney HEK293 cells to arsenic (1 and 5 muM) altered the protein levels of PCNA and DNMT1, parts of a gene expression repressor complex, as well as MAML1.	Arsenic	53-60	mastermind like transcriptional coactivator 1	Homo sapiens	178-183
27165195-9	2016	Also, we show that arsenic exposure affects the expression of PCNA and DNMT1-proteins that are part of a gene expression silencing complex.	Arsenic	19-26	proliferating cell nuclear antigen	Homo sapiens	62-66
27165195-9	2016	Also, we show that arsenic exposure affects the expression of PCNA and DNMT1-proteins that are part of a gene expression silencing complex.	Arsenic	19-26	DNA methyltransferase 1	Homo sapiens	71-76
27297967-0	2016	Arsenic Triglutathione [As(GS)3] Transport by Multidrug Resistance Protein 1 (MRP1/ABCC1) Is Selectively Modified by Phosphorylation of Tyr920/Ser921 and Glycosylation of Asn19/Asn23.	Arsenic	24-26	ATP binding cassette subfamily B member 1	Homo sapiens	46-76
27297967-0	2016	Arsenic Triglutathione [As(GS)3] Transport by Multidrug Resistance Protein 1 (MRP1/ABCC1) Is Selectively Modified by Phosphorylation of Tyr920/Ser921 and Glycosylation of Asn19/Asn23.	Arsenic	24-26	ATP binding cassette subfamily C member 1	Homo sapiens	78-82
27297967-0	2016	Arsenic Triglutathione [As(GS)3] Transport by Multidrug Resistance Protein 1 (MRP1/ABCC1) Is Selectively Modified by Phosphorylation of Tyr920/Ser921 and Glycosylation of Asn19/Asn23.	Arsenic	24-26	ATP binding cassette subfamily C member 1	Homo sapiens	83-88
27297967-2	2016	Arsenic, a human carcinogen, is a high-affinity MRP1 substrate as arsenic triglutathione [As(GS)3].	Arsenic	0-7	ATP binding cassette subfamily C member 1	Homo sapiens	48-52
27477106-10	2016	Collectively, we showed, in presence of arsenic microglia alters cystine/glutamate balance through xCT in extracellular milieu leading to bystander death of immature neurons.	Arsenic	40-47	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	99-102
27217333-9	2016	Furthermore, arsenic decreased hepatic PDK4 expression as well as diminished the induction of PDK4 by BRD in mouse liver and hepatocytes.	Arsenic	13-20	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	94-98
27217333-6	2016	In contrast, arsenic exposure decreased PDK4 expression by inducing G9a and increasing H3K9 di- and tri-methylations levels (H3K9me2/3).	Arsenic	13-20	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	40-44
27217333-10	2016	Overall, the results suggest that arsenic causes aberrant repressive histone modification to silence PDK4 in both HCC cells and in mouse liver.	Arsenic	34-41	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	101-105
27401918-5	2016	RESULTS: We found relatively low levels of arsenic in household tap water (range of 2.48-76.02 mug/L) and in the urine of the participants (7.1 mug/L vs 6.78 mug/L in cases and controls, respectively).	Arsenic	43-50	nuclear RNA export factor 1	Homo sapiens	64-67
27523482-5	2016	A rat model study on the metal stoichiometric analysis of MT1 isoform isolated from the liver of arsenic treated, untreated and zinc treated animals has been carried out using the combination of particle induced X-ray emission (PIXE) and electrospray ionisation mass spectrometry (ESI-MS).	Arsenic	97-104	metallothionein 1	Rattus norvegicus	58-61
27132035-0	2016	Arsenic-induced anti-angiogenesis via miR-425-5p-regulated CCM3.	Arsenic	0-7	microRNA 4255	Homo sapiens	38-48
27132035-0	2016	Arsenic-induced anti-angiogenesis via miR-425-5p-regulated CCM3.	Arsenic	0-7	programmed cell death 10	Homo sapiens	59-63
27310439-2	2016	AsCl3 gives the As-only compound; PCl3 produces compounds having two As atoms with one P atom, or one As atom and two P atoms, and they can exist as two possible isomers, one of which is chiral.	Arsenic	16-18	achaete-scute family bHLH transcription factor 3	Homo sapiens	0-5
26954472-1	2016	Biochar derived from the pyrolysis at 500  C with fresh biogas slurry and residue, was conducted to investigate its potential role in mediating the speciation and mobilization of As(V) and Fe(III) from arsenic-contaminated tailing mine sediment, with consideration of the changes in microbial populations and dissolved organic matter (DOM).	Arsenic	202-209	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	179-184
27140209-1	2016	Cyclic azasulfuryl (As) peptide analogs of the urotensin II (UII, 1, H-Glu-Thr-Pro-Asp-c[Cys-Phe-Trp-Lys-Tyr-Cys]-Val-OH) fragment 4-11 were synthesized to explore the influences of backbone structure on biological activity.	Arsenic	20-22	urotensin 2	Rattus norvegicus	47-67
27208522-4	2016	Traditional methods of classifying these four mechanisms are based on clinically important parameters measured from anterior segment optical coherence tomography (AS-OCT) images, which rely on accurate segmentation of the AS-OCT image and identification of the scleral spur in the segmented AS-OCT images by clinicians.	Arsenic	163-165	plexin A2	Homo sapiens	166-169
26890134-5	2016	Plasma concentrations of Mrp and Oatp substrates were increased in arsenic exposure groups compared with diet-only controls.	Arsenic	67-74	ATP-binding cassette, sub-family C (CFTR/MRP), member 1	Mus musculus	25-28
27208303-6	2016	Peroxule formation is a general response to stimuli such as arsenic and is regulated by peroxin 11a (PEX11a), as Arabidopsis pex11a RNAi lines are unable to produce peroxules under stress conditions.	Arsenic	60-67	peroxin 11A	Arabidopsis thaliana	125-131
26302725-4	2016	Arsenic administration decreased sperm motility, glutathione level, superoxide dismutase and catalase activities in testicular tissue of rats.	Arsenic	0-7	catalase	Rattus norvegicus	93-101
26446860-7	2016	However, the activity of catalase (CAT) decreased in animals exposed to both arsenic compounds.	Arsenic	77-84	catalase	Rattus norvegicus	25-33
26446860-7	2016	However, the activity of catalase (CAT) decreased in animals exposed to both arsenic compounds.	Arsenic	77-84	catalase	Rattus norvegicus	35-38
27038207-4	2016	Amylase (for C cycling), acid phosphatase (for P cycling) and catalase (for redox reaction) activities showed significantly positive correlations (P &lt; 0.05) with Pb, Cd, Zn and As contents.	Arsenic	180-182	catalase	Homo sapiens	47-70
26928318-1	2016	Arsenic (+3 oxidation state) methyltransferase (AS3MT) is the key enzyme in the metabolism of inorganic arsenic (iAs).	Arsenic	104-111	arsenite methyltransferase	Homo sapiens	48-53
26928318-3	2016	The relationships between seven single nucleotide polymorphisms (SNPs) in AS3MT and urinary concentrations of iAs and its methylated metabolites were assessed in mother-infant pairs of the Biomarkers of Exposure to ARsenic (BEAR) cohort.	Arsenic	215-222	arsenite methyltransferase	Homo sapiens	74-79
27230915-10	2016	Concentration of arsenic in home tap water and estimated water consumption were strongly predictive of levels of arsenicals in urine as were smoking, body mass index, and gender.	Arsenic	17-24	nuclear RNA export factor 1	Homo sapiens	33-36
27259345-9	2016	Immunoreactivity for iNOS and eNOS was noted to increase with arsenic treatment.	Arsenic	62-69	nitric oxide synthase 2, inducible	Mus musculus	21-25
27455813-4	2016	We showed that gestational arsenic exposure increased hepatic tumors having activated oncogene Ha-ras by C to A mutation.	Arsenic	27-34	Harvey rat sarcoma virus oncogene	Mus musculus	95-101
27455813-5	2016	We also showed that DNA methylation status of Fosb region is implicated in tumor augmentation by gestational arsenic exposure.	Arsenic	109-116	FBJ osteosarcoma oncogene B	Mus musculus	46-50
27060662-0	2016	Cadmium and arsenic override NF-kappaB developmental regulation of the intestinal UGT1A1 gene and control of hyperbilirubinemia.	Arsenic	12-19	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	82-88
27060662-8	2016	Altering the redox state of the intestines by oral administration of cadmium or arsenic to neonatal hUGT1/Ikkbeta(F/F) and hUGT1/Ikkbeta(DeltaIEC) mice leads to induction of UGT1A1 and a dramatic reduction in TSB levels.	Arsenic	80-87	UDP-glucose glycoprotein glucosyltransferase 1	Homo sapiens	100-105
27060662-8	2016	Altering the redox state of the intestines by oral administration of cadmium or arsenic to neonatal hUGT1/Ikkbeta(F/F) and hUGT1/Ikkbeta(DeltaIEC) mice leads to induction of UGT1A1 and a dramatic reduction in TSB levels.	Arsenic	80-87	inhibitor of kappaB kinase beta	Mus musculus	106-113
27060662-8	2016	Altering the redox state of the intestines by oral administration of cadmium or arsenic to neonatal hUGT1/Ikkbeta(F/F) and hUGT1/Ikkbeta(DeltaIEC) mice leads to induction of UGT1A1 and a dramatic reduction in TSB levels.	Arsenic	80-87	UDP-glucose glycoprotein glucosyltransferase 1	Homo sapiens	123-128
27060662-8	2016	Altering the redox state of the intestines by oral administration of cadmium or arsenic to neonatal hUGT1/Ikkbeta(F/F) and hUGT1/Ikkbeta(DeltaIEC) mice leads to induction of UGT1A1 and a dramatic reduction in TSB levels.	Arsenic	80-87	inhibitor of kappaB kinase beta	Mus musculus	129-136
27250901-5	2016	Here, we propose an adaptation of the recently proposed tetracysteine-arsenic-binding-motif technology to detect and quantitatively characterize the engagement of hTS with one such peptidic inhibitor in cell lysates.	Arsenic	70-77	APC down-regulated 1	Homo sapiens	163-166
26928318-0	2016	Analysis of maternal polymorphisms in arsenic (+3 oxidation state)-methyltransferase AS3MT and fetal sex in relation to arsenic metabolism and infant birth outcomes: Implications for risk analysis.	Arsenic	38-45	arsenite methyltransferase	Homo sapiens	85-90
26928318-0	2016	Analysis of maternal polymorphisms in arsenic (+3 oxidation state)-methyltransferase AS3MT and fetal sex in relation to arsenic metabolism and infant birth outcomes: Implications for risk analysis.	Arsenic	120-127	arsenite methyltransferase	Homo sapiens	85-90
26928318-1	2016	Arsenic (+3 oxidation state) methyltransferase (AS3MT) is the key enzyme in the metabolism of inorganic arsenic (iAs).	Arsenic	104-111	arsenite methyltransferase	Homo sapiens	0-46
26991437-3	2016	A high radioactive concentration of (67) Ga-h-SnF2 particles could be prepared similarly in &gt;=97% RCP with 74% as 3-5 microm and 26% &gt;5 microm in diameter.	Arsenic	114-116	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4	Homo sapiens	46-50
27289040-0	2016	Arsenic-induced dose-dependent modulation of the NF-kappaB/IL-6 axis in thymocytes triggers differential immune responses.	Arsenic	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	49-58
27289040-0	2016	Arsenic-induced dose-dependent modulation of the NF-kappaB/IL-6 axis in thymocytes triggers differential immune responses.	Arsenic	0-7	interleukin 6	Mus musculus	59-63
27289040-10	2016	Our study establishes a novel role of arsenic in regulating immune homeostasis in context to its dose, where, at higher doses, arsenic related upregulation of NF-kappaB cascade takes on an alternative role that is correlated with increased immune-suppression.	Arsenic	38-45	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	159-168
27289040-10	2016	Our study establishes a novel role of arsenic in regulating immune homeostasis in context to its dose, where, at higher doses, arsenic related upregulation of NF-kappaB cascade takes on an alternative role that is correlated with increased immune-suppression.	Arsenic	127-134	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	159-168
27223295-0	2016	Association of Children"s Urinary CC16 Levels with Arsenic Concentrations in Multiple Environmental Media.	Arsenic	51-58	secretoglobin family 1A member 1	Homo sapiens	34-38
27223295-1	2016	Arsenic exposure has been associated with decreased club cell secretory protein (CC16) levels in adults.	Arsenic	0-7	secretoglobin family 1A member 1	Homo sapiens	81-85
27223295-3	2016	Our objective was to determine if urinary CC16 levels in children are associated with arsenic concentrations in environmental media collected from their homes.	Arsenic	86-93	secretoglobin family 1A member 1	Homo sapiens	42-46
27223295-7	2016	There were associations between urinary CC16 and arsenic concentration in soil (b = -0.43, p = 0.001, R2 = 0.08), water (b = -0.22, p = 0.07, R2 = 0.03), house dust (b = -0.37, p = 0.07, R2 = 0.04), and dust loading (b = -0.21, p = 0.04, R2 = 0.04).	Arsenic	49-56	secretoglobin family 1A member 1	Homo sapiens	40-44
27223295-8	2016	In multiple analyses, only the concentration of arsenic in soil was associated with urinary CC16 levels (b = -0.42, p = 0.02, R2 = 0.14 (full model)) after accounting for other factors.	Arsenic	48-55	secretoglobin family 1A member 1	Homo sapiens	92-96
27223295-9	2016	The association between urinary CC16 and soil arsenic may suggest that localized arsenic exposure in the lungs could damage the airway epithelium and predispose children for diminished lung function.	Arsenic	46-53	secretoglobin family 1A member 1	Homo sapiens	32-36
27223295-9	2016	The association between urinary CC16 and soil arsenic may suggest that localized arsenic exposure in the lungs could damage the airway epithelium and predispose children for diminished lung function.	Arsenic	81-88	secretoglobin family 1A member 1	Homo sapiens	32-36
26135927-8	2016	SM22alpha and Rho kinase 2 gene and protein expression were significantly decreased in the aortic tissue of arsenic-exposed mice compared with that of control mice.	Arsenic	108-115	transgelin	Mus musculus	0-9
26878773-0	2016	Antioxidant tert-butylhydroquinone ameliorates arsenic-induced intracellular damages and apoptosis through induction of Nrf2-dependent antioxidant responses as well as stabilization of anti-apoptotic factor Bcl-2 in human keratinocytes.	Arsenic	47-54	NFE2 like bZIP transcription factor 2	Homo sapiens	120-124
26878773-0	2016	Antioxidant tert-butylhydroquinone ameliorates arsenic-induced intracellular damages and apoptosis through induction of Nrf2-dependent antioxidant responses as well as stabilization of anti-apoptotic factor Bcl-2 in human keratinocytes.	Arsenic	47-54	BCL2 apoptosis regulator	Homo sapiens	207-212
26878773-4	2016	Our results demonstrated that tBHQ antagonized arsenic-induced decrease of cell viability, generation of reactive oxygen species (ROS) and lipid peroxidation, as well as reduction of antioxidative enzymes superoxide dismutase (SOD) and catalase (CAT) activities.	Arsenic	47-54	catalase	Homo sapiens	236-244
26878773-4	2016	Our results demonstrated that tBHQ antagonized arsenic-induced decrease of cell viability, generation of reactive oxygen species (ROS) and lipid peroxidation, as well as reduction of antioxidative enzymes superoxide dismutase (SOD) and catalase (CAT) activities.	Arsenic	47-54	catalase	Homo sapiens	246-249
26878773-5	2016	We also found that tBHQ relieved the G2/M phase arrest by arsenic exposure, which was associated with altering the expression of cell cycle regulators cyclin D1 and CDK4.	Arsenic	58-65	cyclin D1	Homo sapiens	151-160
26878773-5	2016	We also found that tBHQ relieved the G2/M phase arrest by arsenic exposure, which was associated with altering the expression of cell cycle regulators cyclin D1 and CDK4.	Arsenic	58-65	cyclin dependent kinase 4	Homo sapiens	165-169
26878773-6	2016	tBHQ treatment further reduced the numbers of arsenic-induced mitochondrial-mediated apoptotic cells, which occurred concomitantly with the effective recovery of mitochondrial membrane potential (DeltaPsim) depolarization, the release of cytochrome c releasing from the mitochondrial as well as the survival signal related factor caspase 3 activation.	Arsenic	46-53	cytochrome c, somatic	Homo sapiens	238-250
26878773-8	2016	More interestingly, arsenic-induced decrease of anti-apoptotic factor B-cell lymphoma-2 (Bcl-2) and increase of pro-apoptotic factor Bcl-2-associated X protein (Bax) could all be reversed by tBHQ pretreatment.	Arsenic	20-27	BCL2 apoptosis regulator	Homo sapiens	70-87
26878773-8	2016	More interestingly, arsenic-induced decrease of anti-apoptotic factor B-cell lymphoma-2 (Bcl-2) and increase of pro-apoptotic factor Bcl-2-associated X protein (Bax) could all be reversed by tBHQ pretreatment.	Arsenic	20-27	BCL2 apoptosis regulator	Homo sapiens	89-94
26878773-8	2016	More interestingly, arsenic-induced decrease of anti-apoptotic factor B-cell lymphoma-2 (Bcl-2) and increase of pro-apoptotic factor Bcl-2-associated X protein (Bax) could all be reversed by tBHQ pretreatment.	Arsenic	20-27	BCL2 associated X, apoptosis regulator	Homo sapiens	133-159
26878773-8	2016	More interestingly, arsenic-induced decrease of anti-apoptotic factor B-cell lymphoma-2 (Bcl-2) and increase of pro-apoptotic factor Bcl-2-associated X protein (Bax) could all be reversed by tBHQ pretreatment.	Arsenic	20-27	BCL2 associated X, apoptosis regulator	Homo sapiens	161-164
26878773-9	2016	These results suggested together that tBHQ could ameliorate arsenic-induced cytotoxicity and apoptosis, which might be linked with the induction of Nrf2-dependent antioxidant responses as well as stabilization of anti-apoptotic factor Bcl-2 in human keratinocytes.	Arsenic	60-67	NFE2 like bZIP transcription factor 2	Homo sapiens	148-152
26878773-9	2016	These results suggested together that tBHQ could ameliorate arsenic-induced cytotoxicity and apoptosis, which might be linked with the induction of Nrf2-dependent antioxidant responses as well as stabilization of anti-apoptotic factor Bcl-2 in human keratinocytes.	Arsenic	60-67	BCL2 apoptosis regulator	Homo sapiens	235-240
26135927-11	2016	Additionally, the expression levels of PDGF-BB and early growth response-1 (Egr-1) were significantly higher in the arsenic group than that in the control group.	Arsenic	116-123	early growth response 1	Mus musculus	76-81
26187899-0	2016	Lutein alleviates arsenic-induced reproductive toxicity in male mice via Nrf2 signaling.	Arsenic	18-25	nuclear factor, erythroid derived 2, like 2	Mus musculus	73-77
26135927-12	2016	These findings reveal biochemical alterations of SM22alpha, PDGF, and Egr-1 in conjunction with decreased SMC area in the aortic wall of arsenic-fed mice.	Arsenic	137-144	transgelin	Mus musculus	49-58
26135927-12	2016	These findings reveal biochemical alterations of SM22alpha, PDGF, and Egr-1 in conjunction with decreased SMC area in the aortic wall of arsenic-fed mice.	Arsenic	137-144	early growth response 1	Mus musculus	70-75
26566708-1	2016	Heme oxygenase (HO)-1 is upregulated by many stressful stimuli, including arsenic.	Arsenic	74-81	heme oxygenase 1	Homo sapiens	0-21
25969347-0	2016	p38alpha MAPK is required for arsenic-induced cell transformation.	Arsenic	30-37	mitogen-activated protein kinase 14	Mus musculus	0-8
25969347-2	2016	In the present study, we show that activation of p38alpha mitogen-activated protein kinase (MAPK) is required for arsenic-induced neoplastic transformation.	Arsenic	114-121	mitogen-activated protein kinase 14	Mus musculus	49-57
25969347-3	2016	Exposure of cells to 0.5 muM arsenic increased CRE and c-Fos promoter activities that were accompanied by increases in p38alpha MAPK and CREB phosphorylation and expression levels concurrently with AP-1 activation.	Arsenic	29-36	FBJ osteosarcoma oncogene	Mus musculus	55-60
25969347-3	2016	Exposure of cells to 0.5 muM arsenic increased CRE and c-Fos promoter activities that were accompanied by increases in p38alpha MAPK and CREB phosphorylation and expression levels concurrently with AP-1 activation.	Arsenic	29-36	mitogen-activated protein kinase 14	Mus musculus	119-127
25969347-3	2016	Exposure of cells to 0.5 muM arsenic increased CRE and c-Fos promoter activities that were accompanied by increases in p38alpha MAPK and CREB phosphorylation and expression levels concurrently with AP-1 activation.	Arsenic	29-36	cAMP responsive element binding protein 1	Mus musculus	137-141
25969347-4	2016	Introduction of short hairpin (sh) RNA-p38alpha into BALB/c 3T3 cells markedly suppressed arsenic-induced colony formation compared with wildtype cells.	Arsenic	90-97	mitogen-activated protein kinase 14	Mus musculus	39-47
25969347-5	2016	CREB phosphorylation and AP-1 activation were decreased in p38alpha knockdown cells after arsenic treatment.	Arsenic	90-97	cAMP responsive element binding protein 1	Mus musculus	0-4
25969347-5	2016	CREB phosphorylation and AP-1 activation were decreased in p38alpha knockdown cells after arsenic treatment.	Arsenic	90-97	mitogen-activated protein kinase 14	Mus musculus	59-67
25969347-6	2016	Arsenic-induced AP-1 activation, measured as c-Fos and CRE promoter activities, and CREB phosphorylation were attenuated by p38 inhibition in BALB/c 3T3 cells.	Arsenic	0-7	FBJ osteosarcoma oncogene	Mus musculus	47-50
25969347-6	2016	Arsenic-induced AP-1 activation, measured as c-Fos and CRE promoter activities, and CREB phosphorylation were attenuated by p38 inhibition in BALB/c 3T3 cells.	Arsenic	0-7	cAMP responsive element binding protein 1	Mus musculus	84-88
25969347-6	2016	Arsenic-induced AP-1 activation, measured as c-Fos and CRE promoter activities, and CREB phosphorylation were attenuated by p38 inhibition in BALB/c 3T3 cells.	Arsenic	0-7	mitogen-activated protein kinase 14	Mus musculus	124-127
25969347-7	2016	Thus, p38alpha MAPK activation is required for arsenic-induced neoplastic transformation mediated through CREB phosphorylation and AP-1 activation.	Arsenic	47-54	mitogen-activated protein kinase 14	Mus musculus	6-14
25969347-7	2016	Thus, p38alpha MAPK activation is required for arsenic-induced neoplastic transformation mediated through CREB phosphorylation and AP-1 activation.	Arsenic	47-54	cAMP responsive element binding protein 1	Mus musculus	106-110
24318767-5	2016	The number of apoptotic germ cell was increased, and the number of proliferating cell nuclear antigen (PCNA)-positive germ cell was decreased in testis after arsenic administration.	Arsenic	158-165	proliferating cell nuclear antigen	Rattus norvegicus	67-101
24318767-5	2016	The number of apoptotic germ cell was increased, and the number of proliferating cell nuclear antigen (PCNA)-positive germ cell was decreased in testis after arsenic administration.	Arsenic	158-165	proliferating cell nuclear antigen	Rattus norvegicus	103-107
24318767-6	2016	Our data indicate a significant reduction in the activity of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling, and there was a rise in the expression of PCNA in testis of arsenic + melatonin group.	Arsenic	213-220	proliferating cell nuclear antigen	Rattus norvegicus	195-199
26566708-4	2016	We prospectively investigated the associations between HO-1 (GT)n polymorphism and cancer risk related to arsenic from drinking water.	Arsenic	106-113	heme oxygenase 1	Homo sapiens	55-59
26566708-13	2016	Associations of HO-1 (GT)n polymorphism with cancer risk differs by histological subtype and the polymorphism should be considered a modifier in the risk assessment of arsenic exposure.	Arsenic	168-175	heme oxygenase 1	Homo sapiens	16-20
26921788-8	2016	A decrease in cyclin D1 protein expression was observed in D1 cells exposed to As(+3) at 500 nM and MMA(+3) starting at 50 nM, suggesting that arsenic at these environmentally-relevant doses suppresses early T cell development through the inhibition of IL-7 signaling pathway.	Arsenic	143-150	cyclin D1	Mus musculus	14-23
26967250-7	2016	We further show that DNA damage, such as exposure to methyl methanesulfonate (MMS), etoposide or arsenic, increases Cdc25A acetylation.	Arsenic	97-104	cell division cycle 25A	Homo sapiens	116-122
26921788-8	2016	A decrease in cyclin D1 protein expression was observed in D1 cells exposed to As(+3) at 500 nM and MMA(+3) starting at 50 nM, suggesting that arsenic at these environmentally-relevant doses suppresses early T cell development through the inhibition of IL-7 signaling pathway.	Arsenic	143-150	interleukin 7	Mus musculus	253-257
26909602-3	2016	In this study, we found miR-222 was upregulated in arsenic-transformed human lung epithelial BEAS-2B cells (As-T cells).	Arsenic	51-58	microRNA 222	Homo sapiens	24-31
26909602-7	2016	These results indicate that miR-222 plays an important role in arsenic-induced tumor growth.	Arsenic	63-70	microRNA 222	Homo sapiens	28-35
26909602-0	2016	Role and mechanism of miR-222 in arsenic-transformed cells for inducing tumor growth.	Arsenic	33-40	microRNA 222	Homo sapiens	22-29
26276563-13	2016	The information regarding the effects of As2O3 on cytokine mRNA expression generated in this study will be important information for arsenic toxicology evaluation.	Arsenic	133-140	TNF receptor superfamily member 8	Homo sapiens	50-58
25731970-0	2016	Association of XRCC1 polymorphisms with arsenic methylation.	Arsenic	40-47	X-ray repair cross complementing 1	Homo sapiens	15-20
25731970-1	2016	The associations of four single nucleotide polymorphisms (p.Arg194Trp, p.Arg280His, p.Pro206Pro, and p.Arg399Gln) in X-ray repair cross-complementing group 1 with urinary arsenic metabolites and 8-hydroxy-2"-deoxyguanosine (8-OHdG) were investigated in a Vietnamese population (n = 100).	Arsenic	171-178	X-ray repair cross complementing 1	Homo sapiens	117-157
26296331-3	2016	And many studies have demonstrated that expressions of PTEN, Akt, and CREB protein were influenced by arsenic, but it is not clear whether this signaling pathway is involved in the nervous system impairment of rats induced by chronic arsenite exposure, and we have addressed this in this study.	Arsenic	102-109	phosphatase and tensin homolog	Rattus norvegicus	55-59
26296331-3	2016	And many studies have demonstrated that expressions of PTEN, Akt, and CREB protein were influenced by arsenic, but it is not clear whether this signaling pathway is involved in the nervous system impairment of rats induced by chronic arsenite exposure, and we have addressed this in this study.	Arsenic	102-109	AKT serine/threonine kinase 1	Rattus norvegicus	61-64
26296331-3	2016	And many studies have demonstrated that expressions of PTEN, Akt, and CREB protein were influenced by arsenic, but it is not clear whether this signaling pathway is involved in the nervous system impairment of rats induced by chronic arsenite exposure, and we have addressed this in this study.	Arsenic	102-109	cAMP responsive element binding protein 1	Rattus norvegicus	70-74
26780347-6	2016	Moreover, we have reported that three kinds of oxidative stress, ultraviolet light-induced stress, osmotic stress and arsenic-induced stress, modulate kinase activity of RET-PTC1 without an extracellular domain as well as c-RET by conformational change of RET protein (dimerization) via disulfide bond formation.	Arsenic	118-125	ret proto-oncogene	Homo sapiens	170-173
26780347-6	2016	Moreover, we have reported that three kinds of oxidative stress, ultraviolet light-induced stress, osmotic stress and arsenic-induced stress, modulate kinase activity of RET-PTC1 without an extracellular domain as well as c-RET by conformational change of RET protein (dimerization) via disulfide bond formation.	Arsenic	118-125	patched 1	Homo sapiens	174-178
26780347-6	2016	Moreover, we have reported that three kinds of oxidative stress, ultraviolet light-induced stress, osmotic stress and arsenic-induced stress, modulate kinase activity of RET-PTC1 without an extracellular domain as well as c-RET by conformational change of RET protein (dimerization) via disulfide bond formation.	Arsenic	118-125	PYD and CARD domain containing	Homo sapiens	219-223
26780347-6	2016	Moreover, we have reported that three kinds of oxidative stress, ultraviolet light-induced stress, osmotic stress and arsenic-induced stress, modulate kinase activity of RET-PTC1 without an extracellular domain as well as c-RET by conformational change of RET protein (dimerization) via disulfide bond formation.	Arsenic	118-125	ret proto-oncogene	Homo sapiens	224-227
26780347-6	2016	Moreover, we have reported that three kinds of oxidative stress, ultraviolet light-induced stress, osmotic stress and arsenic-induced stress, modulate kinase activity of RET-PTC1 without an extracellular domain as well as c-RET by conformational change of RET protein (dimerization) via disulfide bond formation.	Arsenic	118-125	ret proto-oncogene	Homo sapiens	224-227
26970057-0	2016	Influence of MRP1 G1666A and GSTP1 Ile105Val genetic variants on the urinary and blood arsenic levels of Turkish smelter workers.	Arsenic	87-94	ATP binding cassette subfamily C member 1	Homo sapiens	13-17
26775255-7	2016	Taurine could reverse arsenic-inhibited Nrf2 and Trx and inhibit autophagy.	Arsenic	22-29	NFE2 like bZIP transcription factor 2	Rattus norvegicus	40-44
26775255-7	2016	Taurine could reverse arsenic-inhibited Nrf2 and Trx and inhibit autophagy.	Arsenic	22-29	thioredoxin 1	Rattus norvegicus	49-52
26775255-8	2016	In short, inhibition of Nrf2/Trx pathway might play an important role in the pathogenesis of arsenic-related diabetes.	Arsenic	93-100	NFE2 like bZIP transcription factor 2	Rattus norvegicus	24-28
26775255-8	2016	In short, inhibition of Nrf2/Trx pathway might play an important role in the pathogenesis of arsenic-related diabetes.	Arsenic	93-100	thioredoxin 1	Rattus norvegicus	29-32
26782327-6	2016	According to the water quality index, water in the Dan River drainage was suitable for drinking; however, an exposure risk assessment model suggests that As and Sb in the Laojun and Laoguan rivers could pose a high risk to humans in terms of adverse health and potential non-carcinogenic effects.	Arsenic	154-156	NBL1, DAN family BMP antagonist	Homo sapiens	51-54
26803211-11	2016	Concentrations in soil, house dust, tap water, along with floor dust loading were significantly associated with toenail and urinary arsenic but not lead.	Arsenic	132-139	nuclear RNA export factor 1	Homo sapiens	36-39
26803211-12	2016	Mixed models showed that soil and tap water best predicted urinary arsenic.	Arsenic	67-74	nuclear RNA export factor 1	Homo sapiens	34-37
26970057-2	2016	The effect of MRP1 G1666A and GSTP1 Ile105Val polymorphisms on blood and urinary arsenic levels were determined in 95 Turkish smelter workers.	Arsenic	81-88	ATP binding cassette subfamily C member 1	Homo sapiens	14-18
26970057-5	2016	A significant association between MRP1 1666A allele and urinary arsenic levels was found (p=0.001).	Arsenic	64-71	ATP binding cassette subfamily C member 1	Homo sapiens	34-38
26970057-7	2016	Significant association was also detected between MRP1A(-)/GSTP1Val(-) genotypes and urinary arsenic levels (p=0.001).	Arsenic	93-100	glutathione S-transferase pi 1	Homo sapiens	59-64
26970057-8	2016	This study suggested that MRP1 G1666A alone and, also, combined with GSTP1 Ile105Val were associated with inter-individual variations in urinary arsenic levels, but not with blood arsenic levels.	Arsenic	145-152	ATP binding cassette subfamily C member 1	Homo sapiens	26-30
26970057-8	2016	This study suggested that MRP1 G1666A alone and, also, combined with GSTP1 Ile105Val were associated with inter-individual variations in urinary arsenic levels, but not with blood arsenic levels.	Arsenic	145-152	glutathione S-transferase pi 1	Homo sapiens	69-74
27557380-1	2016	OBJECTIVE: To evaluate whether the presence of polymorphisms of peroxisome proliferator-activated receptor gamma PPARgamma (Pro 1 2Ala) and PPARGC1B (Ala203Pro) modifies the association between the inorganic arsenic (iAs) methylation capacity and breast cancer (BC).	Arsenic	208-215	lamin A/C	Homo sapiens	124-129
26771945-6	2016	It has been found that chronic mild stress, but not prenatal stress, acute stress or a combination of PS with AS, decreased the concentration of the mature form of NGF (m-NGF) in the rat hypothalamus.	Arsenic	110-112	nerve growth factor	Rattus norvegicus	164-167
27105409-7	2016	Our estimate is consistent with concentrations expected from other research and is less than 10% of the NSF/ANSI standard of 1 mug/L arsenic in water.	Arsenic	133-140	N-ethylmaleimide sensitive factor, vesicle fusing ATPase	Homo sapiens	104-107
27557380-1	2016	OBJECTIVE: To evaluate whether the presence of polymorphisms of peroxisome proliferator-activated receptor gamma PPARgamma (Pro 1 2Ala) and PPARGC1B (Ala203Pro) modifies the association between the inorganic arsenic (iAs) methylation capacity and breast cancer (BC).	Arsenic	208-215	PPARG coactivator 1 beta	Homo sapiens	140-148
26864988-5	2016	This conceptual self-powered arsenic biosensor demonstrated limits of detection (LODs) of 13 muM for arsenite and 132 muM for arsenate.	Arsenic	29-36	latexin	Homo sapiens	93-96
27471628-0	2016	AIM2 inflammasome mediates Arsenic-induced secretion of IL-1 beta and IL-18.	Arsenic	27-34	absent in melanoma 2	Homo sapiens	0-4
27471628-0	2016	AIM2 inflammasome mediates Arsenic-induced secretion of IL-1 beta and IL-18.	Arsenic	27-34	interleukin 1 beta	Homo sapiens	56-65
27471628-0	2016	AIM2 inflammasome mediates Arsenic-induced secretion of IL-1 beta and IL-18.	Arsenic	27-34	interleukin 18	Homo sapiens	70-75
27471628-7	2016	The data from current study show sub-chronic arsenic exposure activates AIM2 inflammasome which in turn activates caspase-1 and enhances the secretion of IL-1beta and IL-18 in HaCaT cells and the skin of BALB/c mice.	Arsenic	45-52	absent in melanoma 2	Homo sapiens	72-76
27471628-7	2016	The data from current study show sub-chronic arsenic exposure activates AIM2 inflammasome which in turn activates caspase-1 and enhances the secretion of IL-1beta and IL-18 in HaCaT cells and the skin of BALB/c mice.	Arsenic	45-52	caspase 1	Homo sapiens	114-123
27471628-7	2016	The data from current study show sub-chronic arsenic exposure activates AIM2 inflammasome which in turn activates caspase-1 and enhances the secretion of IL-1beta and IL-18 in HaCaT cells and the skin of BALB/c mice.	Arsenic	45-52	interleukin 1 beta	Homo sapiens	154-162
27471628-7	2016	The data from current study show sub-chronic arsenic exposure activates AIM2 inflammasome which in turn activates caspase-1 and enhances the secretion of IL-1beta and IL-18 in HaCaT cells and the skin of BALB/c mice.	Arsenic	45-52	interleukin 18	Homo sapiens	167-172
27471628-8	2016	In addition, arsenic-promoted activation of AIM2 inflammasome and increase of IL-1beta/IL-18 production are inhibited by PKR inhibitor in HaCaT cells or in the skin of PKR mutant mice, indicating a potential role of PKR in arsenic-induced sterile inflammation.	Arsenic	13-20	absent in melanoma 2	Homo sapiens	44-48
27471628-8	2016	In addition, arsenic-promoted activation of AIM2 inflammasome and increase of IL-1beta/IL-18 production are inhibited by PKR inhibitor in HaCaT cells or in the skin of PKR mutant mice, indicating a potential role of PKR in arsenic-induced sterile inflammation.	Arsenic	13-20	interleukin 1 beta	Homo sapiens	78-86
27471628-8	2016	In addition, arsenic-promoted activation of AIM2 inflammasome and increase of IL-1beta/IL-18 production are inhibited by PKR inhibitor in HaCaT cells or in the skin of PKR mutant mice, indicating a potential role of PKR in arsenic-induced sterile inflammation.	Arsenic	13-20	interleukin 18	Homo sapiens	87-92
27471628-8	2016	In addition, arsenic-promoted activation of AIM2 inflammasome and increase of IL-1beta/IL-18 production are inhibited by PKR inhibitor in HaCaT cells or in the skin of PKR mutant mice, indicating a potential role of PKR in arsenic-induced sterile inflammation.	Arsenic	13-20	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	121-124
27471628-8	2016	In addition, arsenic-promoted activation of AIM2 inflammasome and increase of IL-1beta/IL-18 production are inhibited by PKR inhibitor in HaCaT cells or in the skin of PKR mutant mice, indicating a potential role of PKR in arsenic-induced sterile inflammation.	Arsenic	13-20	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	168-171
27471628-8	2016	In addition, arsenic-promoted activation of AIM2 inflammasome and increase of IL-1beta/IL-18 production are inhibited by PKR inhibitor in HaCaT cells or in the skin of PKR mutant mice, indicating a potential role of PKR in arsenic-induced sterile inflammation.	Arsenic	13-20	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	168-171
27471628-8	2016	In addition, arsenic-promoted activation of AIM2 inflammasome and increase of IL-1beta/IL-18 production are inhibited by PKR inhibitor in HaCaT cells or in the skin of PKR mutant mice, indicating a potential role of PKR in arsenic-induced sterile inflammation.	Arsenic	223-230	absent in melanoma 2	Homo sapiens	44-48
27471628-8	2016	In addition, arsenic-promoted activation of AIM2 inflammasome and increase of IL-1beta/IL-18 production are inhibited by PKR inhibitor in HaCaT cells or in the skin of PKR mutant mice, indicating a potential role of PKR in arsenic-induced sterile inflammation.	Arsenic	223-230	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	121-124
26864988-5	2016	This conceptual self-powered arsenic biosensor demonstrated limits of detection (LODs) of 13 muM for arsenite and 132 muM for arsenate.	Arsenic	29-36	latexin	Homo sapiens	118-121
26930347-0	2016	Comment on "Effects of in Utero Exposure to Arsenic during the Second Half of Gestation on Reproductive End Points and Metabolic Parameters in Female CD-1 Mice".	Arsenic	44-51	CD1 antigen complex	Mus musculus	150-154
26231544-1	2016	This study aimed to explore whether Rac1 and Cdc42, representative members of Ras homologue guanosine triphosphatases (Rho GTPases), are involved in neurotoxicity induced by arsenic exposure in rat nervous system.	Arsenic	174-181	Rac family small GTPase 1	Rattus norvegicus	36-40
26231544-1	2016	This study aimed to explore whether Rac1 and Cdc42, representative members of Ras homologue guanosine triphosphatases (Rho GTPases), are involved in neurotoxicity induced by arsenic exposure in rat nervous system.	Arsenic	174-181	cell division cycle 42	Rattus norvegicus	45-50
26581878-4	2016	Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, occurred in an arsenic dose-dependent manner, and persisted for many cell generations following removal of the arsenite, offering a plausible mechanism of persistently genotoxic arsenic action.	Arsenic	206-213	DNA methyltransferase 1	Homo sapiens	62-67
26581878-4	2016	Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, occurred in an arsenic dose-dependent manner, and persisted for many cell generations following removal of the arsenite, offering a plausible mechanism of persistently genotoxic arsenic action.	Arsenic	206-213	DNA methyltransferase 3 alpha	Homo sapiens	69-75
26878367-0	2016	Activation of NADPH-recycling systems in leaves and roots of Arabidopsis thaliana under arsenic-induced stress conditions is accelerated by knock-out of Nudix hydrolase 19 (AtNUDX19) gene.	Arsenic	88-95	nudix hydrolase homolog 19	Arabidopsis thaliana	173-181
26878367-6	2016	In summary, the data reveals a connection between the absence of chloroplastic AtNUDX19 and the rise in all NADP-dehydrogenase activities under physiological and arsenic-induced stress conditions, particularly in roots.	Arsenic	162-169	nudix hydrolase homolog 19	Arabidopsis thaliana	79-87
26551223-4	2016	According to the effect of pH on arsenic removal, the electrostatic interaction between the positively charged surface of Fe3O4-graphene based adsorbents and anionic As(V) species was a major factor to adsorb As(V).	Arsenic	33-40	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	166-171
26551223-4	2016	According to the effect of pH on arsenic removal, the electrostatic interaction between the positively charged surface of Fe3O4-graphene based adsorbents and anionic As(V) species was a major factor to adsorb As(V).	Arsenic	33-40	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	209-214
26942676-6	2016	Genetic ablation of TRIM21 in mice confers protection from oxidative damages caused by arsenic-induced liver insult and pressure overload heart injury.	Arsenic	87-94	tripartite motif-containing 21	Mus musculus	20-26
26295903-0	2016	Effects of in Utero Exposure to Arsenic during the Second Half of Gestation on Reproductive End Points and Metabolic Parameters in Female CD-1 Mice.	Arsenic	32-39	CD1c molecule	Homo sapiens	138-142
26295903-11	2016	CONCLUSION: Our findings revealed unexpected effects of in utero exposure to arsenic: exposure to both a human-relevant low dose and a tumor-inducing level led to early onset of vaginal opening and to obesity in female CD-1 mice.	Arsenic	77-84	CD1c molecule	Homo sapiens	219-223
26930461-0	2016	Response to "Comment on "Effects of in Utero Exposure to Arsenic during the Second Half of Gestation on Reproductive End Points and Metabolic Parameters in Female CD-1 Mice"".	Arsenic	57-64	CD1 antigen complex	Mus musculus	163-167
26791102-4	2016	In the current study, we identified a direct Nrf2 targeting miRNA, miR-214, and demonstrated a protective role of miR-214 in erythroid cells against oxidative stresses generated by radiation, excess iron and arsenic (As) exposure.	Arsenic	208-215	NFE2 like bZIP transcription factor 2	Homo sapiens	45-49
26581878-4	2016	Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, occurred in an arsenic dose-dependent manner, and persisted for many cell generations following removal of the arsenite, offering a plausible mechanism of persistently genotoxic arsenic action.	Arsenic	206-213	DNA methyltransferase 3 beta	Homo sapiens	77-83
26581878-4	2016	Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, occurred in an arsenic dose-dependent manner, and persisted for many cell generations following removal of the arsenite, offering a plausible mechanism of persistently genotoxic arsenic action.	Arsenic	206-213	mutL homolog 1	Homo sapiens	85-90
26581878-4	2016	Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, occurred in an arsenic dose-dependent manner, and persisted for many cell generations following removal of the arsenite, offering a plausible mechanism of persistently genotoxic arsenic action.	Arsenic	206-213	mutS homolog 2	Homo sapiens	96-101
26581878-4	2016	Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, occurred in an arsenic dose-dependent manner, and persisted for many cell generations following removal of the arsenite, offering a plausible mechanism of persistently genotoxic arsenic action.	Arsenic	206-213	DNA methyltransferase 3 alpha	Homo sapiens	151-157
26581878-4	2016	Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, occurred in an arsenic dose-dependent manner, and persisted for many cell generations following removal of the arsenite, offering a plausible mechanism of persistently genotoxic arsenic action.	Arsenic	206-213	DNA methyltransferase 3 beta	Homo sapiens	162-168
26581878-4	2016	Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, occurred in an arsenic dose-dependent manner, and persisted for many cell generations following removal of the arsenite, offering a plausible mechanism of persistently genotoxic arsenic action.	Arsenic	369-376	DNA methyltransferase 1	Homo sapiens	62-67
26581878-4	2016	Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, occurred in an arsenic dose-dependent manner, and persisted for many cell generations following removal of the arsenite, offering a plausible mechanism of persistently genotoxic arsenic action.	Arsenic	369-376	DNA methyltransferase 3 alpha	Homo sapiens	69-75
26581878-4	2016	Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, occurred in an arsenic dose-dependent manner, and persisted for many cell generations following removal of the arsenite, offering a plausible mechanism of persistently genotoxic arsenic action.	Arsenic	369-376	DNA methyltransferase 3 beta	Homo sapiens	77-83
26581878-4	2016	Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, occurred in an arsenic dose-dependent manner, and persisted for many cell generations following removal of the arsenite, offering a plausible mechanism of persistently genotoxic arsenic action.	Arsenic	369-376	mutL homolog 1	Homo sapiens	85-90
26581878-4	2016	Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, occurred in an arsenic dose-dependent manner, and persisted for many cell generations following removal of the arsenite, offering a plausible mechanism of persistently genotoxic arsenic action.	Arsenic	369-376	mutS homolog 2	Homo sapiens	96-101
26581878-4	2016	Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, occurred in an arsenic dose-dependent manner, and persisted for many cell generations following removal of the arsenite, offering a plausible mechanism of persistently genotoxic arsenic action.	Arsenic	369-376	DNA methyltransferase 3 alpha	Homo sapiens	151-157
26581878-4	2016	Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, occurred in an arsenic dose-dependent manner, and persisted for many cell generations following removal of the arsenite, offering a plausible mechanism of persistently genotoxic arsenic action.	Arsenic	369-376	DNA methyltransferase 3 beta	Homo sapiens	162-168
26581878-5	2016	Analyses of promoter methylation status of the DNA mismatch repair genes HMLH1 and HMSH2 show that HMSH2, but not HMLH1, was epigenetically regulated by promoter hypermethylation changes following arsenic treatment.	Arsenic	197-204	mutL homolog 1	Homo sapiens	73-78
26581878-5	2016	Analyses of promoter methylation status of the DNA mismatch repair genes HMLH1 and HMSH2 show that HMSH2, but not HMLH1, was epigenetically regulated by promoter hypermethylation changes following arsenic treatment.	Arsenic	197-204	mutS homolog 2	Homo sapiens	83-88
26581878-5	2016	Analyses of promoter methylation status of the DNA mismatch repair genes HMLH1 and HMSH2 show that HMSH2, but not HMLH1, was epigenetically regulated by promoter hypermethylation changes following arsenic treatment.	Arsenic	197-204	mutS homolog 2	Homo sapiens	99-104
26898223-0	2016	Arabidopsis thaliana NIP7;1 is involved in tissue arsenic distribution and tolerance in response to arsenate.	Arsenic	50-57	NOD26-like intrinsic protein 7;1	Arabidopsis thaliana	21-27
26898223-1	2016	The Arabidopsis aquaglyceroporin NIP7;1 is involved in uptake and tolerance to the trivalent arsenic species arsenite.	Arsenic	93-100	NOD26-like intrinsic protein 7;1	Arabidopsis thaliana	33-39
26898223-3	2016	Loss of function of NIP7;1 improved tolerance to arsenate and reduced arsenic levels in both the phloem and xylem, resulting in altered arsenic distribution between tissues.	Arsenic	70-77	NOD26-like intrinsic protein 7;1	Arabidopsis thaliana	20-26
26898223-3	2016	Loss of function of NIP7;1 improved tolerance to arsenate and reduced arsenic levels in both the phloem and xylem, resulting in altered arsenic distribution between tissues.	Arsenic	136-143	NOD26-like intrinsic protein 7;1	Arabidopsis thaliana	20-26
26791102-4	2016	In the current study, we identified a direct Nrf2 targeting miRNA, miR-214, and demonstrated a protective role of miR-214 in erythroid cells against oxidative stresses generated by radiation, excess iron and arsenic (As) exposure.	Arsenic	208-215	microRNA 214	Homo sapiens	114-121
26791102-4	2016	In the current study, we identified a direct Nrf2 targeting miRNA, miR-214, and demonstrated a protective role of miR-214 in erythroid cells against oxidative stresses generated by radiation, excess iron and arsenic (As) exposure.	Arsenic	217-219	NFE2 like bZIP transcription factor 2	Homo sapiens	45-49
26791102-4	2016	In the current study, we identified a direct Nrf2 targeting miRNA, miR-214, and demonstrated a protective role of miR-214 in erythroid cells against oxidative stresses generated by radiation, excess iron and arsenic (As) exposure.	Arsenic	217-219	microRNA 214	Homo sapiens	114-121
26672074-0	2016	Glutaredoxin S15 Is Involved in Fe-S Cluster Transfer in Mitochondria Influencing Lipoic Acid-Dependent Enzymes, Plant Growth, and Arsenic Tolerance in Arabidopsis.	Arsenic	131-138	CAX-interacting protein 2	Arabidopsis thaliana	0-12
26563149-0	2016	Overexpression of AtPCS1 in tobacco increases arsenic and arsenic plus cadmium accumulation and detoxification.	Arsenic	46-53	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	18-24
26563149-0	2016	Overexpression of AtPCS1 in tobacco increases arsenic and arsenic plus cadmium accumulation and detoxification.	Arsenic	58-65	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	18-24
26563149-1	2016	MAIN CONCLUSION: The heterologous expression of AtPCS1 in tobacco plants exposed to arsenic plus cadmium enhances phytochelatin levels, root As/Cd accumulation and pollutants detoxification, but does not prevent root cyto-histological damages.	Arsenic	84-91	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	48-54
26563149-1	2016	MAIN CONCLUSION: The heterologous expression of AtPCS1 in tobacco plants exposed to arsenic plus cadmium enhances phytochelatin levels, root As/Cd accumulation and pollutants detoxification, but does not prevent root cyto-histological damages.	Arsenic	141-143	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	48-54
26531710-4	2016	At laboratory scale, As and Sb release was much higher under reducing conditions (up to 138 and 1 mug L(-1), respectively) compared to oxic conditions (up to 6 and 0.5 mug L(-1), respectively) and was enhanced by NO3 (-) and PO4 (3-) addition (increased by a factor of 2.3 for As and 1.6 for Sb).	Arsenic	21-23	NBL1, DAN family BMP antagonist	Homo sapiens	213-216
26953705-5	2016	A slight increase in promoter methylation of p53 in cord blood lymphocytes which correlated with arsenic accumulation in nails was observed in these exposed newborns.	Arsenic	97-104	tumor protein p53	Homo sapiens	45-48
26856874-0	2016	Three-dimensional visualization of arsenic stimulated mouse liver sinusoidal by FIB-SEM approach.	Arsenic	35-42	fibrinogen alpha chain	Mus musculus	80-83
26563149-4	2016	Consequently, we analyzed tobacco seedlings overexpressing Arabidopsis phytochelatin synthase1 gene (AtPCS1) exposed to As and/or Cd, to evaluate the levels of PCs and As/Cd, the cyto-histological modifications of the roots and the Cd/As leaf extrusion ability.	Arsenic	120-122	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	101-107
26563149-5	2016	When exposed to As and/or Cd the plants overexpressing AtPCS1 showed higher PC levels, As plus Cd root accumulation, and detoxification ability than the non-overexpressing plants, but a blocked Cd-extrusion from the leaf trichomes.	Arsenic	16-18	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	55-61
26563149-5	2016	When exposed to As and/or Cd the plants overexpressing AtPCS1 showed higher PC levels, As plus Cd root accumulation, and detoxification ability than the non-overexpressing plants, but a blocked Cd-extrusion from the leaf trichomes.	Arsenic	87-89	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	55-61
26563149-9	2016	The latter, however, positively affected accumulation and detoxification to both pollutants, highlighting that Cd/As accumulation and detoxification due to PCS1 activity do not reduce the cyto-histological damage.	Arsenic	114-116	glutathione gamma-glutamylcysteinyltransferase 1-like	Nicotiana tabacum	156-160
26953705-7	2016	In addition, levels of urinary 8-OHdG excretion and salivary hOGG1 expression were significantly decreased in exposed children suggesting a defect in repair of 8-OHdG in arsenic-exposed children.	Arsenic	170-177	8-oxoguanine DNA glycosylase	Homo sapiens	61-66
26760276-9	2016	Carbonic anhydrase (CA) activity was significantly lower in all tested conditions, showing to be affected by both As and low pH, whereas the combined effect of low pH+As was not different from the effect of low pH alone.	Arsenic	114-116	carbonic anhydrase	Crassostrea gigas	0-18
26760276-9	2016	Carbonic anhydrase (CA) activity was significantly lower in all tested conditions, showing to be affected by both As and low pH, whereas the combined effect of low pH+As was not different from the effect of low pH alone.	Arsenic	114-116	carbonic anhydrase	Crassostrea gigas	20-22
26671504-6	2016	Intriguing was the occurrence of post-infusion oxidation of As(III) to As(V) observed in almost all patients and being especially high (&gt;40%) in patient with increased residual As(V).	Arsenic	60-62	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	71-76
24105067-10	2016	Arsenic increased lipid peroxidation (LPO), reduced glutathione content and the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase were depleted significantly in both kidney and brain.	Arsenic	0-7	catalase	Rattus norvegicus	116-124
24105067-10	2016	Arsenic increased lipid peroxidation (LPO), reduced glutathione content and the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase were depleted significantly in both kidney and brain.	Arsenic	0-7	glutathione-disulfide reductase	Rattus norvegicus	154-175
26988683-0	2016	[Relationship of blood aryl hydrocarbon receptor mRNA and cytochrome P450 1A1 mRNA expression with corrected QT interval among residents exposed to arsenic via drinking water].	Arsenic	148-155	aryl hydrocarbon receptor	Homo sapiens	23-48
26988683-0	2016	[Relationship of blood aryl hydrocarbon receptor mRNA and cytochrome P450 1A1 mRNA expression with corrected QT interval among residents exposed to arsenic via drinking water].	Arsenic	148-155	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	58-77
26988683-9	2016	CONCLUSIONS: Long-term exposure to arsenic is associated with upregulated blood AhRmRNA and CYP1A1 mRNA expression.Blood CYP1A1 mRNA expression, but not AhRmRNA expression, is associated with prolonged corrected QT interval.	Arsenic	35-42	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	92-98
26988683-9	2016	CONCLUSIONS: Long-term exposure to arsenic is associated with upregulated blood AhRmRNA and CYP1A1 mRNA expression.Blood CYP1A1 mRNA expression, but not AhRmRNA expression, is associated with prolonged corrected QT interval.	Arsenic	35-42	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	121-127
26772154-0	2016	LincRNAs and base modifications of p53 induced by arsenic methylation in workers.	Arsenic	50-57	tumor protein p53	Homo sapiens	35-38
26772154-1	2016	Arsenic (As) metabolites could induce methylation changes of DNA and base modifications of p53, which play role in the toxicity of As.	Arsenic	0-7	tumor protein p53	Homo sapiens	91-94
26772154-1	2016	Arsenic (As) metabolites could induce methylation changes of DNA and base modifications of p53, which play role in the toxicity of As.	Arsenic	9-11	tumor protein p53	Homo sapiens	91-94
26772154-1	2016	Arsenic (As) metabolites could induce methylation changes of DNA and base modifications of p53, which play role in the toxicity of As.	Arsenic	131-133	tumor protein p53	Homo sapiens	91-94
26772154-11	2016	These findings suggest potentially widespread roles of p53 and relative RNAs in arsenic workers, which may be caused by As metabolism.	Arsenic	80-87	tumor protein p53	Homo sapiens	55-58
26780400-2	2016	In our previous study, we reported that SATB2 gene expression was induced in human bronchial epithelial BEAS-2B cells transformed by arsenic, chromium, nickel and vanadium.	Arsenic	133-140	SATB homeobox 2	Homo sapiens	40-45
26537186-0	2016	Arsenic Promotes NF-Kappab-Mediated Fibroblast Dysfunction and Matrix Remodeling to Impair Muscle Stem Cell Function.	Arsenic	0-7	nuclear factor kappa B subunit 1	Homo sapiens	17-26
26537186-7	2016	Consistent with myomatrix alterations, fibroblasts isolated from arsenic-exposed muscle displayed sustained expression of matrix remodeling genes, the majority of which were mediated by NF-kappaB.	Arsenic	65-72	nuclear factor kappa B subunit 1	Homo sapiens	186-195
26537186-8	2016	Inhibition of NF-kappaB during arsenic exposure preserved normal myofiber structure and functional recovery after injury, suggesting that NF-kappaB signaling serves as an important mechanism of action for the deleterious effects of arsenic on tissue healing.	Arsenic	31-38	nuclear factor kappa B subunit 1	Homo sapiens	14-23
26537186-8	2016	Inhibition of NF-kappaB during arsenic exposure preserved normal myofiber structure and functional recovery after injury, suggesting that NF-kappaB signaling serves as an important mechanism of action for the deleterious effects of arsenic on tissue healing.	Arsenic	31-38	nuclear factor kappa B subunit 1	Homo sapiens	138-147
26537186-8	2016	Inhibition of NF-kappaB during arsenic exposure preserved normal myofiber structure and functional recovery after injury, suggesting that NF-kappaB signaling serves as an important mechanism of action for the deleterious effects of arsenic on tissue healing.	Arsenic	232-239	nuclear factor kappa B subunit 1	Homo sapiens	14-23
26537186-8	2016	Inhibition of NF-kappaB during arsenic exposure preserved normal myofiber structure and functional recovery after injury, suggesting that NF-kappaB signaling serves as an important mechanism of action for the deleterious effects of arsenic on tissue healing.	Arsenic	232-239	nuclear factor kappa B subunit 1	Homo sapiens	138-147
26671504-6	2016	Intriguing was the occurrence of post-infusion oxidation of As(III) to As(V) observed in almost all patients and being especially high (&gt;40%) in patient with increased residual As(V).	Arsenic	60-62	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	180-185
26476769-9	2016	It has been demonstrated that As(V) was the dominant arsenic speciation adsorbed on iron (hydr)oxides.	Arsenic	53-60	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	30-35
26677206-7	2016	PC1 was positively associated (P &lt;0.05) with age, female sex, and BMI, while negatively associated with smoking, arsenic exposure, education, and land ownership.	Arsenic	116-123	proprotein convertase subtilisin/kexin type 1	Homo sapiens	0-3
26140530-5	2016	Here we report the discovery of haloarchaea (Euryarchaeota phylum) biofilms forming under the extreme environmental conditions such as high salinity, pH and arsenic concentration at 4589 m above sea level inside a volcano crater in Diamante Lake, Argentina.	Arsenic	157-164	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	195-198
26606179-1	2016	Embodied study investigates the role of GRX and associated antioxidant enzymes in the detoxification mechanism between arsenic (As) sensitive (Usar-3) and tolerant cultivar (Pant Dhan 11) of Oryza sativa against As(III) and As(V), under GSH enriched, and GSH deprived conditions.	Arsenic	119-126	glutaredoxin	Homo sapiens	40-43
26606179-1	2016	Embodied study investigates the role of GRX and associated antioxidant enzymes in the detoxification mechanism between arsenic (As) sensitive (Usar-3) and tolerant cultivar (Pant Dhan 11) of Oryza sativa against As(III) and As(V), under GSH enriched, and GSH deprived conditions.	Arsenic	128-130	glutaredoxin	Homo sapiens	40-43
26661117-4	2016	Herein, we report on the synthesis of Cs[E3 C2 (trip)2 ] (1 a: E=P; 1 b: E=As; trip=2,4,6-triisopropylphenyl) and Cs[E4 C(trip)] (2 a: E=P; 2 b: E=As).	Arsenic	75-77	mediator complex subunit 1	Homo sapiens	44-54
26661117-4	2016	Herein, we report on the synthesis of Cs[E3 C2 (trip)2 ] (1 a: E=P; 1 b: E=As; trip=2,4,6-triisopropylphenyl) and Cs[E4 C(trip)] (2 a: E=P; 2 b: E=As).	Arsenic	147-149	mediator complex subunit 1	Homo sapiens	44-54
25082665-0	2016	Paraoxonase 1 activity in subchronic low-level inorganic arsenic exposure through drinking water.	Arsenic	57-64	paraoxonase 1	Rattus norvegicus	0-13
25082665-13	2016	Our findings indicate that decreased PON1 activity observed in arsenic exposure may be an incipient biochemical event in the cardiovascular effects of arsenic.	Arsenic	63-70	paraoxonase 1	Rattus norvegicus	37-41
25082665-13	2016	Our findings indicate that decreased PON1 activity observed in arsenic exposure may be an incipient biochemical event in the cardiovascular effects of arsenic.	Arsenic	151-158	paraoxonase 1	Rattus norvegicus	37-41
25082665-14	2016	Modulation of PON1 activity by arsenic may also be mediated through changes in membrane fluidity brought about by changes in the concentration of cholesterol in the microsomes.	Arsenic	31-38	paraoxonase 1	Rattus norvegicus	14-18
26763397-12	2016	Our results showed that arsenic induced the nuclear translocation of FOXO1 and FOXO3a, and altered the cell cycle, with cells accumulating at the G2/M phase.	Arsenic	24-31	forkhead box O1	Homo sapiens	69-74
26763397-12	2016	Our results showed that arsenic induced the nuclear translocation of FOXO1 and FOXO3a, and altered the cell cycle, with cells accumulating at the G2/M phase.	Arsenic	24-31	forkhead box O3	Homo sapiens	79-85
26573582-0	2016	Arsenic Attenuates GLI Signaling, Increasing or Decreasing its Transcriptional Program in a Context-Dependent Manner.	Arsenic	0-7	GLI family zinc finger 1	Homo sapiens	19-22
26688044-9	2016	Furthermore, the resistant phenotype of fps1Delta, snf3Delta and pho81Delta against As(III) links arsenic uptake with the corresponding plasma membrane-bound transporters-aquaglyceroporin (Fps1p), hexose (Snf3p) and phosphate transporters.	Arsenic	98-105	Fps1p	Saccharomyces cerevisiae S288C	189-194
26688044-9	2016	Furthermore, the resistant phenotype of fps1Delta, snf3Delta and pho81Delta against As(III) links arsenic uptake with the corresponding plasma membrane-bound transporters-aquaglyceroporin (Fps1p), hexose (Snf3p) and phosphate transporters.	Arsenic	98-105	glucose sensor	Saccharomyces cerevisiae S288C	205-210
26573582-5	2016	Here we provide in vitro and in vivo evidence that arsenic acts as a modulator of the activity of the HH effector protein glioma-associated oncogene family zinc finger (GLI), activating or inhibiting GLI activity in a context-dependent manner.	Arsenic	51-58	GLI family zinc finger 1	Homo sapiens	122-167
26573582-5	2016	Here we provide in vitro and in vivo evidence that arsenic acts as a modulator of the activity of the HH effector protein glioma-associated oncogene family zinc finger (GLI), activating or inhibiting GLI activity in a context-dependent manner.	Arsenic	51-58	GLI family zinc finger 1	Homo sapiens	169-172
26573582-5	2016	Here we provide in vitro and in vivo evidence that arsenic acts as a modulator of the activity of the HH effector protein glioma-associated oncogene family zinc finger (GLI), activating or inhibiting GLI activity in a context-dependent manner.	Arsenic	51-58	GLI family zinc finger 1	Homo sapiens	200-203
26573582-7	2016	Our results show that arsenic activates GLI signaling when the intrinsic GLI activity is low but inhibits signaling in the presence of high-level GLI activity.	Arsenic	22-29	GLI family zinc finger 1	Homo sapiens	40-43
26573582-7	2016	Our results show that arsenic activates GLI signaling when the intrinsic GLI activity is low but inhibits signaling in the presence of high-level GLI activity.	Arsenic	22-29	GLI family zinc finger 1	Homo sapiens	73-76
26573582-7	2016	Our results show that arsenic activates GLI signaling when the intrinsic GLI activity is low but inhibits signaling in the presence of high-level GLI activity.	Arsenic	22-29	GLI family zinc finger 1	Homo sapiens	73-76
26573582-9	2016	Combining our findings with previous reports, we present an inclusive model in which arsenic plays dual roles in GLI signaling modulation: when GLIs are primarily in their repressor form, arsenic antagonizes their repression capacity, leading to low-level GLI activation, but when GLIs are primarily in their activator form, arsenic attenuates their activity.	Arsenic	85-92	GLI family zinc finger 1	Homo sapiens	113-116
26573582-9	2016	Combining our findings with previous reports, we present an inclusive model in which arsenic plays dual roles in GLI signaling modulation: when GLIs are primarily in their repressor form, arsenic antagonizes their repression capacity, leading to low-level GLI activation, but when GLIs are primarily in their activator form, arsenic attenuates their activity.	Arsenic	85-92	GLI family zinc finger 1	Homo sapiens	144-147
26573582-9	2016	Combining our findings with previous reports, we present an inclusive model in which arsenic plays dual roles in GLI signaling modulation: when GLIs are primarily in their repressor form, arsenic antagonizes their repression capacity, leading to low-level GLI activation, but when GLIs are primarily in their activator form, arsenic attenuates their activity.	Arsenic	188-195	GLI family zinc finger 1	Homo sapiens	113-116
26821021-0	2016	Subchronic Exposure to Arsenic Represses the TH/TRbeta1-CaMK IV Signaling Pathway in Mouse Cerebellum.	Arsenic	23-30	calcium/calmodulin-dependent protein kinase IV	Mus musculus	56-63
26821021-1	2016	We previously reported that arsenic (As) impaired learning and memory by down-regulating calmodulin-dependent protein kinase IV (CaMK IV) in mouse cerebellum.	Arsenic	28-35	calcium/calmodulin-dependent protein kinase IV	Mus musculus	89-127
26821021-1	2016	We previously reported that arsenic (As) impaired learning and memory by down-regulating calmodulin-dependent protein kinase IV (CaMK IV) in mouse cerebellum.	Arsenic	28-35	calcium/calmodulin-dependent protein kinase IV	Mus musculus	129-136
26821021-1	2016	We previously reported that arsenic (As) impaired learning and memory by down-regulating calmodulin-dependent protein kinase IV (CaMK IV) in mouse cerebellum.	Arsenic	37-39	calcium/calmodulin-dependent protein kinase IV	Mus musculus	89-127
26821021-1	2016	We previously reported that arsenic (As) impaired learning and memory by down-regulating calmodulin-dependent protein kinase IV (CaMK IV) in mouse cerebellum.	Arsenic	37-39	calcium/calmodulin-dependent protein kinase IV	Mus musculus	129-136
26821040-0	2016	Divergent Effects of Arsenic on NF-kappaB Signaling in Different Cells or Tissues: A Systematic Review and Meta-Analysis.	Arsenic	21-28	nuclear factor kappa B subunit 1	Homo sapiens	32-41
26821040-3	2016	Herein, a meta-analysis was performed by independently searching databases including the Cochrane Library, PubMed, Springer, Embase, and China National Knowledge Infrastructure, to analyze effects of arsenic exposure on NF-kappaB signaling.	Arsenic	200-207	nuclear factor kappa B subunit 1	Homo sapiens	220-229
26821040-5	2016	Short exposure to high arsenic doses activated the NF-kappaB signaling pathway, while long exposure to low arsenic doses suppressed NF-kappaB signaling pathway activation.	Arsenic	107-114	nuclear factor kappa B subunit 1	Homo sapiens	132-141
27358181-11	2016	In the Cox regression model adjusted for age and gender, adiponectin was significantly associated with mortality in AS, but not in NS, with hazard ratio (95 % CI) of 1.60 (1.14-2.24) comparing the third with first tertile.	Arsenic	116-118	adiponectin, C1Q and collagen domain containing	Homo sapiens	57-68
26783756-1	2016	BACKGROUND: This laboratory previously analyzed the expression of SPARC in the parental UROtsa cells, their arsenite (As(+3)) and cadmium (Cd(+2))-transformed cell lines, and tumor transplants generated from the transformed cells.	Arsenic	118-120	secreted protein acidic and cysteine rich	Homo sapiens	66-71
26784217-9	2016	Additionally, biochemical analysis showed that the individuals exposed to arsenic had higher levels of aspartate aminotransferase and gamma-glutamyl transpeptidase than those who were not exposed.	Arsenic	74-81	inactive glutathione hydrolase 2	Homo sapiens	134-163
26476303-3	2016	The MHCMP shows a maximum adsorption capacity of 82.3 and 49.6 mg As/g adsorbent for As(III) and As(V) ions respectively, and adsorption followed the Langmuir model.	Arsenic	66-68	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	97-102
26537301-5	2016	Among the 5-point mutations in the PML part of PML-RARA identified in patients with relapsed APL, we found that A216V, S214L, and A216T mutations could attenuate the negative regulation of arsenic on PML-RARA, resulting in the retention of oncoproteins.	Arsenic	189-196	PML nuclear body scaffold	Homo sapiens	35-38
26537301-5	2016	Among the 5-point mutations in the PML part of PML-RARA identified in patients with relapsed APL, we found that A216V, S214L, and A216T mutations could attenuate the negative regulation of arsenic on PML-RARA, resulting in the retention of oncoproteins.	Arsenic	189-196	PML nuclear body scaffold	Homo sapiens	47-50
26537301-5	2016	Among the 5-point mutations in the PML part of PML-RARA identified in patients with relapsed APL, we found that A216V, S214L, and A216T mutations could attenuate the negative regulation of arsenic on PML-RARA, resulting in the retention of oncoproteins.	Arsenic	189-196	retinoic acid receptor alpha	Homo sapiens	51-55
26537301-5	2016	Among the 5-point mutations in the PML part of PML-RARA identified in patients with relapsed APL, we found that A216V, S214L, and A216T mutations could attenuate the negative regulation of arsenic on PML-RARA, resulting in the retention of oncoproteins.	Arsenic	189-196	PML nuclear body scaffold	Homo sapiens	47-50
26537301-5	2016	Among the 5-point mutations in the PML part of PML-RARA identified in patients with relapsed APL, we found that A216V, S214L, and A216T mutations could attenuate the negative regulation of arsenic on PML-RARA, resulting in the retention of oncoproteins.	Arsenic	189-196	retinoic acid receptor alpha	Homo sapiens	204-208
26537301-8	2016	In addition to presenting more evidence to reinforce the correlation of genetic mutations in PML-RARA with arsenic efficacy, we provide novel insight into the functional difference of acquired mutations of PML-RARA both in vitro and in the clinical setting.	Arsenic	107-114	PML nuclear body scaffold	Homo sapiens	93-96
26537301-8	2016	In addition to presenting more evidence to reinforce the correlation of genetic mutations in PML-RARA with arsenic efficacy, we provide novel insight into the functional difference of acquired mutations of PML-RARA both in vitro and in the clinical setting.	Arsenic	107-114	retinoic acid receptor alpha	Homo sapiens	97-101
26755550-8	2016	Patients with elevated galectin-3 (n=19, defined as &gt;2 SD above the control group mean value) had a higher risk of nonelective hospitalization or death (hazard ratio 6.0, 95% CI 2.1 to 16.8, P&lt;0.001).	Arsenic	49-51	galectin 3	Homo sapiens	23-33
26760991-4	2016	Furthermore, an increase in lipid peroxidation with depletion of reduced glutathione (GSH) and activities of superoxide dismutase (SOD) and catalase (CAT) occurred in the livers of rats exposed to arsenic.	Arsenic	197-204	catalase	Rattus norvegicus	140-148
26760991-4	2016	Furthermore, an increase in lipid peroxidation with depletion of reduced glutathione (GSH) and activities of superoxide dismutase (SOD) and catalase (CAT) occurred in the livers of rats exposed to arsenic.	Arsenic	197-204	catalase	Rattus norvegicus	150-153
27358181-12	2016	In a model further adjusted for the risk factors, such as diabetes mellitus, hypertension, coronary artery disease, body mass index, LDL-cholesterol and HDL-cholesterol, adiponectin was significantly associated with mortality with hazard ratio of 1.83 (1.28-2.62) and 1.56 (1.15-2.11) for AS and NS, respectively.	Arsenic	289-291	adiponectin, C1Q and collagen domain containing	Homo sapiens	170-181
26446802-3	2016	mRNA for AS3mt, the gene responsible for methylation of arsenic, was detected in all embryonic tissue types studied.	Arsenic	56-63	arsenite methyltransferase	Mus musculus	9-14
26347414-3	2016	Two novel media-injected permeable reactive barrier (MI-PRB) configurations were proposed for removing arsenic from groundwater.	Arsenic	103-110	RB transcriptional corepressor 1	Homo sapiens	56-59
26694653-0	2016	Does maternal MDR1 C1236T polymorphism have an effect on placental arsenic levels?	Arsenic	67-74	ATP binding cassette subfamily B member 1	Homo sapiens	14-18
26482281-0	2016	Aldehyde dehydrogenase induction in arsenic-exposed rat bladder epithelium.	Arsenic	36-43	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	0-22
26362939-1	2016	The adsorption of fluoride and arsenic ions by modified natural materials may have an impact on the removal of F- and As(V) from waters.	Arsenic	31-38	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	111-123
26482281-8	2016	The IHC and western blotting results confirmed that aldehyde dehydrogenase (ALDH) protein was up-regulated in arsenic-treated rat bladder epithelium.	Arsenic	110-117	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	52-74
26482281-8	2016	The IHC and western blotting results confirmed that aldehyde dehydrogenase (ALDH) protein was up-regulated in arsenic-treated rat bladder epithelium.	Arsenic	110-117	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	76-80
26482281-10	2016	In conclusion, the ALDH protein expression could be used as molecular markers for arsenic-induced transformation.	Arsenic	82-89	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	19-23
26745439-0	2016	Removal of arsenic from water using manganese (III) oxide: Adsorption of As(III) and As(V).	Arsenic	11-18	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	85-90
26745439-4	2016	Maximum removal of As(III) and As(V) occurred at pH 3-9 and at pH 2, respectively, while removal of As(V) in the pH range of 6-9 was 93% (pH 6) to 61% (pH 9) of the maximum removal.	Arsenic	19-21	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	100-105
26554512-6	2016	The inhibition of ABC transporters significantly increased the toxicity of paraquat and arsenic, known substrates of ABC transporters.	Arsenic	88-95	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	18-21
27375740-0	2016	Chronic Exposure to Arsenic in Drinking Water Causes Alterations in Locomotor Activity and Decreases Striatal mRNA for the D2 Dopamine Receptor in CD1 Male Mice.	Arsenic	20-27	dopamine receptor D2	Mus musculus	123-143
27375740-0	2016	Chronic Exposure to Arsenic in Drinking Water Causes Alterations in Locomotor Activity and Decreases Striatal mRNA for the D2 Dopamine Receptor in CD1 Male Mice.	Arsenic	20-27	CD1 antigen complex	Mus musculus	147-150
27375740-2	2016	In this study, CD1 mice were exposed to 0.5 or 5.0 mg As/L of drinking water for 6 months.	Arsenic	54-56	CD1 antigen complex	Mus musculus	15-18
26623569-4	2016	The results showed that both CK2 inhibitors, 4,5,6,7-tetrabromobenzotriazole (TBB) and quinalizarin, markedly reduced the toxicity of Zn(ii), Al(iii), Co(ii), Cr(vi) and As(iii).	Arsenic	170-172	casein kinase 2, alpha prime polypeptide	Mus musculus	29-32
26440706-2	2016	Our recent animal studies showed that low dose arsenic (LDA)-induced transient p53 inhibition selectively protected normal tissues from chemotherapy-induced toxicity.	Arsenic	47-54	tumor protein p53	Homo sapiens	79-82
26554512-6	2016	The inhibition of ABC transporters significantly increased the toxicity of paraquat and arsenic, known substrates of ABC transporters.	Arsenic	88-95	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	117-120
26989453-6	2016	Pretreatment of cells with lead, arsenic, aluminum, mercury, or the ethylmercury-containing preservative thimerosal lowered GSH levels and inhibited MS activity in association with decreased uptake of cysteine, which is rate-limiting for GSH synthesis.	Arsenic	33-40	5-methyltetrahydrofolate-homocysteine methyltransferase	Homo sapiens	149-151
26497925-3	2016	Due to its characteristic localization, MRP4 is proposed as a candidate in the elimination of arsenic and may contribute to resistance to As(III).	Arsenic	94-101	ATP binding cassette subfamily C member 4	Homo sapiens	40-44
26497925-5	2016	The IC50 values of As(III) in MRP4 cells were approximately 6-fold higher than those in MRP2 cells, supporting an important role for MRP4 in resistance to As(III).	Arsenic	19-21	ATP binding cassette subfamily C member 4	Homo sapiens	30-34
26497925-5	2016	The IC50 values of As(III) in MRP4 cells were approximately 6-fold higher than those in MRP2 cells, supporting an important role for MRP4 in resistance to As(III).	Arsenic	19-21	ATP binding cassette subfamily C member 4	Homo sapiens	133-137
26497925-8	2016	Given that MRP4 is a major contributor to arsenic resistance in vitro, further investigation into the correlation between MRP4 expression and treatment outcome of leukemia patients treated with arsenic-based regimens is warranted.	Arsenic	42-49	ATP binding cassette subfamily C member 4	Homo sapiens	11-15
26497925-8	2016	Given that MRP4 is a major contributor to arsenic resistance in vitro, further investigation into the correlation between MRP4 expression and treatment outcome of leukemia patients treated with arsenic-based regimens is warranted.	Arsenic	194-201	ATP binding cassette subfamily C member 4	Homo sapiens	122-126
26695265-0	2016	A novel biosensor based on Au@Ag core-shell nanoparticles for SERS detection of arsenic (III).	Arsenic	80-87	seryl-tRNA synthetase 2, mitochondrial	Homo sapiens	62-66
26513487-12	2016	Although the MDA levels were augmented in the arsenic group, SOD, CAT and GSH-Px enzyme activities were lessened than the other groups.	Arsenic	46-53	catalase	Rattus norvegicus	66-69
27244873-4	2016	Since untreated depression is the most powerful risk factor for suicidal behaviour, we postulated that the consumption of arsenic-contaminated tap drinking-water may also be related to suicide.	Arsenic	122-129	nuclear RNA export factor 1	Homo sapiens	143-146
26711267-0	2015	Arsenic Directly Binds to and Activates the Yeast AP-1-Like Transcription Factor Yap8.	Arsenic	0-7	Arr1p	Saccharomyces cerevisiae S288C	81-85
27158593-0	2016	Arsenic inhibits stem cell differentiation by altering the interplay between the Wnt3a and Notch signaling pathways.	Arsenic	0-7	Wnt family member 3A	Homo sapiens	81-86
27158593-3	2016	This study investigated whether arsenic disrupted the Wnt3a signaling pathway, critical in the formation of myotubes and neurons, during the differentiation in P19 mouse embryonic stem cells.	Arsenic	32-39	wingless-type MMTV integration site family, member 3A	Mus musculus	54-59
27158593-5	2016	Arsenic exposure alone inhibits the differentiation of stem cells into neurons and skeletal myotubes, and reduces the expression of both beta-catenin and GSK3beta mRNA to ~55% of control levels.	Arsenic	0-7	catenin beta 1	Homo sapiens	137-149
27158593-5	2016	Arsenic exposure alone inhibits the differentiation of stem cells into neurons and skeletal myotubes, and reduces the expression of both beta-catenin and GSK3beta mRNA to ~55% of control levels.	Arsenic	0-7	glycogen synthase kinase 3 beta	Homo sapiens	154-162
27158593-6	2016	Co-culture of the arsenic-exposed cells with exogenous Wnt3a rescues the morphological phenotype, but does not alter transcript, protein, or phosphorylation status of GSK3beta or beta-catenin.	Arsenic	18-25	Wnt family member 3A	Homo sapiens	55-60
27158593-7	2016	However, arsenic exposure maintains high levels of Hes5 and decreases the expression of MASH1 by 2.2-fold, which are anti- and pro-myogenic and neurogenic genes, respectively, in the Notch signaling pathway.	Arsenic	9-16	hes family bHLH transcription factor 5	Homo sapiens	51-55
27158593-7	2016	However, arsenic exposure maintains high levels of Hes5 and decreases the expression of MASH1 by 2.2-fold, which are anti- and pro-myogenic and neurogenic genes, respectively, in the Notch signaling pathway.	Arsenic	9-16	achaete-scute family bHLH transcription factor 1	Homo sapiens	88-93
27158593-9	2016	Thus, while Wnt3a can partially rescue the inhibition of differentiation from arsenic, it does so by also modulating Notch target genes rather than only working through the canonical Wnt signaling pathway.	Arsenic	78-85	Wnt family member 3A	Homo sapiens	12-17
27158593-9	2016	Thus, while Wnt3a can partially rescue the inhibition of differentiation from arsenic, it does so by also modulating Notch target genes rather than only working through the canonical Wnt signaling pathway.	Arsenic	78-85	Wnt family member 3A	Homo sapiens	12-15
26711267-1	2015	The AP-1-like transcription factor Yap8 is critical for arsenic tolerance in the yeast Saccharomyces cerevisiae.	Arsenic	56-63	Arr1p	Saccharomyces cerevisiae S288C	35-39
26711267-2	2015	However, the mechanism by which Yap8 senses the presence of arsenic and activates transcription of detoxification genes is unknown.	Arsenic	60-67	Arr1p	Saccharomyces cerevisiae S288C	32-36
26535918-8	2015	Silencing of NOX4, addition of N-acetylcystein, or pretreatment with arsenic itself attenuated the initial dose-dependent inhibition of AHR signaling.	Arsenic	69-76	aryl hydrocarbon receptor	Homo sapiens	136-139
26701102-14	2015	This is the first study to show that joint effect of high urinary total arsenic and VEGF-A risk haplotypes may influence the risk of RCC recurrence in humans who live in an area without obvious arsenic exposure.	Arsenic	194-201	vascular endothelial growth factor A	Homo sapiens	84-90
26577531-4	2015	Modulators of hAS3MT activity may be useful for the prevention or treatment of arsenic-related diseases.	Arsenic	79-86	PDS5 cohesin associated factor B	Homo sapiens	14-18
26535918-9	2015	Arsenic pretreatment led to elevated GSH levels and sensitized the cells to ligand-dependent AHR signaling, while silencing of Nrf2 significantly reduced arsenic-mediated activation of the AHR.	Arsenic	0-7	aryl hydrocarbon receptor	Homo sapiens	93-96
26577531-8	2015	These inhibitors may be useful tools for future research in arsenic metabolism and are the starting-point for the development of drugs against hAS3MT.	Arsenic	60-67	arsenite methyltransferase	Homo sapiens	143-149
26535918-0	2015	NADPH Oxidase-Dependent Mechanism Explains How Arsenic and Other Oxidants Can Activate Aryl Hydrocarbon Receptor Signaling.	Arsenic	47-54	aryl hydrocarbon receptor	Homo sapiens	87-112
26535918-9	2015	Arsenic pretreatment led to elevated GSH levels and sensitized the cells to ligand-dependent AHR signaling, while silencing of Nrf2 significantly reduced arsenic-mediated activation of the AHR.	Arsenic	154-161	NFE2 like bZIP transcription factor 2	Homo sapiens	127-131
26535918-1	2015	The mechanisms explaining arsenic toxicity are not well understood, but physiological consequences of stimulated aryl hydrocarbon receptor (AHR) signaling both directly and through cross-talk with other pathways have been indicated.	Arsenic	26-33	aryl hydrocarbon receptor	Homo sapiens	140-143
26535918-2	2015	The aim of this study was to establish how arsenic interacts with AHR-mediated transcription.	Arsenic	43-50	aryl hydrocarbon receptor	Homo sapiens	66-69
26535918-9	2015	Arsenic pretreatment led to elevated GSH levels and sensitized the cells to ligand-dependent AHR signaling, while silencing of Nrf2 significantly reduced arsenic-mediated activation of the AHR.	Arsenic	154-161	aryl hydrocarbon receptor	Homo sapiens	189-192
26535918-5	2015	Arsenic inhibited CYP1A1 enzyme activity and reduced the metabolic clearance of FICZ.	Arsenic	0-7	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	18-24
26535918-6	2015	Arsenic also led to activated CYP1A1 transcription but only in cells grown in medium containing trace amounts of the endogenous ligand FICZ, pointing to an indirect mechanism of activation.	Arsenic	0-7	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	30-36
26535918-7	2015	Initially, arsenic caused dose-dependent inhibition of FICZ-activated AHR signaling, disturbed intracellular GSH status, and increased expression of oxidative stress-related genes.	Arsenic	11-18	aryl hydrocarbon receptor	Homo sapiens	70-73
26598702-0	2015	Systematic identification of arsenic-binding proteins reveals that hexokinase-2 is inhibited by arsenic.	Arsenic	29-36	hexokinase 2	Homo sapiens	67-79
27004129-0	2016	Inositol transporters AtINT2 and AtINT4 regulate arsenic accumulation in Arabidopsis seeds.	Arsenic	49-56	inositol transporter 2	Arabidopsis thaliana	22-28
27004129-0	2016	Inositol transporters AtINT2 and AtINT4 regulate arsenic accumulation in Arabidopsis seeds.	Arsenic	49-56	inositol transporter 4	Arabidopsis thaliana	33-39
27004129-6	2016	Transformation of Saccharomyces cerevisiae with AtINT2 or AtINT4 led to increased arsenic accumulation and increased sensitivity to arsenite.	Arsenic	82-89	inositol transporter 2	Arabidopsis thaliana	48-54
27004129-6	2016	Transformation of Saccharomyces cerevisiae with AtINT2 or AtINT4 led to increased arsenic accumulation and increased sensitivity to arsenite.	Arsenic	82-89	inositol transporter 4	Arabidopsis thaliana	58-64
27004129-8	2016	Disruption of AtINT2 or AtINT4 in Arabidopsis thaliana led to a reduction in phloem, silique and seed arsenic concentrations in plants fed with arsenite through the roots, relative to wild-type plants.	Arsenic	102-109	inositol transporter 2	Arabidopsis thaliana	14-20
27004129-8	2016	Disruption of AtINT2 or AtINT4 in Arabidopsis thaliana led to a reduction in phloem, silique and seed arsenic concentrations in plants fed with arsenite through the roots, relative to wild-type plants.	Arsenic	102-109	inositol transporter 4	Arabidopsis thaliana	24-30
26253796-1	2015	Inorganic mercury and arsenic encompasses a term which includes As(III), As(V) and Hg(II) species.	Arsenic	22-29	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	73-78
26598702-0	2015	Systematic identification of arsenic-binding proteins reveals that hexokinase-2 is inhibited by arsenic.	Arsenic	96-103	hexokinase 2	Homo sapiens	67-79
26598702-5	2015	Detailed biochemical and metabolomics analyses of the highly homologous hexokinase-2 (HK2), which is overexpressed in many cancers, revealed significant inhibition by arsenic.	Arsenic	167-174	hexokinase 2	Homo sapiens	72-84
26598702-5	2015	Detailed biochemical and metabolomics analyses of the highly homologous hexokinase-2 (HK2), which is overexpressed in many cancers, revealed significant inhibition by arsenic.	Arsenic	167-174	hexokinase 2	Homo sapiens	86-89
26598702-6	2015	Furthermore, overexpression of HK2 rescued cells from arsenic-induced apoptosis.	Arsenic	54-61	hexokinase 2	Homo sapiens	31-34
26598702-7	2015	Our results thus strongly implicate glycolysis, and HK2 in particular, as a key target of arsenic.	Arsenic	90-97	hexokinase 2	Homo sapiens	52-55
26485141-9	2015	Treatment of non-toxic doses of AG or NA on alternate days along with arsenic significantly decreased the arsenic induced elevation of the serum level of ALT, AST and ALP, and arsenic deposition in liver.	Arsenic	70-77	glutamic pyruvic transaminase, soluble	Mus musculus	154-157
26485141-9	2015	Treatment of non-toxic doses of AG or NA on alternate days along with arsenic significantly decreased the arsenic induced elevation of the serum level of ALT, AST and ALP, and arsenic deposition in liver.	Arsenic	70-77	transmembrane protease, serine 11d	Mus musculus	159-162
26485141-9	2015	Treatment of non-toxic doses of AG or NA on alternate days along with arsenic significantly decreased the arsenic induced elevation of the serum level of ALT, AST and ALP, and arsenic deposition in liver.	Arsenic	106-113	glutamic pyruvic transaminase, soluble	Mus musculus	154-157
26485141-9	2015	Treatment of non-toxic doses of AG or NA on alternate days along with arsenic significantly decreased the arsenic induced elevation of the serum level of ALT, AST and ALP, and arsenic deposition in liver.	Arsenic	106-113	transmembrane protease, serine 11d	Mus musculus	159-162
26485141-9	2015	Treatment of non-toxic doses of AG or NA on alternate days along with arsenic significantly decreased the arsenic induced elevation of the serum level of ALT, AST and ALP, and arsenic deposition in liver.	Arsenic	106-113	glutamic pyruvic transaminase, soluble	Mus musculus	154-157
26485141-9	2015	Treatment of non-toxic doses of AG or NA on alternate days along with arsenic significantly decreased the arsenic induced elevation of the serum level of ALT, AST and ALP, and arsenic deposition in liver.	Arsenic	106-113	transmembrane protease, serine 11d	Mus musculus	159-162
25537191-0	2015	TG-interacting factor mediates arsenic-induced malignant transformation of keratinocytes via c-Src/EGFR/AKT/FOXO3A and redox signalings.	Arsenic	31-38	TGFB induced factor homeobox 1	Homo sapiens	0-21
26637202-0	2015	Elevated concentrations of serum matrix metalloproteinase-2 and -9 and their associations with circulating markers of cardiovascular diseases in chronic arsenic-exposed individuals.	Arsenic	153-160	matrix metallopeptidase 2	Homo sapiens	33-66
26637202-3	2015	This study has been designed to evaluate the interactions of arsenic exposure with serum MMP-2 and MMP-9 concentrations especially in relation to the circulating biomarkers of CVDs.	Arsenic	61-68	matrix metallopeptidase 2	Homo sapiens	89-94
26637202-3	2015	This study has been designed to evaluate the interactions of arsenic exposure with serum MMP-2 and MMP-9 concentrations especially in relation to the circulating biomarkers of CVDs.	Arsenic	61-68	matrix metallopeptidase 9	Homo sapiens	99-104
26637202-6	2015	RESULTS: Serum MMP-2 and MMP-9 concentrations in arsenic-endemic population were significantly (p &lt; 0.001) higher than those in non-endemic population.	Arsenic	49-56	matrix metallopeptidase 2	Homo sapiens	15-20
26637202-6	2015	RESULTS: Serum MMP-2 and MMP-9 concentrations in arsenic-endemic population were significantly (p &lt; 0.001) higher than those in non-endemic population.	Arsenic	49-56	matrix metallopeptidase 9	Homo sapiens	25-30
26637202-8	2015	MMP-2 concentrations were 1.02, 1.03 and 1.05 times, and MMP-9 concentrations were 1.03, 1.06 and 1.07 times greater for 1 unit increase in log-transformed water, hair and nail arsenic concentrations, respectively, after adjusting for covariates (age, sex, BMI, smoking habit and hypertension).	Arsenic	177-184	matrix metallopeptidase 2	Homo sapiens	0-5
26637202-8	2015	MMP-2 concentrations were 1.02, 1.03 and 1.05 times, and MMP-9 concentrations were 1.03, 1.06 and 1.07 times greater for 1 unit increase in log-transformed water, hair and nail arsenic concentrations, respectively, after adjusting for covariates (age, sex, BMI, smoking habit and hypertension).	Arsenic	177-184	matrix metallopeptidase 9	Homo sapiens	57-62
26637202-12	2015	CONCLUSIONS: This study showed the significant positive associations and dose-response relationships of arsenic exposure with serum MMP-2 and MMP-9 concentrations.	Arsenic	104-111	matrix metallopeptidase 2	Homo sapiens	132-137
26637202-12	2015	CONCLUSIONS: This study showed the significant positive associations and dose-response relationships of arsenic exposure with serum MMP-2 and MMP-9 concentrations.	Arsenic	104-111	matrix metallopeptidase 9	Homo sapiens	142-147
26637202-13	2015	This study also showed the interactions of MMP-2 and MMP-9 concentrations with the circulating markers of CVDs suggesting the MMP-2 and MMP-9 -mediated mechanism of arsenic-induced CVDs.	Arsenic	165-172	matrix metallopeptidase 2	Homo sapiens	43-48
26637202-13	2015	This study also showed the interactions of MMP-2 and MMP-9 concentrations with the circulating markers of CVDs suggesting the MMP-2 and MMP-9 -mediated mechanism of arsenic-induced CVDs.	Arsenic	165-172	matrix metallopeptidase 9	Homo sapiens	53-58
26637202-13	2015	This study also showed the interactions of MMP-2 and MMP-9 concentrations with the circulating markers of CVDs suggesting the MMP-2 and MMP-9 -mediated mechanism of arsenic-induced CVDs.	Arsenic	165-172	matrix metallopeptidase 2	Homo sapiens	126-131
26637202-13	2015	This study also showed the interactions of MMP-2 and MMP-9 concentrations with the circulating markers of CVDs suggesting the MMP-2 and MMP-9 -mediated mechanism of arsenic-induced CVDs.	Arsenic	165-172	matrix metallopeptidase 9	Homo sapiens	136-141
25537191-0	2015	TG-interacting factor mediates arsenic-induced malignant transformation of keratinocytes via c-Src/EGFR/AKT/FOXO3A and redox signalings.	Arsenic	31-38	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	93-98
25537191-0	2015	TG-interacting factor mediates arsenic-induced malignant transformation of keratinocytes via c-Src/EGFR/AKT/FOXO3A and redox signalings.	Arsenic	31-38	epidermal growth factor receptor	Homo sapiens	99-103
25537191-0	2015	TG-interacting factor mediates arsenic-induced malignant transformation of keratinocytes via c-Src/EGFR/AKT/FOXO3A and redox signalings.	Arsenic	31-38	AKT serine/threonine kinase 1	Homo sapiens	104-107
25537191-0	2015	TG-interacting factor mediates arsenic-induced malignant transformation of keratinocytes via c-Src/EGFR/AKT/FOXO3A and redox signalings.	Arsenic	31-38	forkhead box O3	Homo sapiens	108-114
25537191-6	2015	Surprisingly, low-dose arsenic could also transcriptionally increase TG-interacting factor (TGIF) expression via c-Src/EGFR/AKT/FOXO3A signaling involving superoxide production from NADPH oxidase.	Arsenic	23-30	TGFB induced factor homeobox 1	Homo sapiens	69-90
25537191-6	2015	Surprisingly, low-dose arsenic could also transcriptionally increase TG-interacting factor (TGIF) expression via c-Src/EGFR/AKT/FOXO3A signaling involving superoxide production from NADPH oxidase.	Arsenic	23-30	TGFB induced factor homeobox 1	Homo sapiens	92-96
25537191-6	2015	Surprisingly, low-dose arsenic could also transcriptionally increase TG-interacting factor (TGIF) expression via c-Src/EGFR/AKT/FOXO3A signaling involving superoxide production from NADPH oxidase.	Arsenic	23-30	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	113-118
25537191-6	2015	Surprisingly, low-dose arsenic could also transcriptionally increase TG-interacting factor (TGIF) expression via c-Src/EGFR/AKT/FOXO3A signaling involving superoxide production from NADPH oxidase.	Arsenic	23-30	epidermal growth factor receptor	Homo sapiens	119-123
25537191-6	2015	Surprisingly, low-dose arsenic could also transcriptionally increase TG-interacting factor (TGIF) expression via c-Src/EGFR/AKT/FOXO3A signaling involving superoxide production from NADPH oxidase.	Arsenic	23-30	AKT serine/threonine kinase 1	Homo sapiens	124-127
25537191-6	2015	Surprisingly, low-dose arsenic could also transcriptionally increase TG-interacting factor (TGIF) expression via c-Src/EGFR/AKT/FOXO3A signaling involving superoxide production from NADPH oxidase.	Arsenic	23-30	forkhead box O3	Homo sapiens	128-134
25537191-8	2015	Knockdown of TGIF with its specific shRNA abolished the arsenic-induced effects.	Arsenic	56-63	TGFB induced factor homeobox 1	Homo sapiens	13-17
25537191-9	2015	Taken together, we suggest that TGIF plays an important role in low-dose arsenic-induced malignant transformation of HaCaT cells, which is regulated by c-Src/EGFR/AKT/FOXO3A pathway and redox signaling.	Arsenic	73-80	TGFB induced factor homeobox 1	Homo sapiens	32-36
25537191-9	2015	Taken together, we suggest that TGIF plays an important role in low-dose arsenic-induced malignant transformation of HaCaT cells, which is regulated by c-Src/EGFR/AKT/FOXO3A pathway and redox signaling.	Arsenic	73-80	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	152-157
25537191-9	2015	Taken together, we suggest that TGIF plays an important role in low-dose arsenic-induced malignant transformation of HaCaT cells, which is regulated by c-Src/EGFR/AKT/FOXO3A pathway and redox signaling.	Arsenic	73-80	epidermal growth factor receptor	Homo sapiens	158-162
25537191-9	2015	Taken together, we suggest that TGIF plays an important role in low-dose arsenic-induced malignant transformation of HaCaT cells, which is regulated by c-Src/EGFR/AKT/FOXO3A pathway and redox signaling.	Arsenic	73-80	AKT serine/threonine kinase 1	Homo sapiens	163-166
25537191-9	2015	Taken together, we suggest that TGIF plays an important role in low-dose arsenic-induced malignant transformation of HaCaT cells, which is regulated by c-Src/EGFR/AKT/FOXO3A pathway and redox signaling.	Arsenic	73-80	forkhead box O3	Homo sapiens	167-173
26289331-0	2015	Chemical speciation and ecological risk assessment of arsenic in marine sediments from Izmir Bay (Eastern Aegean Sea).	Arsenic	54-61	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	113-116
26511260-2	2015	Source identification analysis indicated that PC1, including Al, Fe, Mn, Cr, Ni, As, Cu, and Zn, can be defined as a sewage component; PC2, including Pb and Sb, can be considered as an atmospheric deposition component; and PC3, containing Cd and Hg, can be considered as an agricultural nonpoint component.	Arsenic	81-83	proprotein convertase subtilisin/kexin type 1	Homo sapiens	46-49
26031227-0	2015	MRP1 expression in bronchoalveolar lavage cells in subjects with lung cancer who were chronically exposed to arsenic.	Arsenic	109-116	ATP binding cassette subfamily C member 1	Homo sapiens	0-4
26031227-2	2015	The aim of this study was to evaluate and compare the expression of MRP1 in bronchoalveolar cells from subjects with and without lung cancer who had been chronically exposed to arsenic through drinking water.	Arsenic	177-184	ATP binding cassette subfamily C member 1	Homo sapiens	68-72
26031227-4	2015	MRP1 expression was significantly decreased in those with arsenic urinary levels &gt;50 mug/L when compared with the controls.	Arsenic	58-65	ATP binding cassette subfamily C member 1	Homo sapiens	0-4
26031227-5	2015	In conclusion, chronic arsenic exposure negatively correlates with the expression of MRP1 in BAL cells in patients with lung cancer.	Arsenic	23-30	ATP binding cassette subfamily C member 1	Homo sapiens	85-89
26549173-6	2015	IL1beta genes were significantly up regulated on exposure to Pb + As (2.01-fold) and inhibited on exposure to Pb + Hg + Cd (0.13-fold).	Arsenic	66-68	interleukin 1, beta	Danio rerio	0-7
26549173-7	2015	TNF-alpha was significantly inhibited on exposure to As (0.40-fold) and Pb + As (0.32-fold) compared to control.	Arsenic	53-55	tumor necrosis factor a (TNF superfamily, member 2)	Danio rerio	0-9
26169724-2	2015	Recently the cytosolic Trx1 system has been shown to be a cellular target of arsenic containing compounds.	Arsenic	77-84	thioredoxin	Homo sapiens	23-27
26823637-5	2015	The tolerance of the acetoclastic and hydrogenotrophic methanogens in the sludge to AsIII increased 47-fold (IC50 = 910 muM) and 12-fold (IC50= 1100 muM), respectively, upon long-term exposure to As.	Arsenic	84-86	latexin	Homo sapiens	120-123
26479948-1	2015	Dithiols such as British anti-lewisite (BAL, rac-2,3-dimercaptopropanol) are an important class of antidotes for the blister agent lewisite (trans-2-chlorovinyldichloroarsine) and, more generally, are chelating agents for arsenic and other toxic metals.	Arsenic	222-229	Rac family small GTPase 2	Homo sapiens	45-50
26823637-5	2015	The tolerance of the acetoclastic and hydrogenotrophic methanogens in the sludge to AsIII increased 47-fold (IC50 = 910 muM) and 12-fold (IC50= 1100 muM), respectively, upon long-term exposure to As.	Arsenic	84-86	latexin	Homo sapiens	149-152
27122327-0	2015	[Changes in mRNA expression of p53 and related downstream genes in peripheral blood lymphocytes in workers occupationally exposed to arsenic].	Arsenic	133-140	tumor protein p53	Homo sapiens	31-34
26569224-5	2015	Notably, PKM2 has a high affinity for arsenic.	Arsenic	38-45	pyruvate kinase M1/2	Homo sapiens	9-13
27122327-1	2015	OBJECTIVE: To investigate the changes in mRNA expression of p53 and related downstream genes in peripheral blood lymphocytes in workers occupationally exposed to arsenic as well as its influencing factors, and to analyze the mechanism of genetic toxicity of arsenic.	Arsenic	162-169	tumor protein p53	Homo sapiens	60-63
27122327-1	2015	OBJECTIVE: To investigate the changes in mRNA expression of p53 and related downstream genes in peripheral blood lymphocytes in workers occupationally exposed to arsenic as well as its influencing factors, and to analyze the mechanism of genetic toxicity of arsenic.	Arsenic	258-265	tumor protein p53	Homo sapiens	60-63
27122327-6	2015	CONCLUSION: The changes in mRNA expression of p53 and related downstream genes are closely related to the metabolic transformation of inorganic arsenic in workers occupationally exposed to arsenic, and it also plays an important role in genetic toxicity and carcinogenic effect in people exposed to arsenic.	Arsenic	144-151	tumor protein p53	Homo sapiens	46-49
27122327-6	2015	CONCLUSION: The changes in mRNA expression of p53 and related downstream genes are closely related to the metabolic transformation of inorganic arsenic in workers occupationally exposed to arsenic, and it also plays an important role in genetic toxicity and carcinogenic effect in people exposed to arsenic.	Arsenic	189-196	tumor protein p53	Homo sapiens	46-49
27122327-6	2015	CONCLUSION: The changes in mRNA expression of p53 and related downstream genes are closely related to the metabolic transformation of inorganic arsenic in workers occupationally exposed to arsenic, and it also plays an important role in genetic toxicity and carcinogenic effect in people exposed to arsenic.	Arsenic	189-196	tumor protein p53	Homo sapiens	46-49
26410455-3	2015	Sporulation-specific glycoamylase (SGA1), which was upregulated in response to arsenic, was fused with the blue fluorescent protein (BFP) for the construction of an oxidative stress-causing chemicals sensor.	Arsenic	79-86	glucan 1,4-alpha-glucosidase	Saccharomyces cerevisiae S288C	35-39
26569224-7	2015	These observations suggest that arsenic-mediated acute promyelocytic leukaemia (APL) suppressive effects involve PKM2.	Arsenic	32-39	pyruvate kinase M1/2	Homo sapiens	113-117
26569224-9	2015	Further investigation into specific signal pathways by which PKM2 mediates APL developments may lead to a better understanding of arsenic effects on APL.	Arsenic	130-137	pyruvate kinase M1/2	Homo sapiens	61-65
26537450-0	2015	Folic acid protects against arsenic-mediated embryo toxicity by up-regulating the expression of Dvr1.	Arsenic	28-35	growth differentiation factor 3	Danio rerio	96-100
26385919-0	2015	Antioncogenic and Oncogenic Properties of Nrf2 in Arsenic-induced Carcinogenesis.	Arsenic	50-57	NFE2 like bZIP transcription factor 2	Homo sapiens	42-46
26537450-2	2015	Our previous study showed that arsenic impairs embryo development by down-regulating Dvr1/GDF1 expression in zebrafish.	Arsenic	31-38	growth differentiation factor 3	Danio rerio	85-89
26537450-2	2015	Our previous study showed that arsenic impairs embryo development by down-regulating Dvr1/GDF1 expression in zebrafish.	Arsenic	31-38	growth differentiation factor 1	Homo sapiens	90-94
26537450-9	2015	Our data demonstrated that folic acid supplementation protected against arsenic-mediated embryo toxicity by up-regulating the expression of Dvr1/GDF1, and folic acid enhanced the expression of GDF1 by decreasing p66Shc expression and subcellular ROS levels.	Arsenic	72-79	growth differentiation factor 3	Danio rerio	140-144
26537450-9	2015	Our data demonstrated that folic acid supplementation protected against arsenic-mediated embryo toxicity by up-regulating the expression of Dvr1/GDF1, and folic acid enhanced the expression of GDF1 by decreasing p66Shc expression and subcellular ROS levels.	Arsenic	72-79	growth differentiation factor 1	Homo sapiens	145-149
25199682-9	2015	A tumor protein p53 (TP53) subnetwork was identified, showing the interactions of TP53 with other genes affected by arsenic.	Arsenic	116-123	tumor protein p53	Homo sapiens	16-19
25199682-9	2015	A tumor protein p53 (TP53) subnetwork was identified, showing the interactions of TP53 with other genes affected by arsenic.	Arsenic	116-123	tumor protein p53	Homo sapiens	21-25
25199682-9	2015	A tumor protein p53 (TP53) subnetwork was identified, showing the interactions of TP53 with other genes affected by arsenic.	Arsenic	116-123	tumor protein p53	Homo sapiens	82-86
25859628-8	2015	Furthermore, liver phosphoenolpyruvate carboxykinase (PEPCK) mRNA expression was increased and liver glycogen content was decreased in arsenic-treated ovariectomized mice compared with arsenic-treated sham mice.	Arsenic	135-142	phosphoenolpyruvate carboxykinase 1, cytosolic	Mus musculus	19-52
25859628-10	2015	Arsenic treatment significantly decreased plasma adiponectin levels in sham and ovariectomized mice.	Arsenic	0-7	adiponectin, C1Q and collagen domain containing	Mus musculus	49-60
25859628-8	2015	Furthermore, liver phosphoenolpyruvate carboxykinase (PEPCK) mRNA expression was increased and liver glycogen content was decreased in arsenic-treated ovariectomized mice compared with arsenic-treated sham mice.	Arsenic	135-142	phosphoenolpyruvate carboxykinase 1, cytosolic	Mus musculus	54-59
26606645-5	2015	Several evidences have shown that mitochondrial disruption, caspase activation, MAPK signaling and p53 are the pathways for arsenic induced apoptosis.	Arsenic	124-131	tumor protein p53	Homo sapiens	99-102
26095615-2	2015	Among the isolates, two of the bacteria (As-9 and As-14) exhibited high resistance to As(V) [MIC &gt;= 700 mM] and As(III) [MIC &gt;= 10 mM] and were selected for further studies.	Arsenic	41-43	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	86-91
25680285-0	2015	Nrf2-dependent repression of interleukin-12 expression in human dendritic cells exposed to inorganic arsenic.	Arsenic	101-108	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
25680285-4	2015	In the present study, we determined if Nrf2 could contribute to these arsenic immunotoxic effects.	Arsenic	70-77	NFE2 like bZIP transcription factor 2	Homo sapiens	39-43
25680285-6	2015	Under these experimental conditions, arsenic rapidly and stably activates Nrf2 and increases the expression of Nrf2 target genes.	Arsenic	37-44	NFE2 like bZIP transcription factor 2	Homo sapiens	74-78
25680285-6	2015	Under these experimental conditions, arsenic rapidly and stably activates Nrf2 and increases the expression of Nrf2 target genes.	Arsenic	37-44	NFE2 like bZIP transcription factor 2	Homo sapiens	111-115
25680285-8	2015	Particularly, arsenic reduces mRNA levels of IL12A and IL12B genes which encodes the p35 and p40 subunits of IL-12p70, respectively.	Arsenic	14-21	interleukin 12A	Homo sapiens	45-50
25680285-8	2015	Particularly, arsenic reduces mRNA levels of IL12A and IL12B genes which encodes the p35 and p40 subunits of IL-12p70, respectively.	Arsenic	14-21	interleukin 12B	Homo sapiens	55-60
25680285-8	2015	Particularly, arsenic reduces mRNA levels of IL12A and IL12B genes which encodes the p35 and p40 subunits of IL-12p70, respectively.	Arsenic	14-21	interleukin 12A	Homo sapiens	85-88
25680285-8	2015	Particularly, arsenic reduces mRNA levels of IL12A and IL12B genes which encodes the p35 and p40 subunits of IL-12p70, respectively.	Arsenic	14-21	interleukin 9	Homo sapiens	93-96
25680285-9	2015	tert-Butylhydroquinone (tBHQ), a reference Nrf2 inducer, mimics arsenic effects and potently inhibits IL-12 expression.	Arsenic	64-71	NFE2 like bZIP transcription factor 2	Homo sapiens	43-47
25680285-10	2015	Genetic inhibition of Nrf2 expression markedly prevents the repression of both IL12 mRNA and IL-12 protein levels triggered by arsenic and tBHQ in human LPS-stimulated DCs.	Arsenic	127-134	NFE2 like bZIP transcription factor 2	Homo sapiens	22-26
25680285-11	2015	In addition, arsenic significantly reduces IL-12 mRNA levels in LPS-activated bone marrow-derived DCs from Nrf2+/+ mice but not in DCs from Nrf2-/- mice.	Arsenic	13-20	nuclear factor, erythroid derived 2, like 2	Mus musculus	107-111
25680285-12	2015	Finally, we show that, besides IL-12, arsenic significantly reduces the expression of IL-23, another heterodimer containing the p40 subunit.	Arsenic	38-45	interleukin 23 subunit alpha	Homo sapiens	86-91
25680285-12	2015	Finally, we show that, besides IL-12, arsenic significantly reduces the expression of IL-23, another heterodimer containing the p40 subunit.	Arsenic	38-45	interleukin 9	Homo sapiens	128-131
25680285-13	2015	In conclusion, our study demonstrated that arsenic represses IL-12 expression in human-activated DCs by specifically stimulating Nrf2 activity.	Arsenic	43-50	NFE2 like bZIP transcription factor 2	Homo sapiens	129-133
26823706-13	2015	The expression of PCNA, MMP-9, and VEGF in the AS-H group decreased significantly compared with the control group (P&lt;0.05).	Arsenic	47-49	proliferating cell nuclear antigen	Oryctolagus cuniculus	18-22
26823706-13	2015	The expression of PCNA, MMP-9, and VEGF in the AS-H group decreased significantly compared with the control group (P&lt;0.05).	Arsenic	47-49	matrix metalloproteinase-9	Oryctolagus cuniculus	24-29
26823706-13	2015	The expression of PCNA, MMP-9, and VEGF in the AS-H group decreased significantly compared with the control group (P&lt;0.05).	Arsenic	47-49	vascular endothelial growth factor A	Oryctolagus cuniculus	35-39
26095615-2	2015	Among the isolates, two of the bacteria (As-9 and As-14) exhibited high resistance to As(V) [MIC &gt;= 700 mM] and As(III) [MIC &gt;= 10 mM] and were selected for further studies.	Arsenic	50-52	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	86-91
26095615-3	2015	Both these bacteria grew well in the presence of arsenic [20 mM As(V) and 5 mM As(III)], but the isolate As-14 strictly required arsenic for its survival and growth and was characterized as a novel arsenic dependent bacterium.	Arsenic	49-56	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	64-69
26095615-5	2015	Quantitative estimation of arsenic through Atomic Absorption Spectrophotometer revealed that there was &gt;60% accumulation of both As(V) and As(III) by the two isolates.	Arsenic	27-34	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	132-137
26395146-5	2015	Our calculations at the MP2 and MP4 levels with basis sets up to the QZVPP+diff quality, and including solvation of the clusters and solvent molecules by the dielectric continuum SMD method, predict the solvation free energy of Li(+) as -116.1, -120.6 and -123.6 kcal mol(-1) in H2O, CH3CN and DMSO solvents, respectively (1 mol L(-1) standard state).	Arsenic	49-51	tryptase pseudogene 1	Homo sapiens	24-27
26209557-5	2015	We also examined the contribution of polymorphisms in the arsenic metabolism gene AS3MT via conditional linkage analysis.	Arsenic	58-65	arsenite methyltransferase	Homo sapiens	82-87
26473953-5	2015	Here we present evidence that suggests As-induced global histone H4K16 acetylation (H4K16ac) partly due to the direct physical interaction between As and histone acetyltransferase (HAT) hMOF (human male absent on first) protein, leading to the loss of hMOF HAT activity.	Arsenic	39-41	lysine acetyltransferase 8	Homo sapiens	186-190
26501310-1	2015	This study reports the concentrations of PM1 trace elements (As, Cd, Co, Cr, Hg, Mn, Ni, Pb, Sb and Se) content in highly mobile (F1), mobile (F2), less mobile (F3) and not mobile (F4) fractions in samples that were collected in the surroundings of power plants in southern Poland.	Arsenic	61-63	transmembrane protein 11	Homo sapiens	41-44
26473953-5	2015	Here we present evidence that suggests As-induced global histone H4K16 acetylation (H4K16ac) partly due to the direct physical interaction between As and histone acetyltransferase (HAT) hMOF (human male absent on first) protein, leading to the loss of hMOF HAT activity.	Arsenic	39-41	lysine acetyltransferase 8	Homo sapiens	252-256
26473953-5	2015	Here we present evidence that suggests As-induced global histone H4K16 acetylation (H4K16ac) partly due to the direct physical interaction between As and histone acetyltransferase (HAT) hMOF (human male absent on first) protein, leading to the loss of hMOF HAT activity.	Arsenic	147-149	lysine acetyltransferase 8	Homo sapiens	186-190
26473953-5	2015	Here we present evidence that suggests As-induced global histone H4K16 acetylation (H4K16ac) partly due to the direct physical interaction between As and histone acetyltransferase (HAT) hMOF (human male absent on first) protein, leading to the loss of hMOF HAT activity.	Arsenic	147-149	lysine acetyltransferase 8	Homo sapiens	252-256
26473953-11	2015	hMOF over-expression not only increased resistance to As and caused less toxicity, but also effectively reversed reduced H4K16ac caused by As exposure.	Arsenic	54-56	lysine acetyltransferase 8	Homo sapiens	0-4
26473953-11	2015	hMOF over-expression not only increased resistance to As and caused less toxicity, but also effectively reversed reduced H4K16ac caused by As exposure.	Arsenic	139-141	lysine acetyltransferase 8	Homo sapiens	0-4
26473898-0	2015	Hepatic and Nephric NRF2 Pathway Up-Regulation, an Early Antioxidant Response, in Acute Arsenic-Exposed Mice.	Arsenic	88-95	nuclear factor, erythroid derived 2, like 2	Mus musculus	20-24
26209128-0	2015	Distributions, sources and ecological risk assessment of arsenic and mercury in the surface sediments of the southwestern coastal Laizhou Bay, Bohai Sea.	Arsenic	57-64	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	149-152
26434351-4	2015	Moreover, our model calculations show that the sign of the cross-shot noise of spin current is negative for all surface states of AS/QD/AS junctions, whereas it oscillates between positive and negative values for two surface states of AB/QD/AB junctions as we sweep the gate voltage.	Arsenic	130-132	spindlin 1	Homo sapiens	79-83
26434351-4	2015	Moreover, our model calculations show that the sign of the cross-shot noise of spin current is negative for all surface states of AS/QD/AS junctions, whereas it oscillates between positive and negative values for two surface states of AB/QD/AB junctions as we sweep the gate voltage.	Arsenic	136-138	spindlin 1	Homo sapiens	79-83
26220687-0	2015	Ethanol enhances arsenic-induced cyclooxygenase-2 expression via both NFAT and NF-kappaB signalings in colorectal cancer cells.	Arsenic	17-24	prostaglandin-endoperoxide synthase 2	Homo sapiens	33-49
26220687-3	2015	In the present study, we hypothesized that ethanol would enhance the function of an environmental carcinogen such as arsenic through increase in COX-2 expression.	Arsenic	117-124	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	145-150
26220687-4	2015	Our in vitro results show that ethanol enhanced arsenic-induced COX-2 expression.	Arsenic	48-55	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	64-69
26220687-6	2015	We demonstrate that antioxidant enzymes have an inhibitory effect on arsenic/ethanol-induced COX-2 expression, indicating that the responsive signaling pathways from co-exposure to arsenic and ethanol relate to ROS generation.	Arsenic	69-76	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	93-98
26220687-6	2015	We demonstrate that antioxidant enzymes have an inhibitory effect on arsenic/ethanol-induced COX-2 expression, indicating that the responsive signaling pathways from co-exposure to arsenic and ethanol relate to ROS generation.	Arsenic	181-188	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	93-98
26220687-7	2015	In vivo results also show that co-exposure to arsenic and ethanol increased COX-2 expression in mice.	Arsenic	46-53	cytochrome c oxidase II, mitochondrial	Mus musculus	76-81
26220687-8	2015	We conclude that ethanol enhances arsenic-induced COX-2 expression in colorectal cancer cells via both the NFAT and NF-kappaB pathways.	Arsenic	34-41	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	50-55
26473898-4	2015	The present investigation aimed to explore the hepatic and nephric NRF2 pathway upregulation in acute arsenic-exposed mice in vivo.	Arsenic	102-109	nuclear factor, erythroid derived 2, like 2	Mus musculus	67-71
26473898-8	2015	A better knowledge about the NRF2 pathway involvment in the cellular response against arsenic could help improve the strategies for reducing the cellular toxicity related to this metalloid.	Arsenic	86-93	nuclear factor, erythroid derived 2, like 2	Mus musculus	29-33
25092181-9	2015	Thus, the highest retention of arsenic was detected in the esophagus after intraperitoneal administration of As(III) to mice, and this appeared to result from multiple factors, including high expression of AQP3, low expression of MRP2, low capacity of glutathione synthesis and low activation of Nrf2.	Arsenic	31-38	aquaporin 3	Mus musculus	206-210
30090333-0	2016	Identification of Id1 as a downstream effector for arsenic-promoted angiogenesis via PI3K/Akt, NF-kappaB and NOS signaling.	Arsenic	51-58	inhibitor of DNA binding 1, HLH protein	Homo sapiens	18-21
30090333-0	2016	Identification of Id1 as a downstream effector for arsenic-promoted angiogenesis via PI3K/Akt, NF-kappaB and NOS signaling.	Arsenic	51-58	AKT serine/threonine kinase 1	Homo sapiens	90-93
30090333-0	2016	Identification of Id1 as a downstream effector for arsenic-promoted angiogenesis via PI3K/Akt, NF-kappaB and NOS signaling.	Arsenic	51-58	nuclear factor kappa B subunit 1	Homo sapiens	95-104
30090333-4	2016	In this study, we aimed at investigating the involvement of inhibitor of DNA binding 1 (Id1) and the associated signal molecules in the arsenic-mediated angiogenesis.	Arsenic	136-143	inhibitor of DNA binding 1, HLH protein	Homo sapiens	60-86
30090333-4	2016	In this study, we aimed at investigating the involvement of inhibitor of DNA binding 1 (Id1) and the associated signal molecules in the arsenic-mediated angiogenesis.	Arsenic	136-143	inhibitor of DNA binding 1, HLH protein	Homo sapiens	88-91
30090333-5	2016	Our initial screening revealed that treatment with low concentrations of arsenic (0.5-1 muM) led to multiple cellular responses, including enhanced endothelial cell viability and angiogenic activity as well as increased protein expression of Id1.	Arsenic	73-80	latexin	Homo sapiens	88-91
30090333-5	2016	Our initial screening revealed that treatment with low concentrations of arsenic (0.5-1 muM) led to multiple cellular responses, including enhanced endothelial cell viability and angiogenic activity as well as increased protein expression of Id1.	Arsenic	73-80	inhibitor of DNA binding 1, HLH protein	Homo sapiens	242-245
30090333-6	2016	The arsenic-induced angiogenesis was suppressed in the Id1-knocked down cells compared to that in control cells.	Arsenic	4-11	inhibitor of DNA binding 1, HLH protein	Homo sapiens	55-58
30090333-7	2016	Furthermore, arsenic-induced Id1 expression and angiogenic activity were regulated by PI3K/Akt, NF-kappaB, and nitric oxide synthase (NOS) signaling.	Arsenic	13-20	inhibitor of DNA binding 1, HLH protein	Homo sapiens	29-32
30090333-7	2016	Furthermore, arsenic-induced Id1 expression and angiogenic activity were regulated by PI3K/Akt, NF-kappaB, and nitric oxide synthase (NOS) signaling.	Arsenic	13-20	AKT serine/threonine kinase 1	Homo sapiens	91-94
30090333-7	2016	Furthermore, arsenic-induced Id1 expression and angiogenic activity were regulated by PI3K/Akt, NF-kappaB, and nitric oxide synthase (NOS) signaling.	Arsenic	13-20	nuclear factor kappa B subunit 1	Homo sapiens	96-105
30090333-7	2016	Furthermore, arsenic-induced Id1 expression and angiogenic activity were regulated by PI3K/Akt, NF-kappaB, and nitric oxide synthase (NOS) signaling.	Arsenic	13-20	nitric oxide synthase 2	Homo sapiens	111-132
30090333-8	2016	In summary, our current data demonstrate for the first time that Id1 mediates the arsenic-promoted angiogenesis, and Id1 may be regarded as an antiangiogenesis target for treatment of arsenic-associated cancer.	Arsenic	82-89	inhibitor of DNA binding 1, HLH protein	Homo sapiens	65-68
25092181-9	2015	Thus, the highest retention of arsenic was detected in the esophagus after intraperitoneal administration of As(III) to mice, and this appeared to result from multiple factors, including high expression of AQP3, low expression of MRP2, low capacity of glutathione synthesis and low activation of Nrf2.	Arsenic	31-38	nuclear factor, erythroid derived 2, like 2	Mus musculus	296-300
25768001-7	2015	Regional heritability analysis confirmed 10q24.32 (AS3MT) as a major arsenic metabolism locus (PVE = 7%, p = 4.4 x 10(-10)), but revealed no additional regions.	Arsenic	69-76	arsenite methyltransferase	Homo sapiens	51-56
26371860-0	2015	Activation of NRF2 pathway in spleen, thymus as well as peripheral blood mononuclear cells by acute arsenic exposure in mice.	Arsenic	100-107	nuclear factor, erythroid derived 2, like 2	Mus musculus	14-18
25768001-10	2015	CONCLUSIONS: Our results suggest that there are common variants outside of the AS3MT region that influence arsenic metabolism in Bangladeshi individuals, but the effects of these variants are very weak compared with variants near AS3MT.	Arsenic	107-114	arsenite methyltransferase	Homo sapiens	79-84
26302178-3	2015	The present study was addressed to explore the molecular link that might exist between arsenic exposure, miR-2909 RNomics involving immunomodulatory genes and effector IgA class switching, revealed that arsenic-exposed Balb/c mice exhibited predominant Th1 immune response coupled with effector IgA class switching thereby tailoring their immune system to ensure increased risk to infections and chronic diseases like cancer.	Arsenic	87-94	negative elongation factor complex member C/D, Th1l	Mus musculus	253-256
26302178-3	2015	The present study was addressed to explore the molecular link that might exist between arsenic exposure, miR-2909 RNomics involving immunomodulatory genes and effector IgA class switching, revealed that arsenic-exposed Balb/c mice exhibited predominant Th1 immune response coupled with effector IgA class switching thereby tailoring their immune system to ensure increased risk to infections and chronic diseases like cancer.	Arsenic	203-210	negative elongation factor complex member C/D, Th1l	Mus musculus	253-256
26371860-1	2015	Arsenic has already been demonstrated to activate the nuclear factor erythroid 2-related factor 2 (NRF2) in many different organs and cell lines.	Arsenic	0-7	nuclear factor, erythroid derived 2, like 2	Mus musculus	54-97
26371860-1	2015	Arsenic has already been demonstrated to activate the nuclear factor erythroid 2-related factor 2 (NRF2) in many different organs and cell lines.	Arsenic	0-7	nuclear factor, erythroid derived 2, like 2	Mus musculus	99-103
26371860-2	2015	The present study tried to explore the expression of NRF2 pathway by acute arsenic exposure in immune system in vivo.	Arsenic	75-82	nuclear factor, erythroid derived 2, like 2	Mus musculus	53-57
26371860-3	2015	Our results showed that treatment with arsenic (sodium arsenite, 5, 10 and 20mg/kg, intra-gastrically) increased the expression of NRF2 and its downstream targets heme oxygenase-1 (HO-1), glutathione-S-transferase (GST), glutamate-cysteine ligase (GCL) and glutathione reductase (GR) consistently in spleen, thymus, as well as peripheral blood mononuclear cells (PBMCs), as early as treatment from 6h.	Arsenic	39-46	nuclear factor, erythroid derived 2, like 2	Mus musculus	131-135
26371860-3	2015	Our results showed that treatment with arsenic (sodium arsenite, 5, 10 and 20mg/kg, intra-gastrically) increased the expression of NRF2 and its downstream targets heme oxygenase-1 (HO-1), glutathione-S-transferase (GST), glutamate-cysteine ligase (GCL) and glutathione reductase (GR) consistently in spleen, thymus, as well as peripheral blood mononuclear cells (PBMCs), as early as treatment from 6h.	Arsenic	39-46	heme oxygenase 1	Mus musculus	163-179
26371860-3	2015	Our results showed that treatment with arsenic (sodium arsenite, 5, 10 and 20mg/kg, intra-gastrically) increased the expression of NRF2 and its downstream targets heme oxygenase-1 (HO-1), glutathione-S-transferase (GST), glutamate-cysteine ligase (GCL) and glutathione reductase (GR) consistently in spleen, thymus, as well as peripheral blood mononuclear cells (PBMCs), as early as treatment from 6h.	Arsenic	39-46	heme oxygenase 1	Mus musculus	181-185
26371860-3	2015	Our results showed that treatment with arsenic (sodium arsenite, 5, 10 and 20mg/kg, intra-gastrically) increased the expression of NRF2 and its downstream targets heme oxygenase-1 (HO-1), glutathione-S-transferase (GST), glutamate-cysteine ligase (GCL) and glutathione reductase (GR) consistently in spleen, thymus, as well as peripheral blood mononuclear cells (PBMCs), as early as treatment from 6h.	Arsenic	39-46	hematopoietic prostaglandin D synthase	Mus musculus	188-213
26371860-3	2015	Our results showed that treatment with arsenic (sodium arsenite, 5, 10 and 20mg/kg, intra-gastrically) increased the expression of NRF2 and its downstream targets heme oxygenase-1 (HO-1), glutathione-S-transferase (GST), glutamate-cysteine ligase (GCL) and glutathione reductase (GR) consistently in spleen, thymus, as well as peripheral blood mononuclear cells (PBMCs), as early as treatment from 6h.	Arsenic	39-46	hematopoietic prostaglandin D synthase	Mus musculus	215-218
26371860-3	2015	Our results showed that treatment with arsenic (sodium arsenite, 5, 10 and 20mg/kg, intra-gastrically) increased the expression of NRF2 and its downstream targets heme oxygenase-1 (HO-1), glutathione-S-transferase (GST), glutamate-cysteine ligase (GCL) and glutathione reductase (GR) consistently in spleen, thymus, as well as peripheral blood mononuclear cells (PBMCs), as early as treatment from 6h.	Arsenic	39-46	glutathione reductase	Mus musculus	257-278
26371860-3	2015	Our results showed that treatment with arsenic (sodium arsenite, 5, 10 and 20mg/kg, intra-gastrically) increased the expression of NRF2 and its downstream targets heme oxygenase-1 (HO-1), glutathione-S-transferase (GST), glutamate-cysteine ligase (GCL) and glutathione reductase (GR) consistently in spleen, thymus, as well as peripheral blood mononuclear cells (PBMCs), as early as treatment from 6h.	Arsenic	39-46	glutathione reductase	Mus musculus	280-282
26371860-6	2015	What"s more, our results also found the imbalanced oxidative redox status under the circumstances that arsenic activated NRF2 pathway, reflected by the generation of lipid peroxidation, as well as the reduction of antioxidative capacities in both spleen and thymus.	Arsenic	103-110	nuclear factor, erythroid derived 2, like 2	Mus musculus	121-125
26371860-7	2015	Taken together, our results here strongly suggested the expression and activation of NRF2 pathway by acute arsenic exposure in immune system in vivo.	Arsenic	107-114	nuclear factor, erythroid derived 2, like 2	Mus musculus	85-89
26413806-6	2015	Cu and As were mainly associated with the second component (PC2).	Arsenic	7-9	chromobox 4	Homo sapiens	60-63
26855884-0	2015	Sex-Dependent effects of developmental arsenic exposure on methylation capacity and methylation regulation of the glucocorticoid receptor system in the embryonic mouse brain.	Arsenic	39-46	nuclear receptor subfamily 3, group C, member 1	Mus musculus	114-137
26855884-1	2015	Previously we have shown that prenatal moderate arsenic exposure (50 ppb) disrupts glucocorticoid receptor (GR) programming and that these changes continue into adolescence in males.	Arsenic	48-55	nuclear receptor subfamily 3, group C, member 1	Mus musculus	83-106
26855884-1	2015	Previously we have shown that prenatal moderate arsenic exposure (50 ppb) disrupts glucocorticoid receptor (GR) programming and that these changes continue into adolescence in males.	Arsenic	48-55	nuclear receptor subfamily 3, group C, member 1	Mus musculus	108-110
26855884-3	2015	In the present studies, we assessed the effects of arsenic on protein and mRNA of the glucocorticoid receptor (GR) and 11beta-hydroxysteroid dehydrogenase (Hsd) isozymes and compared the levels of methylation within the promoters of the Nr3c1 and Hsd11b1 genes in female fetal brain at embryonic days (E) 14 and 18.	Arsenic	51-58	nuclear receptor subfamily 3, group C, member 1	Mus musculus	86-109
26855884-3	2015	In the present studies, we assessed the effects of arsenic on protein and mRNA of the glucocorticoid receptor (GR) and 11beta-hydroxysteroid dehydrogenase (Hsd) isozymes and compared the levels of methylation within the promoters of the Nr3c1 and Hsd11b1 genes in female fetal brain at embryonic days (E) 14 and 18.	Arsenic	51-58	nuclear receptor subfamily 3, group C, member 1	Mus musculus	111-113
26855884-5	2015	Compared to males, females were resistant to arsenic induced changes in GR, 11beta-Hsd-1 and 11beta-Hsd-2 protein levels despite observed elevations in Nr3c1 and Hsd11b2 mRNA.	Arsenic	45-52	nuclear receptor subfamily 3, group C, member 1	Mus musculus	72-74
26855884-5	2015	Compared to males, females were resistant to arsenic induced changes in GR, 11beta-Hsd-1 and 11beta-Hsd-2 protein levels despite observed elevations in Nr3c1 and Hsd11b2 mRNA.	Arsenic	45-52	nuclear receptor subfamily 3, group C, member 1	Mus musculus	152-157
26855884-5	2015	Compared to males, females were resistant to arsenic induced changes in GR, 11beta-Hsd-1 and 11beta-Hsd-2 protein levels despite observed elevations in Nr3c1 and Hsd11b2 mRNA.	Arsenic	45-52	hydroxysteroid 11-beta dehydrogenase 2	Mus musculus	162-169
26855884-7	2015	Arsenic did produce sex and age-specific changes in the methylation of Hsd11b1 gene, producing increased methylation in females at E14 and decreased methylation at E18.	Arsenic	0-7	hydroxysteroid 11-beta dehydrogenase 1	Mus musculus	71-78
26855884-12	2015	Our data suggest that the GR signaling system in female offspring was not as affected by prenatal arsenic and predicts that female arsenic-exposed mice should have normal GR feedback regulation.	Arsenic	131-138	nuclear receptor subfamily 3, group C, member 1	Mus musculus	26-28
26144063-13	2015	Our results demonstrate that the TMAO, modulates AhR-regulated genes which could potentially participate, at least in part, in arsenic induced toxicity and carcinogenicity.	Arsenic	127-134	aryl-hydrocarbon receptor	Mus musculus	49-52
26422469-10	2015	We performed a detailed comparison of the two arsenic-related islands found in CB2, carrying the genes required for arsenite oxidation and As resistance, with those found in K12, 3As, and five other Thiomonas strains also isolated from Carnoules (CB1, CB3, CB6, ACO3 and ACO7).	Arsenic	46-53	cannabinoid receptor 2	Homo sapiens	79-82
26422469-10	2015	We performed a detailed comparison of the two arsenic-related islands found in CB2, carrying the genes required for arsenite oxidation and As resistance, with those found in K12, 3As, and five other Thiomonas strains also isolated from Carnoules (CB1, CB3, CB6, ACO3 and ACO7).	Arsenic	46-53	cannabinoid receptor 1	Homo sapiens	247-250
26049103-0	2015	Solubility shift and SUMOylaltion of promyelocytic leukemia (PML) protein in response to arsenic(III) and fate of the SUMOylated PML.	Arsenic	89-96	PML nuclear body scaffold	Homo sapiens	37-65
26213848-0	2015	Methylated arsenic metabolites bind to PML protein but do not induce cellular differentiation and PML-RARalpha protein degradation.	Arsenic	11-18	PML nuclear body scaffold	Homo sapiens	39-42
26091798-6	2015	The present study has examined activity and expression of 53 and its downstream target protein p21 upon acute or chronic exposure of BEAS-2B cells to arsenic and Cr(VI).	Arsenic	150-157	H3 histone pseudogene 16	Homo sapiens	95-98
26091798-7	2015	The results show that short-term exposure of BEAS-2B cells to arsenic or Cr(VI) was able to activate both p53 and p21.	Arsenic	62-69	tumor protein p53	Homo sapiens	106-109
26091798-7	2015	The results show that short-term exposure of BEAS-2B cells to arsenic or Cr(VI) was able to activate both p53 and p21.	Arsenic	62-69	H3 histone pseudogene 16	Homo sapiens	114-117
26091798-9	2015	In arsenic-transformed BEAS-2B cells reductions in p53 promoter activity, mRNA expression, and phosphorylation of p53 at Ser392 were observed, while the total p53 protein level remained the same compared to those in passage-matched parent ones.	Arsenic	3-10	tumor protein p53	Homo sapiens	51-54
26091798-9	2015	In arsenic-transformed BEAS-2B cells reductions in p53 promoter activity, mRNA expression, and phosphorylation of p53 at Ser392 were observed, while the total p53 protein level remained the same compared to those in passage-matched parent ones.	Arsenic	3-10	tumor protein p53	Homo sapiens	114-117
26049103-0	2015	Solubility shift and SUMOylaltion of promyelocytic leukemia (PML) protein in response to arsenic(III) and fate of the SUMOylated PML.	Arsenic	89-96	PML nuclear body scaffold	Homo sapiens	61-64
26049103-2	2015	We recently developed a simple method to evaluate the modification of PML by As(3+) resulting in a change in solubility and the covalent binding of small ubiquitin-like modifier (SUMO).	Arsenic	77-79	PML nuclear body scaffold	Homo sapiens	70-73
26049103-7	2015	SUMOylated PML decreased after removal of As(3+) from the culture medium.	Arsenic	42-44	PML nuclear body scaffold	Homo sapiens	11-14
26368803-9	2015	The expression of brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP-response element binding protein (pCREB) in the CA1 and dentate gyrus areas (DG) of the dorsal hippocampus were decreased by 3 mg/ kg and 10 mg/ kg, but not by 1 mg/ kg, of arsenic exposure.	Arsenic	256-263	brain derived neurotrophic factor	Mus musculus	18-51
26091798-9	2015	In arsenic-transformed BEAS-2B cells reductions in p53 promoter activity, mRNA expression, and phosphorylation of p53 at Ser392 were observed, while the total p53 protein level remained the same compared to those in passage-matched parent ones.	Arsenic	3-10	tumor protein p53	Homo sapiens	114-117
26091798-13	2015	These results demonstrate that p53 is able to respond to exposure of arsenic or Cr(VI), suggesting that BEAS-2B cells are an appropriate in vitro model to investigate arsenic or Cr(VI) induced lung cancer.	Arsenic	69-76	tumor protein p53	Homo sapiens	31-34
26091798-13	2015	These results demonstrate that p53 is able to respond to exposure of arsenic or Cr(VI), suggesting that BEAS-2B cells are an appropriate in vitro model to investigate arsenic or Cr(VI) induced lung cancer.	Arsenic	167-174	tumor protein p53	Homo sapiens	31-34
26368803-10	2015	The decrease in BDNF and pCREB in the CA1 and DG induced by 3 mg/ kg, but not 10 mg/ kg, of arsenic exposure were prevented by swimming exercise.	Arsenic	92-99	brain derived neurotrophic factor	Mus musculus	16-20
26368803-12	2015	Taken together, these results indicated that swimming exercise prevented the impairment of object recognition LTM induced by arsenic exposure, which may be mediated by BDNF and CREB in the dorsal hippocampus.	Arsenic	125-132	brain derived neurotrophic factor	Mus musculus	168-172
26368803-12	2015	Taken together, these results indicated that swimming exercise prevented the impairment of object recognition LTM induced by arsenic exposure, which may be mediated by BDNF and CREB in the dorsal hippocampus.	Arsenic	125-132	cAMP responsive element binding protein 1	Mus musculus	177-181
26273843-6	2015	Reported results show that glutathione attached CNT-bridged 3D graphene oxide membrane can be used to remove As(III), As(V), and Pb(II) from water sample at 10 ppm level.	Arsenic	109-111	submaxillary gland androgen regulated protein 3B	Homo sapiens	129-135
26359868-8	2015	As2O3 (0.5 and 1 muM) increased the intracellular arsenic content but did not affect the reactive oxygen species (ROS) levels in the myoblasts.	Arsenic	50-57	latexin	Homo sapiens	17-20
25721523-6	2015	Isolates were screened for the presence of arsenic-related genes (arsB, ACR3(1), ACR3(2), aioA, arsM, and arrA).	Arsenic	43-50	arylsulfatase B	Homo sapiens	66-70
26332580-11	2015	We found that arsenic increases adhesion of mononuclear cells via increased CD29 binding to VCAM-1, an adhesion molecule found on activated endothelial cells.	Arsenic	14-21	integrin beta 1 (fibronectin receptor beta)	Mus musculus	76-80
26332580-11	2015	We found that arsenic increases adhesion of mononuclear cells via increased CD29 binding to VCAM-1, an adhesion molecule found on activated endothelial cells.	Arsenic	14-21	vascular cell adhesion molecule 1	Mus musculus	92-98
26332580-12	2015	Similar results were observed in vivo, where arsenic-exposed mice exhibit increased VCAM-1 expression on endothelial cells and increased CD29 on circulating monocytes.	Arsenic	45-52	vascular cell adhesion molecule 1	Mus musculus	84-90
26332580-12	2015	Similar results were observed in vivo, where arsenic-exposed mice exhibit increased VCAM-1 expression on endothelial cells and increased CD29 on circulating monocytes.	Arsenic	45-52	integrin beta 1 (fibronectin receptor beta)	Mus musculus	137-141
25764338-5	2015	There was decrease in mitochondrial superoxide dismutase (MnSOD) activity in arsenic-treated rat brain further showing increased superoxide radical generation in mitochondria.	Arsenic	77-84	superoxide dismutase 2	Rattus norvegicus	22-56
25764338-5	2015	There was decrease in mitochondrial superoxide dismutase (MnSOD) activity in arsenic-treated rat brain further showing increased superoxide radical generation in mitochondria.	Arsenic	77-84	superoxide dismutase 2	Rattus norvegicus	58-63
24615952-8	2015	Only arsenic exposure significantly decreased intestinal superoxide dismutase, catalase activities, and level of soluble thiol with a concomitant increase in malondialdehyde/conjugated dienes.	Arsenic	5-12	catalase	Rattus norvegicus	79-87
26133680-6	2015	This suggests that simply increasing the lipophilicity of a DNA imaging probe to enhance cellular uptake can be counterproductive as, due to increased binding to serum albumin protein, this strategy can actually disrupt nuclear targeting.	Arsenic	31-33	albumin	Homo sapiens	162-175
26048584-9	2015	In conclusion, chronic arsenic exposure of children negatively correlates with sRAGE, and positively correlated with MMP-9 and MMP-9/TIMP-1 levels, and increases the frequency of an abnormal spirometric pattern.	Arsenic	23-30	matrix metallopeptidase 9	Homo sapiens	117-122
26048584-9	2015	In conclusion, chronic arsenic exposure of children negatively correlates with sRAGE, and positively correlated with MMP-9 and MMP-9/TIMP-1 levels, and increases the frequency of an abnormal spirometric pattern.	Arsenic	23-30	matrix metallopeptidase 9	Homo sapiens	127-132
26048584-9	2015	In conclusion, chronic arsenic exposure of children negatively correlates with sRAGE, and positively correlated with MMP-9 and MMP-9/TIMP-1 levels, and increases the frequency of an abnormal spirometric pattern.	Arsenic	23-30	TIMP metallopeptidase inhibitor 1	Homo sapiens	133-139
26008221-0	2015	Arsenic exposure causes epigenetic dysregulation of IL-8 expression leading to proneoplastic changes in kidney cells.	Arsenic	0-7	C-X-C motif chemokine ligand 8	Homo sapiens	52-56
26008221-3	2015	In this work, we have studied the effect of arsenic exposure on renal system using human embryonic kidney cells and prenatally exposed animals and identified Interleukin-8(IL-8) and its homologue (CINC-1) as mediators of arsenic induced renal toxicity.	Arsenic	221-228	C-X-C motif chemokine ligand 8	Homo sapiens	158-171
26008221-3	2015	In this work, we have studied the effect of arsenic exposure on renal system using human embryonic kidney cells and prenatally exposed animals and identified Interleukin-8(IL-8) and its homologue (CINC-1) as mediators of arsenic induced renal toxicity.	Arsenic	221-228	C-X-C motif chemokine ligand 8	Homo sapiens	172-176
26008221-4	2015	We further show that embryonic kidney cells are more responsive to arsenic leading to higher induction of IL-8 as compared to adult cells due to DNA methylation and histone acetylation (H3 acetylation) changes in the IL-8 promoter.	Arsenic	67-74	C-X-C motif chemokine ligand 8	Homo sapiens	106-110
26008221-4	2015	We further show that embryonic kidney cells are more responsive to arsenic leading to higher induction of IL-8 as compared to adult cells due to DNA methylation and histone acetylation (H3 acetylation) changes in the IL-8 promoter.	Arsenic	67-74	C-X-C motif chemokine ligand 8	Homo sapiens	217-221
26008221-5	2015	Through bisulfite analysis of the IL-8 promoter, we have also identified an arsenic modulated CpG site at -168 bases upstream of transcription start site.	Arsenic	76-83	C-X-C motif chemokine ligand 8	Homo sapiens	34-38
26008221-6	2015	This CpG is associated with C/EBP and CREB binding sites in the IL-8 promoter and its demethylation by arsenic coupled with increased H3 histone acetylation and CBP/P300 recruitment could lead to induction of IL-8.	Arsenic	103-110	CCAAT enhancer binding protein alpha	Homo sapiens	28-33
26008221-6	2015	This CpG is associated with C/EBP and CREB binding sites in the IL-8 promoter and its demethylation by arsenic coupled with increased H3 histone acetylation and CBP/P300 recruitment could lead to induction of IL-8.	Arsenic	103-110	cAMP responsive element binding protein 1	Homo sapiens	38-42
26008221-6	2015	This CpG is associated with C/EBP and CREB binding sites in the IL-8 promoter and its demethylation by arsenic coupled with increased H3 histone acetylation and CBP/P300 recruitment could lead to induction of IL-8.	Arsenic	103-110	C-X-C motif chemokine ligand 8	Homo sapiens	64-68
26008221-6	2015	This CpG is associated with C/EBP and CREB binding sites in the IL-8 promoter and its demethylation by arsenic coupled with increased H3 histone acetylation and CBP/P300 recruitment could lead to induction of IL-8.	Arsenic	103-110	CREB binding protein	Homo sapiens	161-169
26008221-6	2015	This CpG is associated with C/EBP and CREB binding sites in the IL-8 promoter and its demethylation by arsenic coupled with increased H3 histone acetylation and CBP/P300 recruitment could lead to induction of IL-8.	Arsenic	103-110	C-X-C motif chemokine ligand 8	Homo sapiens	209-213
26008221-7	2015	Our study shows how epigenetic modulation of IL-8 by arsenic could contribute to increased cell migratory and proliferative capabilities, cell cycle dysregulation and renal toxicity.	Arsenic	53-60	C-X-C motif chemokine ligand 8	Homo sapiens	45-49
26557375-6	2015	However, some differences have been observed: the male:female ratio, the proportion of patients with objective signs of inflammation such as bone marrow oedema as detected by MRI, and the proportion of patients with increased levels of C reactive protein were higher in patients with AS.	Arsenic	284-286	C-reactive protein	Homo sapiens	236-254
26291581-8	2015	In summary, the precise molecular mechanisms through which arsenic is related to diabetes have not been completely elucidated, inactivation of Trx system might provide insights into the underlying mechanisms at the environmental exposure levels.	Arsenic	59-66	thioredoxin 1	Rattus norvegicus	143-146
24665044-9	2015	A significantly higher number of senescent cells, over-expression of p53 and p21 were observed in the As-exposed individuals when compared to unexposed.	Arsenic	102-104	tumor protein p53	Homo sapiens	69-72
24665044-9	2015	A significantly higher number of senescent cells, over-expression of p53 and p21 were observed in the As-exposed individuals when compared to unexposed.	Arsenic	102-104	H3 histone pseudogene 16	Homo sapiens	77-80
26210637-7	2015	As an attempt to eliminate i-As associated toxicity, chronically exposed MEF Ogg1(-/-) cells overexpress the arsenic metabolizing enzyme As3mt.	Arsenic	109-116	8-oxoguanine DNA glycosylase	Homo sapiens	77-81
26312203-5	2015	Mice exposed to arsenic exhibited significant increased in TNF-alpha (4.3-fold), serum Interleukin-1 beta (threefold), Interleukin-6 (3.8-fold) as compared to controls.	Arsenic	16-23	tumor necrosis factor	Mus musculus	59-68
26312203-5	2015	Mice exposed to arsenic exhibited significant increased in TNF-alpha (4.3-fold), serum Interleukin-1 beta (threefold), Interleukin-6 (3.8-fold) as compared to controls.	Arsenic	16-23	interleukin 1 beta	Mus musculus	87-105
26312203-5	2015	Mice exposed to arsenic exhibited significant increased in TNF-alpha (4.3-fold), serum Interleukin-1 beta (threefold), Interleukin-6 (3.8-fold) as compared to controls.	Arsenic	16-23	interleukin 6	Mus musculus	119-132
26276098-0	2015	E4-Ubiquitin ligase Ufd2 stabilizes Yap8 and modulates arsenic stress responses independent of the U-box motif.	Arsenic	55-62	ubiquitin-ubiquitin ligase UFD2	Saccharomyces cerevisiae S288C	20-24
26276098-1	2015	Adaptation of Saccharomyces cerevisiae cells to arsenic stress is mediated through the activation of arsenic detoxification machinery by the Yap8 transcription factor.	Arsenic	48-55	Arr1p	Saccharomyces cerevisiae S288C	141-145
26276098-1	2015	Adaptation of Saccharomyces cerevisiae cells to arsenic stress is mediated through the activation of arsenic detoxification machinery by the Yap8 transcription factor.	Arsenic	101-108	Arr1p	Saccharomyces cerevisiae S288C	141-145
26276098-2	2015	Yap8 is targeted by the ubiquitin proteasome system for degradation under physiological conditions, yet it escapes proteolysis in arsenic-injured cells by a mechanism that remains to be elucidated.	Arsenic	130-137	Arr1p	Saccharomyces cerevisiae S288C	0-4
26148435-0	2015	Arsenic-induced S phase cell cycle lengthening is associated with ROS generation, p53 signaling and CDC25A expression.	Arsenic	0-7	tumor protein p53	Homo sapiens	82-85
26148435-0	2015	Arsenic-induced S phase cell cycle lengthening is associated with ROS generation, p53 signaling and CDC25A expression.	Arsenic	0-7	cell division cycle 25A	Homo sapiens	100-106
26148435-1	2015	Cellular response to arsenic is strongly dependent on p53 functional status.	Arsenic	21-28	tumor protein p53	Homo sapiens	54-57
26148435-2	2015	Primarily arresting the cell cycle in G1 or G2/M phases, arsenic treatment also induces an increase in the S-phase time in wild-type p53 cells.	Arsenic	57-64	tumor protein p53	Homo sapiens	133-136
26148435-3	2015	In contrast, cells with a non-functional p53 display only a subtle increase in the S phase, indicating arsenic differentially affects the cell cycle depending on p53 status.	Arsenic	103-110	tumor protein p53	Homo sapiens	41-44
25982963-0	2015	Insulin attenuates arsenic-induced neurite outgrowth impairments by activating the PI3K/Akt/SIRT1 signaling pathway.	Arsenic	19-26	insulin	Homo sapiens	0-7
26148435-3	2015	In contrast, cells with a non-functional p53 display only a subtle increase in the S phase, indicating arsenic differentially affects the cell cycle depending on p53 status.	Arsenic	103-110	tumor protein p53	Homo sapiens	162-165
26148435-4	2015	Importantly, it has been reported that arsenic induces reactive oxygen species (ROS), a process counteracted by p53.	Arsenic	39-46	tumor protein p53	Homo sapiens	112-115
25982963-0	2015	Insulin attenuates arsenic-induced neurite outgrowth impairments by activating the PI3K/Akt/SIRT1 signaling pathway.	Arsenic	19-26	AKT serine/threonine kinase 1	Homo sapiens	88-91
25982963-0	2015	Insulin attenuates arsenic-induced neurite outgrowth impairments by activating the PI3K/Akt/SIRT1 signaling pathway.	Arsenic	19-26	sirtuin 1	Homo sapiens	92-97
25982963-3	2015	The present study investigated whether insulin can protect neurons from impaired neurite outgrowth induced by arsenic, and examined the signaling pathway involved in this action.	Arsenic	110-117	insulin	Homo sapiens	39-46
26148435-5	2015	To evaluate the participation of p53 in the lengthening of the S phase and the connection between the transient cell cycle arrest and oxidative stress, we evaluated the cell response to arsenic in MCF-7 and H1299 cells, and analyzed p53"s role as a transcription factor in regulating genes involved in ROS reduction and S phase transition.	Arsenic	186-193	tumor protein p53	Homo sapiens	33-36
25982963-10	2015	Taken together, these results show that insulin attenuates arsenic-induced neurite outgrowth impairment possibly via activation of PI3K/Akt/SIRT1 signaling, and arsenic may exert neurite outgrowth inhibition through a mechanism involving reduction of signaling molecules downstream from insulin, PI3K/Akt/SIRT1.	Arsenic	59-66	insulin	Homo sapiens	40-47
26148435-6	2015	Herein, we discovered that arsenic induced an increase in the population of S phase cells that was dependent on the presence and transcriptional activity of p53.	Arsenic	27-34	tumor protein p53	Homo sapiens	157-160
25982963-10	2015	Taken together, these results show that insulin attenuates arsenic-induced neurite outgrowth impairment possibly via activation of PI3K/Akt/SIRT1 signaling, and arsenic may exert neurite outgrowth inhibition through a mechanism involving reduction of signaling molecules downstream from insulin, PI3K/Akt/SIRT1.	Arsenic	59-66	AKT serine/threonine kinase 1	Homo sapiens	136-139
25982963-10	2015	Taken together, these results show that insulin attenuates arsenic-induced neurite outgrowth impairment possibly via activation of PI3K/Akt/SIRT1 signaling, and arsenic may exert neurite outgrowth inhibition through a mechanism involving reduction of signaling molecules downstream from insulin, PI3K/Akt/SIRT1.	Arsenic	59-66	sirtuin 1	Homo sapiens	140-145
26148435-7	2015	Furthermore, for the first time, we demonstrate that arsenic activates p53-dependent transcription of ROS detoxification genes, such as SESN1, and by an indirect mechanism involving ATF3, genes that could be responsible for the S phase cell cycle arrest, such as CDC25A.	Arsenic	53-60	tumor protein p53	Homo sapiens	71-74
25982963-10	2015	Taken together, these results show that insulin attenuates arsenic-induced neurite outgrowth impairment possibly via activation of PI3K/Akt/SIRT1 signaling, and arsenic may exert neurite outgrowth inhibition through a mechanism involving reduction of signaling molecules downstream from insulin, PI3K/Akt/SIRT1.	Arsenic	59-66	insulin	Homo sapiens	287-294
25982963-10	2015	Taken together, these results show that insulin attenuates arsenic-induced neurite outgrowth impairment possibly via activation of PI3K/Akt/SIRT1 signaling, and arsenic may exert neurite outgrowth inhibition through a mechanism involving reduction of signaling molecules downstream from insulin, PI3K/Akt/SIRT1.	Arsenic	59-66	AKT serine/threonine kinase 1	Homo sapiens	301-304
26148435-7	2015	Furthermore, for the first time, we demonstrate that arsenic activates p53-dependent transcription of ROS detoxification genes, such as SESN1, and by an indirect mechanism involving ATF3, genes that could be responsible for the S phase cell cycle arrest, such as CDC25A.	Arsenic	53-60	sestrin 1	Homo sapiens	136-141
25982963-10	2015	Taken together, these results show that insulin attenuates arsenic-induced neurite outgrowth impairment possibly via activation of PI3K/Akt/SIRT1 signaling, and arsenic may exert neurite outgrowth inhibition through a mechanism involving reduction of signaling molecules downstream from insulin, PI3K/Akt/SIRT1.	Arsenic	59-66	sirtuin 1	Homo sapiens	305-310
26148435-7	2015	Furthermore, for the first time, we demonstrate that arsenic activates p53-dependent transcription of ROS detoxification genes, such as SESN1, and by an indirect mechanism involving ATF3, genes that could be responsible for the S phase cell cycle arrest, such as CDC25A.	Arsenic	53-60	activating transcription factor 3	Homo sapiens	182-186
26148435-7	2015	Furthermore, for the first time, we demonstrate that arsenic activates p53-dependent transcription of ROS detoxification genes, such as SESN1, and by an indirect mechanism involving ATF3, genes that could be responsible for the S phase cell cycle arrest, such as CDC25A.	Arsenic	53-60	cell division cycle 25A	Homo sapiens	263-269
26118750-1	2015	The cross-sectional study investigated the impact of chronic low level arsenic (As) exposure (11-50mug/L) on CD14 expression and other inflammatory responses in rural women of West Bengal enrolled from control (As level &lt;10mug/L; N, 131) and exposed area (As level 11-50mug/L, N, 142).	Arsenic	71-78	CD14 molecule	Homo sapiens	109-113
25491248-0	2015	Biological monitoring and the influence of genetic polymorphism of As3MT and GSTs on distribution of urinary arsenic species in occupational exposure workers.	Arsenic	109-116	arsenite methyltransferase	Homo sapiens	67-72
25491248-0	2015	Biological monitoring and the influence of genetic polymorphism of As3MT and GSTs on distribution of urinary arsenic species in occupational exposure workers.	Arsenic	109-116	hematopoietic prostaglandin D synthase	Homo sapiens	77-81
26025778-4	2015	We have previously reported that use of low-dose arsenic (LDA) temporarily and reversibly suppresses p53 activation, thereby ameliorating normal tissue toxicity from exposure to 5-fluorouracil and X rays.	Arsenic	49-56	transformation related protein 53, pseudogene	Mus musculus	101-104
26118750-1	2015	The cross-sectional study investigated the impact of chronic low level arsenic (As) exposure (11-50mug/L) on CD14 expression and other inflammatory responses in rural women of West Bengal enrolled from control (As level &lt;10mug/L; N, 131) and exposed area (As level 11-50mug/L, N, 142).	Arsenic	80-82	CD14 molecule	Homo sapiens	109-113
26067210-11	2015	A possible interpretation of this finding is that when AS3MT is higher, excretion of MMA + DMA + TMAO is more efficient, leaving lower concentrations in the tissues, with the opposite effect (less excretion) when AS3MT is lower; alternatively, other enzymes or linked genes may affect the methylation of As.	Arsenic	304-306	arsenite methyltransferase, gene 1	Xenopus tropicalis	55-60
25736215-4	2015	In RET G691S polymorphism, the overall distribution of variant alleles (GA + AA) in cases was 62.9% as against 44.5% in controls (P &lt; 0.05) whereas frequency of RET L769L variant alleles (TG + GG) in cases was 70% versus 88% in controls (P &lt; 0.05).	Arsenic	85-87	ret proto-oncogene	Homo sapiens	3-6
25979314-0	2015	Arsenic Induces Insulin Resistance in Mouse Adipocytes and Myotubes Via Oxidative Stress-Regulated Mitochondrial Sirt3-FOXO3a Signaling Pathway.	Arsenic	0-7	sirtuin 3	Mus musculus	113-118
25979314-0	2015	Arsenic Induces Insulin Resistance in Mouse Adipocytes and Myotubes Via Oxidative Stress-Regulated Mitochondrial Sirt3-FOXO3a Signaling Pathway.	Arsenic	0-7	forkhead box O3	Mus musculus	119-125
25979314-6	2015	Reduced FOXO3a activity by arsenic exhibited a decreased binding affinity to the promoters of both manganese superoxide dismutase (MnSOD) and peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1alpha, a broad and powerful regulator of reactive oxygen species (ROS) metabolism.	Arsenic	27-34	forkhead box O3	Mus musculus	8-14
25979314-2	2015	This study investigates the role of mitochondrial oxidative stress protein Sirtuin 3 (Sirt3) and its targeting proteins in chronic arsenic-induced T2DM in mouse adipocytes and myotubes.	Arsenic	131-138	sirtuin 3	Mus musculus	75-84
25979314-6	2015	Reduced FOXO3a activity by arsenic exhibited a decreased binding affinity to the promoters of both manganese superoxide dismutase (MnSOD) and peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1alpha, a broad and powerful regulator of reactive oxygen species (ROS) metabolism.	Arsenic	27-34	superoxide dismutase 2, mitochondrial	Mus musculus	99-129
25979314-6	2015	Reduced FOXO3a activity by arsenic exhibited a decreased binding affinity to the promoters of both manganese superoxide dismutase (MnSOD) and peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1alpha, a broad and powerful regulator of reactive oxygen species (ROS) metabolism.	Arsenic	27-34	superoxide dismutase 2, mitochondrial	Mus musculus	131-136
25979314-6	2015	Reduced FOXO3a activity by arsenic exhibited a decreased binding affinity to the promoters of both manganese superoxide dismutase (MnSOD) and peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1alpha, a broad and powerful regulator of reactive oxygen species (ROS) metabolism.	Arsenic	27-34	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	142-215
25979314-7	2015	Forced expression of Sirt3 or MnSOD in mouse myotubes elevated Deltapsim and restored ISGU inhibited by arsenic exposure.	Arsenic	104-111	sirtuin 3	Mus musculus	21-26
25979314-7	2015	Forced expression of Sirt3 or MnSOD in mouse myotubes elevated Deltapsim and restored ISGU inhibited by arsenic exposure.	Arsenic	104-111	superoxide dismutase 2, mitochondrial	Mus musculus	30-35
25979314-2	2015	This study investigates the role of mitochondrial oxidative stress protein Sirtuin 3 (Sirt3) and its targeting proteins in chronic arsenic-induced T2DM in mouse adipocytes and myotubes.	Arsenic	131-138	sirtuin 3	Mus musculus	86-91
25979314-8	2015	Our results suggest that Sirt3/FOXO3a/MnSOD signaling plays a significant role in the inhibition of ISGU induced by chronic arsenic exposure.	Arsenic	124-131	sirtuin 3	Mus musculus	25-30
25979314-8	2015	Our results suggest that Sirt3/FOXO3a/MnSOD signaling plays a significant role in the inhibition of ISGU induced by chronic arsenic exposure.	Arsenic	124-131	forkhead box O3	Mus musculus	31-37
25979314-3	2015	The results show that chronic arsenic exposure significantly decreased insulin-stimulated glucose uptake (ISGU) in correlation with reduced expression of insulin-regulated glucose transporter type 4 (Glut4).	Arsenic	30-37	solute carrier family 2 (facilitated glucose transporter), member 4	Mus musculus	200-205
25979314-8	2015	Our results suggest that Sirt3/FOXO3a/MnSOD signaling plays a significant role in the inhibition of ISGU induced by chronic arsenic exposure.	Arsenic	124-131	superoxide dismutase 2, mitochondrial	Mus musculus	38-43
26024302-3	2015	Thus, P19 mouse embryonic stem cells were used to investigate the mechanisms by which arsenic could inhibit cellular differentiation.	Arsenic	86-93	interleukin 23, alpha subunit p19	Mus musculus	6-9
25997655-0	2015	Interactive Effects of N6AMT1 and As3MT in Arsenic Biomethylation.	Arsenic	43-50	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	23-29
25997655-0	2015	Interactive Effects of N6AMT1 and As3MT in Arsenic Biomethylation.	Arsenic	43-50	arsenite methyltransferase	Homo sapiens	34-39
25997655-1	2015	In humans, arsenic is primarily metabolized by arsenic (+3 oxidation state) methyltransferase (As3MT) to yield both trivalent and pentavalent methylated metabolites.	Arsenic	11-18	arsenite methyltransferase	Homo sapiens	47-93
25997655-1	2015	In humans, arsenic is primarily metabolized by arsenic (+3 oxidation state) methyltransferase (As3MT) to yield both trivalent and pentavalent methylated metabolites.	Arsenic	11-18	arsenite methyltransferase	Homo sapiens	95-100
25997655-2	2015	We recently reported that the putative N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) can biotransform monomethylarsonous acid (MMA(III)) to dimethylarsinic acid, conferring resistance of human cells to arsenic exposure.	Arsenic	210-217	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	39-83
25997655-2	2015	We recently reported that the putative N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) can biotransform monomethylarsonous acid (MMA(III)) to dimethylarsinic acid, conferring resistance of human cells to arsenic exposure.	Arsenic	210-217	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	85-91
26079204-0	2015	Arsenic causes aortic dysfunction and systemic hypertension in rats: Augmentation of angiotensin II signaling.	Arsenic	0-7	angiotensinogen	Rattus norvegicus	85-99
26079204-3	2015	We investigated whether modulation of angiotensin II signaling and redox homeostasis could be a mechanism contributing to arsenic-induced vascular disorder.	Arsenic	122-129	angiotensinogen	Rattus norvegicus	38-52
26079204-11	2015	Arsenic caused concentration-dependent enhancement of the angiotensin II-induced aortic contractile response.	Arsenic	0-7	angiotensinogen	Rattus norvegicus	58-72
26079204-12	2015	Arsenic also caused concentration-dependent increase in the plasma levels of angiotensin II and angiotensin converting enzyme and the expression of aortic AT1 receptor and Galphaq/11 proteins.	Arsenic	0-7	angiotensinogen	Rattus norvegicus	77-125
26079204-12	2015	Arsenic also caused concentration-dependent increase in the plasma levels of angiotensin II and angiotensin converting enzyme and the expression of aortic AT1 receptor and Galphaq/11 proteins.	Arsenic	0-7	angiotensin II receptor, type 1a	Rattus norvegicus	155-158
26079204-12	2015	Arsenic also caused concentration-dependent increase in the plasma levels of angiotensin II and angiotensin converting enzyme and the expression of aortic AT1 receptor and Galphaq/11 proteins.	Arsenic	0-7	G protein subunit alpha q	Rattus norvegicus	172-179
26079204-13	2015	Arsenic increased aortic protein kinase C activity and the concentrations of protein tyrosine kinase, extracellular signal-regulated kinase-1/2 and vascular endothelial growth factor.	Arsenic	0-7	mitogen activated protein kinase 3	Rattus norvegicus	102-143
26079204-14	2015	Further, arsenic increased aortic mRNA expression of Nox2, Nox4 and p22phox, NADPH oxidase activity and ROS generation.	Arsenic	9-16	cytochrome b-245 beta chain	Rattus norvegicus	53-57
26079204-14	2015	Further, arsenic increased aortic mRNA expression of Nox2, Nox4 and p22phox, NADPH oxidase activity and ROS generation.	Arsenic	9-16	NADPH oxidase 4	Rattus norvegicus	59-63
26079204-14	2015	Further, arsenic increased aortic mRNA expression of Nox2, Nox4 and p22phox, NADPH oxidase activity and ROS generation.	Arsenic	9-16	cytochrome b-245 alpha chain	Rattus norvegicus	68-75
26079204-15	2015	The results suggest that arsenic-mediated enhancement of angiotensin II signaling could be an important mechanism in the arsenic-induced vascular disorder, where ROS could augment the angiotensin II signaling through activation of MAP kinase pathway.	Arsenic	25-32	angiotensinogen	Rattus norvegicus	57-71
26079204-15	2015	The results suggest that arsenic-mediated enhancement of angiotensin II signaling could be an important mechanism in the arsenic-induced vascular disorder, where ROS could augment the angiotensin II signaling through activation of MAP kinase pathway.	Arsenic	25-32	angiotensinogen	Rattus norvegicus	184-198
26079204-15	2015	The results suggest that arsenic-mediated enhancement of angiotensin II signaling could be an important mechanism in the arsenic-induced vascular disorder, where ROS could augment the angiotensin II signaling through activation of MAP kinase pathway.	Arsenic	121-128	angiotensinogen	Rattus norvegicus	57-71
26024302-12	2015	All three arsenic species reduced the nuclear localization of MyoD and NeuroD1 in a similar manner.	Arsenic	10-17	myogenic differentiation 1	Mus musculus	62-66
26024302-12	2015	All three arsenic species reduced the nuclear localization of MyoD and NeuroD1 in a similar manner.	Arsenic	10-17	neurogenic differentiation 1	Mus musculus	71-78
26024302-6	2015	Early during differentiation, arsenic significantly reduced the transcript and protein expression of Msx1 and Pax3, both needed for NPBS cell formation.	Arsenic	30-37	msh homeobox 1	Mus musculus	101-105
26024302-6	2015	Early during differentiation, arsenic significantly reduced the transcript and protein expression of Msx1 and Pax3, both needed for NPBS cell formation.	Arsenic	30-37	paired box 3	Mus musculus	110-114
26024302-7	2015	Arsenic also significantly reduced the protein expression of Sox 10, needed for neural crest progenitor cell production, by 31-50%, and downregulated the protein and mRNA levels of NeuroD1, needed for neural crest cell differentiation, in a time- and dose-dependent manner.	Arsenic	0-7	SRY (sex determining region Y)-box 10	Mus musculus	61-67
26024302-7	2015	Arsenic also significantly reduced the protein expression of Sox 10, needed for neural crest progenitor cell production, by 31-50%, and downregulated the protein and mRNA levels of NeuroD1, needed for neural crest cell differentiation, in a time- and dose-dependent manner.	Arsenic	0-7	neurogenic differentiation 1	Mus musculus	181-188
25804789-6	2015	Adsorption equilibrium data were evaluated using the Langmuir isotherm model, and the maximum adsorption capacity qmax was 18.25 and 4.97 mg g(-1) for As(III) on AAB and GAB, respectively, and 21.79 and 10.92 mg g(-1) for As(V) on AAB and GAB, respectively.	Arsenic	151-153	alpha-1-B glycoprotein	Homo sapiens	170-173
26396915-0	2015	Optimized mixture of As, Cd and Pb induce mitochondria-mediated apoptosis in C6-glioma via astroglial activation, inflammation and P38-MAPK.	Arsenic	21-23	mitogen activated protein kinase 14	Rattus norvegicus	131-139
25963571-6	2015	The concentrations of As and Hg exceeded the wet threshold safety values (MEC, PEC) indicating possible As and Hg contamination.	Arsenic	22-24	C-C motif chemokine ligand 28	Homo sapiens	74-77
25804789-6	2015	Adsorption equilibrium data were evaluated using the Langmuir isotherm model, and the maximum adsorption capacity qmax was 18.25 and 4.97 mg g(-1) for As(III) on AAB and GAB, respectively, and 21.79 and 10.92 mg g(-1) for As(V) on AAB and GAB, respectively.	Arsenic	151-153	alpha-1-B glycoprotein	Homo sapiens	239-242
25866076-2	2015	As(III) S-adenosylmethionine methyltransferases (AS3MT in mammals and ArsM in microbes) methylate As(III) three times in consecutive steps and play a central role in arsenic metabolism from bacteria to humans.	Arsenic	166-173	arsenite methyltransferase	Homo sapiens	49-54
24961358-6	2015	Small molecule inhibitors of NF-kappaB and p38 MAPK blocked arsenic-induced COX-2 expression, suggesting arsenic-induced COX-2 up-regulation was NF-kappaB- and p38 MAPK-dependent.	Arsenic	60-67	prostaglandin-endoperoxide synthase 2	Homo sapiens	76-81
25851633-10	2015	In the meta-analysis of placebo-controlled studies comparing G-CSF primary prophylaxis with placebo in the as-treated analysis sets, the HR (95% CI) for OS was 0.77 (0.58-1.03).	Arsenic	107-109	colony stimulating factor 3	Homo sapiens	61-66
24961358-6	2015	Small molecule inhibitors of NF-kappaB and p38 MAPK blocked arsenic-induced COX-2 expression, suggesting arsenic-induced COX-2 up-regulation was NF-kappaB- and p38 MAPK-dependent.	Arsenic	60-67	prostaglandin-endoperoxide synthase 2	Homo sapiens	121-126
24961358-6	2015	Small molecule inhibitors of NF-kappaB and p38 MAPK blocked arsenic-induced COX-2 expression, suggesting arsenic-induced COX-2 up-regulation was NF-kappaB- and p38 MAPK-dependent.	Arsenic	105-112	prostaglandin-endoperoxide synthase 2	Homo sapiens	76-81
24961358-6	2015	Small molecule inhibitors of NF-kappaB and p38 MAPK blocked arsenic-induced COX-2 expression, suggesting arsenic-induced COX-2 up-regulation was NF-kappaB- and p38 MAPK-dependent.	Arsenic	105-112	prostaglandin-endoperoxide synthase 2	Homo sapiens	121-126
25825128-8	2015	Unexpectedly, urinary arsenic concentrations were inversely associated with both systolic (p=0.081), and diastolic (p=0.002) blood pressure, and with the ratio of apolipoproteins B/A (p&lt;0.001).	Arsenic	22-29	apolipoprotein B	Homo sapiens	163-182
25759212-0	2015	A distinct and replicable variant of the squamous cell carcinoma gene inositol polyphosphate-5-phosphatase modifies the susceptibility of arsenic-associated skin lesions in Bangladesh.	Arsenic	138-145	inositol polyphosphate-5-phosphatase A	Homo sapiens	70-106
25759212-8	2015	CONCLUSIONS: Minor allele carriers of the skin cancer gene INPP5A modified the odds of arsenic-induced skin lesions in both main and replicative populations.	Arsenic	87-94	inositol polyphosphate-5-phosphatase A	Homo sapiens	59-65
26057048-5	2015	In mice, acute immobilized stress (AS) caused a biphasic effect on CDK5 activity, initially reducing but increasing afterwards in prefrontal cortex (PFC) and hippocampus (HIPPO), whereas chronic unpredictable stress (CS) strongly increased it in these brain areas, indicating that AS and CS differentially regulate this kinase activity in a brain region-specific fashion.	Arsenic	35-37	cyclin-dependent kinase 5	Mus musculus	67-71
25967284-12	2015	A statistically significant interaction was observed in the relationship between dimethylarsinic acid (DMA) levels in urinary arsenic and SGA between strata of GSTO1 A104A (p for interaction=0.02).	Arsenic	126-133	glutathione S-transferase omega 1	Homo sapiens	160-165
25804888-3	2015	After 38 weeks of continuous arsenic exposure, secreted matrix metalloproteinase-2 (MMP2) activity increased to over 200% of control, levels linked to arsenic-induced cancer phenotypes in other cell lines.	Arsenic	29-36	matrix metallopeptidase 2	Homo sapiens	56-82
25804888-3	2015	After 38 weeks of continuous arsenic exposure, secreted matrix metalloproteinase-2 (MMP2) activity increased to over 200% of control, levels linked to arsenic-induced cancer phenotypes in other cell lines.	Arsenic	29-36	matrix metallopeptidase 2	Homo sapiens	84-88
25804888-3	2015	After 38 weeks of continuous arsenic exposure, secreted matrix metalloproteinase-2 (MMP2) activity increased to over 200% of control, levels linked to arsenic-induced cancer phenotypes in other cell lines.	Arsenic	151-158	matrix metallopeptidase 2	Homo sapiens	56-82
25804888-3	2015	After 38 weeks of continuous arsenic exposure, secreted matrix metalloproteinase-2 (MMP2) activity increased to over 200% of control, levels linked to arsenic-induced cancer phenotypes in other cell lines.	Arsenic	151-158	matrix metallopeptidase 2	Homo sapiens	84-88
25804888-10	2015	Increased transcript expression of metallothioneins, MT1A and MT2A and the stress response genes HMOX1 (690%) and HIF1A (247%) occurred in CATLE cells possibly in adaptation to chronic arsenic exposure.	Arsenic	185-192	metallothionein 2A	Homo sapiens	62-66
25804888-10	2015	Increased transcript expression of metallothioneins, MT1A and MT2A and the stress response genes HMOX1 (690%) and HIF1A (247%) occurred in CATLE cells possibly in adaptation to chronic arsenic exposure.	Arsenic	185-192	heme oxygenase 1	Homo sapiens	97-102
25804888-10	2015	Increased transcript expression of metallothioneins, MT1A and MT2A and the stress response genes HMOX1 (690%) and HIF1A (247%) occurred in CATLE cells possibly in adaptation to chronic arsenic exposure.	Arsenic	185-192	hypoxia inducible factor 1 subunit alpha	Homo sapiens	114-119
25909687-9	2015	When using urine osmolality to adjust for urine concentration, a log-unit increase in total arsenic and DMA was associated with a 0.4 mL/min/1.73 m(2) (95% CI -1.8 to 1.1 mL/min/1.73 m(2)) and 0.01 (95% CI -1.9 to 1.9 mL/min/1.73 m(2)) lower eGFR, respectively.	Arsenic	92-99	CD59 molecule (CD59 blood group)	Homo sapiens	137-142
25909687-9	2015	When using urine osmolality to adjust for urine concentration, a log-unit increase in total arsenic and DMA was associated with a 0.4 mL/min/1.73 m(2) (95% CI -1.8 to 1.1 mL/min/1.73 m(2)) and 0.01 (95% CI -1.9 to 1.9 mL/min/1.73 m(2)) lower eGFR, respectively.	Arsenic	92-99	CD59 molecule (CD59 blood group)	Homo sapiens	174-179
25909687-9	2015	When using urine osmolality to adjust for urine concentration, a log-unit increase in total arsenic and DMA was associated with a 0.4 mL/min/1.73 m(2) (95% CI -1.8 to 1.1 mL/min/1.73 m(2)) and 0.01 (95% CI -1.9 to 1.9 mL/min/1.73 m(2)) lower eGFR, respectively.	Arsenic	92-99	CD59 molecule (CD59 blood group)	Homo sapiens	174-179
25876999-0	2015	Associations between the polymorphisms of GSTT1, GSTM1 and methylation of arsenic in the residents exposed to low-level arsenic in drinking water in China.	Arsenic	74-81	glutathione S-transferase theta 1	Homo sapiens	42-47
25876999-0	2015	Associations between the polymorphisms of GSTT1, GSTM1 and methylation of arsenic in the residents exposed to low-level arsenic in drinking water in China.	Arsenic	74-81	glutathione S-transferase mu 1	Homo sapiens	49-54
25876999-0	2015	Associations between the polymorphisms of GSTT1, GSTM1 and methylation of arsenic in the residents exposed to low-level arsenic in drinking water in China.	Arsenic	120-127	glutathione S-transferase theta 1	Homo sapiens	42-47
25876999-1	2015	We carry out a study to analyze the relation between polymorphisms of GSTT1, GSTM1 and the capacity of arsenic methylation in a human population exposed to arsenic in drinking water.	Arsenic	103-110	glutathione S-transferase theta 1	Homo sapiens	70-75
25876999-1	2015	We carry out a study to analyze the relation between polymorphisms of GSTT1, GSTM1 and the capacity of arsenic methylation in a human population exposed to arsenic in drinking water.	Arsenic	103-110	glutathione S-transferase mu 1	Homo sapiens	77-82
25876999-1	2015	We carry out a study to analyze the relation between polymorphisms of GSTT1, GSTM1 and the capacity of arsenic methylation in a human population exposed to arsenic in drinking water.	Arsenic	156-163	glutathione S-transferase theta 1	Homo sapiens	70-75
25876999-1	2015	We carry out a study to analyze the relation between polymorphisms of GSTT1, GSTM1 and the capacity of arsenic methylation in a human population exposed to arsenic in drinking water.	Arsenic	156-163	glutathione S-transferase mu 1	Homo sapiens	77-82
25876999-2	2015	230 randomly chose subjects were divided into four subgroups based on the arsenic levels, and then the associations between the polymorphisms of GSTT1, GSTM1 and methylation of arsenic were investigated.	Arsenic	177-184	glutathione S-transferase theta 1	Homo sapiens	145-150
25876999-7	2015	Our results suggested that the polymorphisms of GSTT1 and GSTM1 were associated with the methylation of arsenic, especially the levels of DMA and SMI.	Arsenic	104-111	glutathione S-transferase theta 1	Homo sapiens	48-53
25876999-7	2015	Our results suggested that the polymorphisms of GSTT1 and GSTM1 were associated with the methylation of arsenic, especially the levels of DMA and SMI.	Arsenic	104-111	glutathione S-transferase mu 1	Homo sapiens	58-63
26100807-4	2015	Compound formulations are supported by a range of characterization techniques, and theoretical calculations suggest the presence of polarized covalent one-, two- and threefold bonding interactions between uranium and arsenic in parent arsenide [U-AsH2], terminal arsinidene [U=AsH] and arsenido [U AsK2] complexes, respectively.	Arsenic	217-224	arylsulfatase family member H	Homo sapiens	247-250
26100807-4	2015	Compound formulations are supported by a range of characterization techniques, and theoretical calculations suggest the presence of polarized covalent one-, two- and threefold bonding interactions between uranium and arsenic in parent arsenide [U-AsH2], terminal arsinidene [U=AsH] and arsenido [U AsK2] complexes, respectively.	Arsenic	217-224	mitogen-activated protein kinase kinase kinase 6	Homo sapiens	298-302
26454960-6	2015	RESULTS: The activity of ALT, AST and the contents of MDA of 70 d control group were significantly lower than that arsenic exposure group.	Arsenic	115-122	glutamic pyruvic transaminase, soluble	Mus musculus	25-28
26439596-8	2015	Histopathological and immunohistochemical examination revealed that telmisartan markedly attenuated testicular tissue changes, and decreased the arsenic-induced expression of vascular endothelial growth factor, inducible nitric oxide synthase, tumor necrosis factor-alpha, cyclooxygenase-2, nuclear factor-kappaB, and caspase-3.	Arsenic	145-152	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	273-289
26439596-8	2015	Histopathological and immunohistochemical examination revealed that telmisartan markedly attenuated testicular tissue changes, and decreased the arsenic-induced expression of vascular endothelial growth factor, inducible nitric oxide synthase, tumor necrosis factor-alpha, cyclooxygenase-2, nuclear factor-kappaB, and caspase-3.	Arsenic	145-152	caspase 3	Rattus norvegicus	318-327
25869292-9	2015	The toxic effect of arsenic was also indicated by significantly decreased activities of enzymatic antioxidants such as superoxide dismutase, catalase, and glutathione peroxidase along with non-enzymatic antioxidant such as reduced glutathione.	Arsenic	20-27	catalase	Rattus norvegicus	141-149
26060329-0	2015	SUMO deconjugation is required for arsenic-triggered ubiquitylation of PML.	Arsenic	35-42	PML nuclear body scaffold	Homo sapiens	71-74
25652692-3	2015	Here, we characterized Tg(hsp70:gfp) medaka for inducible GFP expression by seven environment-relevant heavy metals, including mercury, arsenic, lead, cadmium, copper, chromium, and zinc.	Arsenic	136-143	Heat shock 70 kDa protein-like	Oryzias latipes	26-31
25907674-0	2015	Arsenic Inhibits DNA Mismatch Repair by Promoting EGFR Expression and PCNA Phosphorylation.	Arsenic	0-7	epidermal growth factor receptor	Homo sapiens	50-54
25907674-3	2015	Using a model non-genotoxic carcinogen, arsenic, we show here that exposure to arsenic inhibits mismatch repair (MMR) in human cells, possibly through its ability to stimulate epidermal growth factor receptor (EGFR)-dependent tyrosine phosphorylation of proliferating cellular nuclear antigen (PCNA).	Arsenic	79-86	epidermal growth factor receptor	Homo sapiens	176-208
25907674-3	2015	Using a model non-genotoxic carcinogen, arsenic, we show here that exposure to arsenic inhibits mismatch repair (MMR) in human cells, possibly through its ability to stimulate epidermal growth factor receptor (EGFR)-dependent tyrosine phosphorylation of proliferating cellular nuclear antigen (PCNA).	Arsenic	79-86	epidermal growth factor receptor	Homo sapiens	210-214
25907674-3	2015	Using a model non-genotoxic carcinogen, arsenic, we show here that exposure to arsenic inhibits mismatch repair (MMR) in human cells, possibly through its ability to stimulate epidermal growth factor receptor (EGFR)-dependent tyrosine phosphorylation of proliferating cellular nuclear antigen (PCNA).	Arsenic	79-86	proliferating cell nuclear antigen	Homo sapiens	254-292
25907674-4	2015	HeLa cells exposed to exogenous arsenic demonstrate a dose- and time-dependent increase in the levels of EGFR and tyrosine 211-phosphorylated PCNA.	Arsenic	32-39	epidermal growth factor receptor	Homo sapiens	105-109
25907674-6	2015	These results suggest a model in which arsenic induces expression of EGFR, which in turn phosphorylates PCNA, and phosphorylated PCNA then inhibits MMR, leading to increased susceptibility to carcinogenesis.	Arsenic	39-46	epidermal growth factor receptor	Homo sapiens	69-73
25788710-2	2015	The most sensitive target of arsenic toxicity in the vasculature is the endothelium, and incubation of these cells with low concentrations of arsenite, a naturally occurring and highly toxic inorganic form of arsenic, rapidly induces reactive oxygen species (ROS) formation via activation of a specific NADPH oxidase (Nox2).	Arsenic	29-36	cytochrome b-245 beta chain	Homo sapiens	318-322
25788710-7	2015	This review is a comprehensive analysis of the mechanisms that mediate arsenic effects associated with Nox2 activation, ROS activity, and endothelial dysfunction, and also considers future avenues of research into what is a relatively poorly understood topic with major implications for human health.	Arsenic	71-78	cytochrome b-245 beta chain	Homo sapiens	103-107
25845984-2	2015	Insulin resistance (IR) has been proposed as a mechanism of arsenic-related diabetes.	Arsenic	60-67	insulin	Homo sapiens	0-7
25845984-4	2015	We examined the association between urinary arsenic and insulin resistance in US adolescents.	Arsenic	44-51	insulin	Homo sapiens	56-63
25752797-5	2015	In rats, the related canalicular transporter Mrp2/Abcc2 is required for biliary excretion of arsenic as As(GS)(3) and MMA(GS)(2).	Arsenic	93-100	ATP binding cassette subfamily C member 2	Rattus norvegicus	45-49
25739736-3	2015	We genotyped women from this population for 4,301,332 single nucleotide polymorphisms (SNPs) and found a strong association between the AS3MT (arsenic [+3 oxidation state] methyltransferase) gene and mono- and dimethylated arsenic in urine, suggesting that AS3MT functions as the major gene for arsenic metabolism in humans.	Arsenic	143-150	arsenite methyltransferase	Homo sapiens	136-141
25739736-3	2015	We genotyped women from this population for 4,301,332 single nucleotide polymorphisms (SNPs) and found a strong association between the AS3MT (arsenic [+3 oxidation state] methyltransferase) gene and mono- and dimethylated arsenic in urine, suggesting that AS3MT functions as the major gene for arsenic metabolism in humans.	Arsenic	223-230	arsenite methyltransferase	Homo sapiens	136-189
25739736-3	2015	We genotyped women from this population for 4,301,332 single nucleotide polymorphisms (SNPs) and found a strong association between the AS3MT (arsenic [+3 oxidation state] methyltransferase) gene and mono- and dimethylated arsenic in urine, suggesting that AS3MT functions as the major gene for arsenic metabolism in humans.	Arsenic	223-230	arsenite methyltransferase	Homo sapiens	136-141
25739736-7	2015	Our data show that adaptation to tolerate the environmental stressor arsenic has likely driven an increase in the frequencies of protective variants of AS3MT, providing the first evidence of human adaptation to a toxic chemical.	Arsenic	69-76	arsenite methyltransferase	Homo sapiens	152-157
25752797-5	2015	In rats, the related canalicular transporter Mrp2/Abcc2 is required for biliary excretion of arsenic as As(GS)(3) and MMA(GS)(2).	Arsenic	93-100	ATP binding cassette subfamily C member 2	Rattus norvegicus	50-55
25752797-8	2015	Basolateral transport of arsenic was temperature- and GSH-dependent and inhibited by the MRP inhibitor MK-571.	Arsenic	25-32	ATP binding cassette subfamily C member 1	Homo sapiens	89-92
25752797-11	2015	Treatment of SCHH with oltipraz (Nrf2 activator) increased MRP4 levels and basolateral efflux of arsenic.	Arsenic	97-104	NFE2 like bZIP transcription factor 2	Homo sapiens	33-37
25752797-13	2015	These results suggest arsenic basolateral transport prevails over biliary excretion and is mediated at least in part by MRPs, most likely including MRP4.	Arsenic	22-29	ATP binding cassette subfamily C member 4	Homo sapiens	148-152
25795919-6	2015	We also show that PML intracellular distribution is altered in NPM1-mutated AML cells and reverted by arsenic through oxidative stress induction.	Arsenic	102-109	PML nuclear body scaffold	Homo sapiens	18-21
25800051-5	2015	Combined RA/arsenic treatment significantly reduced bone marrow blasts in 3 patients and restored the subnuclear localization of both NPM1 and PML.	Arsenic	12-19	nucleophosmin 1	Homo sapiens	134-138
25800051-5	2015	Combined RA/arsenic treatment significantly reduced bone marrow blasts in 3 patients and restored the subnuclear localization of both NPM1 and PML.	Arsenic	12-19	PML nuclear body scaffold	Homo sapiens	143-146
25953102-7	2015	RESULTS: As2O3-induced cytotoxicity in AML cell lines was significantly enhanced after azacytidine pre-treatment as a result of AQP9 up-regulation, leading to increased arsenic uptake and hence intracellular concentration.	Arsenic	169-176	aquaporin 9	Homo sapiens	128-132
25944616-0	2015	Filamin A phosphorylation by Akt promotes cell migration in response to arsenic.	Arsenic	72-79	filamin A	Homo sapiens	0-9
25944616-0	2015	Filamin A phosphorylation by Akt promotes cell migration in response to arsenic.	Arsenic	72-79	AKT serine/threonine kinase 1	Homo sapiens	29-32
25944616-1	2015	We had previously reported that trivalent arsenic (As(3+)), a well-known environmental carcinogen, induces phosphorylation of several putative Akt substrates.	Arsenic	42-49	AKT serine/threonine kinase 1	Homo sapiens	143-146
25944616-9	2015	Antagonizing Akt signaling can ameliorate As(3+)-induced filamin A phosphorylation and cell migration, which may serve as a molecular targeting strategy for malignancies associated with environmental As(3+) exposure.	Arsenic	42-44	AKT serine/threonine kinase 1	Homo sapiens	13-16
25944616-9	2015	Antagonizing Akt signaling can ameliorate As(3+)-induced filamin A phosphorylation and cell migration, which may serve as a molecular targeting strategy for malignancies associated with environmental As(3+) exposure.	Arsenic	42-44	filamin A	Homo sapiens	57-66
26090138-4	2015	CsCrAs2O7 is isotypic with the monoclinic A (I) M (III) X 2O7 (A (I) = alkali metal; M (III) = Al, Cr, Fe; X = As, P) type I family of compounds crystallizing in the space group P21/c.	Arsenic	4-6	H3 histone pseudogene 16	Homo sapiens	178-183
25595679-6	2015	On the other hand, one could speculate that GSH reduces arsenic-induced TPO inhibition by interacting directly with arsenic or TPO, consequently limiting arsenic"s ability to inhibit TPO activity.	Arsenic	56-63	thyroid peroxidase	Homo sapiens	72-75
25595679-6	2015	On the other hand, one could speculate that GSH reduces arsenic-induced TPO inhibition by interacting directly with arsenic or TPO, consequently limiting arsenic"s ability to inhibit TPO activity.	Arsenic	56-63	thyroid peroxidase	Homo sapiens	127-130
25595679-6	2015	On the other hand, one could speculate that GSH reduces arsenic-induced TPO inhibition by interacting directly with arsenic or TPO, consequently limiting arsenic"s ability to inhibit TPO activity.	Arsenic	56-63	thyroid peroxidase	Homo sapiens	127-130
25595679-6	2015	On the other hand, one could speculate that GSH reduces arsenic-induced TPO inhibition by interacting directly with arsenic or TPO, consequently limiting arsenic"s ability to inhibit TPO activity.	Arsenic	116-123	thyroid peroxidase	Homo sapiens	72-75
25595679-6	2015	On the other hand, one could speculate that GSH reduces arsenic-induced TPO inhibition by interacting directly with arsenic or TPO, consequently limiting arsenic"s ability to inhibit TPO activity.	Arsenic	116-123	thyroid peroxidase	Homo sapiens	72-75
25595679-11	2015	When 0.1 ppm As2O3 (i.e., the lowest dose of arsenic able to partially inhibit TPO activity) is combined with 0.01, 0.1, 1.0, or 10 ppm GSH inhibition of in vitro TPO activity is augmented as indicated by complete inhibition of TPO.	Arsenic	45-52	thyroid peroxidase	Homo sapiens	79-82
26288817-6	2015	In particular, expression of the HEDGEHOG pathway component, GLI3, in female placentae was both negatively associated with arsenic exposure and positively associated with infant birth weight.	Arsenic	123-130	GLI family zinc finger 3	Homo sapiens	61-65
25732093-5	2015	Arsenic species in kelp and laver were identified using electrospray ionization ion trap time of flight mass spectrometry (ESI-IT-TOF).	Arsenic	0-7	FEZ family zinc finger 2	Homo sapiens	130-133
26288817-8	2015	We showed previously that arsenic-exposed NIH3T3 cells have reduced GLI3 repressor protein.	Arsenic	26-33	GLI family zinc finger 3	Homo sapiens	68-72
24347089-8	2015	Arsenic increased the activities of serum alanine aminotransferase and aspartate aminotransferase and caused histological alterations in liver indicating hepatotoxicity.	Arsenic	0-7	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	71-97
24347089-9	2015	Arsenic increased lipid peroxidation, depleted reduced glutathione and decreased the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase in liver.	Arsenic	0-7	catalase	Rattus norvegicus	121-129
24347089-9	2015	Arsenic increased lipid peroxidation, depleted reduced glutathione and decreased the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase in liver.	Arsenic	0-7	glutathione-disulfide reductase	Rattus norvegicus	158-179
26288817-9	2015	Together, these studies identify GLI3 as a key signaling node that is affected by arsenic, mediating a subset of its effects on developmental signaling and fetal health.	Arsenic	82-89	GLI family zinc finger 3	Homo sapiens	33-37
25575156-6	2015	RESULTS: Of the 170 SNPs tested, multiplicative interactions between well-water arsenic and two SNPs, rs281432 in ICAM1 (padj = 0.0002) and rs3176867 in VCAM1 (padj = 0.035), were significant for CVD after adjustment for multiple testing.	Arsenic	80-87	intercellular adhesion molecule 1	Homo sapiens	114-119
25430011-5	2015	Furthermore, in tap water from Osijek, levels of arsenic exceeded the WHO guidelines and EPA regulations.	Arsenic	49-56	nuclear RNA export factor 1	Homo sapiens	16-19
25575156-6	2015	RESULTS: Of the 170 SNPs tested, multiplicative interactions between well-water arsenic and two SNPs, rs281432 in ICAM1 (padj = 0.0002) and rs3176867 in VCAM1 (padj = 0.035), were significant for CVD after adjustment for multiple testing.	Arsenic	80-87	vascular cell adhesion molecule 1	Homo sapiens	153-158
25732589-0	2015	Arabidopsis NIP3;1 Plays an Important Role in Arsenic Uptake and Root-to-Shoot Translocation under Arsenite Stress Conditions.	Arsenic	46-53	NOD26-like intrinsic protein 3;1	Arabidopsis thaliana	12-18
25893757-7	2015	Spatial principle component analysis showed that the first principal component (PC1) including Cd, As, and Pb could explain 56.18 % of the non-residual fraction.	Arsenic	99-101	polycystin 1, transient receptor potential channel interacting	Homo sapiens	80-83
25893757-8	2015	High values of PC1 were observed mostly in the southern part of Weishan Lake, which indicated greater bioavailability and toxicity of Cd, As, and Pb in this area.	Arsenic	138-140	polycystin 1, transient receptor potential channel interacting	Homo sapiens	15-18
25760782-9	2015	However, elevated risks for hormone receptor-negative tumors were observed for higher exposure to cadmium compounds and possibly inorganic arsenic among never-smoking non-movers.	Arsenic	139-146	nuclear receptor subfamily 4 group A member 1	Homo sapiens	28-44
25732589-3	2015	In this study, using reverse genetic strategies, Arabidopsis NIP3;1 was identified to play an important role in both the arsenic uptake and root-to-shoot distribution under arsenite stress conditions.	Arsenic	121-128	NOD26-like intrinsic protein 3;1	Arabidopsis thaliana	61-67
25732589-4	2015	The nip3;1 loss-of-function mutants displayed obvious improvements in arsenite tolerance for aboveground growth and accumulated less arsenic in shoots than those of the wild-type plants, whereas the nip3;1 nip1;1 double mutant showed strong arsenite tolerance and improved growth of both roots and shoots under arsenite stress conditions.	Arsenic	133-140	NOD26-like intrinsic protein 3;1	Arabidopsis thaliana	4-10
25600998-12	2015	Taken together, these results indicate that root uptake of arsenate is probably not via sulfate transporters, but the poor growth of the double mutant of sultr1;1 and sultr1;2 was due to its poor sulfate status and decreased levels of thiols, which had pleiotropic effects on the root uptake and translocation of potassium and phosphorus and arsenic tolerance.	Arsenic	342-349	sulfate transporter 1;1	Arabidopsis thaliana	154-175
25929406-0	2015	Purine nucleoside phosphorylase and the enzymatic antioxidant defense system in breast milk from women with different levels of arsenic exposure.	Arsenic	128-135	purine nucleoside phosphorylase	Homo sapiens	0-31
25929406-1	2015	Purine nucleoside phosphorylase (PNP) is an ubiquitous enzyme which plays an important role in arsenic (As) detoxification.	Arsenic	95-102	purine nucleoside phosphorylase	Homo sapiens	0-31
25929406-1	2015	Purine nucleoside phosphorylase (PNP) is an ubiquitous enzyme which plays an important role in arsenic (As) detoxification.	Arsenic	95-102	purine nucleoside phosphorylase	Homo sapiens	33-36
25929406-1	2015	Purine nucleoside phosphorylase (PNP) is an ubiquitous enzyme which plays an important role in arsenic (As) detoxification.	Arsenic	104-106	purine nucleoside phosphorylase	Homo sapiens	0-31
25929406-1	2015	Purine nucleoside phosphorylase (PNP) is an ubiquitous enzyme which plays an important role in arsenic (As) detoxification.	Arsenic	104-106	purine nucleoside phosphorylase	Homo sapiens	33-36
25783758-4	2015	The effect of lattice strain, implemented by a 3.2% change in the As-Si nearest-neighbour bond length, further shifts the value of eta2 to -1.87 x 10(-3) microm(2) V(-2), resulting in an excellent agreement of theory with the experimentally measured value of -1.9 +- 0.2 x 10(-3) microm(2) V(-2).	Arsenic	66-68	DNA polymerase iota	Homo sapiens	131-135
26137629-0	2015	[Dynamic changes of ROS, MDA and SOD during arsenic-induced neoplastic transformation in human keratinocytes].	Arsenic	44-51	superoxide dismutase 1	Homo sapiens	33-36
26137629-1	2015	OBJECTIVE: To investigate the level of ROS, MDA and SOD in different stages of arsenic-induced neoplastic transformation in human keratinocytes.	Arsenic	79-86	superoxide dismutase 1	Homo sapiens	52-55
26137629-5	2015	RESULTS: A marked increase in the secretion of active MMP-9 in the arsenic-treated (1.0 mumol/L NaAsO2) cells was observed in comparison to the passage-matched untreated control (0.0 mumol/L NaAsO2) cells at 28 and 35 passages.	Arsenic	67-74	matrix metallopeptidase 9	Homo sapiens	54-59
26137629-11	2015	CONCLUSION: Long-term exposure to low concentrations of inorganic arsenic-induced malignant transformation of HaCaT cells is accompanied by intracellular imbalance between oxidative-antioxidant, which increased expression of SOD and low levels of ROS found in the later-stage of arsenite-induced transformation.	Arsenic	66-73	superoxide dismutase 1	Homo sapiens	225-228
25575490-8	2015	In the soleus muscle of the T group, AS-160(Thr-642) (AKT substrate of 160 kDa) and AMPK(Thr-172) (AMP-Activated Protein Kinase) phosphorylation was increased by exercise in both basal and insulin-stimulated conditions, but it was reduced in TL mice with insulin stimulation compared with the T group.	Arsenic	37-39	TBC1 domain family, member 4	Mus musculus	54-78
25660332-5	2015	METHODS AND RESULTS: Ultra-performance liquid chromatography-quadrupole time-of-flight-mass spectrometry (UPLC-QTOF-MS) coupled with pattern recognition methods was integrated to examine the cerebral metabolic signature of human alpha-synuclein transgenic mice and the effects of AS on central nervous system (CNS) in pathology and physiology.	Arsenic	280-282	synuclein alpha	Homo sapiens	229-244
25600320-5	2015	Arsenic immobilization can be favorably obtained at solution pH in the range of 4.0-6.0 and Fe(II) concentration from 250 to 1000 muM.	Arsenic	0-7	latexin	Homo sapiens	130-133
25539033-10	2015	Additionally arsenic treatment significantly increased testicular thiobarbituric acid reactive substance (TBARS) levels while catalase (CAT), superoxide dismutase (SOD), peroxidase (POD), and glutathione reductase (GSR) activities, and plasma and intra-testicular testosterone concentrations, were decreased significantly.	Arsenic	13-20	glutathione-disulfide reductase	Rattus norvegicus	192-213
25493652-3	2015	Our fieldwork in Bangladesh demonstrated that levels of placental growth factor (PlGF) in urine samples from residents of cancer-prone areas with arsenic-polluted drinking water were higher than those in urine samples from residents of an area that was not polluted with arsenic.	Arsenic	146-153	placental growth factor	Homo sapiens	56-79
25493652-3	2015	Our fieldwork in Bangladesh demonstrated that levels of placental growth factor (PlGF) in urine samples from residents of cancer-prone areas with arsenic-polluted drinking water were higher than those in urine samples from residents of an area that was not polluted with arsenic.	Arsenic	146-153	placental growth factor	Homo sapiens	81-85
25493652-3	2015	Our fieldwork in Bangladesh demonstrated that levels of placental growth factor (PlGF) in urine samples from residents of cancer-prone areas with arsenic-polluted drinking water were higher than those in urine samples from residents of an area that was not polluted with arsenic.	Arsenic	271-278	placental growth factor	Homo sapiens	56-79
25355491-0	2015	MiR-133b contributes to arsenic-induced apoptosis in U251 glioma cells by targeting the hERG channel.	Arsenic	24-31	microRNA 133b	Homo sapiens	0-8
25355491-0	2015	MiR-133b contributes to arsenic-induced apoptosis in U251 glioma cells by targeting the hERG channel.	Arsenic	24-31	ETS transcription factor ERG	Homo sapiens	88-92
25827134-1	2015	BACKGROUND: Growth hormone-releasing hormone agonists (GHRH-As) stimulate cardiac repair following myocardial infarction (MI) in rats through the activation of the GHRH signaling pathway within the heart.	Arsenic	60-62	growth hormone releasing hormone	Rattus norvegicus	12-44
25827134-1	2015	BACKGROUND: Growth hormone-releasing hormone agonists (GHRH-As) stimulate cardiac repair following myocardial infarction (MI) in rats through the activation of the GHRH signaling pathway within the heart.	Arsenic	60-62	growth hormone releasing hormone	Rattus norvegicus	55-59
25827134-1	2015	BACKGROUND: Growth hormone-releasing hormone agonists (GHRH-As) stimulate cardiac repair following myocardial infarction (MI) in rats through the activation of the GHRH signaling pathway within the heart.	Arsenic	60-62	growth hormone releasing hormone	Rattus norvegicus	164-168
25639566-9	2015	Moreover, autophagy and subsequent reduction in alpha-synuclein levels may be a vicious cycle in arsenics-induced neurotoxicity.	Arsenic	97-105	synuclein alpha	Rattus norvegicus	48-63
25799109-9	2015	Selected bacterial strains incubated anaerobically over 300 days using natural orange sand of Pleistocene aquifer showed release of soluble As mostly as As3+ along with several other elements (Al, Fe, Mn, K, etc.).	Arsenic	140-142	PDS5 cohesin associated factor B	Homo sapiens	153-156
25625412-5	2015	Among the identified arsenic-responsive miRNAs, several are predicted to target Nfe2l2-regulated antioxidant genes, including glutamate-cysteine ligase (GCL) catalytic subunit (GCLC) and modifier subunit (GCLM) which are involved in glutathione (GSH) synthesis.	Arsenic	21-28	nuclear factor, erythroid 2	Rattus norvegicus	80-84
25411909-4	2015	Our previous studies recognized a protective role for the heme-regulated eIF2alpha kinase (Hri) in erythroid cells against oxidative stress exerted by arsenic and cadmium.	Arsenic	151-158	eukaryotic translation initiation factor 2 alpha kinase 1	Mus musculus	58-89
25411909-4	2015	Our previous studies recognized a protective role for the heme-regulated eIF2alpha kinase (Hri) in erythroid cells against oxidative stress exerted by arsenic and cadmium.	Arsenic	151-158	eukaryotic translation initiation factor 2 alpha kinase 1	Mus musculus	91-94
25799405-10	2015	CONCLUSIONS: Our results support the hypothesis that polymorphisms of the EDNRB gene may influence the susceptibility to obesity and can interact with plasma arsenic levels.	Arsenic	158-165	endothelin receptor type B	Homo sapiens	74-79
25625412-5	2015	Among the identified arsenic-responsive miRNAs, several are predicted to target Nfe2l2-regulated antioxidant genes, including glutamate-cysteine ligase (GCL) catalytic subunit (GCLC) and modifier subunit (GCLM) which are involved in glutathione (GSH) synthesis.	Arsenic	21-28	glutamate-cysteine ligase, catalytic subunit	Rattus norvegicus	177-181
25625412-5	2015	Among the identified arsenic-responsive miRNAs, several are predicted to target Nfe2l2-regulated antioxidant genes, including glutamate-cysteine ligase (GCL) catalytic subunit (GCLC) and modifier subunit (GCLM) which are involved in glutathione (GSH) synthesis.	Arsenic	21-28	glutamate cysteine ligase, modifier subunit	Rattus norvegicus	205-209
25625412-6	2015	Exposure to low concentrations of arsenic increased mRNA expression for Gclc and Gclm, while high concentrations significantly reduced their expression, which were correlated to changes in hepatic GCL activity and GSH level.	Arsenic	34-41	glutamate-cysteine ligase, catalytic subunit	Rattus norvegicus	72-76
25625412-6	2015	Exposure to low concentrations of arsenic increased mRNA expression for Gclc and Gclm, while high concentrations significantly reduced their expression, which were correlated to changes in hepatic GCL activity and GSH level.	Arsenic	34-41	glutamate cysteine ligase, modifier subunit	Rattus norvegicus	81-85
25586904-0	2015	Involvement of epigenetics and EMT-related miRNA in arsenic-induced neoplastic transformation and their potential clinical use.	Arsenic	52-59	IL2 inducible T cell kinase	Homo sapiens	31-34
25586904-8	2015	Western blot analysis demonstrated decreased PTEN and increased AKT and mTOR in arsenic-treated HUC1 cells.	Arsenic	80-87	phosphatase and tensin homolog	Homo sapiens	45-49
25586904-8	2015	Western blot analysis demonstrated decreased PTEN and increased AKT and mTOR in arsenic-treated HUC1 cells.	Arsenic	80-87	mechanistic target of rapamycin kinase	Homo sapiens	72-76
25586904-8	2015	Western blot analysis demonstrated decreased PTEN and increased AKT and mTOR in arsenic-treated HUC1 cells.	Arsenic	80-87	AKT serine/threonine kinase 1	Homo sapiens	64-67
25763302-0	2015	Phosphate fertilizer is a main source of arsenic in areas affected with chronic kidney disease of unknown etiology in Sri Lanka.	Arsenic	41-48	sorcin	Homo sapiens	118-121
25586904-9	2015	Levels of miR-200a, miR-200b, and miR-200c were downregulated in arsenic-exposed HUC1 cells by quantitative RT-PCR.	Arsenic	65-72	microRNA 200a	Homo sapiens	10-18
25586904-9	2015	Levels of miR-200a, miR-200b, and miR-200c were downregulated in arsenic-exposed HUC1 cells by quantitative RT-PCR.	Arsenic	65-72	microRNA 200b	Homo sapiens	20-28
25586904-9	2015	Levels of miR-200a, miR-200b, and miR-200c were downregulated in arsenic-exposed HUC1 cells by quantitative RT-PCR.	Arsenic	65-72	microRNA 200c	Homo sapiens	34-42
25586904-10	2015	Furthermore, in human urine, miR-200c and miR-205 were inversely associated with arsenic exposure (P = 0.005 and 0.009, respectively).	Arsenic	81-88	microRNA 200c	Homo sapiens	29-37
25586904-10	2015	Furthermore, in human urine, miR-200c and miR-205 were inversely associated with arsenic exposure (P = 0.005 and 0.009, respectively).	Arsenic	81-88	microRNA 205	Homo sapiens	42-49
25586904-12	2015	Our study suggests that exposure to arsenic rapidly induces a multifaceted dedifferentiation program and miR-205 has potential to be used as a marker of arsenic exposure as well as a maker of early urothelial carcinoma detection.	Arsenic	153-160	microRNA 205	Homo sapiens	105-112
25895260-2	2015	While arsenic caused a significant increase in AChE, DDVP produced marked depletion.	Arsenic	6-13	acetylcholinesterase	Rattus norvegicus	47-51
25701463-4	2015	We tried to explore the roles UPK1A plays in BTCC via the transfection of its antisense nucleotides (AS) into T24 cells to observe their changes of proliferation and apoptosis.	Arsenic	101-103	uroplakin 1A	Homo sapiens	30-35
25405958-9	2015	The balance between MMPs and TIMPs is important in maintaining the dynamic equilibrium between the ECM, and the renin-angiotensin-aldosterone system, which is involved in the pathologenesis of AS, and in which AngII has a central role.	Arsenic	193-195	matrix metallopeptidase 9	Rattus norvegicus	20-24
25618704-0	2015	Evaluation and modelling of dissolved organic matter reactivity toward As(III) and As(V) - implication in environmental arsenic speciation.	Arsenic	120-127	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	83-88
25924428-0	2015	[Gender-dependent expression of ERalpha in arsenic exposed mice offspring"s lung tissue].	Arsenic	43-50	estrogen receptor 1 (alpha)	Mus musculus	32-39
25924428-8	2015	CONCLUSION: Arsenic infected during pregnancy can increase the lung tissue"s ERalpha expression level of female offspring in infancy and adulthood.	Arsenic	12-19	estrogen receptor 1 (alpha)	Mus musculus	77-84
25763302-7	2015	Also TSP is a rich source of other nephrotoxic metals including Cr, Co, Ni, Pb and V. Annually more than 0.1 million tons of TSP is imported to Sri Lanka containing approximately 2100 kg of arsenic.	Arsenic	190-197	sorcin	Homo sapiens	144-147
25763302-10	2015	Arsenic contamination in pesticides varied from 0.18 mg/kg to 2.53 mg/kg although arsenic containing pesticides are banned in Sri Lanka.	Arsenic	82-89	sorcin	Homo sapiens	126-129
25763302-11	2015	Glyphosate the most widely used pesticide in Sri Lanka contains average of 1.9 mg/kg arsenic.	Arsenic	85-92	sorcin	Homo sapiens	45-48
25797979-3	2015	In this study, we evaluated the protective effects of Phyllanthus emblica (Indian gooseberry or Amla) leaf extract (PLE) on arsenic-mediated toxicity in experimental mice.	Arsenic	124-131	perinatal lethality	Mus musculus	116-119
25180936-0	2015	Associations of total arsenic in drinking water, hair and nails with serum vascular endothelial growth factor in arsenic-endemic individuals in Bangladesh.	Arsenic	22-29	vascular endothelial growth factor A	Homo sapiens	75-109
25180936-0	2015	Associations of total arsenic in drinking water, hair and nails with serum vascular endothelial growth factor in arsenic-endemic individuals in Bangladesh.	Arsenic	113-120	vascular endothelial growth factor A	Homo sapiens	75-109
25180936-4	2015	However, human study showing the association between arsenic exposure and serum VEGF levels has not yet been documented.	Arsenic	53-60	vascular endothelial growth factor A	Homo sapiens	80-84
25180936-5	2015	This study was aimed to investigate the association between arsenic exposure and serum VEGF levels in the arsenic-endemic individuals in Bangladesh.	Arsenic	60-67	vascular endothelial growth factor A	Homo sapiens	87-91
25180936-5	2015	This study was aimed to investigate the association between arsenic exposure and serum VEGF levels in the arsenic-endemic individuals in Bangladesh.	Arsenic	106-113	vascular endothelial growth factor A	Homo sapiens	87-91
25180936-9	2015	Serum VEGF levels were correlated with water (rs = 0.363, p &lt; 0.001), hair (rs = 0.205, p &lt; 0.01) and nail (rs = 0.190, p &lt; 0.01) arsenic.	Arsenic	139-146	vascular endothelial growth factor A	Homo sapiens	6-10
25180936-10	2015	Further, VEGF levels showed dose-response relationships with water, hair and nail arsenic.	Arsenic	82-89	vascular endothelial growth factor A	Homo sapiens	9-13
25180936-12	2015	Significant associations of arsenic exposure with VEGF levels were found even after adjusting with relevant covariates.	Arsenic	28-35	vascular endothelial growth factor A	Homo sapiens	50-54
25561743-5	2015	In response to arsenic exposure, nucleolin-SUMO was induced and promoted its binding with gadd45alpha mRNA, which increased gadd45alpha mRNA stability and protein expression, subsequently causing GADD45alpha-mediated cell death.	Arsenic	15-22	nucleolin	Homo sapiens	33-42
25561743-5	2015	In response to arsenic exposure, nucleolin-SUMO was induced and promoted its binding with gadd45alpha mRNA, which increased gadd45alpha mRNA stability and protein expression, subsequently causing GADD45alpha-mediated cell death.	Arsenic	15-22	growth arrest and DNA damage inducible alpha	Homo sapiens	90-101
25561743-5	2015	In response to arsenic exposure, nucleolin-SUMO was induced and promoted its binding with gadd45alpha mRNA, which increased gadd45alpha mRNA stability and protein expression, subsequently causing GADD45alpha-mediated cell death.	Arsenic	15-22	growth arrest and DNA damage inducible alpha	Homo sapiens	124-135
25561743-5	2015	In response to arsenic exposure, nucleolin-SUMO was induced and promoted its binding with gadd45alpha mRNA, which increased gadd45alpha mRNA stability and protein expression, subsequently causing GADD45alpha-mediated cell death.	Arsenic	15-22	growth arrest and DNA damage inducible alpha	Homo sapiens	196-207
25559853-0	2015	STAT3-dependent VEGF production from keratinocytes abrogates dendritic cell activation and migration by arsenic: a plausible regional mechanism of immunosuppression in arsenical cancers.	Arsenic	104-111	signal transducer and activator of transcription 3	Homo sapiens	0-5
25559853-0	2015	STAT3-dependent VEGF production from keratinocytes abrogates dendritic cell activation and migration by arsenic: a plausible regional mechanism of immunosuppression in arsenical cancers.	Arsenic	104-111	vascular endothelial growth factor A	Homo sapiens	16-20
25559853-10	2015	Arsenic induced STAT3 activation and the production of VEGF in keratinocytes.	Arsenic	0-7	signal transducer and activator of transcription 3	Homo sapiens	16-21
25559853-10	2015	Arsenic induced STAT3 activation and the production of VEGF in keratinocytes.	Arsenic	0-7	vascular endothelial growth factor A	Homo sapiens	55-59
25559853-12	2015	While VEGF by itself minimally induced the expression of CD86 and MHC-II in MDDC, arsenic induced-MDDC activation was abolished by VEGF pretreatment.	Arsenic	82-89	vascular endothelial growth factor A	Homo sapiens	131-135
25797979-11	2015	These results indicated that PLE may not block arsenic deposition in tissue directly but rather may play a protective role to reduce arsenic-induced toxicity.	Arsenic	47-54	perinatal lethality	Mus musculus	29-32
25797979-11	2015	These results indicated that PLE may not block arsenic deposition in tissue directly but rather may play a protective role to reduce arsenic-induced toxicity.	Arsenic	133-140	perinatal lethality	Mus musculus	29-32
25797979-12	2015	Therefore, co-administration of PLE in arsenic-exposed animals might have a future therapeutic application for protecting against arsenic-mediated toxicity.	Arsenic	39-46	perinatal lethality	Mus musculus	32-35
25797979-12	2015	Therefore, co-administration of PLE in arsenic-exposed animals might have a future therapeutic application for protecting against arsenic-mediated toxicity.	Arsenic	130-137	perinatal lethality	Mus musculus	32-35
25485709-5	2015	In WT cells arsenic caused concentration-dependent increases in MT expression (transcript and protein), and in the metal-responsive transcription factor-1 (MTF-1), which is required to induce the MT gene.	Arsenic	12-19	metal regulatory transcription factor 1	Homo sapiens	115-154
25465483-4	2015	For as-made Mg substituted STA-2, the positive charge of the organocation template is balanced by the substitution of Mg(2+) for Al(3+) and, where required, by hydroxide anions coordinated to the framework [27] Al MAS NMR spectra show that Al is present in both tetrahedral and five-fold coordination, with the latter dependent on the amount of substituted cations, and confirms the bridging nature of the hydroxyl groups, while high-resolution MQMAS spectra are able to show that Mg appears to preferentially substitute on the Al1 site.	Arsenic	4-6	ephrin A5	Homo sapiens	528-531
23282998-4	2015	Results of the present study also showed that arsenic caused cytotoxicity by elevating morphological alterations, TUNEL-positive nuclei, caspase-3 activity and DNA damage and reducing cell adhesion and cell proliferation in a time-dependent manner.	Arsenic	46-53	caspase 3	Rattus norvegicus	137-146
25485709-5	2015	In WT cells arsenic caused concentration-dependent increases in MT expression (transcript and protein), and in the metal-responsive transcription factor-1 (MTF-1), which is required to induce the MT gene.	Arsenic	12-19	metal regulatory transcription factor 1	Homo sapiens	156-161
25485709-8	2015	The transport genes, Abcc1 and Abcc2 were increased by arsenic in WT cells but either showed no or very limited increases in MT-null cells.	Arsenic	55-62	ATP binding cassette subfamily C member 1	Homo sapiens	21-26
25485709-8	2015	The transport genes, Abcc1 and Abcc2 were increased by arsenic in WT cells but either showed no or very limited increases in MT-null cells.	Arsenic	55-62	ATP binding cassette subfamily C member 2	Homo sapiens	31-36
26788513-0	2015	Arsenic and Mercury Containing Traditional Chinese Medicine (Realgar and Cinnabar) Strongly Inhibit Organic Anion Transporters, Oat1 and Oat3, In Vivo in Mice.	Arsenic	0-7	solute carrier family 22 (organic anion transporter), member 6	Mus musculus	128-132
25585981-4	2015	The surface characterization revealed that laser polishing reduced the surface roughness of stent by 34-64% compared to that of the as-received stent surface condition depending on the treatment time (i.e., 700-1600 mum).	Arsenic	44-46	latexin	Homo sapiens	216-219
25482150-2	2015	Based on the nanostructures developed, we performed the ultrasensitive detection of arsenic ions by SERS and monitored the catalyzed reactions using real-time SERS.	Arsenic	84-91	seryl-tRNA synthetase 2, mitochondrial	Homo sapiens	100-104
25499816-8	2015	In the present study, we used expressions of catalase (antioxidant against H2O2) and superoxide dismutase 2 (SOD2, antioxidant against O2(-)) to decrease ROS level and investigated their role in the process of arsenic-induced cell transformation.	Arsenic	210-217	superoxide dismutase 2	Homo sapiens	85-107
25499816-12	2015	The inhibition of catalase to increase ROS level restored apoptosis capability of arsenic-transformed BEAS-2B cells, further showing that ROS levels are low in these cells.	Arsenic	82-89	catalase	Homo sapiens	18-26
25290577-7	2015	These results indicate that the epidermis of human skin and resulting malignancies express high level of MT-3 and potentially impact on the known association of arsenic exposure and the development of skin disorders and related cancers.	Arsenic	161-168	metallothionein 3	Homo sapiens	105-109
26170775-0	2015	Arsenic Primes Human Bone Marrow CD34+ Cells for Erythroid Differentiation.	Arsenic	0-7	CD34 molecule	Homo sapiens	33-37
26788513-0	2015	Arsenic and Mercury Containing Traditional Chinese Medicine (Realgar and Cinnabar) Strongly Inhibit Organic Anion Transporters, Oat1 and Oat3, In Vivo in Mice.	Arsenic	0-7	solute carrier family 22 (organic anion transporter), member 8	Mus musculus	137-141
26295053-8	2015	In conclusion, GSTs, EPHX1, and XPD are potential genetic factors for arsenic-induced skin cancers.	Arsenic	70-77	hematopoietic prostaglandin D synthase	Homo sapiens	15-19
26295053-8	2015	In conclusion, GSTs, EPHX1, and XPD are potential genetic factors for arsenic-induced skin cancers.	Arsenic	70-77	epoxide hydrolase 1	Homo sapiens	21-26
26788513-9	2015	Arsenic and mercury containing traditional Chinese medicine (Realgar and Cinnabar) probably induce kidney damage through inhibiting several members of the organic anion transporters (such as OAT1 and OAT3).	Arsenic	0-7	solute carrier family 22 (organic anion transporter), member 6	Mus musculus	191-195
26295053-8	2015	In conclusion, GSTs, EPHX1, and XPD are potential genetic factors for arsenic-induced skin cancers.	Arsenic	70-77	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	32-35
26788513-9	2015	Arsenic and mercury containing traditional Chinese medicine (Realgar and Cinnabar) probably induce kidney damage through inhibiting several members of the organic anion transporters (such as OAT1 and OAT3).	Arsenic	0-7	solute carrier family 22 (organic anion transporter), member 8	Mus musculus	200-204
26292025-0	2015	Low-dose arsenic-mediated metabolic shift is associated with activation of Polo-like kinase 1 (Plk1).	Arsenic	9-16	polo like kinase 1	Homo sapiens	75-93
26114099-5	2015	In summary, in this present study, we demonstrated that subchronic arsenic exposure induces only the anxiety-like behaviors in normal mice and enhances the depression-like behaviors in the reserpine induced mouse model of depression, in which the cerebral prefrontal cortex BDNF-TrkB signaling pathway is involved.	Arsenic	67-74	brain derived neurotrophic factor	Mus musculus	274-278
26114099-5	2015	In summary, in this present study, we demonstrated that subchronic arsenic exposure induces only the anxiety-like behaviors in normal mice and enhances the depression-like behaviors in the reserpine induced mouse model of depression, in which the cerebral prefrontal cortex BDNF-TrkB signaling pathway is involved.	Arsenic	67-74	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	279-283
25815309-0	2015	Lutein has a protective effect on hepatotoxicity induced by arsenic via Nrf2 signaling.	Arsenic	60-67	nuclear factor, erythroid derived 2, like 2	Mus musculus	72-76
26292025-0	2015	Low-dose arsenic-mediated metabolic shift is associated with activation of Polo-like kinase 1 (Plk1).	Arsenic	9-16	polo like kinase 1	Homo sapiens	95-99
26292025-4	2015	It was recently shown that low-dose arsenic leads to a metabolic shift from mitochondrial respiration to aerobic glycolysis via inactivation of tumor suppressor p53 and activation of NF-kappaB.	Arsenic	36-43	tumor protein p53	Homo sapiens	161-164
26292025-4	2015	It was recently shown that low-dose arsenic leads to a metabolic shift from mitochondrial respiration to aerobic glycolysis via inactivation of tumor suppressor p53 and activation of NF-kappaB.	Arsenic	36-43	nuclear factor kappa B subunit 1	Homo sapiens	183-192
26292025-5	2015	However, how inactivation of p53, activation of NF-kappaB, and metabolic change are coordinated in response to low-dose arsenic exposure is still not completely understood.	Arsenic	120-127	tumor protein p53	Homo sapiens	29-32
26292025-5	2015	However, how inactivation of p53, activation of NF-kappaB, and metabolic change are coordinated in response to low-dose arsenic exposure is still not completely understood.	Arsenic	120-127	nuclear factor kappa B subunit 1	Homo sapiens	48-57
26292025-7	2015	Herein, we showed that low-dose arsenic leads to elevation of Plk1 in an NF-kappaB-dependent manner and that elevation of Plk1 contributes to the metabolic change from oxidative phosphorylation to glycolysis via activation of the PI3K/AKT/mTOR pathway.	Arsenic	32-39	polo like kinase 1	Homo sapiens	62-66
26292025-7	2015	Herein, we showed that low-dose arsenic leads to elevation of Plk1 in an NF-kappaB-dependent manner and that elevation of Plk1 contributes to the metabolic change from oxidative phosphorylation to glycolysis via activation of the PI3K/AKT/mTOR pathway.	Arsenic	32-39	nuclear factor kappa B subunit 1	Homo sapiens	73-82
26292025-7	2015	Herein, we showed that low-dose arsenic leads to elevation of Plk1 in an NF-kappaB-dependent manner and that elevation of Plk1 contributes to the metabolic change from oxidative phosphorylation to glycolysis via activation of the PI3K/AKT/mTOR pathway.	Arsenic	32-39	AKT serine/threonine kinase 1	Homo sapiens	235-238
26292025-7	2015	Herein, we showed that low-dose arsenic leads to elevation of Plk1 in an NF-kappaB-dependent manner and that elevation of Plk1 contributes to the metabolic change from oxidative phosphorylation to glycolysis via activation of the PI3K/AKT/mTOR pathway.	Arsenic	32-39	mechanistic target of rapamycin kinase	Homo sapiens	239-243
26292025-8	2015	Furthermore, we showed that inhibition/depletion of Plk1 reverses low-dose arsenic-associated phenotypes, including enhanced cell proliferation, activation of the PI3K/AKT/mTOR pathway, and increased glycolysis.	Arsenic	75-82	polo like kinase 1	Homo sapiens	52-56
26292025-8	2015	Furthermore, we showed that inhibition/depletion of Plk1 reverses low-dose arsenic-associated phenotypes, including enhanced cell proliferation, activation of the PI3K/AKT/mTOR pathway, and increased glycolysis.	Arsenic	75-82	AKT serine/threonine kinase 1	Homo sapiens	168-171
26292025-8	2015	Furthermore, we showed that inhibition/depletion of Plk1 reverses low-dose arsenic-associated phenotypes, including enhanced cell proliferation, activation of the PI3K/AKT/mTOR pathway, and increased glycolysis.	Arsenic	75-82	mechanistic target of rapamycin kinase	Homo sapiens	172-176
26292025-9	2015	Finally, inhibition of the PI3K/AKT/mTOR pathway also antagonizes the enhanced glycolytic influx due to low-dose arsenic exposure.	Arsenic	113-120	AKT serine/threonine kinase 1	Homo sapiens	32-35
26292025-9	2015	Finally, inhibition of the PI3K/AKT/mTOR pathway also antagonizes the enhanced glycolytic influx due to low-dose arsenic exposure.	Arsenic	113-120	mechanistic target of rapamycin kinase	Homo sapiens	36-40
26292025-10	2015	Our studies support the notion that Plk1 likely plays a critical role in cellular responses to low-dose arsenic.	Arsenic	104-111	polo like kinase 1	Homo sapiens	36-40
27054085-0	2015	Arsenic-exposed Keratinocytes Exhibit Differential microRNAs Expression Profile; Potential Implication of miR-21, miR-200a and miR-141 in Melanoma Pathway.	Arsenic	0-7	microRNA 21	Homo sapiens	106-112
27054085-0	2015	Arsenic-exposed Keratinocytes Exhibit Differential microRNAs Expression Profile; Potential Implication of miR-21, miR-200a and miR-141 in Melanoma Pathway.	Arsenic	0-7	microRNA 200a	Homo sapiens	114-122
27054085-0	2015	Arsenic-exposed Keratinocytes Exhibit Differential microRNAs Expression Profile; Potential Implication of miR-21, miR-200a and miR-141 in Melanoma Pathway.	Arsenic	0-7	microRNA 141	Homo sapiens	127-134
27054085-2	2015	Here, non-malignant human keratinocytes (HaCaT) were exposed to arsenic and its effects on microRNAs (miRNAs; miR) expression were analyzed via miRCURY LNA array analyses.	Arsenic	64-71	membrane associated ring-CH-type finger 8	Homo sapiens	102-105
25325195-7	2015	Methylation of PLA2G2C (probe cg04605617) was the most significantly associated locus in relation to both urinary (p = 3.40 x 10(-11)) and blood arsenic concentrations (p = 1.48 x 10(-11)).	Arsenic	145-152	phospholipase A2 group IIC	Homo sapiens	15-22
25460635-0	2015	Association between maternal urinary arsenic species and infant cord blood leptin levels in a New Hampshire Pregnancy Cohort.	Arsenic	37-44	leptin	Homo sapiens	75-81
25156000-0	2015	Genetic variation in arsenic (+3 oxidation state) methyltransferase (AS3MT), arsenic metabolism and risk of basal cell carcinoma in a European population.	Arsenic	21-28	arsenite methyltransferase	Homo sapiens	69-74
25156000-2	2015	Arsenic metabolism is a susceptibility factor for arsenic toxicity, and specific haplotypes in arsenic (+3 oxidation state) methyltransferase (AS3MT) have been associated with increased urinary fractions of the most toxic arsenic metabolite, methylarsonic acid (MMA).	Arsenic	0-7	arsenite methyltransferase	Homo sapiens	143-148
25325195-8	2015	Three additional novel methylation loci-SQSTM1 (cg01225779), SLC4A4 (cg06121226), and IGH (cg13651690)--were also significantly associated with arsenic exposure.	Arsenic	144-151	sequestosome 1	Homo sapiens	40-46
25156000-2	2015	Arsenic metabolism is a susceptibility factor for arsenic toxicity, and specific haplotypes in arsenic (+3 oxidation state) methyltransferase (AS3MT) have been associated with increased urinary fractions of the most toxic arsenic metabolite, methylarsonic acid (MMA).	Arsenic	50-57	arsenite methyltransferase	Homo sapiens	143-148
25156000-2	2015	Arsenic metabolism is a susceptibility factor for arsenic toxicity, and specific haplotypes in arsenic (+3 oxidation state) methyltransferase (AS3MT) have been associated with increased urinary fractions of the most toxic arsenic metabolite, methylarsonic acid (MMA).	Arsenic	95-102	arsenite methyltransferase	Homo sapiens	143-148
25156000-3	2015	The aim of this study is to elucidate the association of AS3MT haplotypes with arsenic metabolism and the risk of BCC.	Arsenic	79-86	arsenite methyltransferase	Homo sapiens	57-62
25460635-3	2015	This study aimed to investigate the association between in utero arsenic exposure and infant cord blood leptin concentrations within 156 mother-infant pairs from the New Hampshire Birth Cohort Study (NHBCS) who were exposed to low to moderate levels of arsenic through well water and diet.	Arsenic	65-72	leptin	Homo sapiens	104-110
25460635-5	2015	Results indicate that urinary arsenic species concentrations were predictive of infant cord blood leptin levels following adjustment for creatinine, infant birth weight for gestational age percentile, infant sex, maternal pregnancy-related weight gain, and maternal education level amongst 149 white mother-infant pairs in multivariate linear regression models.	Arsenic	30-37	leptin	Homo sapiens	98-104
25460635-6	2015	A doubling or 100% increase in total urinary arsenic concentration (iAs+MMA+DMA) was associated with a 10.3% (95% CI: 0.8-20.7%) increase in cord blood leptin levels.	Arsenic	45-52	leptin	Homo sapiens	152-158
25156000-9	2015	The results suggest that carriage of AS3MT haplotypes associated with less-efficient arsenic methylation, or lack of AS3MT haplotypes associated with a more-efficient arsenic methylation, results in higher risk of arsenic-related BCC.	Arsenic	85-92	arsenite methyltransferase	Homo sapiens	37-42
25460635-8	2015	The association between inorganic arsenic (iAs) and cord blood leptin was of similar magnitude and direction as other arsenic species (a 100% increase in iAs was associated with a 6.5% (95% CI: -3.4-17.5%) increase in cord blood leptin levels), albeit not significant.	Arsenic	34-41	leptin	Homo sapiens	63-69
25156000-9	2015	The results suggest that carriage of AS3MT haplotypes associated with less-efficient arsenic methylation, or lack of AS3MT haplotypes associated with a more-efficient arsenic methylation, results in higher risk of arsenic-related BCC.	Arsenic	167-174	arsenite methyltransferase	Homo sapiens	117-122
25325195-8	2015	Three additional novel methylation loci-SQSTM1 (cg01225779), SLC4A4 (cg06121226), and IGH (cg13651690)--were also significantly associated with arsenic exposure.	Arsenic	144-151	solute carrier family 4 member 4	Homo sapiens	61-67
25156000-10	2015	The fact that AS3MT haplotype status modified arsenic metabolism, and in turn the arsenic-related BCC risk, supports a causal relationship between low-level arsenic exposure and BCC.	Arsenic	46-53	arsenite methyltransferase	Homo sapiens	14-19
25460635-9	2015	These results suggest in utero exposure to low levels of arsenic influences cord blood leptin concentration and presents a potential mechanism by which arsenic may impact early childhood growth.	Arsenic	57-64	leptin	Homo sapiens	87-93
25156000-10	2015	The fact that AS3MT haplotype status modified arsenic metabolism, and in turn the arsenic-related BCC risk, supports a causal relationship between low-level arsenic exposure and BCC.	Arsenic	82-89	arsenite methyltransferase	Homo sapiens	14-19
25325195-8	2015	Three additional novel methylation loci-SQSTM1 (cg01225779), SLC4A4 (cg06121226), and IGH (cg13651690)--were also significantly associated with arsenic exposure.	Arsenic	144-151	immunoglobulin heavy locus	Homo sapiens	86-89
25156000-10	2015	The fact that AS3MT haplotype status modified arsenic metabolism, and in turn the arsenic-related BCC risk, supports a causal relationship between low-level arsenic exposure and BCC.	Arsenic	82-89	arsenite methyltransferase	Homo sapiens	14-19
25460668-6	2015	RESULTS: Urinary arsenic was positively associated with expression of WRN, and negatively associated with TERF2, DKC1, TERF2IP and OBFC1 (all P&lt;0.00035, Bonferroni-corrected threshold).	Arsenic	17-24	WRN RecQ like helicase	Homo sapiens	70-73
25460668-6	2015	RESULTS: Urinary arsenic was positively associated with expression of WRN, and negatively associated with TERF2, DKC1, TERF2IP and OBFC1 (all P&lt;0.00035, Bonferroni-corrected threshold).	Arsenic	17-24	telomeric repeat binding factor 2	Homo sapiens	106-111
25460668-6	2015	RESULTS: Urinary arsenic was positively associated with expression of WRN, and negatively associated with TERF2, DKC1, TERF2IP and OBFC1 (all P&lt;0.00035, Bonferroni-corrected threshold).	Arsenic	17-24	dyskerin pseudouridine synthase 1	Homo sapiens	113-117
25413109-1	2015	The objective of this work was to investigate the interaction of arsenic species (As(III) and As(V)) with tropical peat.	Arsenic	65-72	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	94-99
25460668-6	2015	RESULTS: Urinary arsenic was positively associated with expression of WRN, and negatively associated with TERF2, DKC1, TERF2IP and OBFC1 (all P&lt;0.00035, Bonferroni-corrected threshold).	Arsenic	17-24	TERF2 interacting protein	Homo sapiens	119-126
25460668-6	2015	RESULTS: Urinary arsenic was positively associated with expression of WRN, and negatively associated with TERF2, DKC1, TERF2IP and OBFC1 (all P&lt;0.00035, Bonferroni-corrected threshold).	Arsenic	17-24	STN1 subunit of CST complex	Homo sapiens	131-136
25460668-7	2015	We detected interaction between urinary arsenic and arsenic metabolism efficiency in relation to expression of WRN (P for interaction =0.00008).	Arsenic	40-47	WRN RecQ like helicase	Homo sapiens	111-114
25787108-0	2015	Subchronic exposure to arsenic induces apoptosis in the hippocampus of the mouse brains through the Bcl-2/Bax pathway.	Arsenic	23-30	B cell leukemia/lymphoma 2	Mus musculus	100-105
26366023-1	2015	Efflux is by far the most common means of arsenic detoxification is by methylation catalyzed by a family of As(III) S-adenosylmethionine (SAM) methyltransferases (MTs) enzymes designated ArsM in microbes or AS3MT in higher eukaryotes.	Arsenic	42-49	arsenite methyltransferase	Homo sapiens	207-212
25218889-0	2015	Interaction study of arsenic (III and V) ions with metallothionein gene (MT2A) fragment.	Arsenic	21-28	metallothionein 2A	Homo sapiens	73-77
25755798-1	2015	BACKGROUND: As a susceptibility gene for AS, the polymorphsims of PTPN22 associated with disease susceptibility.	Arsenic	41-43	protein tyrosine phosphatase non-receptor type 22	Homo sapiens	66-72
25155036-6	2015	Hepatic expression of SREBP-1c was reduced in arsenic-exposed fed animals, with a 16-fold change in reduction.	Arsenic	46-53	sterol regulatory element binding transcription factor 1	Mus musculus	22-30
25438126-4	2015	In this region, water contained total arsenic concentrations up to 1250 mug L(-1), which was almost exclusively As(V).	Arsenic	38-45	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	112-117
25438126-7	2015	In urine 93% of the arsenic was found as methylated arsenic species, such as monomethylarsonic acid [MMA(V)] and dimethylarsinic acid [DMA(V)].	Arsenic	20-27	major histocompatibility complex, class II, DM alpha	Homo sapiens	135-138
25438126-8	2015	The original ingested inorganic species [As(V)], represent less than 1% of the total urinary arsenic.	Arsenic	93-100	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	41-46
25438126-10	2015	Both methylation indexes were 0.06, indicating a high biological converting capability of As(V) into MMA and then MMA into DMA, compared with the control population and other arsenic exposed populations previously reported.	Arsenic	175-182	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	90-95
26056846-2	2015	The typical method for arsenic removal from groundwater is to oxidize trivalent (As(III)) to pentavalent (As(V)) followed by the As(V) removal.	Arsenic	23-30	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	105-111
26637766-2	2015	Acute promyelocytic leukemia (APL) is characterized commonly by a fusion between the PML gene and the RARA gene, genes targetable by arsenic (ATO) and retinoic acid (ATRA), respectively.	Arsenic	133-140	PML nuclear body scaffold	Homo sapiens	85-88
26637766-2	2015	Acute promyelocytic leukemia (APL) is characterized commonly by a fusion between the PML gene and the RARA gene, genes targetable by arsenic (ATO) and retinoic acid (ATRA), respectively.	Arsenic	133-140	retinoic acid receptor alpha	Homo sapiens	102-106
25787108-0	2015	Subchronic exposure to arsenic induces apoptosis in the hippocampus of the mouse brains through the Bcl-2/Bax pathway.	Arsenic	23-30	BCL2-associated X protein	Mus musculus	106-109
25787108-12	2015	However, the expressions of the Bax gene and its protein, and the expression ratio of Bax/Bcl-2 in the hippocampus were significantly higher in the groups exposed to As than in the control group (p&lt;0.05).	Arsenic	166-168	BCL2-associated X protein	Mus musculus	32-35
25787108-12	2015	However, the expressions of the Bax gene and its protein, and the expression ratio of Bax/Bcl-2 in the hippocampus were significantly higher in the groups exposed to As than in the control group (p&lt;0.05).	Arsenic	166-168	BCL2-associated X protein	Mus musculus	86-89
25787108-12	2015	However, the expressions of the Bax gene and its protein, and the expression ratio of Bax/Bcl-2 in the hippocampus were significantly higher in the groups exposed to As than in the control group (p&lt;0.05).	Arsenic	166-168	B cell leukemia/lymphoma 2	Mus musculus	90-95
25344585-4	2015	This inhibition of AMPK by arsenic is required in part for its cytotoxic effects on primitive leukemic progenitors from patients with AML, while concomitant treatment with an AMPK activator antagonizes in vivo the arsenic-induced antileukemic effects in a xenograft AML mouse model.	Arsenic	27-34	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	19-23
25240912-6	2015	Vitamin E supplementation alleviated the toxic effects caused by arsenic on serum alanine aminotransferase and aspartate aminotransferase and lipid peroxidation.	Arsenic	65-72	aspartate aminotransferase, cytoplasmic	Capra hircus	111-137
25344585-4	2015	This inhibition of AMPK by arsenic is required in part for its cytotoxic effects on primitive leukemic progenitors from patients with AML, while concomitant treatment with an AMPK activator antagonizes in vivo the arsenic-induced antileukemic effects in a xenograft AML mouse model.	Arsenic	214-221	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	19-23
25344585-4	2015	This inhibition of AMPK by arsenic is required in part for its cytotoxic effects on primitive leukemic progenitors from patients with AML, while concomitant treatment with an AMPK activator antagonizes in vivo the arsenic-induced antileukemic effects in a xenograft AML mouse model.	Arsenic	214-221	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	175-179
25344585-6	2015	However, when AMPK expression is lost, arsenic-dependent activation of the kinase RSK downstream of MAPK activity compensates the generation of regulatory feedback signals through phosphorylation of downstream mTOR targets.	Arsenic	39-46	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	14-18
25344585-6	2015	However, when AMPK expression is lost, arsenic-dependent activation of the kinase RSK downstream of MAPK activity compensates the generation of regulatory feedback signals through phosphorylation of downstream mTOR targets.	Arsenic	39-46	ribosomal protein S6 kinase A2	Homo sapiens	82-85
25344585-6	2015	However, when AMPK expression is lost, arsenic-dependent activation of the kinase RSK downstream of MAPK activity compensates the generation of regulatory feedback signals through phosphorylation of downstream mTOR targets.	Arsenic	39-46	mechanistic target of rapamycin kinase	Homo sapiens	210-214
26411935-8	2015	We also showed that the Fosb expression level significantly increased following gestational arsenic exposure.	Arsenic	92-99	FBJ osteosarcoma oncogene B	Mus musculus	24-28
25459689-2	2015	In previous work we have developed and characterized a prenatal moderate arsenic exposure (50ppb) model and identified several deficits in learning and memory and mood disorders, as well as alterations within the glucocorticoid receptor signaling system in the adolescent mouse.	Arsenic	73-80	nuclear receptor subfamily 3, group C, member 1	Mus musculus	213-236
25459689-3	2015	In these present studies we assessed the effects of arsenic on the glucocorticoid receptor (GR) pathway in both the placenta and the fetal brain in response at two critical periods, embryonic days 14 and 18.	Arsenic	52-59	nuclear receptor subfamily 3, group C, member 1	Mus musculus	67-90
25459689-3	2015	In these present studies we assessed the effects of arsenic on the glucocorticoid receptor (GR) pathway in both the placenta and the fetal brain in response at two critical periods, embryonic days 14 and 18.	Arsenic	52-59	nuclear receptor subfamily 3, group C, member 1	Mus musculus	92-94
26411936-2	2015	Genetic polymorphisms such as single nucleotide polymorphisms (SNPs) in arsenic (+3 oxidation state) methyltransferase (AS3MT), which can methylate arsenic compounds using S-adenosyl-l-methionine (AdoMet), have been reported to modify arsenic methylation.	Arsenic	72-79	arsenite methyltransferase	Homo sapiens	120-125
25459689-6	2015	At E14 we found arsenic exposure significantly decreased expression of both protein and message in brain of GR and the 11beta-HSD1, while 11beta-HSD2 enzyme protein levels were increased but mRNA levels were decreased in the brain.	Arsenic	16-23	nuclear receptor subfamily 3, group C, member 1	Mus musculus	108-110
26411936-2	2015	Genetic polymorphisms such as single nucleotide polymorphisms (SNPs) in arsenic (+3 oxidation state) methyltransferase (AS3MT), which can methylate arsenic compounds using S-adenosyl-l-methionine (AdoMet), have been reported to modify arsenic methylation.	Arsenic	148-155	arsenite methyltransferase	Homo sapiens	72-118
25459689-6	2015	At E14 we found arsenic exposure significantly decreased expression of both protein and message in brain of GR and the 11beta-HSD1, while 11beta-HSD2 enzyme protein levels were increased but mRNA levels were decreased in the brain.	Arsenic	16-23	hydroxysteroid 11-beta dehydrogenase 1	Mus musculus	119-130
25459689-10	2015	This suggests that arsenic exposure may alter GR expression levels as a consequence of a prolonged developmental imbalance between 11beta-HSD1 and 11beta-HSD2 protein expression despite decreased 11HSDB2 mRNA.	Arsenic	19-26	nuclear receptor subfamily 3, group C, member 1	Mus musculus	46-48
26411936-2	2015	Genetic polymorphisms such as single nucleotide polymorphisms (SNPs) in arsenic (+3 oxidation state) methyltransferase (AS3MT), which can methylate arsenic compounds using S-adenosyl-l-methionine (AdoMet), have been reported to modify arsenic methylation.	Arsenic	148-155	arsenite methyltransferase	Homo sapiens	120-125
25459689-10	2015	This suggests that arsenic exposure may alter GR expression levels as a consequence of a prolonged developmental imbalance between 11beta-HSD1 and 11beta-HSD2 protein expression despite decreased 11HSDB2 mRNA.	Arsenic	19-26	hydroxysteroid 11-beta dehydrogenase 1	Mus musculus	131-142
26411936-3	2015	In this review, we summarize studies conducted by us in Vietnam and by others on the association of AS3MT genetic polymorphisms with arsenic metabolism as well as human health effects.	Arsenic	133-140	arsenite methyltransferase	Homo sapiens	100-105
25459689-10	2015	This suggests that arsenic exposure may alter GR expression levels as a consequence of a prolonged developmental imbalance between 11beta-HSD1 and 11beta-HSD2 protein expression despite decreased 11HSDB2 mRNA.	Arsenic	19-26	hydroxysteroid 11-beta dehydrogenase 2	Mus musculus	147-158
26411936-4	2015	Most of the SNPs in AS3MT showed inconsistent results in terms of genotype-dependent differences in arsenic metabolism among the studies.	Arsenic	100-107	arsenite methyltransferase	Homo sapiens	20-25
25868784-5	2015	Silibinin with 0.5 or 5 microM arsenic induced G1 or G2/M phase arrest, respectively, and decreased the protein levels of CDK2, -4, and -6 and cyclin D1, D3, and E and increased CDK inhibitors p21 and p27.	Arsenic	31-38	cyclin dependent kinase 2	Homo sapiens	122-138
25868784-5	2015	Silibinin with 0.5 or 5 microM arsenic induced G1 or G2/M phase arrest, respectively, and decreased the protein levels of CDK2, -4, and -6 and cyclin D1, D3, and E and increased CDK inhibitors p21 and p27.	Arsenic	31-38	cyclin D1	Homo sapiens	143-152
25868784-6	2015	Arsenic alone increased cyclin B1 level and Cdc2 kinase activity which were reduced in silibinin combination.	Arsenic	0-7	cyclin B1	Homo sapiens	24-33
26411936-5	2015	However, AS3MT 12390 (rs3740393) and 14458 (rs11191439) were consistently related to arsenic methylation regardless of the study population: AS3MT 12390 (rs3740393) affected the second step of methylation of arsenic, whereas 14458 (rs11191439) affected the first methylation step.	Arsenic	85-92	arsenite methyltransferase	Homo sapiens	9-14
26411936-5	2015	However, AS3MT 12390 (rs3740393) and 14458 (rs11191439) were consistently related to arsenic methylation regardless of the study population: AS3MT 12390 (rs3740393) affected the second step of methylation of arsenic, whereas 14458 (rs11191439) affected the first methylation step.	Arsenic	85-92	arsenite methyltransferase	Homo sapiens	141-146
26411936-5	2015	However, AS3MT 12390 (rs3740393) and 14458 (rs11191439) were consistently related to arsenic methylation regardless of the study population: AS3MT 12390 (rs3740393) affected the second step of methylation of arsenic, whereas 14458 (rs11191439) affected the first methylation step.	Arsenic	208-215	arsenite methyltransferase	Homo sapiens	141-146
25448440-4	2014	The purpose of this study was to investigate whether arsenic can disrupt Shh signaling in P19 mouse embryonic stem cells, leading to changes muscle and neuronal cell differentiation.	Arsenic	53-60	sonic hedgehog	Mus musculus	73-76
25288670-0	2015	Exposure to As-, Cd-, and Pb-mixture induces Abeta, amyloidogenic APP processing and cognitive impairments via oxidative stress-dependent neuroinflammation in young rats.	Arsenic	12-15	amyloid beta precursor protein	Rattus norvegicus	45-50
25598836-0	2014	Arsenic exposure is associated with DNA hypermethylation of the tumor suppressor gene p16.	Arsenic	0-7	cyclin dependent kinase inhibitor 2A	Homo sapiens	86-89
25598836-3	2014	Laboratory studies suggest that arsenic is a poor mutagen but may cause epigenetic silencing of key tumor suppressor genes such as p16 through DNA hypermethylation.	Arsenic	32-39	cyclin dependent kinase inhibitor 2A	Homo sapiens	131-134
25598836-7	2014	Conditional logistic regression analysis showed that DNA hypermethylation of p16 gene was significantly associated with high arsenic exposure (Odds Ratio = 10.0, P = 0.0019) independently of the development of arsenicosis (Odds Ratio = 2.0, P = 0.1343).	Arsenic	125-132	cyclin dependent kinase inhibitor 2A	Homo sapiens	77-80
25598836-8	2014	CONCLUSIONS: High exposure of arsenic in human is positively linked to DNA hypermethylation of p16 gene, suggesting that epigenetic silencing of key tumor suppressor may be an important mechanism by which arsenic promotes cancer initiation.	Arsenic	30-37	cyclin dependent kinase inhibitor 2A	Homo sapiens	95-98
25598836-8	2014	CONCLUSIONS: High exposure of arsenic in human is positively linked to DNA hypermethylation of p16 gene, suggesting that epigenetic silencing of key tumor suppressor may be an important mechanism by which arsenic promotes cancer initiation.	Arsenic	205-212	cyclin dependent kinase inhibitor 2A	Homo sapiens	95-98
25425339-1	2014	Bioreduction of As(V) and As-bearing iron oxides is considered to be one of the key processes leading to arsenic pollution in groundwaters in South and Southeast Asia.	Arsenic	105-112	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	16-21
25425339-3	2014	The aim of the present study was to follow arsenic speciation during the abiotic Fe(II)-induced transformation of As(III)- and As(V)-doped lepidocrocite to magnetite, and to evaluate the influence of arsenic on the transformation kinetics and pathway.	Arsenic	43-50	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	127-132
25448440-10	2014	Moreover, additional extracellular SHH rescued the inhibitory effects of arsenic on cellular differentiation due to an increase in GLI binding activity.	Arsenic	73-80	sonic hedgehog signaling molecule	Homo sapiens	35-38
25448440-10	2014	Moreover, additional extracellular SHH rescued the inhibitory effects of arsenic on cellular differentiation due to an increase in GLI binding activity.	Arsenic	73-80	GLI family zinc finger 1	Homo sapiens	131-134
25448440-11	2014	Taken together, we conclude that arsenic exposure affected Shh signaling, ultimately decreasing the expression of the Gli2 transcription factor.	Arsenic	33-40	sonic hedgehog signaling molecule	Homo sapiens	59-62
25448440-11	2014	Taken together, we conclude that arsenic exposure affected Shh signaling, ultimately decreasing the expression of the Gli2 transcription factor.	Arsenic	33-40	GLI family zinc finger 2	Homo sapiens	118-122
25227780-0	2014	DNA fragmentation, caspase 3 and prostate-specific antigen genes expression induced by arsenic, cadmium, and chromium on nontumorigenic human prostate cells.	Arsenic	87-94	caspase 3	Homo sapiens	19-28
25258343-8	2014	Thus, APL differentiation is a default program triggered by clearance of PML/RARA-bound promoters, rather than obligatory active transcriptional activation, explaining how arsenic elicits APL maturation through PML/RARA degradation.	Arsenic	172-179	PML nuclear body scaffold	Homo sapiens	73-76
25258343-8	2014	Thus, APL differentiation is a default program triggered by clearance of PML/RARA-bound promoters, rather than obligatory active transcriptional activation, explaining how arsenic elicits APL maturation through PML/RARA degradation.	Arsenic	172-179	retinoic acid receptor alpha	Homo sapiens	77-81
25258343-8	2014	Thus, APL differentiation is a default program triggered by clearance of PML/RARA-bound promoters, rather than obligatory active transcriptional activation, explaining how arsenic elicits APL maturation through PML/RARA degradation.	Arsenic	172-179	PML nuclear body scaffold	Homo sapiens	211-214
25258343-8	2014	Thus, APL differentiation is a default program triggered by clearance of PML/RARA-bound promoters, rather than obligatory active transcriptional activation, explaining how arsenic elicits APL maturation through PML/RARA degradation.	Arsenic	172-179	retinoic acid receptor alpha	Homo sapiens	215-219
25479081-0	2014	Prenatal exposure to arsenic and cadmium impacts infectious disease-related genes within the glucocorticoid receptor signal transduction pathway.	Arsenic	21-28	nuclear receptor subfamily 3 group C member 1	Homo sapiens	93-116
25463133-13	2014	Also, MPO/PON1 ratio may be a predictor of AS.	Arsenic	43-45	myeloperoxidase	Mus musculus	6-9
25463133-13	2014	Also, MPO/PON1 ratio may be a predictor of AS.	Arsenic	43-45	paraoxonase 1	Mus musculus	10-14
25464340-11	2014	Furthermore, ACR2 does not interact epistatically with HAC1, since arsenic metabolism in the acr2 hac1 double mutant is disrupted in an identical manner to that described for the hac1 single mutant.	Arsenic	67-74	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	93-97
25227780-0	2014	DNA fragmentation, caspase 3 and prostate-specific antigen genes expression induced by arsenic, cadmium, and chromium on nontumorigenic human prostate cells.	Arsenic	87-94	kallikrein related peptidase 3	Homo sapiens	33-58
25319007-4	2014	Although DR expression was similar in the cerebral cortex of As-treated mice, DRD1 to DRD4 expression significantly increased in the striatum of 100 mg/L As-exposed mice.	Arsenic	154-156	dopamine receptor D1	Mus musculus	78-82
25227780-3	2014	This in vitro study demonstrates the relative death sensitivity of prostatic (RWPE-1) cells to arsenic (As), cadmium (Cd), and chromium (Cr) as environmental pollutants through its apoptotic effects and the effect of these chemicals on prostate-specific antigen (PSA) gene expression as a marker for their carcinogecity.	Arsenic	95-102	kallikrein related peptidase 3	Homo sapiens	236-267
25273567-12	2014	Mice lacking LXRalpha are resistant to arsenic-enhanced atherosclerosis, but arsenic-exposed LXRalpha(-/-)apoE(-/-) mice still present a different plaque composition pattern than the arsenic-exposed apoE(-/-) mice.	Arsenic	77-84	nuclear receptor subfamily 1, group H, member 3	Mus musculus	93-101
25319007-4	2014	Although DR expression was similar in the cerebral cortex of As-treated mice, DRD1 to DRD4 expression significantly increased in the striatum of 100 mg/L As-exposed mice.	Arsenic	154-156	dopamine receptor D4	Mus musculus	86-90
25241017-0	2014	Arsenic methylation capacity and obesity are associated with insulin resistance in obese children and adolescents.	Arsenic	0-7	insulin	Homo sapiens	61-68
25229165-1	2014	Arsenic has wide-ranging effects on human health and there is evidence that it alters the immune response by influencing CD4+/CD8+ T cell ratios, IL-2 cytokine levels, and the expression of immune-response genes.	Arsenic	0-7	CD4 molecule	Homo sapiens	121-124
25229165-1	2014	Arsenic has wide-ranging effects on human health and there is evidence that it alters the immune response by influencing CD4+/CD8+ T cell ratios, IL-2 cytokine levels, and the expression of immune-response genes.	Arsenic	0-7	CD8a molecule	Homo sapiens	126-129
25229165-1	2014	Arsenic has wide-ranging effects on human health and there is evidence that it alters the immune response by influencing CD4+/CD8+ T cell ratios, IL-2 cytokine levels, and the expression of immune-response genes.	Arsenic	0-7	interleukin 2	Homo sapiens	146-150
25229165-3	2014	Our results showed that maternal urinary arsenic concentrations were inversely related to absolute total CD45RA+ CD4+ cord blood CD69+ T cell counts (N=116, p=0.04) and positively associated with CD45RA+ CD69- CD294+ cell counts (p=0.01).	Arsenic	41-48	CD4 molecule	Homo sapiens	105-108
25229165-3	2014	Our results showed that maternal urinary arsenic concentrations were inversely related to absolute total CD45RA+ CD4+ cord blood CD69+ T cell counts (N=116, p=0.04) and positively associated with CD45RA+ CD69- CD294+ cell counts (p=0.01).	Arsenic	41-48	CD69 molecule	Homo sapiens	129-133
25229165-3	2014	Our results showed that maternal urinary arsenic concentrations were inversely related to absolute total CD45RA+ CD4+ cord blood CD69+ T cell counts (N=116, p=0.04) and positively associated with CD45RA+ CD69- CD294+ cell counts (p=0.01).	Arsenic	41-48	CD69 molecule	Homo sapiens	204-208
25229165-3	2014	Our results showed that maternal urinary arsenic concentrations were inversely related to absolute total CD45RA+ CD4+ cord blood CD69+ T cell counts (N=116, p=0.04) and positively associated with CD45RA+ CD69- CD294+ cell counts (p=0.01).	Arsenic	41-48	prostaglandin D2 receptor 2	Homo sapiens	210-215
25229165-4	2014	In placental samples (N=70), higher in utero urinary arsenic concentrations were positively associated with the expression of IL1beta (p=0.03).	Arsenic	53-60	interleukin 1 beta	Homo sapiens	126-133
25273566-0	2014	Silencing KRAS overexpression in arsenic-transformed prostate epithelial and stem cells partially mitigates malignant phenotype.	Arsenic	33-40	KRAS proto-oncogene, GTPase	Homo sapiens	10-14
25273566-5	2014	Thus, we hypothesize KRAS activation is key in causing and maintaining an arsenic-induced malignant phenotype, and hence, KRAS knockdown (KD) may reverse this malignant phenotype.	Arsenic	74-81	KRAS proto-oncogene, GTPase	Homo sapiens	21-25
25273566-8	2014	KRAS KD decreased phosphorylated ERK, indicating inhibition of RAS/ERK signaling, a proliferation/survival pathway activated with arsenic transformation.	Arsenic	130-137	KRAS proto-oncogene, GTPase	Homo sapiens	0-4
25273566-8	2014	KRAS KD decreased phosphorylated ERK, indicating inhibition of RAS/ERK signaling, a proliferation/survival pathway activated with arsenic transformation.	Arsenic	130-137	mitogen-activated protein kinase 1	Homo sapiens	33-36
25273566-8	2014	KRAS KD decreased phosphorylated ERK, indicating inhibition of RAS/ERK signaling, a proliferation/survival pathway activated with arsenic transformation.	Arsenic	130-137	mitogen-activated protein kinase 1	Homo sapiens	67-70
25273566-9	2014	Secreted metalloproteinase (MMP) activity was increased by arsenic-induced malignant transformation, but KRAS KD from 4 weeks on decreased secreted MMP-9 activity by 50% in As-CSCs.	Arsenic	59-66	matrix metallopeptidase 9	Homo sapiens	28-31
25273566-14	2014	Thus, KRAS silencing impacts aspects of arsenic-induced malignant phenotype, inducing loss of many typical cancer characteristics particularly in As-CSCs.	Arsenic	40-47	KRAS proto-oncogene, GTPase	Homo sapiens	6-10
25273567-0	2014	Genetic deletion of LXRalpha prevents arsenic-enhanced atherosclerosis, but not arsenic-altered plaque composition.	Arsenic	38-45	nuclear receptor subfamily 1, group H, member 3	Mus musculus	20-28
25273567-4	2014	Indeed, deletion of LXRalpha protected apoE(-/-) mice against the proatherogenic effects of arsenic.	Arsenic	92-99	nuclear receptor subfamily 1, group H, member 3	Mus musculus	20-28
25273567-12	2014	Mice lacking LXRalpha are resistant to arsenic-enhanced atherosclerosis, but arsenic-exposed LXRalpha(-/-)apoE(-/-) mice still present a different plaque composition pattern than the arsenic-exposed apoE(-/-) mice.	Arsenic	77-84	apolipoprotein E	Mus musculus	106-110
25273567-4	2014	Indeed, deletion of LXRalpha protected apoE(-/-) mice against the proatherogenic effects of arsenic.	Arsenic	92-99	apolipoprotein E	Mus musculus	39-43
25273567-5	2014	We have previously shown that arsenic changes the plaque composition in apoE(-/-) mice.	Arsenic	30-37	apolipoprotein E	Mus musculus	72-76
25273567-12	2014	Mice lacking LXRalpha are resistant to arsenic-enhanced atherosclerosis, but arsenic-exposed LXRalpha(-/-)apoE(-/-) mice still present a different plaque composition pattern than the arsenic-exposed apoE(-/-) mice.	Arsenic	77-84	apolipoprotein E	Mus musculus	199-203
25273567-6	2014	Arsenic decreased collagen content in the apoE(-/-) model, and we have observed the same diminution in LXRalpha(-/-)apoE(-/-) mice.	Arsenic	0-7	apolipoprotein E	Mus musculus	42-46
25273567-12	2014	Mice lacking LXRalpha are resistant to arsenic-enhanced atherosclerosis, but arsenic-exposed LXRalpha(-/-)apoE(-/-) mice still present a different plaque composition pattern than the arsenic-exposed apoE(-/-) mice.	Arsenic	77-84	nuclear receptor subfamily 1, group H, member 3	Mus musculus	93-101
25273567-8	2014	Although transcriptional activation of collagen remained the same in SMC from both genotypes, arsenic-exposed LXRalpha(-/-)apoE(-/-) plaques had increased matrix metalloproteinase activity compared with both control LXRalpha(-/-)apoE(-/-) and apoE(-/-), which could be responsible for both the decrease in plaque collagen and the SMC invasion.	Arsenic	94-101	nuclear receptor subfamily 1, group H, member 3	Mus musculus	110-118
25273567-12	2014	Mice lacking LXRalpha are resistant to arsenic-enhanced atherosclerosis, but arsenic-exposed LXRalpha(-/-)apoE(-/-) mice still present a different plaque composition pattern than the arsenic-exposed apoE(-/-) mice.	Arsenic	77-84	apolipoprotein E	Mus musculus	106-110
25273567-8	2014	Although transcriptional activation of collagen remained the same in SMC from both genotypes, arsenic-exposed LXRalpha(-/-)apoE(-/-) plaques had increased matrix metalloproteinase activity compared with both control LXRalpha(-/-)apoE(-/-) and apoE(-/-), which could be responsible for both the decrease in plaque collagen and the SMC invasion.	Arsenic	94-101	apolipoprotein E	Mus musculus	123-127
25273567-8	2014	Although transcriptional activation of collagen remained the same in SMC from both genotypes, arsenic-exposed LXRalpha(-/-)apoE(-/-) plaques had increased matrix metalloproteinase activity compared with both control LXRalpha(-/-)apoE(-/-) and apoE(-/-), which could be responsible for both the decrease in plaque collagen and the SMC invasion.	Arsenic	94-101	nuclear receptor subfamily 1, group H, member 3	Mus musculus	216-224
25273567-12	2014	Mice lacking LXRalpha are resistant to arsenic-enhanced atherosclerosis, but arsenic-exposed LXRalpha(-/-)apoE(-/-) mice still present a different plaque composition pattern than the arsenic-exposed apoE(-/-) mice.	Arsenic	77-84	apolipoprotein E	Mus musculus	199-203
25273567-8	2014	Although transcriptional activation of collagen remained the same in SMC from both genotypes, arsenic-exposed LXRalpha(-/-)apoE(-/-) plaques had increased matrix metalloproteinase activity compared with both control LXRalpha(-/-)apoE(-/-) and apoE(-/-), which could be responsible for both the decrease in plaque collagen and the SMC invasion.	Arsenic	94-101	apolipoprotein E	Mus musculus	229-233
25273567-8	2014	Although transcriptional activation of collagen remained the same in SMC from both genotypes, arsenic-exposed LXRalpha(-/-)apoE(-/-) plaques had increased matrix metalloproteinase activity compared with both control LXRalpha(-/-)apoE(-/-) and apoE(-/-), which could be responsible for both the decrease in plaque collagen and the SMC invasion.	Arsenic	94-101	apolipoprotein E	Mus musculus	229-233
25173797-5	2014	In addition, the dysregulation of other molecular targets such as nuclear factor kappa B, Hippo signaling protein Yap, and the mineral dust-induced proto-oncogene may orchestrate the pathogenesis of arsenic-mediated health effects.	Arsenic	199-206	Yes1 associated transcriptional regulator	Homo sapiens	114-117
25402141-0	2014	Effects of gamma-ray irradiation on optical absorption and laser damage performance of KDP crystals containing arsenic impurities.	Arsenic	111-118	WNK lysine deficient protein kinase 1	Homo sapiens	87-90
25257954-3	2014	We found the concentrations of IL-8, TNF-alpha, and TGF-alpha presented in urine were significantly elevated in the high urinary arsenic workers compared with the low urinary arsenic workers.	Arsenic	129-136	C-X-C motif chemokine ligand 8	Homo sapiens	31-35
25257954-3	2014	We found the concentrations of IL-8, TNF-alpha, and TGF-alpha presented in urine were significantly elevated in the high urinary arsenic workers compared with the low urinary arsenic workers.	Arsenic	129-136	tumor necrosis factor	Homo sapiens	37-46
25257954-3	2014	We found the concentrations of IL-8, TNF-alpha, and TGF-alpha presented in urine were significantly elevated in the high urinary arsenic workers compared with the low urinary arsenic workers.	Arsenic	129-136	transforming growth factor alpha	Homo sapiens	52-61
25257954-8	2014	These data indicated that arsenic increased the secretion of inflammatory factors and IL-8, TNF-alpha, and TGF-alpha expression may be a useful biomarker of the effect of arsenic exposure.	Arsenic	26-33	C-X-C motif chemokine ligand 8	Homo sapiens	86-90
25257954-8	2014	These data indicated that arsenic increased the secretion of inflammatory factors and IL-8, TNF-alpha, and TGF-alpha expression may be a useful biomarker of the effect of arsenic exposure.	Arsenic	26-33	tumor necrosis factor	Homo sapiens	92-101
25257954-8	2014	These data indicated that arsenic increased the secretion of inflammatory factors and IL-8, TNF-alpha, and TGF-alpha expression may be a useful biomarker of the effect of arsenic exposure.	Arsenic	26-33	transforming growth factor alpha	Homo sapiens	107-116
25257954-8	2014	These data indicated that arsenic increased the secretion of inflammatory factors and IL-8, TNF-alpha, and TGF-alpha expression may be a useful biomarker of the effect of arsenic exposure.	Arsenic	171-178	C-X-C motif chemokine ligand 8	Homo sapiens	86-90
25257954-8	2014	These data indicated that arsenic increased the secretion of inflammatory factors and IL-8, TNF-alpha, and TGF-alpha expression may be a useful biomarker of the effect of arsenic exposure.	Arsenic	171-178	transforming growth factor alpha	Homo sapiens	107-116
25281835-8	2014	We have found that arsenic alters epigenetic regulation of SIRT1 expression via structural reorganisation of chromatin at the miR-34a gene promoter in the initial 24h of exposure; and over time, through shifts in miR-34a and SIRT1 gene methylation.	Arsenic	19-26	sirtuin 1	Homo sapiens	59-64
25281835-8	2014	We have found that arsenic alters epigenetic regulation of SIRT1 expression via structural reorganisation of chromatin at the miR-34a gene promoter in the initial 24h of exposure; and over time, through shifts in miR-34a and SIRT1 gene methylation.	Arsenic	19-26	microRNA 34a	Homo sapiens	126-133
25281835-0	2014	Arsenic exposure disrupts epigenetic regulation of SIRT1 in human keratinocytes.	Arsenic	0-7	sirtuin 1	Homo sapiens	51-56
25281835-8	2014	We have found that arsenic alters epigenetic regulation of SIRT1 expression via structural reorganisation of chromatin at the miR-34a gene promoter in the initial 24h of exposure; and over time, through shifts in miR-34a and SIRT1 gene methylation.	Arsenic	19-26	microRNA 34a	Homo sapiens	213-220
25281835-3	2014	Expression of the histone deacetylase SIRT1 is altered in solid tumours and haematological malignancies; however its role in arsenic-induced pathology is unknown.	Arsenic	125-132	sirtuin 1	Homo sapiens	38-43
25281835-8	2014	We have found that arsenic alters epigenetic regulation of SIRT1 expression via structural reorganisation of chromatin at the miR-34a gene promoter in the initial 24h of exposure; and over time, through shifts in miR-34a and SIRT1 gene methylation.	Arsenic	19-26	sirtuin 1	Homo sapiens	225-230
25281835-4	2014	In this study we investigated the effect of arsenic on epigenetic regulation of SIRT1 and its targeting microRNA, miR-34a in primary human keratinocytes.	Arsenic	44-51	sirtuin 1	Homo sapiens	80-85
25281835-9	2014	Taken together, this investigation demonstrates that arsenic produces cumulative disruptions to epigenetic regulation of miR-34a expression, and this is associated with impaired coordination of SIRT1 functional activity.	Arsenic	53-60	microRNA 34a	Homo sapiens	121-128
25281835-4	2014	In this study we investigated the effect of arsenic on epigenetic regulation of SIRT1 and its targeting microRNA, miR-34a in primary human keratinocytes.	Arsenic	44-51	microRNA 34a	Homo sapiens	114-121
25201354-5	2014	In one strategy, acute arsenic exposure (20 muM, 24 h) was applied, as MAPK signaling is generally considered to be transient.	Arsenic	23-30	mitogen-activated protein kinase 3	Homo sapiens	71-75
25266719-0	2014	Arsenic induces polyadenylation of canonical histone mRNA by down-regulating stem-loop-binding protein gene expression.	Arsenic	0-7	stem-loop binding protein	Homo sapiens	77-102
25266719-4	2014	Here we report that exposure to arsenic, a carcinogenic metal, decreased cellular levels of SLBP by inducing its proteasomal degradation and inhibiting SLBP transcription via epigenetic mechanisms.	Arsenic	32-39	stem-loop binding protein	Homo sapiens	92-96
25266719-4	2014	Here we report that exposure to arsenic, a carcinogenic metal, decreased cellular levels of SLBP by inducing its proteasomal degradation and inhibiting SLBP transcription via epigenetic mechanisms.	Arsenic	32-39	stem-loop binding protein	Homo sapiens	152-156
25266719-5	2014	Notably, arsenic exposure dramatically increased polyadenylation of canonical histone H3.1 mRNA possibly through down-regulation of SLBP expression.	Arsenic	9-16	stem-loop binding protein	Homo sapiens	132-136
25452698-6	2014	Gene neighborhood analysis of the arsenic resistance operon in the genome of Bacteroides thetaiotaomicron VPI-5482, a human gut symbiont, revealed the adjacent arrangement of genes for arsenite binding/transfer (ArsD) and cytochrome c biosynthesis (DsbD_2).	Arsenic	34-41	arylsulfatase D	Homo sapiens	212-216
25452698-6	2014	Gene neighborhood analysis of the arsenic resistance operon in the genome of Bacteroides thetaiotaomicron VPI-5482, a human gut symbiont, revealed the adjacent arrangement of genes for arsenite binding/transfer (ArsD) and cytochrome c biosynthesis (DsbD_2).	Arsenic	34-41	cytochrome c, somatic	Homo sapiens	222-234
25201354-7	2014	We found that acute arsenic exposure activated extracellular signal-regulated 1/2 kinases (ERK1/2) and c-Jun N-terminal kinase (JNK) in parallel with increased transcription and nuclear translocation of factor-erythroid 2-related factor 2 (NRF2) and enhanced expression of gamma-glutamyl cysteine ligase catalytic subunit (GCLC), resulting in elevated intracellular GSH levels.	Arsenic	20-27	mitogen-activated protein kinase 3	Homo sapiens	91-97
25201354-7	2014	We found that acute arsenic exposure activated extracellular signal-regulated 1/2 kinases (ERK1/2) and c-Jun N-terminal kinase (JNK) in parallel with increased transcription and nuclear translocation of factor-erythroid 2-related factor 2 (NRF2) and enhanced expression of gamma-glutamyl cysteine ligase catalytic subunit (GCLC), resulting in elevated intracellular GSH levels.	Arsenic	20-27	mitogen-activated protein kinase 8	Homo sapiens	103-126
25201354-7	2014	We found that acute arsenic exposure activated extracellular signal-regulated 1/2 kinases (ERK1/2) and c-Jun N-terminal kinase (JNK) in parallel with increased transcription and nuclear translocation of factor-erythroid 2-related factor 2 (NRF2) and enhanced expression of gamma-glutamyl cysteine ligase catalytic subunit (GCLC), resulting in elevated intracellular GSH levels.	Arsenic	20-27	mitogen-activated protein kinase 8	Homo sapiens	128-131
25201354-7	2014	We found that acute arsenic exposure activated extracellular signal-regulated 1/2 kinases (ERK1/2) and c-Jun N-terminal kinase (JNK) in parallel with increased transcription and nuclear translocation of factor-erythroid 2-related factor 2 (NRF2) and enhanced expression of gamma-glutamyl cysteine ligase catalytic subunit (GCLC), resulting in elevated intracellular GSH levels.	Arsenic	20-27	NFE2 like bZIP transcription factor 2	Homo sapiens	240-244
25201354-7	2014	We found that acute arsenic exposure activated extracellular signal-regulated 1/2 kinases (ERK1/2) and c-Jun N-terminal kinase (JNK) in parallel with increased transcription and nuclear translocation of factor-erythroid 2-related factor 2 (NRF2) and enhanced expression of gamma-glutamyl cysteine ligase catalytic subunit (GCLC), resulting in elevated intracellular GSH levels.	Arsenic	20-27	glutamate-cysteine ligase catalytic subunit	Homo sapiens	273-321
25201354-7	2014	We found that acute arsenic exposure activated extracellular signal-regulated 1/2 kinases (ERK1/2) and c-Jun N-terminal kinase (JNK) in parallel with increased transcription and nuclear translocation of factor-erythroid 2-related factor 2 (NRF2) and enhanced expression of gamma-glutamyl cysteine ligase catalytic subunit (GCLC), resulting in elevated intracellular GSH levels.	Arsenic	20-27	glutamate-cysteine ligase catalytic subunit	Homo sapiens	323-327
25201354-8	2014	Specific ERK inhibitor abolished arsenic-induced NRF2 nuclear translocation and GSH synthesis.	Arsenic	33-40	mitogen-activated protein kinase 1	Homo sapiens	9-12
25201354-8	2014	Specific ERK inhibitor abolished arsenic-induced NRF2 nuclear translocation and GSH synthesis.	Arsenic	33-40	NFE2 like bZIP transcription factor 2	Homo sapiens	49-53
25201354-9	2014	During chronic arsenic exposure which induced a malignant cellular phenotype, continuous p38 activation and NRF2 nuclear translocation were observed with enhanced GSH synthesis.	Arsenic	15-22	mitogen-activated protein kinase 1	Homo sapiens	89-92
25201354-9	2014	During chronic arsenic exposure which induced a malignant cellular phenotype, continuous p38 activation and NRF2 nuclear translocation were observed with enhanced GSH synthesis.	Arsenic	15-22	NFE2 like bZIP transcription factor 2	Homo sapiens	108-112
25201354-10	2014	Specific p38 inhibitor attenuated arsenic-enhanced GSH synthesis without changing NRF2 nuclear translocation.	Arsenic	34-41	mitogen-activated protein kinase 1	Homo sapiens	9-12
25201354-11	2014	Taken together, our results indicate MAPK pathways play an important role in cellular GSH homeostasis in response to arsenic.	Arsenic	117-124	mitogen-activated protein kinase 3	Homo sapiens	37-41
25201354-12	2014	However, the specific activation of certain MAPK is different between acute and chronic arsenic exposure.	Arsenic	88-95	mitogen-activated protein kinase 3	Homo sapiens	44-48
25201354-13	2014	Furthermore, it appears that during chronic arsenic exposure, GSH synthesis is regulated by p38 at least in part independent of NRF2.	Arsenic	44-51	mitogen-activated protein kinase 1	Homo sapiens	92-95
25201354-13	2014	Furthermore, it appears that during chronic arsenic exposure, GSH synthesis is regulated by p38 at least in part independent of NRF2.	Arsenic	44-51	NFE2 like bZIP transcription factor 2	Homo sapiens	128-132
25092648-0	2014	Arsenic exposure disrupts the normal function of the FA/BRCA repair pathway.	Arsenic	0-7	BRCA1 DNA repair associated	Homo sapiens	56-60
25194983-5	2014	The results suggested that DMPS competitively coordinated with As(3+) and monomethylarsonous acid (MMA(3+)) to inhibit the up-regulation of arsenic on the expression of hAS3MT and block arsenic involving in the enzymatic methylation.	Arsenic	140-147	PDS5 cohesin associated factor B	Homo sapiens	169-173
25568664-8	2014	The activation of STAT5 was reduced upon the exposure to Arsenic which was accompanied by apoptosis in both PML/RARalpha- and DEK/NUP214-positive leukemic cells.	Arsenic	57-64	signal transducer and activator of transcription 5A	Homo sapiens	18-23
25568664-8	2014	The activation of STAT5 was reduced upon the exposure to Arsenic which was accompanied by apoptosis in both PML/RARalpha- and DEK/NUP214-positive leukemic cells.	Arsenic	57-64	PML nuclear body scaffold	Homo sapiens	108-111
25568664-8	2014	The activation of STAT5 was reduced upon the exposure to Arsenic which was accompanied by apoptosis in both PML/RARalpha- and DEK/NUP214-positive leukemic cells.	Arsenic	57-64	retinoic acid receptor alpha	Homo sapiens	112-129
25568664-8	2014	The activation of STAT5 was reduced upon the exposure to Arsenic which was accompanied by apoptosis in both PML/RARalpha- and DEK/NUP214-positive leukemic cells.	Arsenic	57-64	nucleoporin 214	Homo sapiens	130-136
25395130-3	2014	As-PC were detected from As(PC2) to As(PC5) with an increasing number of isomers that differ in the position of thiol groups bound to As.	Arsenic	0-2	chromobox 4	Homo sapiens	28-31
25395130-3	2014	As-PC were detected from As(PC2) to As(PC5) with an increasing number of isomers that differ in the position of thiol groups bound to As.	Arsenic	0-2	proprotein convertase subtilisin/kexin type 5	Homo sapiens	39-42
25092648-8	2014	Overall, our data demonstrate that environmentally relevant arsenic exposures disrupt the normal function of the FA/BRCA activity, supporting a novel source of arsenic co- and carcinogenic effects.	Arsenic	60-67	BRCA1 DNA repair associated	Homo sapiens	116-120
25092648-8	2014	Overall, our data demonstrate that environmentally relevant arsenic exposures disrupt the normal function of the FA/BRCA activity, supporting a novel source of arsenic co- and carcinogenic effects.	Arsenic	160-167	BRCA1 DNA repair associated	Homo sapiens	116-120
25092648-9	2014	This is the first study linking arsenic exposure with the FA/BRCA DNA repair pathway.	Arsenic	32-39	BRCA1 DNA repair associated	Homo sapiens	61-65
25299175-5	2014	The distribution, diversity and abundance of functional genes (including arsC, arrA, aioA, arsB and ACR3) were much higher for the samples containing higher As and Sb concentrations.	Arsenic	157-159	steroid sulfatase	Homo sapiens	73-77
25349987-1	2014	Arsenic (III) methyltransferase (AS3MT) is a cysteine (Cys)-rich enzyme that catalyzes the biomethylation of arsenic.	Arsenic	109-116	arsenite methyltransferase	Homo sapiens	33-38
25349987-8	2014	In recovery experiments, we confirmed that trivalent arsenicals were substrates for hAS3MT, methylation of arsenic occurred on the enzyme, and an intramolecular disulfide bond might be formed after iAs3+ was methylated to dimethylarsinous acid (DMA3+).	Arsenic	53-60	arsenite methyltransferase	Homo sapiens	84-90
25218292-9	2014	Arsenic down-regulated eNOS and up-regulated iNOS protein expression and increased basal NO and 3-nitrotyrosine level.	Arsenic	0-7	nitric oxide synthase 3	Rattus norvegicus	23-27
25218292-9	2014	Arsenic down-regulated eNOS and up-regulated iNOS protein expression and increased basal NO and 3-nitrotyrosine level.	Arsenic	0-7	nitric oxide synthase 2	Rattus norvegicus	45-49
25218292-10	2014	Arsenic increased aortic Nox-4 and p22Phox mRNA expression, Nox activity, ROS generation and lipid peroxidation.	Arsenic	0-7	NADPH oxidase 4	Rattus norvegicus	25-30
25218292-10	2014	Arsenic increased aortic Nox-4 and p22Phox mRNA expression, Nox activity, ROS generation and lipid peroxidation.	Arsenic	0-7	cytochrome b-245 alpha chain	Rattus norvegicus	35-42
25218292-11	2014	Further, arsenic decreased the activities of superoxide dismutase, catalase, and glutathione peroxidase and depleted aortic GSH content.	Arsenic	9-16	catalase	Rattus norvegicus	67-75
25156962-6	2014	This method was successfully used to determine arsenic speciation in the guano samples collected from the Xisha Islands of the South China Sea, and the results indicated that As(III) and As(V) were the dominant arsenic species in modern and ancient guano, respectively.	Arsenic	211-218	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	187-192
25299175-5	2014	The distribution, diversity and abundance of functional genes (including arsC, arrA, aioA, arsB and ACR3) were much higher for the samples containing higher As and Sb concentrations.	Arsenic	157-159	arylsulfatase B	Homo sapiens	91-95
25218703-7	2014	Significant interactions are detected between XRCC3 T241M and sunlight exposure at work, and between XRCC3 T241M and exposure to arsenic in drinking water (p-value for interaction &lt;0.10).	Arsenic	129-136	X-ray repair cross complementing 3	Homo sapiens	101-106
24927198-10	2014	The adjusted incidence rate ratios (IRRs) per 1-mug/L increment in arsenic levels in drinking water were as follows: IRR = 1.03 (95% CI: 1.01, 1.06) and IRR = 1.02 (95% CI: 0.99, 1.05) for all and strict diabetes cases, respectively.	Arsenic	67-74	insulin receptor related receptor	Homo sapiens	36-39
24927198-10	2014	The adjusted incidence rate ratios (IRRs) per 1-mug/L increment in arsenic levels in drinking water were as follows: IRR = 1.03 (95% CI: 1.01, 1.06) and IRR = 1.02 (95% CI: 0.99, 1.05) for all and strict diabetes cases, respectively.	Arsenic	67-74	insulin receptor related receptor	Homo sapiens	117-120
25089838-0	2014	The novel regulations of MEF2A, CAMKK2, CALM3, and TNNI3 in ventricular hypertrophy induced by arsenic exposure in rats.	Arsenic	95-102	myocyte enhancer factor 2a	Rattus norvegicus	25-30
25089838-0	2014	The novel regulations of MEF2A, CAMKK2, CALM3, and TNNI3 in ventricular hypertrophy induced by arsenic exposure in rats.	Arsenic	95-102	calcium/calmodulin-dependent protein kinase kinase 2	Rattus norvegicus	32-38
25089838-0	2014	The novel regulations of MEF2A, CAMKK2, CALM3, and TNNI3 in ventricular hypertrophy induced by arsenic exposure in rats.	Arsenic	95-102	calmodulin 3	Rattus norvegicus	40-45
25089838-0	2014	The novel regulations of MEF2A, CAMKK2, CALM3, and TNNI3 in ventricular hypertrophy induced by arsenic exposure in rats.	Arsenic	95-102	troponin I3, cardiac type	Rattus norvegicus	51-56
25286945-5	2014	In the human liver, hAS3MT converts inorganic arsenic into more toxic and carcinogenic forms.	Arsenic	46-53	PDS5 cohesin associated factor B	Homo sapiens	20-24
24995390-10	2014	In addition, presence of MK571 significantly increased the specific cellular arsenic content, suggesting that Mrp1 may also be involved in arsenic export from astrocytes.	Arsenic	77-84	ATP binding cassette subfamily C member 1	Rattus norvegicus	110-114
27867209-0	2014	Adsorption and desorption of arsenic to aquifer sediment on the Red River floodplain at Nam Du, Vietnam.	Arsenic	29-36	SH3 and cysteine rich domain 3	Homo sapiens	88-91
25587330-5	2014	The repetitive unit was likely composed of 3 As, 3 Cs, 13 Bs and 1 D. Together with the average molecular weight, it was predictable that HB-1 consisted of about seven of the repetitive unit.	Arsenic	45-47	histocompatibility minor HB-1	Homo sapiens	138-142
25417402-14	2014	SAQ scores of QOL were negatively associated with the inflammatory index (IL-6/IL-10), and there was a significant negative association of IL-10 with AS (r = - 0.15, P &lt; 0.05).	Arsenic	150-152	interleukin 10	Homo sapiens	139-144
24995390-10	2014	In addition, presence of MK571 significantly increased the specific cellular arsenic content, suggesting that Mrp1 may also be involved in arsenic export from astrocytes.	Arsenic	139-146	ATP binding cassette subfamily C member 1	Rattus norvegicus	110-114
28962283-4	2014	This study aims to clarify the correlation between arsenic pollution and functional defect of p15INK4b gene in arsenic exposure residents from a region of Guizhou Province, China.	Arsenic	51-58	cyclin dependent kinase inhibitor 2B	Homo sapiens	94-102
24996682-10	2014	CONCLUSIONS: Urinary VEGF and PGE2 levels increased in arsenic exposure copper smelting workers, and urinary VEGF levels are well associated with the urinary arsenicals.	Arsenic	55-62	vascular endothelial growth factor A	Homo sapiens	21-25
24472713-3	2014	The arsenic removal isotherms were expressed by the Langmuir type equations, and the highest removal capacity was observed for the adsorbent prepared from concrete sludge with heat treatment at 105 C, the maximum removal capacity being 175 mg-As(V)/g.	Arsenic	4-11	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	243-248
24821849-11	2014	IR was higher in RA patients with anti-TNF monoclonal antibodies [307.71 (95% CI 184.79, 454.93)] than in those with rituximab [20.0 (95% CI 0.10, 60)] and etanercept [67.58 (95% CI 12.1, 163.94)] or AS, PsA and psoriasis with etanercept [60.01 (95% CI 3.6, 184.79)].	Arsenic	200-202	tumor necrosis factor	Homo sapiens	39-42
28962283-4	2014	This study aims to clarify the correlation between arsenic pollution and functional defect of p15INK4b gene in arsenic exposure residents from a region of Guizhou Province, China.	Arsenic	111-118	cyclin dependent kinase inhibitor 2B	Homo sapiens	94-102
28962283-7	2014	Subjects with higher arsenic concentrations are more likely to have p15INK4b methylation and gene deletion (chi2 = 4.28, P = 0.04 and chi2 = 4.31, P = 0.04).	Arsenic	21-28	cyclin dependent kinase inhibitor 2B	Homo sapiens	68-76
28962283-9	2014	These observations indicate that inactivation of p15INK4b through genetic alteration or epigenetic modification is a common event that is associated with arsenic exposure and the development of arsenicosis.	Arsenic	154-161	cyclin dependent kinase inhibitor 2B	Homo sapiens	49-57
24952339-3	2014	Exposure to arsenic (20mg/kg body weight, p.o) for 28 days in rats resulted to decrease the expression of CHRM2 receptor gene associated with mitochondrial dysfunctions as evident by decrease in the mitochondrial membrane potential, activity of mitochondrial complexes and enhanced apoptosis both in the frontal cortex and hippocampus in comparison to controls.	Arsenic	12-19	cholinergic receptor, muscarinic 2	Rattus norvegicus	106-111
24995641-2	2014	In this work, we show that size-resolved concentrations of As and Pb generally follow a bimodal distribution with the majority of contaminants in the fine size fraction (&lt;1 mum) around mining activities that include smelting operations at various sites in Australia and Arizona.	Arsenic	59-61	latexin	Homo sapiens	176-179
25018058-10	2014	Our results suggest that the XRCC1 399 Gln/Gln and 194 Arg/Arg DNA repair genes play an important role in poor arsenic methylation capacity, thereby increasing the risk of UC in non-obvious arsenic exposure areas.	Arsenic	111-118	X-ray repair cross complementing 1	Homo sapiens	29-34
25010156-0	2014	Speciation analysis of inorganic arsenic in river water by Amberlite IRA 910 resin immobilized in a polyacrylamide gel as a selective binding agent for As(V) in diffusive gradient thin film technique.	Arsenic	33-40	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	152-157
25010156-3	2014	Subsequently, the concentration of As(III) was obtained by determining the difference between the total As and As(V).	Arsenic	35-37	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	111-116
25064658-3	2014	The purpose of this study was to investigate the involvement of ADH in the oral health pathology of smoking (AS) and non-smoking (ANS) alcohol-dependent males.	Arsenic	109-111	aldo-keto reductase family 1 member A1	Homo sapiens	64-67
24448713-9	2014	PP2A activity was significantly higher in the arsenic-fed mice compared with the control group.	Arsenic	46-53	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	0-4
24448713-10	2014	These findings indicate that microvessels generally respond to vasoactive agents, and that the increased PP2A activity is involved in mustard oil-induced vascular leakage in arsenic-fed mice.	Arsenic	174-181	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	105-109
24643503-1	2014	TNF-alpha promoter polymorphisms may be associated with the severity rather than the susceptibility of AS.	Arsenic	103-105	tumor necrosis factor	Homo sapiens	0-9
24924402-13	2014	In conclusion, elevated childhood arsenic exposure appeared to reduce cell-mediated immunity, possibly linked to reduced concentrations of Th1 cytokines.	Arsenic	34-41	negative elongation factor complex member C/D	Homo sapiens	139-142
25221743-7	2014	There was mixed evidence of an association between arsenic exposure and chronic kidney disease (CKD), beta-2 microglobulin (beta2MG), and N-acetyl-beta-D-glucosaminidase (NAG) outcomes.	Arsenic	51-58	beta-2-microglobulin	Homo sapiens	102-122
25221743-7	2014	There was mixed evidence of an association between arsenic exposure and chronic kidney disease (CKD), beta-2 microglobulin (beta2MG), and N-acetyl-beta-D-glucosaminidase (NAG) outcomes.	Arsenic	51-58	beta-2-microglobulin	Homo sapiens	124-131
25221743-7	2014	There was mixed evidence of an association between arsenic exposure and chronic kidney disease (CKD), beta-2 microglobulin (beta2MG), and N-acetyl-beta-D-glucosaminidase (NAG) outcomes.	Arsenic	51-58	O-GlcNAcase	Homo sapiens	138-169
25128769-11	2014	Arsenic did not modify paracetamol"s effect on 5-HT1A expression, but reduced paracetamol-mediated down-regulation of 5-HT2A and reversed up-regulation of CB1 receptors.	Arsenic	0-7	5-hydroxytryptamine receptor 2A	Rattus norvegicus	118-124
25128769-11	2014	Arsenic did not modify paracetamol"s effect on 5-HT1A expression, but reduced paracetamol-mediated down-regulation of 5-HT2A and reversed up-regulation of CB1 receptors.	Arsenic	0-7	cannabinoid receptor 1	Rattus norvegicus	155-158
25128769-12	2014	Results suggest arsenic reduced paracetamol-induced analgesia possibly by interfering with pronociceptive 5-HT2A and antinociceptive CB1 receptors.	Arsenic	16-23	5-hydroxytryptamine receptor 2A	Rattus norvegicus	106-112
25128769-12	2014	Results suggest arsenic reduced paracetamol-induced analgesia possibly by interfering with pronociceptive 5-HT2A and antinociceptive CB1 receptors.	Arsenic	16-23	cannabinoid receptor 1	Rattus norvegicus	133-136
24926533-2	2014	It has been known for a while now that some invertebrates also possess functional phytochelatin synthase (PCS) enzymes, and that at least one species, the nematode Caenorhabditis elegans, produces phytochelatins to help detoxify cadmium, and probably also other metal and metalloid ions including arsenic, zinc, selenium, silver, and copper.	Arsenic	297-304	Glutathione gamma-glutamylcysteinyltransferase	Caenorhabditis elegans	82-104
24926533-2	2014	It has been known for a while now that some invertebrates also possess functional phytochelatin synthase (PCS) enzymes, and that at least one species, the nematode Caenorhabditis elegans, produces phytochelatins to help detoxify cadmium, and probably also other metal and metalloid ions including arsenic, zinc, selenium, silver, and copper.	Arsenic	297-304	Glutathione gamma-glutamylcysteinyltransferase	Caenorhabditis elegans	106-109
24959978-8	2014	In the morphine-treated animals, AS and SS increased apoptotic factors remarkably (except for the Bax/Bcl-2 ratio after AS and SS in the Str and caspase-3 activation after AS in the NAc) and also decreased conditioning scores.	Arsenic	33-35	BCL2, apoptosis regulator	Rattus norvegicus	102-107
24905690-11	2014	The expression of uncoupling protein 2 (Ucp2), an important mitochondrial enzyme was also subdued in arsenic exposed zebrafish.	Arsenic	101-108	uncoupling protein 2	Danio rerio	18-38
24905690-11	2014	The expression of uncoupling protein 2 (Ucp2), an important mitochondrial enzyme was also subdued in arsenic exposed zebrafish.	Arsenic	101-108	uncoupling protein 2	Danio rerio	40-44
25093545-10	2014	A broad adaptation pH range for both As(V) and As(III) adsorbed by the resulting product indicates its promising application perspective for decontamination of arsenic-polluted water.	Arsenic	160-167	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	37-42
28962272-4	2014	The methylation of As is catalyzed by arsenic (+3 oxidation state) methyltransferase (AS3MT).	Arsenic	19-21	arsenite methyltransferase	Homo sapiens	38-84
25258480-7	2014	The complex structure revealed the mode of arsenic binding efficiency with the receptor aquaporine 9 and ABCC1 channel protein.	Arsenic	43-50	ATP binding cassette subfamily C member 1	Homo sapiens	105-110
28962272-4	2014	The methylation of As is catalyzed by arsenic (+3 oxidation state) methyltransferase (AS3MT).	Arsenic	19-21	arsenite methyltransferase	Homo sapiens	86-91
25101770-3	2014	We investigated the association between GST genotypes and whole blood arsenic concentrations (BASC) in Jamaican children with and without autism spectrum disorder (ASD).	Arsenic	70-77	glutathione S-transferase kappa 1	Homo sapiens	40-43
28962272-11	2014	We conclude that AS3MT catalyzes the methylation of As and not other biomethylatable metalloids, such as Se and Te.	Arsenic	52-54	arsenite methyltransferase	Homo sapiens	17-22
25099865-5	2014	Here we identify a quantitative trait locus that encodes a novel arsenate reductase critical for arsenic tolerance in plants.	Arsenic	97-104	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	65-83
24570342-3	2014	Because the expression of lipocalin-2 (LCN2) was highly enhanced by promoter hypomethylation in inorganic arsenic (iAs)-HUCs cells as well as bladder cancer tissues, we further showed that mutations at the binding sequences for NF-kappaB and C/EBP-alpha significantly reduced LCN2 promoter activity.	Arsenic	106-113	lipocalin 2	Homo sapiens	26-37
24570342-3	2014	Because the expression of lipocalin-2 (LCN2) was highly enhanced by promoter hypomethylation in inorganic arsenic (iAs)-HUCs cells as well as bladder cancer tissues, we further showed that mutations at the binding sequences for NF-kappaB and C/EBP-alpha significantly reduced LCN2 promoter activity.	Arsenic	106-113	lipocalin 2	Homo sapiens	39-43
24570342-7	2014	Taken together, our results show that sustained low-dose arsenic exposure results in epigenetic changes and enhanced oncogenic potential via LCN2 overexpression.	Arsenic	57-64	lipocalin 2	Homo sapiens	141-145
24831965-12	2014	Among these differentially expressed genes, significant decreases in the mRNA expressions of CaMKII, Gria1, Gria2, Grin1, Itpr1, Grm1 and PLCbeta4 related to the LTP and LTD were found at the PSD of mouse cerebellum exposed to arsenic.	Arsenic	227-234	calcium/calmodulin-dependent protein kinase II, delta	Mus musculus	93-99
24831965-12	2014	Among these differentially expressed genes, significant decreases in the mRNA expressions of CaMKII, Gria1, Gria2, Grin1, Itpr1, Grm1 and PLCbeta4 related to the LTP and LTD were found at the PSD of mouse cerebellum exposed to arsenic.	Arsenic	227-234	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	101-106
24831965-12	2014	Among these differentially expressed genes, significant decreases in the mRNA expressions of CaMKII, Gria1, Gria2, Grin1, Itpr1, Grm1 and PLCbeta4 related to the LTP and LTD were found at the PSD of mouse cerebellum exposed to arsenic.	Arsenic	227-234	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	108-113
24831965-12	2014	Among these differentially expressed genes, significant decreases in the mRNA expressions of CaMKII, Gria1, Gria2, Grin1, Itpr1, Grm1 and PLCbeta4 related to the LTP and LTD were found at the PSD of mouse cerebellum exposed to arsenic.	Arsenic	227-234	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	115-120
24831965-12	2014	Among these differentially expressed genes, significant decreases in the mRNA expressions of CaMKII, Gria1, Gria2, Grin1, Itpr1, Grm1 and PLCbeta4 related to the LTP and LTD were found at the PSD of mouse cerebellum exposed to arsenic.	Arsenic	227-234	inositol 1,4,5-trisphosphate receptor 1	Mus musculus	122-127
24831965-12	2014	Among these differentially expressed genes, significant decreases in the mRNA expressions of CaMKII, Gria1, Gria2, Grin1, Itpr1, Grm1 and PLCbeta4 related to the LTP and LTD were found at the PSD of mouse cerebellum exposed to arsenic.	Arsenic	227-234	glutamate receptor, metabotropic 1	Mus musculus	129-133
25005685-10	2014	Thus, in CD1 mice whole-life arsenic exposure induced lung tumors at human-relevant doses (i.e., 50 and 500 ppb).	Arsenic	29-36	CD1 antigen complex	Mus musculus	9-12
25101770-9	2014	These findings suggest a possible role of GSTP1 in the detoxification of arsenic.	Arsenic	73-80	glutathione S-transferase pi 1	Homo sapiens	42-47
24970285-0	2014	Tert-butylhydroquinone as a phenolic activator of Nrf2 antagonizes arsenic-induced oxidative cytotoxicity but promotes arsenic methylation and detoxication in human hepatocyte cell line.	Arsenic	67-74	telomerase reverse transcriptase	Homo sapiens	0-4
24970285-0	2014	Tert-butylhydroquinone as a phenolic activator of Nrf2 antagonizes arsenic-induced oxidative cytotoxicity but promotes arsenic methylation and detoxication in human hepatocyte cell line.	Arsenic	67-74	NFE2 like bZIP transcription factor 2	Homo sapiens	50-54
24970285-3	2014	The objective of this study was to test whether tert-butylhydroquinone (tBHQ), a well-known synthetic Nrf2 inducer, could protect human hepatocytes against arsenic-induced cytotoxicity and oxidative injuries.	Arsenic	156-163	telomerase reverse transcriptase	Homo sapiens	48-52
24970285-0	2014	Tert-butylhydroquinone as a phenolic activator of Nrf2 antagonizes arsenic-induced oxidative cytotoxicity but promotes arsenic methylation and detoxication in human hepatocyte cell line.	Arsenic	119-126	telomerase reverse transcriptase	Homo sapiens	0-4
24970285-0	2014	Tert-butylhydroquinone as a phenolic activator of Nrf2 antagonizes arsenic-induced oxidative cytotoxicity but promotes arsenic methylation and detoxication in human hepatocyte cell line.	Arsenic	119-126	NFE2 like bZIP transcription factor 2	Homo sapiens	50-54
24970285-6	2014	Collectively, we suspected that Nrf2 signaling pathway may be involved in the protective effects of tBHQ against arsenic invasion in hepatocytes.	Arsenic	113-120	NFE2 like bZIP transcription factor 2	Homo sapiens	32-36
24726863-1	2014	Inorganic arsenic(As) is metabolized through a series of methylation reactions catalyzed by arsenic(III)-methyltransferase (AS3MT), resulting in the generation of monomethylarsonic (MMAs) and dimethylarsinic acids (DMAs).	Arsenic	18-20	arsenite methyltransferase	Homo sapiens	124-129
25069452-0	2014	Importance of Arsenic and pesticides in epidemic chronic kidney disease in Sri Lanka.	Arsenic	14-21	sorcin	Homo sapiens	75-78
24870404-0	2014	A novel pathway for arsenic elimination: human multidrug resistance protein 4 (MRP4/ABCC4) mediates cellular export of dimethylarsinic acid (DMAV) and the diglutathione conjugate of monomethylarsonous acid (MMAIII).	Arsenic	20-27	ATP binding cassette subfamily C member 4	Homo sapiens	79-83
24870404-0	2014	A novel pathway for arsenic elimination: human multidrug resistance protein 4 (MRP4/ABCC4) mediates cellular export of dimethylarsinic acid (DMAV) and the diglutathione conjugate of monomethylarsonous acid (MMAIII).	Arsenic	20-27	ATP binding cassette subfamily C member 4	Homo sapiens	84-89
24870404-6	2014	Human multidrug resistance protein 1 (MRP1/ABCC1) and MRP2 (ABCC2) are established arsenic efflux pumps, but unlike the related MRP4 (ABCC4) are not present at the basolateral membrane of hepatocytes.	Arsenic	83-90	ATP binding cassette subfamily B member 1	Homo sapiens	6-36
24870404-6	2014	Human multidrug resistance protein 1 (MRP1/ABCC1) and MRP2 (ABCC2) are established arsenic efflux pumps, but unlike the related MRP4 (ABCC4) are not present at the basolateral membrane of hepatocytes.	Arsenic	83-90	ATP binding cassette subfamily C member 1	Homo sapiens	38-42
24870404-6	2014	Human multidrug resistance protein 1 (MRP1/ABCC1) and MRP2 (ABCC2) are established arsenic efflux pumps, but unlike the related MRP4 (ABCC4) are not present at the basolateral membrane of hepatocytes.	Arsenic	83-90	ATP binding cassette subfamily C member 1	Homo sapiens	43-48
24870404-6	2014	Human multidrug resistance protein 1 (MRP1/ABCC1) and MRP2 (ABCC2) are established arsenic efflux pumps, but unlike the related MRP4 (ABCC4) are not present at the basolateral membrane of hepatocytes.	Arsenic	83-90	ATP binding cassette subfamily C member 2	Homo sapiens	54-58
24870404-6	2014	Human multidrug resistance protein 1 (MRP1/ABCC1) and MRP2 (ABCC2) are established arsenic efflux pumps, but unlike the related MRP4 (ABCC4) are not present at the basolateral membrane of hepatocytes.	Arsenic	83-90	ATP binding cassette subfamily C member 2	Homo sapiens	60-65
24870404-7	2014	MRP4 is also found at the apical membrane of renal proximal tubule cells, making it an ideal candidate for urinary arsenic elimination.	Arsenic	115-122	ATP binding cassette subfamily C member 4	Homo sapiens	0-4
24870404-12	2014	These results suggest that human MRP4 could be a major player in the elimination of arsenic.	Arsenic	84-91	ATP binding cassette subfamily C member 4	Homo sapiens	33-37
24792412-0	2014	AS3MT, GSTO, and PNP polymorphisms: impact on arsenic methylation and implications for disease susceptibility.	Arsenic	46-53	arsenite methyltransferase	Homo sapiens	0-5
24830721-4	2014	We found that sustained overexpression of the pro-inflammatory IL6 promoted arsenic-induced cell transformation by inhibiting autophagy.	Arsenic	76-83	interleukin 6	Homo sapiens	63-66
24677489-10	2014	One of the validated CpG site (cg03333116; change of %methylation was 13.2 in New Cases versus -0.09 in Persistent Controls; P &lt; 0.001) belonged to the RHBDF1 gene, which was previously reported to be hypermethylated in arsenic-exposed cases.	Arsenic	223-230	rhomboid 5 homolog 1	Homo sapiens	155-161
24694939-5	2014	Speciation of As in water samples from Holocene sediments revealed the dominant species to be As(III), with ratios of As(III):AsT ranging from 0.55 to 0.98 (average 0.74).	Arsenic	14-16	solute carrier family 17 member 5	Homo sapiens	126-129
24792412-0	2014	AS3MT, GSTO, and PNP polymorphisms: impact on arsenic methylation and implications for disease susceptibility.	Arsenic	46-53	purine nucleoside phosphorylase	Homo sapiens	17-20
25079991-0	2014	Effect of CaO on retention of S, Cl, Br, As, Mn, V, Cr, Ni, Cu, Zn, W and Pb in bottom ashes from fluidized-bed coal combustion power station.	Arsenic	41-43	mummy	Drosophila melanogaster	10-13
25079991-8	2014	It was also discovered that major enrichment of CaO in the finest bottom ash fractions could be advantageously used for simple separation of elements strongly associated with these fractions, mainly S and As, but also Cl or Br.	Arsenic	205-207	mummy	Drosophila melanogaster	48-51
25079991-5	2014	Strong positive correlations with CaO content in bottom ashes were observed (for all four combustion tests) for S, As, Cl and Br (R=0.917-0.999).	Arsenic	115-117	mummy	Drosophila melanogaster	34-37
22859221-3	2014	Among several effects of arsenic, it has been suggested that arsenic-induced vascular endothelial growth factor (VEGF) expression plays a critical role in arsenic carcinogenesis.	Arsenic	25-32	vascular endothelial growth factor A	Homo sapiens	77-111
24841200-0	2014	MicroRNA-200b suppresses arsenic-transformed cell migration by targeting protein kinase Calpha and Wnt5b-protein kinase Calpha positive feedback loop and inhibiting Rac1 activation.	Arsenic	25-32	microRNA 200b	Homo sapiens	0-13
24841200-0	2014	MicroRNA-200b suppresses arsenic-transformed cell migration by targeting protein kinase Calpha and Wnt5b-protein kinase Calpha positive feedback loop and inhibiting Rac1 activation.	Arsenic	25-32	protein kinase C alpha	Homo sapiens	73-94
24841200-0	2014	MicroRNA-200b suppresses arsenic-transformed cell migration by targeting protein kinase Calpha and Wnt5b-protein kinase Calpha positive feedback loop and inhibiting Rac1 activation.	Arsenic	25-32	Wnt family member 5B	Homo sapiens	99-104
24841200-0	2014	MicroRNA-200b suppresses arsenic-transformed cell migration by targeting protein kinase Calpha and Wnt5b-protein kinase Calpha positive feedback loop and inhibiting Rac1 activation.	Arsenic	25-32	protein kinase C alpha	Homo sapiens	105-126
24841200-0	2014	MicroRNA-200b suppresses arsenic-transformed cell migration by targeting protein kinase Calpha and Wnt5b-protein kinase Calpha positive feedback loop and inhibiting Rac1 activation.	Arsenic	25-32	Rac family small GTPase 1	Homo sapiens	165-169
24841200-3	2014	This study was performed to investigate how miR-200b inhibits arsenic-transformed cell migration.	Arsenic	62-69	microRNA 200b	Homo sapiens	44-52
24841200-8	2014	In addition, we also found a positive feedback loop between Wnt5b and PKCalpha in arsenic-transformed cells.	Arsenic	82-89	Wnt family member 5B	Homo sapiens	60-65
24841200-8	2014	In addition, we also found a positive feedback loop between Wnt5b and PKCalpha in arsenic-transformed cells.	Arsenic	82-89	protein kinase C alpha	Homo sapiens	70-78
24841200-11	2014	Further mechanistic studies revealed that Rac1 is highly activated in arsenic-transformed cells and stably expressing miR-200b abolishes Rac1 activation changing actin cytoskeleton organization.	Arsenic	70-77	Rac family small GTPase 1	Homo sapiens	42-46
24841200-11	2014	Further mechanistic studies revealed that Rac1 is highly activated in arsenic-transformed cells and stably expressing miR-200b abolishes Rac1 activation changing actin cytoskeleton organization.	Arsenic	70-77	microRNA 200b	Homo sapiens	118-126
24841200-11	2014	Further mechanistic studies revealed that Rac1 is highly activated in arsenic-transformed cells and stably expressing miR-200b abolishes Rac1 activation changing actin cytoskeleton organization.	Arsenic	70-77	Rac family small GTPase 1	Homo sapiens	137-141
24841200-13	2014	Together, these findings indicate that miR-200b suppresses arsenic-transformed cell migration by targeting PKCalpha and Wnt5b-PKCalpha positive feedback loop and subsequently inhibiting Rac1 activation.	Arsenic	59-66	microRNA 200b	Homo sapiens	39-47
24841200-13	2014	Together, these findings indicate that miR-200b suppresses arsenic-transformed cell migration by targeting PKCalpha and Wnt5b-PKCalpha positive feedback loop and subsequently inhibiting Rac1 activation.	Arsenic	59-66	protein kinase C alpha	Homo sapiens	107-115
24841200-13	2014	Together, these findings indicate that miR-200b suppresses arsenic-transformed cell migration by targeting PKCalpha and Wnt5b-PKCalpha positive feedback loop and subsequently inhibiting Rac1 activation.	Arsenic	59-66	Wnt family member 5B	Homo sapiens	120-125
24841200-13	2014	Together, these findings indicate that miR-200b suppresses arsenic-transformed cell migration by targeting PKCalpha and Wnt5b-PKCalpha positive feedback loop and subsequently inhibiting Rac1 activation.	Arsenic	59-66	protein kinase C alpha	Homo sapiens	126-134
24841200-13	2014	Together, these findings indicate that miR-200b suppresses arsenic-transformed cell migration by targeting PKCalpha and Wnt5b-PKCalpha positive feedback loop and subsequently inhibiting Rac1 activation.	Arsenic	59-66	Rac family small GTPase 1	Homo sapiens	186-190
24531206-11	2014	CONCLUSIONS: Our results suggest that arsenic is capable of inhibiting osteoblast differentiation of BMSCs via an ERK-dependent signaling pathway and thus increasing bone loss.	Arsenic	38-45	Eph receptor B1	Rattus norvegicus	114-117
24970117-5	2014	Arsenic, mercury and lead exposure led to a significant inhibition of blood delta:aminolevulinic acid dehydratase (ALAD) activity and glutathione level supported by increased thiobarbituric acid reactive substance (TBARS).	Arsenic	0-7	aminolevulinate dehydratase	Rattus norvegicus	76-113
24970117-5	2014	Arsenic, mercury and lead exposure led to a significant inhibition of blood delta:aminolevulinic acid dehydratase (ALAD) activity and glutathione level supported by increased thiobarbituric acid reactive substance (TBARS).	Arsenic	0-7	aminolevulinate dehydratase	Rattus norvegicus	115-119
25004251-0	2014	Sequential activation of Elk-1/Egr-1/GADD45alpha by arsenic.	Arsenic	52-59	ETS transcription factor ELK1	Homo sapiens	25-30
25004251-0	2014	Sequential activation of Elk-1/Egr-1/GADD45alpha by arsenic.	Arsenic	52-59	early growth response 1	Homo sapiens	31-36
25004251-0	2014	Sequential activation of Elk-1/Egr-1/GADD45alpha by arsenic.	Arsenic	52-59	growth arrest and DNA damage inducible alpha	Homo sapiens	37-48
24634002-5	2014	Arsenic resulted in a time dependent inhibition of GR mediated by the superoxide anion.	Arsenic	0-7	glutathione-disulfide reductase	Rattus norvegicus	51-53
24634002-8	2014	Furthermore, arsenic induced free radical mediated inhibition of GR was found to be partially uncompetitive and associated with time dependent decrease in the substrate binding rate.	Arsenic	13-20	glutathione-disulfide reductase	Rattus norvegicus	65-67
24473067-10	2014	Regional mean concentrations were highest in the Maldives, Seychelles and Sri Lanka with 3.5, 2.5, and 2.4mug/g ww, respectively, raising concern for arsenic pollution in the Indian Ocean.	Arsenic	150-157	sorcin	Physeter catodon	74-77
24531206-7	2014	After arsenic treatment during differentiation, expression of runt-related transcription factor-2 (Runx2), bone morphogenetic protein-2 (BMP-2), and osteocalcin in BMSCs was inhibited and phosphorylation of enhanced extracellular signal-regulated kinase (ERK) was increased.	Arsenic	6-13	RUNX family transcription factor 2	Rattus norvegicus	62-97
24531206-7	2014	After arsenic treatment during differentiation, expression of runt-related transcription factor-2 (Runx2), bone morphogenetic protein-2 (BMP-2), and osteocalcin in BMSCs was inhibited and phosphorylation of enhanced extracellular signal-regulated kinase (ERK) was increased.	Arsenic	6-13	RUNX family transcription factor 2	Rattus norvegicus	99-104
24531206-7	2014	After arsenic treatment during differentiation, expression of runt-related transcription factor-2 (Runx2), bone morphogenetic protein-2 (BMP-2), and osteocalcin in BMSCs was inhibited and phosphorylation of enhanced extracellular signal-regulated kinase (ERK) was increased.	Arsenic	6-13	bone morphogenetic protein 2	Rattus norvegicus	107-135
24531206-7	2014	After arsenic treatment during differentiation, expression of runt-related transcription factor-2 (Runx2), bone morphogenetic protein-2 (BMP-2), and osteocalcin in BMSCs was inhibited and phosphorylation of enhanced extracellular signal-regulated kinase (ERK) was increased.	Arsenic	6-13	bone morphogenetic protein 2	Rattus norvegicus	137-142
24531206-7	2014	After arsenic treatment during differentiation, expression of runt-related transcription factor-2 (Runx2), bone morphogenetic protein-2 (BMP-2), and osteocalcin in BMSCs was inhibited and phosphorylation of enhanced extracellular signal-regulated kinase (ERK) was increased.	Arsenic	6-13	bone gamma-carboxyglutamate protein	Rattus norvegicus	149-160
22859221-3	2014	Among several effects of arsenic, it has been suggested that arsenic-induced vascular endothelial growth factor (VEGF) expression plays a critical role in arsenic carcinogenesis.	Arsenic	25-32	vascular endothelial growth factor A	Homo sapiens	113-117
22859221-3	2014	Among several effects of arsenic, it has been suggested that arsenic-induced vascular endothelial growth factor (VEGF) expression plays a critical role in arsenic carcinogenesis.	Arsenic	61-68	vascular endothelial growth factor A	Homo sapiens	77-111
24531206-7	2014	After arsenic treatment during differentiation, expression of runt-related transcription factor-2 (Runx2), bone morphogenetic protein-2 (BMP-2), and osteocalcin in BMSCs was inhibited and phosphorylation of enhanced extracellular signal-regulated kinase (ERK) was increased.	Arsenic	6-13	Eph receptor B1	Rattus norvegicus	216-253
24531206-7	2014	After arsenic treatment during differentiation, expression of runt-related transcription factor-2 (Runx2), bone morphogenetic protein-2 (BMP-2), and osteocalcin in BMSCs was inhibited and phosphorylation of enhanced extracellular signal-regulated kinase (ERK) was increased.	Arsenic	6-13	Eph receptor B1	Rattus norvegicus	255-258
22859221-3	2014	Among several effects of arsenic, it has been suggested that arsenic-induced vascular endothelial growth factor (VEGF) expression plays a critical role in arsenic carcinogenesis.	Arsenic	61-68	vascular endothelial growth factor A	Homo sapiens	113-117
24905533-2	2014	Nineteen 2"-hydroxy-4"-isoprenyloxychalcone derivatives (a-s) were evaluated the inhibition CDC25B activity.	Arsenic	57-60	cell division cycle 25B	Homo sapiens	92-98
24632381-0	2014	Nrf2 expression and activity in human T lymphocytes: stimulation by T cell receptor activation and priming by inorganic arsenic and tert-butylhydroquinone.	Arsenic	120-127	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
24632381-11	2014	Inhibition of Nrf2 expression abrogates the effects of inorganic arsenic on mRNA levels of antioxidant genes, but does not alter the expression of IL-2, TNF-alpha, interferon-gamma, or IL-17 in Th cells activated in the absence or presence of the metalloid.	Arsenic	65-72	NFE2 like bZIP transcription factor 2	Homo sapiens	14-18
24107458-0	2014	Nuclear factor erythroid 2-related factor gene variants and susceptibility of arsenic-related skin lesions.	Arsenic	78-85	NFE2 like bZIP transcription factor 2	Homo sapiens	0-41
24107458-11	2014	This is the first report studying the association between NRF2 polymorphisms and susceptibility of As-related skin lesions.	Arsenic	99-101	NFE2 like bZIP transcription factor 2	Homo sapiens	58-62
24434654-4	2014	By using human bronchial epithelial cells and human lung cancer cell lines, we showed that arsenic was able to induce expression of mdig.	Arsenic	91-98	ribosomal oxygenase 2	Homo sapiens	132-136
24642100-1	2014	High concentrations of arsenic (&gt;50mug L(-1)) have been detected for the first time in groundwater of the wave-dominated Paraiba do Sul delta, Brazil.	Arsenic	23-30	immunoglobulin kappa variable 1-16	Homo sapiens	42-48
24675094-0	2014	Prenatal arsenic exposure and shifts in the newborn proteome: interindividual differences in tumor necrosis factor (TNF)-responsive signaling.	Arsenic	9-16	tumor necrosis factor	Homo sapiens	93-114
24675094-0	2014	Prenatal arsenic exposure and shifts in the newborn proteome: interindividual differences in tumor necrosis factor (TNF)-responsive signaling.	Arsenic	9-16	tumor necrosis factor	Homo sapiens	116-119
24779916-1	2014	An analysis of 70 wells that tap groundwater from depths of up to 260 m in and around the town of Cremona, N. Italy, shows that 50 of them contain more than 10 mug/L of arsenic.	Arsenic	169-176	nuclear RNA export factor 1	Homo sapiens	29-32
24754514-10	2014	Proinflammatory cytokines (IL-6 and TNF-alpha) were upregulated following arsenic treatment as in the case of the LPS stimulated group without alterations in anti-inflammatory IL-10.	Arsenic	74-81	interleukin 6	Mus musculus	27-31
24754514-10	2014	Proinflammatory cytokines (IL-6 and TNF-alpha) were upregulated following arsenic treatment as in the case of the LPS stimulated group without alterations in anti-inflammatory IL-10.	Arsenic	74-81	tumor necrosis factor	Mus musculus	36-45
24816914-4	2014	Treatment with 3 microM of arsenic promoted cell invasion via upregulation of expression of MT1-MMP and downregulation of expression of p14ARF and simultaneously induced cell apoptosis through inhibition of expression of N-cadherin and increase of expression of p21(WAF1/CIP1) at both transcript and protein levels in HSC5 cells.	Arsenic	27-34	matrix metallopeptidase 14	Homo sapiens	92-99
24816914-4	2014	Treatment with 3 microM of arsenic promoted cell invasion via upregulation of expression of MT1-MMP and downregulation of expression of p14ARF and simultaneously induced cell apoptosis through inhibition of expression of N-cadherin and increase of expression of p21(WAF1/CIP1) at both transcript and protein levels in HSC5 cells.	Arsenic	27-34	cyclin dependent kinase inhibitor 2A	Homo sapiens	136-142
24816914-4	2014	Treatment with 3 microM of arsenic promoted cell invasion via upregulation of expression of MT1-MMP and downregulation of expression of p14ARF and simultaneously induced cell apoptosis through inhibition of expression of N-cadherin and increase of expression of p21(WAF1/CIP1) at both transcript and protein levels in HSC5 cells.	Arsenic	27-34	cadherin 2	Homo sapiens	221-231
24816914-4	2014	Treatment with 3 microM of arsenic promoted cell invasion via upregulation of expression of MT1-MMP and downregulation of expression of p14ARF and simultaneously induced cell apoptosis through inhibition of expression of N-cadherin and increase of expression of p21(WAF1/CIP1) at both transcript and protein levels in HSC5 cells.	Arsenic	27-34	cyclin dependent kinase inhibitor 1A	Homo sapiens	262-265
24816914-4	2014	Treatment with 3 microM of arsenic promoted cell invasion via upregulation of expression of MT1-MMP and downregulation of expression of p14ARF and simultaneously induced cell apoptosis through inhibition of expression of N-cadherin and increase of expression of p21(WAF1/CIP1) at both transcript and protein levels in HSC5 cells.	Arsenic	27-34	cyclin dependent kinase inhibitor 1A	Homo sapiens	266-270
24816914-4	2014	Treatment with 3 microM of arsenic promoted cell invasion via upregulation of expression of MT1-MMP and downregulation of expression of p14ARF and simultaneously induced cell apoptosis through inhibition of expression of N-cadherin and increase of expression of p21(WAF1/CIP1) at both transcript and protein levels in HSC5 cells.	Arsenic	27-34	cyclin dependent kinase inhibitor 1A	Homo sapiens	271-275
24816914-5	2014	We also showed that inhibition of MT1-MMP expression by NSC405020 resulted in decrease of arsenic-mediated invasion of HSC5 cells involving decrease in phosphorylated extracellular signal-regulated kinases (pERK).	Arsenic	90-97	matrix metallopeptidase 14	Homo sapiens	34-41
24434654-5	2014	We further demonstrated that this mdig induction by arsenic was partially dependent on the JNK and STAT3 signaling pathways.	Arsenic	52-59	ribosomal oxygenase 2	Homo sapiens	34-38
24434654-5	2014	We further demonstrated that this mdig induction by arsenic was partially dependent on the JNK and STAT3 signaling pathways.	Arsenic	52-59	mitogen-activated protein kinase 8	Homo sapiens	91-94
24434654-5	2014	We further demonstrated that this mdig induction by arsenic was partially dependent on the JNK and STAT3 signaling pathways.	Arsenic	52-59	signal transducer and activator of transcription 3	Homo sapiens	99-104
24434654-6	2014	Disruption of the JNK or STAT3 by either chemical inhibitors or siRNAs diminished arsenic-induced accumulation of mdig mRNA and protein.	Arsenic	82-89	mitogen-activated protein kinase 8	Homo sapiens	18-21
24434654-6	2014	Disruption of the JNK or STAT3 by either chemical inhibitors or siRNAs diminished arsenic-induced accumulation of mdig mRNA and protein.	Arsenic	82-89	signal transducer and activator of transcription 3	Homo sapiens	25-30
24434654-6	2014	Disruption of the JNK or STAT3 by either chemical inhibitors or siRNAs diminished arsenic-induced accumulation of mdig mRNA and protein.	Arsenic	82-89	ribosomal oxygenase 2	Homo sapiens	114-118
24315179-1	2014	A microcosm experiment was conducted to examine the effects of hydrogen peroxide (at a concentration range of 5-50 muM) on the release of arsenic from the dissolution of arsenopyrite, a dominant arsenic-bearing mineral occurring in natural environments.	Arsenic	138-145	latexin	Homo sapiens	115-118
24434654-7	2014	Furthermore, we also showed that microRNA-21 (miR-21) and Akt were down-stream effectors of the JNK and STAT3 signaling pathways in arsenic-induced mdig expression.	Arsenic	132-139	microRNA 21	Homo sapiens	33-44
24434654-7	2014	Furthermore, we also showed that microRNA-21 (miR-21) and Akt were down-stream effectors of the JNK and STAT3 signaling pathways in arsenic-induced mdig expression.	Arsenic	132-139	microRNA 21	Homo sapiens	46-52
24434654-7	2014	Furthermore, we also showed that microRNA-21 (miR-21) and Akt were down-stream effectors of the JNK and STAT3 signaling pathways in arsenic-induced mdig expression.	Arsenic	132-139	AKT serine/threonine kinase 1	Homo sapiens	58-61
24434654-7	2014	Furthermore, we also showed that microRNA-21 (miR-21) and Akt were down-stream effectors of the JNK and STAT3 signaling pathways in arsenic-induced mdig expression.	Arsenic	132-139	mitogen-activated protein kinase 8	Homo sapiens	96-99
24434654-7	2014	Furthermore, we also showed that microRNA-21 (miR-21) and Akt were down-stream effectors of the JNK and STAT3 signaling pathways in arsenic-induced mdig expression.	Arsenic	132-139	signal transducer and activator of transcription 3	Homo sapiens	104-109
24434654-7	2014	Furthermore, we also showed that microRNA-21 (miR-21) and Akt were down-stream effectors of the JNK and STAT3 signaling pathways in arsenic-induced mdig expression.	Arsenic	132-139	ribosomal oxygenase 2	Homo sapiens	148-152
24434654-8	2014	Transfection of the cells with anti-miR-21 or pre-treatment of the cells with Akt inhibitor blunted mdig induction by arsenic.	Arsenic	118-125	microRNA 21	Homo sapiens	36-42
24434654-8	2014	Transfection of the cells with anti-miR-21 or pre-treatment of the cells with Akt inhibitor blunted mdig induction by arsenic.	Arsenic	118-125	AKT serine/threonine kinase 1	Homo sapiens	78-81
24434654-8	2014	Transfection of the cells with anti-miR-21 or pre-treatment of the cells with Akt inhibitor blunted mdig induction by arsenic.	Arsenic	118-125	ribosomal oxygenase 2	Homo sapiens	100-104
24434654-10	2014	Taken together, our data suggest that mdig may play important roles on the pathogenesis of arsenic-induced lung cancer and that JNK and STAT3 signaling pathways are essential in mediating arsenic-induced mdig expression.	Arsenic	91-98	ribosomal oxygenase 2	Homo sapiens	38-42
24434654-10	2014	Taken together, our data suggest that mdig may play important roles on the pathogenesis of arsenic-induced lung cancer and that JNK and STAT3 signaling pathways are essential in mediating arsenic-induced mdig expression.	Arsenic	188-195	mitogen-activated protein kinase 8	Homo sapiens	128-131
24434654-10	2014	Taken together, our data suggest that mdig may play important roles on the pathogenesis of arsenic-induced lung cancer and that JNK and STAT3 signaling pathways are essential in mediating arsenic-induced mdig expression.	Arsenic	188-195	signal transducer and activator of transcription 3	Homo sapiens	136-141
24434654-10	2014	Taken together, our data suggest that mdig may play important roles on the pathogenesis of arsenic-induced lung cancer and that JNK and STAT3 signaling pathways are essential in mediating arsenic-induced mdig expression.	Arsenic	188-195	ribosomal oxygenase 2	Homo sapiens	204-208
24813017-2	2014	Analysis of 100 drinking water samples revealed that arsenic concentration was below 10 mug l-1 in 60% samples, 10-50 mug l-1 in 6%, 100 mug l-1 in 24% and 200 mug l-1 in 10% samples, respectively.	Arsenic	53-60	immunoglobulin kappa variable 1-16	Homo sapiens	92-95
24525453-10	2014	In adjusted models, every log 10 increase in maternal drinking water arsenic exposure was estimated to increase CD8+ T cells by 7.4% (P = 0.0004) and decrease in CD4+ T cells by 9.2% (P = 0.0002).	Arsenic	69-76	CD8a molecule	Homo sapiens	112-115
24525453-10	2014	In adjusted models, every log 10 increase in maternal drinking water arsenic exposure was estimated to increase CD8+ T cells by 7.4% (P = 0.0004) and decrease in CD4+ T cells by 9.2% (P = 0.0002).	Arsenic	69-76	CD4 molecule	Homo sapiens	162-165
24517892-0	2014	Reversibility of changes in brain cholinergic receptors and acetylcholinesterase activity in rats following early life arsenic exposure.	Arsenic	119-126	acetylcholinesterase	Rattus norvegicus	60-80
24671580-9	2014	The increases in ADG during the P2 and final BW obtained with NSP enzyme supplementation were greater in pigs fed the AS than those fed the AL (barley x enzyme, P &lt; 0.05).	Arsenic	118-120	ADG	Sus scrofa	17-20
24813017-3	2014	The arsenic concentration in drinking water ranged from 12.8 to 132.2 mug l-1.	Arsenic	4-11	immunoglobulin kappa variable 1-16	Homo sapiens	74-77
24813017-4	2014	The depth of source of drinking water (10-60 m) was also found with a mean of 36.12 +- 13.61 mug l-1 arsenic concentration.	Arsenic	101-108	immunoglobulin kappa variable 1-16	Homo sapiens	97-100
24813017-5	2014	Observations revealed that at depth ranging from 10 to 20 m, the mean level of arsenic concentration was 17.398 +- 21.796 mug l-1, while at 21 to 40 m depth As level was 39.685 +- 40.832 mug l-1 and at 41 to 60 m As level was 46.89 +- 52.80 mug l-1, respectively.	Arsenic	79-86	immunoglobulin kappa variable 1-16	Homo sapiens	126-129
24813017-9	2014	Results showed that group 21-30 years having maximum arsenic concentration with mean value of 52.57 +- 53.79 mug l-1.	Arsenic	53-60	immunoglobulin kappa variable 1-16	Homo sapiens	113-116
24813017-10	2014	Correlation analysis also showed a significant positive correlation (r = 0.801, t = 5.66, P &lt; 0.05) between age of drinking water sources and their respective arsenic concentration (mug l-1).	Arsenic	162-169	immunoglobulin kappa variable 1-16	Homo sapiens	189-192
24598884-3	2014	Both reactions are catalyzed by arsenic (+3 oxidation state) methyltransferase (AS3MT) using S-adenosylmethionine (SAM) as the methyl donor, yielding the methylated product and S-adenosylhomocysteine (SAH), a potent product-inhibitor of AS3MT.	Arsenic	32-39	arsenite methyltransferase	Homo sapiens	80-85
24598884-3	2014	Both reactions are catalyzed by arsenic (+3 oxidation state) methyltransferase (AS3MT) using S-adenosylmethionine (SAM) as the methyl donor, yielding the methylated product and S-adenosylhomocysteine (SAH), a potent product-inhibitor of AS3MT.	Arsenic	32-39	arsenite methyltransferase	Homo sapiens	237-242
24582688-0	2014	Reactive oxygen species contribute to arsenic-induced EZH2 phosphorylation in human bronchial epithelial cells and lung cancer cells.	Arsenic	38-45	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	54-58
23255470-0	2014	Aberrant overexpression of FOXM1 transcription factor plays a critical role in lung carcinogenesis induced by low doses of arsenic.	Arsenic	123-130	forkhead box M1	Homo sapiens	27-32
24656378-4	2014	The expressions of osteocalcin (OC) and osteopontin (OPN) for the HSTC were also detected to be about twice as high as those on the as-sprayed TC.	Arsenic	108-110	bone gamma-carboxyglutamate protein	Homo sapiens	19-30
24656378-4	2014	The expressions of osteocalcin (OC) and osteopontin (OPN) for the HSTC were also detected to be about twice as high as those on the as-sprayed TC.	Arsenic	108-110	bone gamma-carboxyglutamate protein	Homo sapiens	32-34
24656378-4	2014	The expressions of osteocalcin (OC) and osteopontin (OPN) for the HSTC were also detected to be about twice as high as those on the as-sprayed TC.	Arsenic	108-110	secreted phosphoprotein 1	Homo sapiens	40-51
24656378-4	2014	The expressions of osteocalcin (OC) and osteopontin (OPN) for the HSTC were also detected to be about twice as high as those on the as-sprayed TC.	Arsenic	108-110	secreted phosphoprotein 1	Homo sapiens	53-56
24593923-6	2014	Additionally, the at-risk genotypes of the AS3MT SNPs were positively related to the proportion of monomethylarsonic acid (MMA) in urine, which is indicative of arsenic methylation capacity.	Arsenic	161-168	arsenite methyltransferase	Homo sapiens	43-48
24582688-1	2014	Our previous studies suggested that arsenic is able to induce serine 21 phosphorylation of the EZH2 protein through activation of JNK, STAT3, and Akt signaling pathways in the bronchial epithelial cell line, BEAS-2B.	Arsenic	36-43	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	95-99
24582688-1	2014	Our previous studies suggested that arsenic is able to induce serine 21 phosphorylation of the EZH2 protein through activation of JNK, STAT3, and Akt signaling pathways in the bronchial epithelial cell line, BEAS-2B.	Arsenic	36-43	mitogen-activated protein kinase 8	Homo sapiens	130-133
24582688-1	2014	Our previous studies suggested that arsenic is able to induce serine 21 phosphorylation of the EZH2 protein through activation of JNK, STAT3, and Akt signaling pathways in the bronchial epithelial cell line, BEAS-2B.	Arsenic	36-43	signal transducer and activator of transcription 3	Homo sapiens	135-140
24582688-1	2014	Our previous studies suggested that arsenic is able to induce serine 21 phosphorylation of the EZH2 protein through activation of JNK, STAT3, and Akt signaling pathways in the bronchial epithelial cell line, BEAS-2B.	Arsenic	36-43	AKT serine/threonine kinase 1	Homo sapiens	146-149
24582688-2	2014	In the present report, we further demonstrated that reactive oxygen species (ROS) were involved in the arsenic-induced protein kinase activation that leads to EZH2 phosphorylation.	Arsenic	103-110	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	159-163
24964631-0	2014	[Expression and significance of ERalpha mRNA of residents exposed to arsenic via drinking water].	Arsenic	69-76	estrogen receptor 1	Homo sapiens	32-39
24964631-1	2014	OBJECTIVE: To detect ERbeta mRNA expression of subjects exposed to different arsenic drinking water, and to analyze the potential relationship between their abnormal expression and heart injury caused by arsenic in order to study the endocrine disturbing effect of arsenic.	Arsenic	77-84	estrogen receptor 2	Homo sapiens	21-27
24964631-8	2014	CONCLUSION: chronic arsenic exposure can potentially disturb ERbeta mRNA expression, as well as there are possible relationship between ERbeta mRNA abnormal expression and Q-Tc interval prolongation and Tp-Te interval prolonged caused by arsenic.	Arsenic	20-27	estrogen receptor 2	Homo sapiens	61-67
24964631-8	2014	CONCLUSION: chronic arsenic exposure can potentially disturb ERbeta mRNA expression, as well as there are possible relationship between ERbeta mRNA abnormal expression and Q-Tc interval prolongation and Tp-Te interval prolonged caused by arsenic.	Arsenic	238-245	estrogen receptor 2	Homo sapiens	136-142
24582688-4	2014	First, the pretreatment of the cells with N-acetyl-l-cysteine (NAC), a potent antioxidant, abolishes arsenic-induced EZH2 phosphorylation along with the inhibition of JNK, STAT3, and Akt.	Arsenic	101-108	X-linked Kx blood group	Homo sapiens	63-66
24582688-4	2014	First, the pretreatment of the cells with N-acetyl-l-cysteine (NAC), a potent antioxidant, abolishes arsenic-induced EZH2 phosphorylation along with the inhibition of JNK, STAT3, and Akt.	Arsenic	101-108	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	117-121
24582688-4	2014	First, the pretreatment of the cells with N-acetyl-l-cysteine (NAC), a potent antioxidant, abolishes arsenic-induced EZH2 phosphorylation along with the inhibition of JNK, STAT3, and Akt.	Arsenic	101-108	mitogen-activated protein kinase 8	Homo sapiens	167-170
24582688-4	2014	First, the pretreatment of the cells with N-acetyl-l-cysteine (NAC), a potent antioxidant, abolishes arsenic-induced EZH2 phosphorylation along with the inhibition of JNK, STAT3, and Akt.	Arsenic	101-108	signal transducer and activator of transcription 3	Homo sapiens	172-177
24582688-4	2014	First, the pretreatment of the cells with N-acetyl-l-cysteine (NAC), a potent antioxidant, abolishes arsenic-induced EZH2 phosphorylation along with the inhibition of JNK, STAT3, and Akt.	Arsenic	101-108	AKT serine/threonine kinase 1	Homo sapiens	183-186
24582688-6	2014	By ectopic expression of the myc-tagged EZH2, we additionally identified direct interaction and phosphorylation of the EZH2 protein by Akt in response to arsenic and H2O2.	Arsenic	154-161	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	40-44
24964631-8	2014	CONCLUSION: chronic arsenic exposure can potentially disturb ERbeta mRNA expression, as well as there are possible relationship between ERbeta mRNA abnormal expression and Q-Tc interval prolongation and Tp-Te interval prolonged caused by arsenic.	Arsenic	238-245	transmembrane phosphatase with tensin homology	Homo sapiens	203-208
24582688-6	2014	By ectopic expression of the myc-tagged EZH2, we additionally identified direct interaction and phosphorylation of the EZH2 protein by Akt in response to arsenic and H2O2.	Arsenic	154-161	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	119-123
24582688-6	2014	By ectopic expression of the myc-tagged EZH2, we additionally identified direct interaction and phosphorylation of the EZH2 protein by Akt in response to arsenic and H2O2.	Arsenic	154-161	AKT serine/threonine kinase 1	Homo sapiens	135-138
24582688-7	2014	Furthermore, both arsenic and H2O2 were able to induce the translocation of ectopically expressed or endogenous EZH2 from nucleus to cytoplasm.	Arsenic	18-25	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	112-116
24582688-8	2014	In summary, the data presented in this report indicate that oxidative stress due to ROS generation plays an important role in the arsenic-induced EZH2 phosphorylation.	Arsenic	130-137	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	146-150
24669248-6	2014	Of the 123 miRNAs, 15 miRNAs were differentially expressed between the AS and CS groups, of which four were significantly upregulated (rno-miR-296, rno-miR-141, rno-miR-382 and rno-miR-219-5p) and 11 were downregulated (significantly downregulated, rno-miR-135a and rno-miR-466b).	Arsenic	71-73	microRNA 296	Rattus norvegicus	135-146
24759735-0	2014	Fluoride and arsenic exposure impairs learning and memory and decreases mGluR5 expression in the hippocampus and cortex in rats.	Arsenic	13-20	glutamate receptor, ionotropic, kainate 1	Mus musculus	72-78
24759735-11	2014	mGluR5 mRNA and protein expressions in the hippocampus and mGluR5 protein expression in the cortex decreased in rats exposed to arsenic alone.	Arsenic	128-135	glutamate receptor, ionotropic, kainate 1	Mus musculus	0-6
24759735-11	2014	mGluR5 mRNA and protein expressions in the hippocampus and mGluR5 protein expression in the cortex decreased in rats exposed to arsenic alone.	Arsenic	128-135	glutamate receptor, ionotropic, kainate 1	Mus musculus	59-65
24759735-12	2014	Interestingly, compared with fluoride and arsenic exposure alone, fluoride and arsenic combination decreased mGluR5 mRNA expression in the cortex and protein expression in the hippocampus, suggesting a synergistic effect of fluoride and arsenic.	Arsenic	42-49	glutamate receptor, ionotropic, kainate 1	Mus musculus	109-115
24759735-12	2014	Interestingly, compared with fluoride and arsenic exposure alone, fluoride and arsenic combination decreased mGluR5 mRNA expression in the cortex and protein expression in the hippocampus, suggesting a synergistic effect of fluoride and arsenic.	Arsenic	79-86	glutamate receptor, ionotropic, kainate 1	Mus musculus	109-115
24759735-12	2014	Interestingly, compared with fluoride and arsenic exposure alone, fluoride and arsenic combination decreased mGluR5 mRNA expression in the cortex and protein expression in the hippocampus, suggesting a synergistic effect of fluoride and arsenic.	Arsenic	79-86	glutamate receptor, ionotropic, kainate 1	Mus musculus	109-115
24552478-0	2014	ATP-binding cassette transporter A1 (ABCA1) promotes arsenic tolerance in human cells by reducing cellular arsenic accumulation.	Arsenic	53-60	ATP binding cassette subfamily A member 1	Homo sapiens	0-35
24552478-0	2014	ATP-binding cassette transporter A1 (ABCA1) promotes arsenic tolerance in human cells by reducing cellular arsenic accumulation.	Arsenic	53-60	ATP binding cassette subfamily A member 1	Homo sapiens	37-42
24552478-0	2014	ATP-binding cassette transporter A1 (ABCA1) promotes arsenic tolerance in human cells by reducing cellular arsenic accumulation.	Arsenic	107-114	ATP binding cassette subfamily A member 1	Homo sapiens	0-35
24552478-0	2014	ATP-binding cassette transporter A1 (ABCA1) promotes arsenic tolerance in human cells by reducing cellular arsenic accumulation.	Arsenic	107-114	ATP binding cassette subfamily A member 1	Homo sapiens	37-42
24552478-8	2014	We found that among the three ABC genes, only when ABCA1 gene expression was silenced did cells obviously lose their arsenic tolerance.	Arsenic	117-124	ATP binding cassette subfamily A member 1	Homo sapiens	51-56
24552478-10	2014	Overexpression of ABCA1 in HeLa cells decreased arsenic accumulation in the cells and the cells were more resistant to As(III) than control cells transfected with empty vector.	Arsenic	48-55	ATP binding cassette subfamily A member 1	Homo sapiens	18-23
24552478-11	2014	These results suggest a new functional role for ABCA1 in the development of arsenic resistance in human cells.	Arsenic	76-83	ATP binding cassette subfamily A member 1	Homo sapiens	48-53
24617811-5	2014	On the other hand, alkaline pH that favors the photoinduced transformation of NO3(-) to NO2(-) significantly facilitated the catalytic reduction/oxidation cycling, which enabled the complete oxidation of As(III) at the condition of [As(III)]/[NO2(-)] &gt;&gt; 1 and markedly accelerated NO3(-)-sensitized oxidation of As(III).	Arsenic	204-206	NBL1, DAN family BMP antagonist	Homo sapiens	78-81
24617811-5	2014	On the other hand, alkaline pH that favors the photoinduced transformation of NO3(-) to NO2(-) significantly facilitated the catalytic reduction/oxidation cycling, which enabled the complete oxidation of As(III) at the condition of [As(III)]/[NO2(-)] &gt;&gt; 1 and markedly accelerated NO3(-)-sensitized oxidation of As(III).	Arsenic	204-206	NBL1, DAN family BMP antagonist	Homo sapiens	287-290
24617811-5	2014	On the other hand, alkaline pH that favors the photoinduced transformation of NO3(-) to NO2(-) significantly facilitated the catalytic reduction/oxidation cycling, which enabled the complete oxidation of As(III) at the condition of [As(III)]/[NO2(-)] &gt;&gt; 1 and markedly accelerated NO3(-)-sensitized oxidation of As(III).	Arsenic	233-235	NBL1, DAN family BMP antagonist	Homo sapiens	78-81
24617811-5	2014	On the other hand, alkaline pH that favors the photoinduced transformation of NO3(-) to NO2(-) significantly facilitated the catalytic reduction/oxidation cycling, which enabled the complete oxidation of As(III) at the condition of [As(III)]/[NO2(-)] &gt;&gt; 1 and markedly accelerated NO3(-)-sensitized oxidation of As(III).	Arsenic	233-235	NBL1, DAN family BMP antagonist	Homo sapiens	287-290
24617811-5	2014	On the other hand, alkaline pH that favors the photoinduced transformation of NO3(-) to NO2(-) significantly facilitated the catalytic reduction/oxidation cycling, which enabled the complete oxidation of As(III) at the condition of [As(III)]/[NO2(-)] &gt;&gt; 1 and markedly accelerated NO3(-)-sensitized oxidation of As(III).	Arsenic	233-235	NBL1, DAN family BMP antagonist	Homo sapiens	78-81
24617811-5	2014	On the other hand, alkaline pH that favors the photoinduced transformation of NO3(-) to NO2(-) significantly facilitated the catalytic reduction/oxidation cycling, which enabled the complete oxidation of As(III) at the condition of [As(III)]/[NO2(-)] &gt;&gt; 1 and markedly accelerated NO3(-)-sensitized oxidation of As(III).	Arsenic	233-235	NBL1, DAN family BMP antagonist	Homo sapiens	287-290
24851051-9	2014	As many as 41% and 13% of patients had LDL-C levels &gt;=0.5 mmol/L (&gt;=20 mg/dL) above LDL-C 1.8 mmol/L (70 mg/dL) and 2.6 mmol/L (100 mg/dL), respectively, in both cohorts; these percentages were generally similar across atorvastatin doses.	Arsenic	8-10	component of oligomeric golgi complex 2	Homo sapiens	39-44
24851051-9	2014	As many as 41% and 13% of patients had LDL-C levels &gt;=0.5 mmol/L (&gt;=20 mg/dL) above LDL-C 1.8 mmol/L (70 mg/dL) and 2.6 mmol/L (100 mg/dL), respectively, in both cohorts; these percentages were generally similar across atorvastatin doses.	Arsenic	8-10	component of oligomeric golgi complex 2	Homo sapiens	90-95
24669248-6	2014	Of the 123 miRNAs, 15 miRNAs were differentially expressed between the AS and CS groups, of which four were significantly upregulated (rno-miR-296, rno-miR-141, rno-miR-382 and rno-miR-219-5p) and 11 were downregulated (significantly downregulated, rno-miR-135a and rno-miR-466b).	Arsenic	71-73	microRNA 141	Rattus norvegicus	148-159
24669248-6	2014	Of the 123 miRNAs, 15 miRNAs were differentially expressed between the AS and CS groups, of which four were significantly upregulated (rno-miR-296, rno-miR-141, rno-miR-382 and rno-miR-219-5p) and 11 were downregulated (significantly downregulated, rno-miR-135a and rno-miR-466b).	Arsenic	71-73	microRNA 382	Rattus norvegicus	161-172
24669248-6	2014	Of the 123 miRNAs, 15 miRNAs were differentially expressed between the AS and CS groups, of which four were significantly upregulated (rno-miR-296, rno-miR-141, rno-miR-382 and rno-miR-219-5p) and 11 were downregulated (significantly downregulated, rno-miR-135a and rno-miR-466b).	Arsenic	71-73	microRNA 135a	Rattus norvegicus	249-261
24413338-8	2014	Re-expression of miR-199a-5p impaired arsenic-induced angiogenesis and tumor growth through its direct targets HIF-1alpha and COX-2.	Arsenic	38-45	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	126-131
24473091-0	2014	Arsenic-induced promoter hypomethylation and over-expression of ERCC2 reduces DNA repair capacity in humans by non-disjunction of the ERCC2-Cdk7 complex.	Arsenic	0-7	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	64-69
24473091-0	2014	Arsenic-induced promoter hypomethylation and over-expression of ERCC2 reduces DNA repair capacity in humans by non-disjunction of the ERCC2-Cdk7 complex.	Arsenic	0-7	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	134-139
24473091-0	2014	Arsenic-induced promoter hypomethylation and over-expression of ERCC2 reduces DNA repair capacity in humans by non-disjunction of the ERCC2-Cdk7 complex.	Arsenic	0-7	cyclin dependent kinase 7	Homo sapiens	140-144
24473091-4	2014	Arsenic metabolism alters epigenetic regulation; we tried to elucidate the regulation of ERCC2 in arsenic-exposed humans.	Arsenic	0-7	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	89-94
24473091-4	2014	Arsenic metabolism alters epigenetic regulation; we tried to elucidate the regulation of ERCC2 in arsenic-exposed humans.	Arsenic	98-105	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	89-94
24473091-8	2014	Bisulfite-modified methylation specific PCR showed a significant (p &lt; 0.0001) hypomethylation of the ERCC2 promoter in the arsenic-exposed individuals.	Arsenic	126-133	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	104-109
24473091-10	2014	Immuno-precipitation and western blotting revealed an increased (p &lt; 0.001) association of Cdk7 with ERCC2 in highly arsenic exposed individuals.	Arsenic	120-127	cyclin dependent kinase 7	Homo sapiens	94-98
24473091-10	2014	Immuno-precipitation and western blotting revealed an increased (p &lt; 0.001) association of Cdk7 with ERCC2 in highly arsenic exposed individuals.	Arsenic	120-127	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	104-109
24473091-12	2014	Thus we infer that arsenic biotransformation leads to promoter hypomethylation of ERCC2, which in turn inhibits the normal functioning of the CAK-complex, thus affecting DNA-repair; this effect was highest among the arsenic exposed individuals with dermatological lesions.	Arsenic	19-26	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	82-87
24473091-12	2014	Thus we infer that arsenic biotransformation leads to promoter hypomethylation of ERCC2, which in turn inhibits the normal functioning of the CAK-complex, thus affecting DNA-repair; this effect was highest among the arsenic exposed individuals with dermatological lesions.	Arsenic	216-223	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	82-87
24621105-5	2014	Among those with the AA genotype of the AS3MT gene, arsenic levels were negatively associated with language (p &lt; 0.001), attention (p = 0.01), and executive functioning (p = 0.04).	Arsenic	52-59	arsenite methyltransferase	Homo sapiens	40-45
24621105-8	2014	CONCLUSIONS: Low-level arsenic exposure is associated with cognitive functioning; however, this association is modified by an AS3MT gene.	Arsenic	23-30	arsenite methyltransferase	Homo sapiens	126-131
24413338-0	2014	Chronic arsenic exposure and angiogenesis in human bronchial epithelial cells via the ROS/miR-199a-5p/HIF-1alpha/COX-2 pathway.	Arsenic	8-15	hypoxia inducible factor 1 subunit alpha	Homo sapiens	102-112
24413338-0	2014	Chronic arsenic exposure and angiogenesis in human bronchial epithelial cells via the ROS/miR-199a-5p/HIF-1alpha/COX-2 pathway.	Arsenic	8-15	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	113-118
24413338-8	2014	Re-expression of miR-199a-5p impaired arsenic-induced angiogenesis and tumor growth through its direct targets HIF-1alpha and COX-2.	Arsenic	38-45	hypoxia inducible factor 1 subunit alpha	Homo sapiens	111-121
23993414-13	2014	In the number of cells that stained positive for BMP-2, the LAS group was significantly larger than that in the AS group after 1 (P &lt; 0.0001) and 2 weeks (P = 0.0113).	Arsenic	61-63	bone morphogenetic protein 2	Oryctolagus cuniculus	49-54
24675390-0	2014	Arsenic-induced sub-lethal stress reprograms human bronchial epithelial cells to CD61  cancer stem cells.	Arsenic	0-7	integrin subunit beta 3	Homo sapiens	81-85
23524579-0	2014	Low-dose arsenic induces chemotherapy protection via p53/NF-kappaB-mediated metabolic regulation.	Arsenic	9-16	tumor protein p53	Homo sapiens	53-56
23524579-0	2014	Low-dose arsenic induces chemotherapy protection via p53/NF-kappaB-mediated metabolic regulation.	Arsenic	9-16	nuclear factor kappa B subunit 1	Homo sapiens	57-66
23524579-3	2014	Pretreatment of untransformed cells with low doses of arsenic induced concerted p53 suppression and NF-kappaB activation, which elicited a marked induction of glycolysis.	Arsenic	54-61	tumor protein p53	Homo sapiens	80-83
23524579-3	2014	Pretreatment of untransformed cells with low doses of arsenic induced concerted p53 suppression and NF-kappaB activation, which elicited a marked induction of glycolysis.	Arsenic	54-61	nuclear factor kappa B subunit 1	Homo sapiens	100-109
23524579-5	2014	Using both in vitro and in vivo models, we demonstrated an absolute requirement of functional p53 in arsenic-mediated protection.	Arsenic	101-108	tumor protein p53	Homo sapiens	94-97
24190502-0	2014	Ogg1 genetic background determines the genotoxic potential of environmentally relevant arsenic exposures.	Arsenic	87-94	8-oxoguanine DNA glycosylase	Homo sapiens	0-4
24413338-9	2014	We further showed that arsenic induced COX-2 expression through HIF-1 regulation at the transcriptional level.	Arsenic	23-30	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	39-44
24413338-9	2014	We further showed that arsenic induced COX-2 expression through HIF-1 regulation at the transcriptional level.	Arsenic	23-30	hypoxia inducible factor 1 subunit alpha	Homo sapiens	64-69
24413338-11	2014	CONCLUSION: The findings establish critical roles of miR-199a-5p and its downstream targets HIF-1/COX-2 in arsenic-induced tumor growth and angiogenesis.	Arsenic	107-114	hypoxia inducible factor 1 subunit alpha	Homo sapiens	92-97
24413338-11	2014	CONCLUSION: The findings establish critical roles of miR-199a-5p and its downstream targets HIF-1/COX-2 in arsenic-induced tumor growth and angiogenesis.	Arsenic	107-114	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	98-103
24413338-14	2014	Chronic arsenic exposure and angiogenesis in human bronchial epithelial cells via the ROS/miR-199a-5p/HIF-1alpha/COX-2 Pathway.	Arsenic	8-15	hypoxia inducible factor 1 subunit alpha	Homo sapiens	102-112
24413338-14	2014	Chronic arsenic exposure and angiogenesis in human bronchial epithelial cells via the ROS/miR-199a-5p/HIF-1alpha/COX-2 Pathway.	Arsenic	8-15	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	113-118
24711750-10	2014	It was evident from the results of drinking of the arsenic contaminated water of shallow tube wells that the levels of DBH activity decreased significantly as compared to the control healthy persons.	Arsenic	51-58	dopamine beta-hydroxylase	Homo sapiens	119-122
24391088-0	2014	A low-dose arsenic-induced p53 protein-mediated metabolic mechanism of radiotherapy protection.	Arsenic	11-18	tumor protein p53	Homo sapiens	27-30
24361962-0	2014	Arsenic programmes cellular genomic-immunity through miR-2909 RNomics.	Arsenic	0-7	microRNA 2909	Homo sapiens	53-61
24361962-2	2014	Although arsenic has been shown to have paradoxical effect on one arm of this armour involving APOBEC3G, the exact molecular mechanism of its action in this regard is far from clear.	Arsenic	9-16	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	95-103
23838883-3	2014	The objective of this study was to determine whether arsenic exposure is associated with changes in airway AAT concentration and whether this relationship is modified by selenium.	Arsenic	53-60	serpin family A member 1	Homo sapiens	107-110
23838883-6	2014	Household tap-water arsenic, toenail arsenic and urinary inorganic arsenic and metabolites were significantly higher in Ajo (20.6+-3.5 mug/l, 0.54+-0.77 mug/g and 27.7+-21.2 mug/l, respectively) than in Tucson (3.9+-2.5 mug/l, 0.16+-0.20 mug/g and 13.0+-13.8 mug/l, respectively).	Arsenic	20-27	nuclear RNA export factor 1	Homo sapiens	10-13
23838883-9	2014	Reduction in AAT may be a means by which arsenic induces respiratory disease, and selenium may protect against this adverse effect.	Arsenic	41-48	serpin family A member 1	Homo sapiens	13-16
23860400-7	2014	Among subjects living in homes with tap water As &lt;=10, 5 or 3 p.p.b., aggregate inorganic As exposure was 8.6-11.8 mug/day, with 54-85% of intake from food.	Arsenic	46-48	nuclear RNA export factor 1	Homo sapiens	36-39
24473123-0	2014	Arsenic-induced suppression of kidney cell proliferation and the transcriptional coregulator MAML1.	Arsenic	0-7	mastermind like transcriptional coactivator 1	Homo sapiens	93-98
24473123-5	2014	Exposure of HEK293 cells to inorganic arsenic (arsenite) showed reduced levels of MAML1, in combination with a decreased proliferation rate.	Arsenic	38-45	mastermind like transcriptional coactivator 1	Homo sapiens	82-87
24473123-6	2014	Our findings provide evidence that arsenic can inhibit proliferation of embryonic kidney cells, possibly through reduction of MAML1 gene expression.	Arsenic	35-42	mastermind like transcriptional coactivator 1	Homo sapiens	126-131
23961884-2	2014	The reduction in protein amount and enzyme activity caused by disruption of mitochondrial LIPOAMIDE DEHYDROGENASE2 enhanced the arsenic sensitivity of Arabidopsis thaliana.	Arsenic	128-135	lipoamide dehydrogenase 2	Arabidopsis thaliana	90-114
24391088-3	2014	We showed that low doses of arsenic induce HIF-1alpha, which activates a metabolic shift from oxidative phosphorylation to glycolysis, resulting in increased cellular resistance to radiation.	Arsenic	28-35	hypoxia inducible factor 1 subunit alpha	Homo sapiens	43-53
24391088-4	2014	Of importance is that low-dose arsenic-induced HIF-1alpha requires functional p53, limiting the glycolytic shift to normal cells.	Arsenic	31-38	hypoxia inducible factor 1 subunit alpha	Homo sapiens	47-57
24391088-4	2014	Of importance is that low-dose arsenic-induced HIF-1alpha requires functional p53, limiting the glycolytic shift to normal cells.	Arsenic	31-38	tumor protein p53	Homo sapiens	78-81
24516582-0	2014	The NRF2-KEAP1 pathway is an early responsive gene network in arsenic exposed lymphoblastoid cells.	Arsenic	62-69	NFE2 like bZIP transcription factor 2	Homo sapiens	4-8
24384392-0	2014	Mthfr gene ablation enhances susceptibility to arsenic prenatal toxicity.	Arsenic	47-54	methylenetetrahydrofolate reductase	Mus musculus	0-5
24384392-5	2014	RESULTS: When the dams in Mthfr(+/-)xMthfr(+/-) matings were treated with 7.2 mg/kg As, the resorption rate increased to 43.4%, from a background frequency of 7.2%.	Arsenic	84-86	methylenetetrahydrofolate reductase	Mus musculus	26-31
24516582-0	2014	The NRF2-KEAP1 pathway is an early responsive gene network in arsenic exposed lymphoblastoid cells.	Arsenic	62-69	kelch like ECH associated protein 1	Homo sapiens	9-14
23892647-5	2014	Moreover, arsenic activated UPR, leading to phosphorylation of eukaryotic translation initiation factor 2 subunit alpha (eIF2alpha), induction of ATF4, and processing of ATF6.	Arsenic	10-17	eukaryotic translation initiation factor 2, subunit 1 alpha	Mus musculus	63-119
24068038-0	2014	Arsenic-induced cancer cell phenotype in human breast epithelia is estrogen receptor-independent but involves aromatase activation.	Arsenic	0-7	estrogen receptor 1	Homo sapiens	67-84
24154821-4	2014	In this study, we evaluated AS3MT promoter methylation according to exposure, assessed by urinary arsenic excretion in a stratified random sample of 48 participants from the Strong Heart Study who had urine arsenic measured at baseline and DNA available from 1989 to 1991 and 1998-1999.	Arsenic	98-105	arsenite methyltransferase	Homo sapiens	28-33
24154821-8	2014	A hypomethylated region in the AS3MT promoter was associated with higher arsenic exposure.	Arsenic	73-80	arsenite methyltransferase	Homo sapiens	31-36
24154821-9	2014	In vitro, arsenic induced AS3MT promoter hypomethylation, and it increased AS3MT expression in human peripheral blood mononuclear cells.	Arsenic	10-17	arsenite methyltransferase	Homo sapiens	26-31
24154821-9	2014	In vitro, arsenic induced AS3MT promoter hypomethylation, and it increased AS3MT expression in human peripheral blood mononuclear cells.	Arsenic	10-17	arsenite methyltransferase	Homo sapiens	75-80
22120977-6	2014	Arsenic did not alter basal and inducible nitric oxide synthase (iNOS)-mediated NO production, but decreased constitutive NOS (cNOS)-mediated NO release.	Arsenic	0-7	nitric oxide synthase 3	Rattus norvegicus	109-125
22120977-6	2014	Arsenic did not alter basal and inducible nitric oxide synthase (iNOS)-mediated NO production, but decreased constitutive NOS (cNOS)-mediated NO release.	Arsenic	0-7	nitric oxide synthase 3	Rattus norvegicus	127-131
22120977-7	2014	Arsenic reduced expression of endothelial NOS (eNOS) and iNOS genes.	Arsenic	0-7	nitric oxide synthase 3	Rattus norvegicus	30-45
22120977-7	2014	Arsenic reduced expression of endothelial NOS (eNOS) and iNOS genes.	Arsenic	0-7	nitric oxide synthase 2	Rattus norvegicus	57-61
24161444-9	2014	In conclusion, this study demonstrates for the first time that methylated pentavalent arsenic metabolites are bifunctional inducers, as they increase CYP1A1 by activating the AhR/XRE signaling pathway and they increase NQO1 by activating the Nrf2/ARE signaling pathway in addition to the AhR/XRE pathway.	Arsenic	86-93	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	150-156
24161444-9	2014	In conclusion, this study demonstrates for the first time that methylated pentavalent arsenic metabolites are bifunctional inducers, as they increase CYP1A1 by activating the AhR/XRE signaling pathway and they increase NQO1 by activating the Nrf2/ARE signaling pathway in addition to the AhR/XRE pathway.	Arsenic	86-93	aryl hydrocarbon receptor	Homo sapiens	175-178
24161444-9	2014	In conclusion, this study demonstrates for the first time that methylated pentavalent arsenic metabolites are bifunctional inducers, as they increase CYP1A1 by activating the AhR/XRE signaling pathway and they increase NQO1 by activating the Nrf2/ARE signaling pathway in addition to the AhR/XRE pathway.	Arsenic	86-93	NAD(P)H quinone dehydrogenase 1	Homo sapiens	219-223
24161444-9	2014	In conclusion, this study demonstrates for the first time that methylated pentavalent arsenic metabolites are bifunctional inducers, as they increase CYP1A1 by activating the AhR/XRE signaling pathway and they increase NQO1 by activating the Nrf2/ARE signaling pathway in addition to the AhR/XRE pathway.	Arsenic	86-93	NFE2 like bZIP transcription factor 2	Homo sapiens	242-246
24161444-9	2014	In conclusion, this study demonstrates for the first time that methylated pentavalent arsenic metabolites are bifunctional inducers, as they increase CYP1A1 by activating the AhR/XRE signaling pathway and they increase NQO1 by activating the Nrf2/ARE signaling pathway in addition to the AhR/XRE pathway.	Arsenic	86-93	aryl hydrocarbon receptor	Homo sapiens	288-291
23892647-10	2014	In addition, pretreatment with salubrinal, a selective inhibitor of eIF2alpha dephosphorylation, enhanced arsenic-induced GRP78 and CHOP expression and partially prevented arsenic cytotoxicity in SVEC4-10 cells.	Arsenic	106-113	heat shock protein 5	Mus musculus	122-127
23892647-10	2014	In addition, pretreatment with salubrinal, a selective inhibitor of eIF2alpha dephosphorylation, enhanced arsenic-induced GRP78 and CHOP expression and partially prevented arsenic cytotoxicity in SVEC4-10 cells.	Arsenic	106-113	DNA-damage inducible transcript 3	Mus musculus	132-136
22120977-3	2014	Arsenic increased lipid peroxidation and reactive oxygen species (ROS) generation, depleted glutathione (GSH), and decreased superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glutathione reductase (GR) activities.	Arsenic	0-7	catalase	Rattus norvegicus	153-161
22120977-3	2014	Arsenic increased lipid peroxidation and reactive oxygen species (ROS) generation, depleted glutathione (GSH), and decreased superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glutathione reductase (GR) activities.	Arsenic	0-7	glutathione-disulfide reductase	Rattus norvegicus	197-218
22120977-3	2014	Arsenic increased lipid peroxidation and reactive oxygen species (ROS) generation, depleted glutathione (GSH), and decreased superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glutathione reductase (GR) activities.	Arsenic	0-7	glutathione-disulfide reductase	Rattus norvegicus	220-222
24161444-0	2014	Methylated pentavalent arsenic metabolites are bifunctional inducers, as they induce cytochrome P450 1A1 and NAD(P)H:quinone oxidoreductase through AhR- and Nrf2-dependent mechanisms.	Arsenic	23-30	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	85-104
24161444-0	2014	Methylated pentavalent arsenic metabolites are bifunctional inducers, as they induce cytochrome P450 1A1 and NAD(P)H:quinone oxidoreductase through AhR- and Nrf2-dependent mechanisms.	Arsenic	23-30	crystallin zeta	Homo sapiens	117-139
24161444-0	2014	Methylated pentavalent arsenic metabolites are bifunctional inducers, as they induce cytochrome P450 1A1 and NAD(P)H:quinone oxidoreductase through AhR- and Nrf2-dependent mechanisms.	Arsenic	23-30	aryl hydrocarbon receptor	Homo sapiens	148-151
24161444-0	2014	Methylated pentavalent arsenic metabolites are bifunctional inducers, as they induce cytochrome P450 1A1 and NAD(P)H:quinone oxidoreductase through AhR- and Nrf2-dependent mechanisms.	Arsenic	23-30	NFE2 like bZIP transcription factor 2	Homo sapiens	157-161
23892647-5	2014	Moreover, arsenic activated UPR, leading to phosphorylation of eukaryotic translation initiation factor 2 subunit alpha (eIF2alpha), induction of ATF4, and processing of ATF6.	Arsenic	10-17	eukaryotic translation initiation factor 2, subunit 1 alpha	Mus musculus	121-130
23892647-5	2014	Moreover, arsenic activated UPR, leading to phosphorylation of eukaryotic translation initiation factor 2 subunit alpha (eIF2alpha), induction of ATF4, and processing of ATF6.	Arsenic	10-17	activating transcription factor 4	Mus musculus	146-150
23892647-5	2014	Moreover, arsenic activated UPR, leading to phosphorylation of eukaryotic translation initiation factor 2 subunit alpha (eIF2alpha), induction of ATF4, and processing of ATF6.	Arsenic	10-17	activating transcription factor 6	Mus musculus	170-174
23892647-6	2014	Treatment with arsenic also triggered the expression of endoplasmic reticulum (ER) stress markers, GRP78 (glucose-regulated protein), and CHOP (C/EBP homologous protein).	Arsenic	15-22	heat shock protein 5	Mus musculus	99-104
23892647-6	2014	Treatment with arsenic also triggered the expression of endoplasmic reticulum (ER) stress markers, GRP78 (glucose-regulated protein), and CHOP (C/EBP homologous protein).	Arsenic	15-22	DNA-damage inducible transcript 3	Mus musculus	138-142
23892647-6	2014	Treatment with arsenic also triggered the expression of endoplasmic reticulum (ER) stress markers, GRP78 (glucose-regulated protein), and CHOP (C/EBP homologous protein).	Arsenic	15-22	DNA-damage inducible transcript 3	Mus musculus	144-168
23892647-7	2014	The activation of eIF2alpha, ATF4 and ATF6 and expression of GRP78 and CHOP are repressed by both LA and tiron, indicating arsenic-induced UPR is mediated through ROS-dependent and ROS-independent pathways.	Arsenic	123-130	eukaryotic translation initiation factor 2, subunit 1 alpha	Mus musculus	18-27
23892647-7	2014	The activation of eIF2alpha, ATF4 and ATF6 and expression of GRP78 and CHOP are repressed by both LA and tiron, indicating arsenic-induced UPR is mediated through ROS-dependent and ROS-independent pathways.	Arsenic	123-130	activating transcription factor 4	Mus musculus	29-33
23892647-7	2014	The activation of eIF2alpha, ATF4 and ATF6 and expression of GRP78 and CHOP are repressed by both LA and tiron, indicating arsenic-induced UPR is mediated through ROS-dependent and ROS-independent pathways.	Arsenic	123-130	activating transcription factor 6	Mus musculus	38-42
23892647-7	2014	The activation of eIF2alpha, ATF4 and ATF6 and expression of GRP78 and CHOP are repressed by both LA and tiron, indicating arsenic-induced UPR is mediated through ROS-dependent and ROS-independent pathways.	Arsenic	123-130	heat shock protein 5	Mus musculus	61-66
23892647-7	2014	The activation of eIF2alpha, ATF4 and ATF6 and expression of GRP78 and CHOP are repressed by both LA and tiron, indicating arsenic-induced UPR is mediated through ROS-dependent and ROS-independent pathways.	Arsenic	123-130	DNA-damage inducible transcript 3	Mus musculus	71-75
24382825-2	2014	Crystallinity of HAp nanoparticles was reduced because of the interference of the surface layers of chitosan with the dissolution/reprecipitation-mediated recrystallization mechanism that conditions the transition from the as-precipitated amorphous calcium phosphate phase to the most thermodynamically stable one--HAp.	Arsenic	36-38	retinoic acid receptor, beta	Mus musculus	17-20
24456662-9	2014	Additionally, there was a lower percentage of CD25- and CD40-positive cells in the group of 6- to 8-year-old children exposed to the highest concentrations of both As and F when compared to the 9- to 12-year-old group (CD25: 0.7+-0.8 vs. 1.1+-0.9, p&lt;0.0014; CD40: 16.0+-7.0 vs. 21.8+-5.8, p&lt;0.0003).	Arsenic	164-166	interleukin 2 receptor subunit alpha	Homo sapiens	46-50
24456662-9	2014	Additionally, there was a lower percentage of CD25- and CD40-positive cells in the group of 6- to 8-year-old children exposed to the highest concentrations of both As and F when compared to the 9- to 12-year-old group (CD25: 0.7+-0.8 vs. 1.1+-0.9, p&lt;0.0014; CD40: 16.0+-7.0 vs. 21.8+-5.8, p&lt;0.0003).	Arsenic	164-166	CD40 molecule	Homo sapiens	56-60
24456662-9	2014	Additionally, there was a lower percentage of CD25- and CD40-positive cells in the group of 6- to 8-year-old children exposed to the highest concentrations of both As and F when compared to the 9- to 12-year-old group (CD25: 0.7+-0.8 vs. 1.1+-0.9, p&lt;0.0014; CD40: 16.0+-7.0 vs. 21.8+-5.8, p&lt;0.0003).	Arsenic	164-166	interleukin 2 receptor subunit alpha	Homo sapiens	219-223
24456662-9	2014	Additionally, there was a lower percentage of CD25- and CD40-positive cells in the group of 6- to 8-year-old children exposed to the highest concentrations of both As and F when compared to the 9- to 12-year-old group (CD25: 0.7+-0.8 vs. 1.1+-0.9, p&lt;0.0014; CD40: 16.0+-7.0 vs. 21.8+-5.8, p&lt;0.0003).	Arsenic	164-166	CD40 molecule	Homo sapiens	261-265
24275069-2	2014	Poly(ADP-ribose) polymerase-1 (PARP-1), a zinc finger DNA repair protein, has been identified as a sensitive molecular target for arsenic.	Arsenic	130-137	poly(ADP-ribose) polymerase 1	Homo sapiens	0-29
24028894-3	2014	Down-regulation of the mutant Kras gene by siRNA caused defective abilities of proliferation, clonal formation, migration, and invasion of pancreatic cancer cells, as well as cell cycle arrest at the G0/G1 phase, which substantially enhanced the apoptosis-inducing effect of arsenic administration.	Arsenic	275-282	KRAS proto-oncogene, GTPase	Homo sapiens	30-34
24028894-4	2014	Consequently, co-administration of the two nanomedicines encapsulating siRNA or arsenic showed ideal tumor growth inhibition both in vitro and in vivo as a result of synergistic effect of the siRNA-directed Kras oncogene silencing and arsenic-induced cell apoptosis.	Arsenic	80-87	KRAS proto-oncogene, GTPase	Homo sapiens	207-211
24028894-4	2014	Consequently, co-administration of the two nanomedicines encapsulating siRNA or arsenic showed ideal tumor growth inhibition both in vitro and in vivo as a result of synergistic effect of the siRNA-directed Kras oncogene silencing and arsenic-induced cell apoptosis.	Arsenic	235-242	KRAS proto-oncogene, GTPase	Homo sapiens	207-211
24499085-7	2014	The receiver-operating characteristic curve analysis, comparing AS and the control group, showed area under the curve for cysC-umb, cysC-3, Cr-umb and Cr-3 (0.918; 0.698; 0.692; 0.660).	Arsenic	64-66	cystatin C	Homo sapiens	122-126
24499085-7	2014	The receiver-operating characteristic curve analysis, comparing AS and the control group, showed area under the curve for cysC-umb, cysC-3, Cr-umb and Cr-3 (0.918; 0.698; 0.692; 0.660).	Arsenic	64-66	cystatin C	Homo sapiens	132-136
24338963-5	2014	RESULTS: The separation capability between the analytical signals of arsenic species, AsB-As(III), As(III)-DMA, DMA-MMA and MMA-As(V), was 1.3, 1.1, 5.1 and 4.6, respectively.	Arsenic	69-76	arylsulfatase B	Homo sapiens	86-89
24359134-4	2014	Arsenic redox changes by Synechocystis under P-limited conditions is a dynamic cyclic process that includes the following: surface As(III) oxidation (either in the periplasm or near the outer membrane), As(V) uptake, intracellular As(V) reduction, and As(III) efflux.	Arsenic	0-7	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	203-208
24359134-4	2014	Arsenic redox changes by Synechocystis under P-limited conditions is a dynamic cyclic process that includes the following: surface As(III) oxidation (either in the periplasm or near the outer membrane), As(V) uptake, intracellular As(V) reduction, and As(III) efflux.	Arsenic	0-7	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	231-236
24190887-0	2014	PML isoforms in response to arsenic: high-resolution analysis of PML body structure and degradation.	Arsenic	28-35	PML nuclear body scaffold	Homo sapiens	0-3
24190887-0	2014	PML isoforms in response to arsenic: high-resolution analysis of PML body structure and degradation.	Arsenic	28-35	PML nuclear body scaffold	Homo sapiens	65-68
24190887-1	2014	Arsenic is a clinically effective treatment for acute promyelocytic leukaemia (APL) in which the promyelocytic leukaemia (PML) protein is fused to retinoic receptor alpha (RARalpha).	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	122-125
24190887-1	2014	Arsenic is a clinically effective treatment for acute promyelocytic leukaemia (APL) in which the promyelocytic leukaemia (PML) protein is fused to retinoic receptor alpha (RARalpha).	Arsenic	0-7	retinoic acid receptor alpha	Homo sapiens	172-180
24190887-2	2014	PML-RARalpha is degraded by the proteasome by a SUMO-dependent, ubiquitin-mediated pathway in response to arsenic treatment, curing the disease.	Arsenic	106-113	PML nuclear body scaffold	Homo sapiens	0-3
24190887-2	2014	PML-RARalpha is degraded by the proteasome by a SUMO-dependent, ubiquitin-mediated pathway in response to arsenic treatment, curing the disease.	Arsenic	106-113	retinoic acid receptor alpha	Homo sapiens	4-12
24190887-4	2014	Using a system in which only a single EYFP-linked PML isoform is expressed, we demonstrate that PMLI, PMLII and PMLVI accumulate in the cytoplasm following arsenic treatment, whereas PMLIII, PMLIV and PMLV do not.	Arsenic	156-163	PML nuclear body scaffold	Homo sapiens	50-53
24190887-6	2014	Arsenic treatment results in dramatic isoform-specific changes to PML body ultrastructure.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	66-69
24190887-7	2014	After extended arsenic treatment most PML isoforms are degraded, leaving SUMO at the core of the nuclear bodies.	Arsenic	15-22	PML nuclear body scaffold	Homo sapiens	38-41
24190887-9	2014	Immunoprecipitation analysis demonstrates that all PML isoforms are modified by SUMO and ubiquitin after arsenic treatment, and by using siRNA, we demonstrate that arsenic-induced degradation of all PML isoforms is dependent on the ubiquitin E3 ligase RNF4.	Arsenic	105-112	PML nuclear body scaffold	Homo sapiens	51-54
24190887-9	2014	Immunoprecipitation analysis demonstrates that all PML isoforms are modified by SUMO and ubiquitin after arsenic treatment, and by using siRNA, we demonstrate that arsenic-induced degradation of all PML isoforms is dependent on the ubiquitin E3 ligase RNF4.	Arsenic	164-171	PML nuclear body scaffold	Homo sapiens	51-54
24190887-9	2014	Immunoprecipitation analysis demonstrates that all PML isoforms are modified by SUMO and ubiquitin after arsenic treatment, and by using siRNA, we demonstrate that arsenic-induced degradation of all PML isoforms is dependent on the ubiquitin E3 ligase RNF4.	Arsenic	164-171	PML nuclear body scaffold	Homo sapiens	199-202
24190887-9	2014	Immunoprecipitation analysis demonstrates that all PML isoforms are modified by SUMO and ubiquitin after arsenic treatment, and by using siRNA, we demonstrate that arsenic-induced degradation of all PML isoforms is dependent on the ubiquitin E3 ligase RNF4.	Arsenic	164-171	ring finger protein 4	Homo sapiens	252-256
24190887-11	2014	Thus the variable C-terminal domain influences the rate and location of degradation of PML isoforms following arsenic treatment.	Arsenic	110-117	PML nuclear body scaffold	Homo sapiens	87-90
24296302-2	2014	The trivalent form of MMA is highly toxic in vitro and previous studies have identified associations between the proportion of urinary arsenic as MMA (%MMA) and several arsenic-related diseases.	Arsenic	135-142	monocyte to macrophage differentiation associated	Homo sapiens	22-25
24296302-2	2014	The trivalent form of MMA is highly toxic in vitro and previous studies have identified associations between the proportion of urinary arsenic as MMA (%MMA) and several arsenic-related diseases.	Arsenic	135-142	monocyte to macrophage differentiation associated	Homo sapiens	146-149
24296302-2	2014	The trivalent form of MMA is highly toxic in vitro and previous studies have identified associations between the proportion of urinary arsenic as MMA (%MMA) and several arsenic-related diseases.	Arsenic	135-142	monocyte to macrophage differentiation associated	Homo sapiens	146-149
24296302-2	2014	The trivalent form of MMA is highly toxic in vitro and previous studies have identified associations between the proportion of urinary arsenic as MMA (%MMA) and several arsenic-related diseases.	Arsenic	169-176	monocyte to macrophage differentiation associated	Homo sapiens	22-25
24296302-2	2014	The trivalent form of MMA is highly toxic in vitro and previous studies have identified associations between the proportion of urinary arsenic as MMA (%MMA) and several arsenic-related diseases.	Arsenic	169-176	monocyte to macrophage differentiation associated	Homo sapiens	146-149
24296302-2	2014	The trivalent form of MMA is highly toxic in vitro and previous studies have identified associations between the proportion of urinary arsenic as MMA (%MMA) and several arsenic-related diseases.	Arsenic	169-176	monocyte to macrophage differentiation associated	Homo sapiens	146-149
24296302-1	2014	In humans, ingested inorganic arsenic is metabolized to monomethylarsenic (MMA) then to dimethylarsenic (DMA), although this process is not complete in most people.	Arsenic	30-37	monocyte to macrophage differentiation associated	Homo sapiens	75-78
24275069-2	2014	Poly(ADP-ribose) polymerase-1 (PARP-1), a zinc finger DNA repair protein, has been identified as a sensitive molecular target for arsenic.	Arsenic	130-137	poly(ADP-ribose) polymerase 1	Homo sapiens	31-37
24275069-9	2014	These findings suggest that arsenite binding to PARP-1 protein created similar adverse biological effects as zinc deficiency, which establishes the molecular mechanism for zinc supplementation as a potentially effective treatment to reverse the detrimental outcomes of arsenic exposure.	Arsenic	269-276	poly(ADP-ribose) polymerase 1	Homo sapiens	48-54
24188932-7	2014	In conclusion, these results define a unique mechanism of HIF-1alpha accumulation following arsenic exposure, that is, arsenic activates NADPH oxidase-mitochondria axis to produce ROS, which deplete intracellular ascorbate and Fe(II) to inactivate PHDs, leading to HIF-1alpha stabilization.	Arsenic	92-99	hypoxia inducible factor 1 subunit alpha	Homo sapiens	58-68
24188932-1	2014	Arsenic exposure has been shown to induce hypoxia inducible factor 1alpha (HIF-1alpha) accumulation, however the underlying mechanism remains unknown.	Arsenic	0-7	hypoxia inducible factor 1 subunit alpha	Homo sapiens	42-73
24188932-1	2014	Arsenic exposure has been shown to induce hypoxia inducible factor 1alpha (HIF-1alpha) accumulation, however the underlying mechanism remains unknown.	Arsenic	0-7	hypoxia inducible factor 1 subunit alpha	Homo sapiens	75-85
24188932-2	2014	In the present study, we tested the hypothesis that arsenic exposure triggered the interaction between NADPH oxidase and mitochondria to promote reactive oxygen species (ROS) production, which inactivate prolyl hydroxylases (PHDs) activity, leading to the stabilization of HIF-1alpha protein.	Arsenic	52-59	hypoxia inducible factor 1 subunit alpha	Homo sapiens	273-283
24188932-7	2014	In conclusion, these results define a unique mechanism of HIF-1alpha accumulation following arsenic exposure, that is, arsenic activates NADPH oxidase-mitochondria axis to produce ROS, which deplete intracellular ascorbate and Fe(II) to inactivate PHDs, leading to HIF-1alpha stabilization.	Arsenic	119-126	hypoxia inducible factor 1 subunit alpha	Homo sapiens	58-68
24801890-3	2014	We demonstrate that Notch1 function contributes to the arsenic-induced keratinocyte transformation.	Arsenic	55-62	notch receptor 1	Homo sapiens	20-26
24244939-1	2014	Rapid and sensitive SERS identification and quantification of arsenic species in multiple matrices have been realized using a Fe3O4@Ag magnetic substrate.	Arsenic	62-69	seryl-tRNA synthetase 2, mitochondrial	Homo sapiens	20-24
24244939-2	2014	The molecular structure of arsenic on Fe3O4@Ag characterized using EXAFS spectroscopy and DFT confirms the existence of a chemical effect on SERS enhancement.	Arsenic	27-34	seryl-tRNA synthetase 2, mitochondrial	Homo sapiens	141-145
24244939-0	2014	Rapid in situ identification of arsenic species using a portable Fe3O4@Ag SERS sensor.	Arsenic	32-39	seryl-tRNA synthetase 2, mitochondrial	Homo sapiens	74-78
24157283-0	2014	Arsenic induces reactive oxygen species-caused neuronal cell apoptosis through JNK/ERK-mediated mitochondria-dependent and GRP 78/CHOP-regulated pathways.	Arsenic	0-7	mitogen-activated protein kinase 8	Mus musculus	79-82
24157283-0	2014	Arsenic induces reactive oxygen species-caused neuronal cell apoptosis through JNK/ERK-mediated mitochondria-dependent and GRP 78/CHOP-regulated pathways.	Arsenic	0-7	mitogen-activated protein kinase 1	Mus musculus	83-86
24157283-0	2014	Arsenic induces reactive oxygen species-caused neuronal cell apoptosis through JNK/ERK-mediated mitochondria-dependent and GRP 78/CHOP-regulated pathways.	Arsenic	0-7	heat shock protein 5	Mus musculus	123-129
24157283-0	2014	Arsenic induces reactive oxygen species-caused neuronal cell apoptosis through JNK/ERK-mediated mitochondria-dependent and GRP 78/CHOP-regulated pathways.	Arsenic	0-7	DNA-damage inducible transcript 3	Mus musculus	130-134
23818078-12	2014	Median arsenic levels in urine of groups I and II males were 124 and 61 mug L(-1) (p = 0.052) and in females 130 and 52 mug L(-1) (p = 0.0001), respectively.	Arsenic	7-14	immunoglobulin kappa variable 1-16	Homo sapiens	76-81
24268366-8	2014	Significant associations between cumulative arsenic exposure and DNA methylation levels of 28 patients were observed in nine CpG sites of nine gens including PDGFD (Spearman rank correlation, 0.54), CTNNA2 (0.48), KCNK17 (0.52), PCDHB2 (0.57), ZNF132 (0.48), DCDC2 (0.48), KLK7 (0.48), FBXO39 (0.49), and NPY2R (0.45).	Arsenic	44-51	platelet derived growth factor D	Homo sapiens	158-163
23784053-7	2014	The kinetic data showed that a sharp initial uptake of arsenic reached its equilibrium state within about 50 min of contact time, and the sorption kinetics followed a pseudo-second-order rate law both for As(III) and As(V) sorption.	Arsenic	55-62	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	217-222
23818078-13	2014	When arsenic levels in the water were reduced to below 50 mug L(-1) (Indian permissible limit), total arsenic intake and arsenic intake through the water significantly decreased, but arsenic uptake through the diet was found to be not significantly affected.	Arsenic	5-12	immunoglobulin kappa variable 1-16	Homo sapiens	62-67
24268366-8	2014	Significant associations between cumulative arsenic exposure and DNA methylation levels of 28 patients were observed in nine CpG sites of nine gens including PDGFD (Spearman rank correlation, 0.54), CTNNA2 (0.48), KCNK17 (0.52), PCDHB2 (0.57), ZNF132 (0.48), DCDC2 (0.48), KLK7 (0.48), FBXO39 (0.49), and NPY2R (0.45).	Arsenic	44-51	catenin alpha 2	Homo sapiens	199-205
24448467-0	2014	Arsenic reduces the antipyretic activity of paracetamol in rats: modulation of brain COX-2 activity and CB1 receptor expression.	Arsenic	0-7	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	85-90
24268366-8	2014	Significant associations between cumulative arsenic exposure and DNA methylation levels of 28 patients were observed in nine CpG sites of nine gens including PDGFD (Spearman rank correlation, 0.54), CTNNA2 (0.48), KCNK17 (0.52), PCDHB2 (0.57), ZNF132 (0.48), DCDC2 (0.48), KLK7 (0.48), FBXO39 (0.49), and NPY2R (0.45).	Arsenic	44-51	potassium two pore domain channel subfamily K member 17	Homo sapiens	214-220
24268366-8	2014	Significant associations between cumulative arsenic exposure and DNA methylation levels of 28 patients were observed in nine CpG sites of nine gens including PDGFD (Spearman rank correlation, 0.54), CTNNA2 (0.48), KCNK17 (0.52), PCDHB2 (0.57), ZNF132 (0.48), DCDC2 (0.48), KLK7 (0.48), FBXO39 (0.49), and NPY2R (0.45).	Arsenic	44-51	protocadherin beta 2	Homo sapiens	229-235
24268366-8	2014	Significant associations between cumulative arsenic exposure and DNA methylation levels of 28 patients were observed in nine CpG sites of nine gens including PDGFD (Spearman rank correlation, 0.54), CTNNA2 (0.48), KCNK17 (0.52), PCDHB2 (0.57), ZNF132 (0.48), DCDC2 (0.48), KLK7 (0.48), FBXO39 (0.49), and NPY2R (0.45).	Arsenic	44-51	zinc finger protein 132	Homo sapiens	244-250
24361700-0	2014	Arsenic may be involved in fluoride-induced bone toxicity through PTH/PKA/AP1 signaling pathway.	Arsenic	0-7	parathyroid hormone	Homo sapiens	66-69
24361700-0	2014	Arsenic may be involved in fluoride-induced bone toxicity through PTH/PKA/AP1 signaling pathway.	Arsenic	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	74-77
24268366-8	2014	Significant associations between cumulative arsenic exposure and DNA methylation levels of 28 patients were observed in nine CpG sites of nine gens including PDGFD (Spearman rank correlation, 0.54), CTNNA2 (0.48), KCNK17 (0.52), PCDHB2 (0.57), ZNF132 (0.48), DCDC2 (0.48), KLK7 (0.48), FBXO39 (0.49), and NPY2R (0.45).	Arsenic	44-51	doublecortin domain containing 2	Homo sapiens	259-264
24268366-8	2014	Significant associations between cumulative arsenic exposure and DNA methylation levels of 28 patients were observed in nine CpG sites of nine gens including PDGFD (Spearman rank correlation, 0.54), CTNNA2 (0.48), KCNK17 (0.52), PCDHB2 (0.57), ZNF132 (0.48), DCDC2 (0.48), KLK7 (0.48), FBXO39 (0.49), and NPY2R (0.45).	Arsenic	44-51	kallikrein related peptidase 7	Homo sapiens	273-277
24268366-8	2014	Significant associations between cumulative arsenic exposure and DNA methylation levels of 28 patients were observed in nine CpG sites of nine gens including PDGFD (Spearman rank correlation, 0.54), CTNNA2 (0.48), KCNK17 (0.52), PCDHB2 (0.57), ZNF132 (0.48), DCDC2 (0.48), KLK7 (0.48), FBXO39 (0.49), and NPY2R (0.45).	Arsenic	44-51	F-box protein 39	Homo sapiens	286-292
24268366-8	2014	Significant associations between cumulative arsenic exposure and DNA methylation levels of 28 patients were observed in nine CpG sites of nine gens including PDGFD (Spearman rank correlation, 0.54), CTNNA2 (0.48), KCNK17 (0.52), PCDHB2 (0.57), ZNF132 (0.48), DCDC2 (0.48), KLK7 (0.48), FBXO39 (0.49), and NPY2R (0.45).	Arsenic	44-51	neuropeptide Y receptor Y2	Homo sapiens	305-310
24268366-10	2014	CONCLUSIONS: Significant associations between cumulative arsenic exposure and methylation level of CTNNA2, KLK7, NPY2R, ZNF132 and KCNK17 were found in smoking-unrelated urothelial carcinoma.	Arsenic	57-64	catenin alpha 2	Homo sapiens	99-105
24268366-10	2014	CONCLUSIONS: Significant associations between cumulative arsenic exposure and methylation level of CTNNA2, KLK7, NPY2R, ZNF132 and KCNK17 were found in smoking-unrelated urothelial carcinoma.	Arsenic	57-64	kallikrein related peptidase 7	Homo sapiens	107-111
24268366-10	2014	CONCLUSIONS: Significant associations between cumulative arsenic exposure and methylation level of CTNNA2, KLK7, NPY2R, ZNF132 and KCNK17 were found in smoking-unrelated urothelial carcinoma.	Arsenic	57-64	neuropeptide Y receptor Y2	Homo sapiens	113-118
24268366-10	2014	CONCLUSIONS: Significant associations between cumulative arsenic exposure and methylation level of CTNNA2, KLK7, NPY2R, ZNF132 and KCNK17 were found in smoking-unrelated urothelial carcinoma.	Arsenic	57-64	zinc finger protein 132	Homo sapiens	120-126
24361700-6	2014	By observing the changes in gene and protein expression of PTH/PKA/AP1 signaling pathway, the results show that fluoride can increase the expression levels of PTH, PKA, and AP1, but arsenic can only affect the expression of AP1; fluoride and arsenic have an interaction on the expression of AP1.	Arsenic	182-189	parathyroid hormone	Homo sapiens	59-62
24361700-6	2014	By observing the changes in gene and protein expression of PTH/PKA/AP1 signaling pathway, the results show that fluoride can increase the expression levels of PTH, PKA, and AP1, but arsenic can only affect the expression of AP1; fluoride and arsenic have an interaction on the expression of AP1.	Arsenic	182-189	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	67-70
24361700-7	2014	Further study found that fluoride and arsenic can affect the mRNA expression level of c-fos gene (AP1 family members), and have an interaction on the expression of c-fos, but not c-jun.	Arsenic	38-45	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	86-91
24361700-7	2014	Further study found that fluoride and arsenic can affect the mRNA expression level of c-fos gene (AP1 family members), and have an interaction on the expression of c-fos, but not c-jun.	Arsenic	38-45	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	98-101
24268366-10	2014	CONCLUSIONS: Significant associations between cumulative arsenic exposure and methylation level of CTNNA2, KLK7, NPY2R, ZNF132 and KCNK17 were found in smoking-unrelated urothelial carcinoma.	Arsenic	57-64	potassium two pore domain channel subfamily K member 17	Homo sapiens	131-137
24448467-0	2014	Arsenic reduces the antipyretic activity of paracetamol in rats: modulation of brain COX-2 activity and CB1 receptor expression.	Arsenic	0-7	cannabinoid receptor 1	Rattus norvegicus	104-107
24361700-7	2014	Further study found that fluoride and arsenic can affect the mRNA expression level of c-fos gene (AP1 family members), and have an interaction on the expression of c-fos, but not c-jun.	Arsenic	38-45	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	164-169
24361700-9	2014	Arsenic can affect the expression of c-fos, thereby affecting the expression of transcription factor AP1, indirectly involved in fluoride-induced bone toxicity.	Arsenic	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	37-42
24361700-9	2014	Arsenic can affect the expression of c-fos, thereby affecting the expression of transcription factor AP1, indirectly involved in fluoride-induced bone toxicity.	Arsenic	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	101-104
24448467-1	2014	We examined whether subacute arsenic exposure can reduce paracetamol-mediated antipyretic activity by affecting COX pathway and cannabinoid CB1 receptor regulation.	Arsenic	29-36	cannabinoid receptor 1	Rattus norvegicus	140-143
24478546-4	2014	An increase in the lipid peroxidation and decrease in the levels of reduced glutathione and activity of superoxide dismutase, catalase, and glutathione peroxidase were observed in arsenic treated mice as compared to controls.	Arsenic	180-187	catalase	Mus musculus	126-134
24448467-9	2014	In the arsenic-preexposed rats, paracetamol-mediated effects were attenuated, while CB1 receptor up-regulation was reversed to down-regulation.	Arsenic	7-14	cannabinoid receptor 1	Rattus norvegicus	84-87
24448467-10	2014	Results suggest that elevated COX-2 activity and reduced CB1 expression could be involved in the arsenic-mediated attenuation of the antipyretic activity of paracetamol.	Arsenic	97-104	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	30-35
24448467-10	2014	Results suggest that elevated COX-2 activity and reduced CB1 expression could be involved in the arsenic-mediated attenuation of the antipyretic activity of paracetamol.	Arsenic	97-104	cannabinoid receptor 1	Rattus norvegicus	57-60
24679086-8	2014	In group of smelters from Departments of Furnace exposed to arsenic above current TLV, excreted arsenic species As(+3) and As(+5) seemed to reduce the level of Clara cell protein (CC16), thereby reducing anti-inflammatory potential of the lungs and increasing the levels of renal biomarker (beta2M) and copper in urine (CuU).	Arsenic	60-67	secretoglobin family 1A member 1	Homo sapiens	180-184
25436473-0	2014	Chemoprevention against arsenic-induced mutagenic DNA breakage and apoptotic liver damage in rat via antioxidant and SOD1 upregulation by green tea (Camellia sinensis) which recovers broken DNA resulted from arsenic-H2O2 related in vitro oxidant stress.	Arsenic	24-31	superoxide dismutase 1	Rattus norvegicus	117-121
25436473-0	2014	Chemoprevention against arsenic-induced mutagenic DNA breakage and apoptotic liver damage in rat via antioxidant and SOD1 upregulation by green tea (Camellia sinensis) which recovers broken DNA resulted from arsenic-H2O2 related in vitro oxidant stress.	Arsenic	208-215	superoxide dismutase 1	Rattus norvegicus	117-121
25436473-3	2014	In this study, arsenic-induced (0.6 ppm/100 g body weight/day for 28 days) impairment of cytosolic superoxide-dismutase (SOD1), catalase, xanthine-oxidase, thiol, and urate activities/levels led to increase in tissue levels of damaging malondialdehyde, conjugated dienes, serum necrotic-marker lactate-dehydrogenase, and metabolic inflammatory-marker c-reactive protein suggesting dysregulation at the transcriptional/signal-transduction level.	Arsenic	15-22	superoxide dismutase 1	Rattus norvegicus	121-125
24679086-8	2014	In group of smelters from Departments of Furnace exposed to arsenic above current TLV, excreted arsenic species As(+3) and As(+5) seemed to reduce the level of Clara cell protein (CC16), thereby reducing anti-inflammatory potential of the lungs and increasing the levels of renal biomarker (beta2M) and copper in urine (CuU).	Arsenic	96-103	secretoglobin family 1A member 1	Homo sapiens	180-184
23700971-4	2014	Expression of OsNRAMP1 in yeast mutant (fet3fet4) rescued iron (Fe) uptake and exhibited enhanced accumulation of As and Cd.	Arsenic	114-116	ferroxidase FET3	Saccharomyces cerevisiae S288C	40-48
24189653-8	2014	Real-time PCR quantification of functional genes and transcripts revealed that arsenic induced the transcription of functional arsenic resistance and speciation genes (arsB, ACR3 and aioA), while no transcription of PAH-degradation genes (PAH-dioxygenase and catechol-dioxygenase) was detected with phenanthrene.	Arsenic	79-86	arylsulfatase B	Homo sapiens	168-172
24189653-8	2014	Real-time PCR quantification of functional genes and transcripts revealed that arsenic induced the transcription of functional arsenic resistance and speciation genes (arsB, ACR3 and aioA), while no transcription of PAH-degradation genes (PAH-dioxygenase and catechol-dioxygenase) was detected with phenanthrene.	Arsenic	127-134	arylsulfatase B	Homo sapiens	168-172
24361376-0	2014	Micronucleus frequency in copper-mine workers exposed to arsenic is modulated by the AS3MT Met287Thr polymorphism.	Arsenic	57-64	arsenite methyltransferase	Homo sapiens	85-90
24361376-1	2014	Arsenic(III)methyltransferase (AS3MT) has been demonstrated to be the key enzyme in the metabolism of arsenic as it catalyses the methylation of arsenite and monomethylarsonic acid (MMA) to form methylated arsenic species, which have higher toxic and genotoxic potential than the parent compounds.	Arsenic	102-109	arsenite methyltransferase	Homo sapiens	31-36
24361376-1	2014	Arsenic(III)methyltransferase (AS3MT) has been demonstrated to be the key enzyme in the metabolism of arsenic as it catalyses the methylation of arsenite and monomethylarsonic acid (MMA) to form methylated arsenic species, which have higher toxic and genotoxic potential than the parent compounds.	Arsenic	206-213	arsenite methyltransferase	Homo sapiens	31-36
24361376-2	2014	The aim of this study is to evaluate if genetic variation in the AS3MT gene influences arsenic-induced cytogenetic damage, measured by the micronucleus (MN) assay.	Arsenic	87-94	arsenite methyltransferase	Homo sapiens	65-70
24361376-7	2014	To our knowledge, these results are the first to show that genetic variation in AS3MT, especially the Met287Thr polymorphism, may play a role in modulating the levels of arsenic-induced cytogenetic damage among individuals chronically exposed to arsenic.	Arsenic	170-177	arsenite methyltransferase	Homo sapiens	80-85
24361376-7	2014	To our knowledge, these results are the first to show that genetic variation in AS3MT, especially the Met287Thr polymorphism, may play a role in modulating the levels of arsenic-induced cytogenetic damage among individuals chronically exposed to arsenic.	Arsenic	246-253	arsenite methyltransferase	Homo sapiens	80-85
24239724-5	2014	The percent MMA of individuals with the A2B/A2B genotype of arsenic (+3 oxidation state) methyltransferase (AS3MT) was significantly lower than those with AB/A2B.	Arsenic	60-67	arsenite methyltransferase	Homo sapiens	108-113
24184494-2	2014	Previously, we have shown that arsenic can apparently induce 2-cell arrest in mouse preimplantation embryo and the expression of oxidative stress adaptor protein p66(Shc) is up-regulated in this process.	Arsenic	31-38	src homology 2 domain-containing transforming protein C1	Mus musculus	162-165
24184494-2	2014	Previously, we have shown that arsenic can apparently induce 2-cell arrest in mouse preimplantation embryo and the expression of oxidative stress adaptor protein p66(Shc) is up-regulated in this process.	Arsenic	31-38	src homology 2 domain-containing transforming protein C1	Mus musculus	166-169
23933432-2	2014	Microorganism-mediated redox reactions have a crucial role in the As cycle; the microbial oxidation of As (As(III) to As(V)) is a critical transformation because it favors the immobilization of As in the solid phase.	Arsenic	66-68	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	118-123
23933432-2	2014	Microorganism-mediated redox reactions have a crucial role in the As cycle; the microbial oxidation of As (As(III) to As(V)) is a critical transformation because it favors the immobilization of As in the solid phase.	Arsenic	103-105	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	118-123
25494643-9	2014	And the test of reducing ability of stably transfected cells revealed that the concentration of accumulated trivalent arsenic increased by 25% in HepG2-pCI-ArsC cells.	Arsenic	118-125	steroid sulfatase	Homo sapiens	156-160
25494643-12	2014	Taken together, these results demonstrated that prokaryotic arsenic resistant gene arsC integrated successfully into HepG2 genome and enhanced arsenate resistance of HepG2, which brought new insights of arsenic detoxification in mammalian cells.	Arsenic	60-67	steroid sulfatase	Homo sapiens	83-87
25494643-12	2014	Taken together, these results demonstrated that prokaryotic arsenic resistant gene arsC integrated successfully into HepG2 genome and enhanced arsenate resistance of HepG2, which brought new insights of arsenic detoxification in mammalian cells.	Arsenic	203-210	steroid sulfatase	Homo sapiens	83-87
24748729-3	2014	RESULTS: Arsenic exposures (3 mg/kg body weight p.o for 30 days) in mice caused an increase production of ROS (76%), lipid peroxidation (84%) and decrease in the levels of superoxide dismutase (53%) and catalase (54%) in spleen as compared to controls.	Arsenic	9-16	catalase	Mus musculus	203-211
24748729-4	2014	Arsenic exposure to mice also caused a significant increase in caspases-3 activity (2.8 fold) and decreases cell viability (44%), mitochondrial membrane potential (47%) linked with apoptosis assessed by the cell cycle analysis (subG1-28.72%) and annexin V/PI binding in spleen as compared to controls.	Arsenic	0-7	annexin A5	Mus musculus	246-255
24748729-5	2014	Simultaneous treatment of arsenic and amla (500 mg/kg body weight p.o for 30 days) in mice decreased the levels of lipid peroxidation (33%), ROS production (24%), activity of caspase-3 (1.4 fold), apoptosis (subG1 12.72%) and increased cell viability (63%), levels superoxide dismutase (80%), catalase (77%) and mitochondrial membrane potential (66%) as compared to mice treated with arsenic alone.	Arsenic	26-33	caspase 3	Mus musculus	175-184
24094730-1	2014	Arsenic exists in ground water as oxyanions having two oxidation states, As(III) and As(V), and its concentrations vary widely and regionally across the United States (USA).	Arsenic	0-7	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	85-90
24748729-5	2014	Simultaneous treatment of arsenic and amla (500 mg/kg body weight p.o for 30 days) in mice decreased the levels of lipid peroxidation (33%), ROS production (24%), activity of caspase-3 (1.4 fold), apoptosis (subG1 12.72%) and increased cell viability (63%), levels superoxide dismutase (80%), catalase (77%) and mitochondrial membrane potential (66%) as compared to mice treated with arsenic alone.	Arsenic	26-33	catalase	Mus musculus	293-301
24391030-1	2013	To study the relationship between arsenic resistance of 293T cells and overexpression of ARG1, the ARG1 gene in a recombinant plasmid was transfected into 293T cells via liposomes, and then ARG1 overexpression was examined by real-time PCR and immunocytochemistry.	Arsenic	34-41	arginase 1	Homo sapiens	89-93
24094730-2	2014	Because of the difference in toxicity and removability of As(III) and As(V), arsenic speciation is important in the selection and design of an arsenic treatment systems.	Arsenic	77-84	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	70-75
24391919-1	2013	Arsenic (III) methyltransferase (AS3MT) catalyzes the process of arsenic methylation.	Arsenic	65-72	arsenite methyltransferase	Homo sapiens	33-38
24391919-3	2013	However, only two As-binding sites (Cys156 and Cys206) have been confirmed on human AS3MT (hAS3MT).	Arsenic	18-20	arsenite methyltransferase	Homo sapiens	84-89
24391919-3	2013	However, only two As-binding sites (Cys156 and Cys206) have been confirmed on human AS3MT (hAS3MT).	Arsenic	18-20	arsenite methyltransferase	Homo sapiens	91-97
24391919-17	2013	The distances between S(C61) and arsenic in WT-hAS3MT-As and WT-hAS3MT-SAM-As models are 7.5 A and 4.1 A, respectively.	Arsenic	33-40	arsenite methyltransferase	Homo sapiens	47-53
24391919-17	2013	The distances between S(C61) and arsenic in WT-hAS3MT-As and WT-hAS3MT-SAM-As models are 7.5 A and 4.1 A, respectively.	Arsenic	33-40	arsenite methyltransferase	Homo sapiens	64-70
24391919-18	2013	This indicates that SAM-binding to hAS3MT shortens the distance between S(C61) and arsenic and promotes As-binding to hAS3MT.	Arsenic	83-90	arsenite methyltransferase	Homo sapiens	35-41
24391919-18	2013	This indicates that SAM-binding to hAS3MT shortens the distance between S(C61) and arsenic and promotes As-binding to hAS3MT.	Arsenic	104-106	arsenite methyltransferase	Homo sapiens	35-41
24391919-18	2013	This indicates that SAM-binding to hAS3MT shortens the distance between S(C61) and arsenic and promotes As-binding to hAS3MT.	Arsenic	104-106	arsenite methyltransferase	Homo sapiens	118-124
24391919-20	2013	Model of WT-hAS3MT-SAM-As and the experimental results indicate that Cys61 is the third As-binding site.	Arsenic	23-25	arsenite methyltransferase	Homo sapiens	12-18
24391030-6	2013	We conclude that the ARG1 gene increases arsenic resistance of 293T cells.	Arsenic	41-48	arginase 1	Homo sapiens	21-25
24358276-1	2013	In Saccharomyces cerevisiae, the transcription factor Yap8 is a key determinant in arsenic stress response.	Arsenic	83-90	Arr1p	Saccharomyces cerevisiae S288C	54-58
24145059-10	2013	Taken together, our results indicate that arsenic upregulates LOX-1 expression through the reactive oxygen species-mediated NF-kappaB signaling pathway, followed by augmented cellular oxLDL uptake, thus highlighting a critical role of the aberrant LOX-1 signaling pathway in the pathogenesis of arsenic-induced atherosclerosis.	Arsenic	42-49	oxidized low density lipoprotein (lectin-like) receptor 1	Mus musculus	62-67
24135626-0	2013	Effects of arsenic on modification of promyelocytic leukemia (PML): PML responds to low levels of arsenite.	Arsenic	11-18	PML nuclear body scaffold	Homo sapiens	38-66
24135626-0	2013	Effects of arsenic on modification of promyelocytic leukemia (PML): PML responds to low levels of arsenite.	Arsenic	11-18	PML nuclear body scaffold	Homo sapiens	62-65
24145059-10	2013	Taken together, our results indicate that arsenic upregulates LOX-1 expression through the reactive oxygen species-mediated NF-kappaB signaling pathway, followed by augmented cellular oxLDL uptake, thus highlighting a critical role of the aberrant LOX-1 signaling pathway in the pathogenesis of arsenic-induced atherosclerosis.	Arsenic	42-49	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	124-133
24145059-10	2013	Taken together, our results indicate that arsenic upregulates LOX-1 expression through the reactive oxygen species-mediated NF-kappaB signaling pathway, followed by augmented cellular oxLDL uptake, thus highlighting a critical role of the aberrant LOX-1 signaling pathway in the pathogenesis of arsenic-induced atherosclerosis.	Arsenic	42-49	oxidized low density lipoprotein (lectin-like) receptor 1	Mus musculus	248-253
24145059-10	2013	Taken together, our results indicate that arsenic upregulates LOX-1 expression through the reactive oxygen species-mediated NF-kappaB signaling pathway, followed by augmented cellular oxLDL uptake, thus highlighting a critical role of the aberrant LOX-1 signaling pathway in the pathogenesis of arsenic-induced atherosclerosis.	Arsenic	295-302	oxidized low density lipoprotein (lectin-like) receptor 1	Mus musculus	62-67
24349408-6	2013	Immunofluorescent staining of arsenic-treated MTE cells showed altered patterns of localization of the transmembrane tight junction proteins claudin (Cl) Cl-1, Cl-4, Cl-7 and occludin at cell-cell contacts when compared with untreated controls.	Arsenic	30-37	adhesion G protein-coupled receptor L1	Homo sapiens	154-158
24349408-6	2013	Immunofluorescent staining of arsenic-treated MTE cells showed altered patterns of localization of the transmembrane tight junction proteins claudin (Cl) Cl-1, Cl-4, Cl-7 and occludin at cell-cell contacts when compared with untreated controls.	Arsenic	30-37	endogenous retrovirus group W member 3	Homo sapiens	160-164
24349408-6	2013	Immunofluorescent staining of arsenic-treated MTE cells showed altered patterns of localization of the transmembrane tight junction proteins claudin (Cl) Cl-1, Cl-4, Cl-7 and occludin at cell-cell contacts when compared with untreated controls.	Arsenic	30-37	occludin	Homo sapiens	175-183
24349408-8	2013	We found that arsenic exposure significantly increased the protein expression of Cl-4 and occludin as well as the mRNA levels of Cl-4 and Cl-7 in these cells.	Arsenic	14-21	endogenous retrovirus group W member 3	Homo sapiens	81-85
24349408-8	2013	We found that arsenic exposure significantly increased the protein expression of Cl-4 and occludin as well as the mRNA levels of Cl-4 and Cl-7 in these cells.	Arsenic	14-21	occludin	Homo sapiens	90-98
24349408-8	2013	We found that arsenic exposure significantly increased the protein expression of Cl-4 and occludin as well as the mRNA levels of Cl-4 and Cl-7 in these cells.	Arsenic	14-21	endogenous retrovirus group W member 3	Homo sapiens	129-133
24349408-9	2013	Additionally, arsenic exposure resulted in altered phosphorylation of occludin.	Arsenic	14-21	occludin	Homo sapiens	70-78
24367140-5	2013	In addition to elevated As levels in surface and shallow groundwater of Tibet, hot spring and alkaline salt lake waters displayed very high As levels, reaching a maximum value of 5,985 mug/L and 10,626 mug/L As, respectively.	Arsenic	140-142	lipoic acid synthetase	Homo sapiens	206-210
23917727-6	2013	PIXE analysis shows that some copper along with zinc is also present in the rabbit as well as rat MT1 which could not be assessed with ESI-MS. During As metallation reaction with rabbit MT1, with increase in arsenic concentration, the amount of arsenic bound to MT1 also increases, though not proportionally.	Arsenic	208-215	metallothionein 1	Rattus norvegicus	98-101
23917727-6	2013	PIXE analysis shows that some copper along with zinc is also present in the rabbit as well as rat MT1 which could not be assessed with ESI-MS. During As metallation reaction with rabbit MT1, with increase in arsenic concentration, the amount of arsenic bound to MT1 also increases, though not proportionally.	Arsenic	208-215	metallothionein 1	Rattus norvegicus	186-189
23917727-6	2013	PIXE analysis shows that some copper along with zinc is also present in the rabbit as well as rat MT1 which could not be assessed with ESI-MS. During As metallation reaction with rabbit MT1, with increase in arsenic concentration, the amount of arsenic bound to MT1 also increases, though not proportionally.	Arsenic	208-215	metallothionein 1	Rattus norvegicus	186-189
23917727-6	2013	PIXE analysis shows that some copper along with zinc is also present in the rabbit as well as rat MT1 which could not be assessed with ESI-MS. During As metallation reaction with rabbit MT1, with increase in arsenic concentration, the amount of arsenic bound to MT1 also increases, though not proportionally.	Arsenic	245-252	metallothionein 1	Rattus norvegicus	98-101
23917727-6	2013	PIXE analysis shows that some copper along with zinc is also present in the rabbit as well as rat MT1 which could not be assessed with ESI-MS. During As metallation reaction with rabbit MT1, with increase in arsenic concentration, the amount of arsenic bound to MT1 also increases, though not proportionally.	Arsenic	245-252	metallothionein 1	Rattus norvegicus	186-189
23917727-6	2013	PIXE analysis shows that some copper along with zinc is also present in the rabbit as well as rat MT1 which could not be assessed with ESI-MS. During As metallation reaction with rabbit MT1, with increase in arsenic concentration, the amount of arsenic bound to MT1 also increases, though not proportionally.	Arsenic	245-252	metallothionein 1	Rattus norvegicus	186-189
24164099-5	2013	Especially, release of cytochrome c or activation of the caspase cascades and apoptosis-related proteins by arsenic is thought to occur by directly targeting mitochondria.	Arsenic	108-115	cytochrome c, somatic	Homo sapiens	23-35
24118411-7	2013	Among such regions, we showed that a gene body region of the oncogene Fosb underwent alteration in DNA methylation by gestational arsenic exposure.	Arsenic	130-137	FBJ osteosarcoma oncogene B	Mus musculus	70-74
24118411-8	2013	We also showed that Fosb expression significantly increased corresponding to the DNA methylation level of the gene body in the arsenic-exposed group.	Arsenic	127-134	FBJ osteosarcoma oncogene B	Mus musculus	20-24
23921152-0	2013	Arsenic toxicity induced endothelial dysfunction and dementia: pharmacological interdiction by histone deacetylase and inducible nitric oxide synthase inhibitors.	Arsenic	0-7	nitric oxide synthase 2	Rattus norvegicus	119-150
24303053-0	2013	Arsenic exposure affects plasma insulin-like growth factor 1 (IGF-1) in children in rural Bangladesh.	Arsenic	0-7	insulin like growth factor 1	Homo sapiens	32-60
24303053-0	2013	Arsenic exposure affects plasma insulin-like growth factor 1 (IGF-1) in children in rural Bangladesh.	Arsenic	0-7	insulin like growth factor 1	Homo sapiens	62-67
23009795-7	2013	Moreover, ever smokers with high arsenic exposure carrying 1 or 2 risk genotypes of the VEGF gene had a significantly increased risk of 6.6 for bladder cancer and a strikingly higher risk of 9.9 for UUTUC.	Arsenic	33-40	vascular endothelial growth factor A	Homo sapiens	88-92
23009795-8	2013	Additionally, UUTUC cases with high arsenic exposure carrying 1 or 2 risk genotypes of the VEGF gene had a non-significant increased risk of advanced tumor stage.	Arsenic	36-43	vascular endothelial growth factor A	Homo sapiens	91-95
24597041-4	2013	The genesis of arsenic was investigated by principal component analyses involving total dissolved solids, Ca(+2), Mg(+2), Na(+), K(+), HCO3-, Cl(-1), SO4(-2), NO3-, Fetotal, and Astotal and analyzed for 57 groundwater samples, hydrochemical facies analyses, aquifer-aquitard configuration, and water-level behaviour.	Arsenic	15-22	NBL1, DAN family BMP antagonist	Homo sapiens	159-162
24312089-2	2013	The arsenic islands included the AsIII oxidase structural genes aioBA, ars operons (e.g., arsRCB) which code for arsenic resistance, and pho, pst, and phn genes known to be part of the classical phosphate stress response and that encode functions associated with regulating and acquiring organic and inorganic phosphorus.	Arsenic	113-120	RIEG2	Homo sapiens	4-7
24025636-6	2013	Exposure to chromium and arsenic induced significant modifications in the redox state of the test organisms, evidenced by significant alterations in GSTs and GPx activities.	Arsenic	25-32	peroxiredoxin 6 pseudogene 2	Mus musculus	158-161
24044897-6	2013	cPLA2alpha upregulation led to activation of neutral sphingomyelinase (N-SMase) as its activity was inhibited in the presence of AS, and could be restored by addition of arachidonic acid.	Arsenic	129-131	phospholipase A2 group IVA	Homo sapiens	0-10
24184500-3	2013	Arsenic exposure significantly decreased the activities of superoxide dismutase (SOD) isoforms, catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) with increase in glutathione s transferase (GST) while lipid peroxidation (LPx), arsenic levels, mRNA expression of caspase 3 and 9 were significantly increased in different brain regions.	Arsenic	253-260	glutathione-disulfide reductase	Rattus norvegicus	168-170
24128716-7	2013	RESULTS: The arsenic-related tumor exhibited alterations common in LUSC, such as the increased number of copies at 3q26 (SOX2 locus).	Arsenic	13-20	SRY-box transcription factor 2	Homo sapiens	121-125
24184500-3	2013	Arsenic exposure significantly decreased the activities of superoxide dismutase (SOD) isoforms, catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) with increase in glutathione s transferase (GST) while lipid peroxidation (LPx), arsenic levels, mRNA expression of caspase 3 and 9 were significantly increased in different brain regions.	Arsenic	0-7	catalase	Rattus norvegicus	96-104
24184500-3	2013	Arsenic exposure significantly decreased the activities of superoxide dismutase (SOD) isoforms, catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) with increase in glutathione s transferase (GST) while lipid peroxidation (LPx), arsenic levels, mRNA expression of caspase 3 and 9 were significantly increased in different brain regions.	Arsenic	0-7	catalase	Rattus norvegicus	106-109
24184500-3	2013	Arsenic exposure significantly decreased the activities of superoxide dismutase (SOD) isoforms, catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) with increase in glutathione s transferase (GST) while lipid peroxidation (LPx), arsenic levels, mRNA expression of caspase 3 and 9 were significantly increased in different brain regions.	Arsenic	0-7	glutathione-disulfide reductase	Rattus norvegicus	145-166
24184500-3	2013	Arsenic exposure significantly decreased the activities of superoxide dismutase (SOD) isoforms, catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) with increase in glutathione s transferase (GST) while lipid peroxidation (LPx), arsenic levels, mRNA expression of caspase 3 and 9 were significantly increased in different brain regions.	Arsenic	0-7	glutathione-disulfide reductase	Rattus norvegicus	168-170
24184500-3	2013	Arsenic exposure significantly decreased the activities of superoxide dismutase (SOD) isoforms, catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) with increase in glutathione s transferase (GST) while lipid peroxidation (LPx), arsenic levels, mRNA expression of caspase 3 and 9 were significantly increased in different brain regions.	Arsenic	0-7	caspase 3	Rattus norvegicus	288-297
24044897-6	2013	cPLA2alpha upregulation led to activation of neutral sphingomyelinase (N-SMase) as its activity was inhibited in the presence of AS, and could be restored by addition of arachidonic acid.	Arsenic	129-131	sphingomyelin phosphodiesterase 2	Homo sapiens	45-69
24044897-6	2013	cPLA2alpha upregulation led to activation of neutral sphingomyelinase (N-SMase) as its activity was inhibited in the presence of AS, and could be restored by addition of arachidonic acid.	Arsenic	129-131	sphingomyelin phosphodiesterase 2	Homo sapiens	71-78
23804311-0	2013	Chronic exposure to arsenic, estrogen, and their combination causes increased growth and transformation in human prostate epithelial cells potentially by hypermethylation-mediated silencing of MLH1.	Arsenic	20-27	mutL homolog 1	Homo sapiens	193-197
24214398-10	2013	Under As toxicity, the overexpression lines showed minimal changes in de novo Glu synthesis, while the ggct2;1 mutant increased nitrogen assimilation by severalfold, resulting in a very low As/N ratio in tissue.	Arsenic	190-192	ChaC-like family protein	Arabidopsis thaliana	103-110
24214398-6	2013	5-OP levels were further increased by the addition of arsenite and GSH to the medium, indicating that GGCT2;1 participates in the cellular response to arsenic (As) via GSH degradation.	Arsenic	151-158	ChaC-like family protein	Arabidopsis thaliana	102-109
24214398-6	2013	5-OP levels were further increased by the addition of arsenite and GSH to the medium, indicating that GGCT2;1 participates in the cellular response to arsenic (As) via GSH degradation.	Arsenic	160-162	ChaC-like family protein	Arabidopsis thaliana	102-109
24214398-8	2013	GGCT2;1 transcripts were upregulated in As-treated Arabidopsis, and ggct2;1 knockout mutants were more tolerant to As and cadmium than the wild type.	Arsenic	40-42	ChaC-like family protein	Arabidopsis thaliana	0-7
24214398-8	2013	GGCT2;1 transcripts were upregulated in As-treated Arabidopsis, and ggct2;1 knockout mutants were more tolerant to As and cadmium than the wild type.	Arsenic	115-117	ChaC-like family protein	Arabidopsis thaliana	0-7
24214398-8	2013	GGCT2;1 transcripts were upregulated in As-treated Arabidopsis, and ggct2;1 knockout mutants were more tolerant to As and cadmium than the wild type.	Arsenic	115-117	ChaC-like family protein	Arabidopsis thaliana	68-75
23804311-10	2013	Hypermethylation of MLH1 promoter further suggested the epigenetic inactivation of MLH1 expression in arsenic and estrogen treated cells.	Arsenic	102-109	mutL homolog 1	Homo sapiens	20-24
23804311-10	2013	Hypermethylation of MLH1 promoter further suggested the epigenetic inactivation of MLH1 expression in arsenic and estrogen treated cells.	Arsenic	102-109	mutL homolog 1	Homo sapiens	83-87
23804311-12	2013	CONCLUSIONS: Findings of this study for the first time suggest that arsenic and estrogen exposures cause increased cell growth and survival potentially through epigenetic inactivation of MLH1 resulting in decreased MLH1-mediated apoptotic response, and consequently increased cellular transformation.	Arsenic	68-75	mutL homolog 1	Homo sapiens	187-191
23804311-12	2013	CONCLUSIONS: Findings of this study for the first time suggest that arsenic and estrogen exposures cause increased cell growth and survival potentially through epigenetic inactivation of MLH1 resulting in decreased MLH1-mediated apoptotic response, and consequently increased cellular transformation.	Arsenic	68-75	mutL homolog 1	Homo sapiens	215-219
23968725-0	2013	Arsenic induces the expressions of angiogenesis-related factors through PI3K and MAPK pathways in SV-HUC-1 human uroepithelial cells.	Arsenic	0-7	mitogen-activated protein kinase 3	Homo sapiens	81-85
24205341-1	2013	The presence of the arsenic oxidation, reduction, and extrusion genes arsC, arrA, aioA, and acr3 was explored in a range of natural environments in northern Chile, with arsenic concentrations spanning six orders of magnitude.	Arsenic	20-27	steroid sulfatase	Homo sapiens	70-74
24205341-3	2013	Enterobacterial related arsC genes appeared only in the environments with the lowest As concentration, while Firmicutes-like genes were present throughout the range of As concentrations.	Arsenic	85-87	steroid sulfatase	Homo sapiens	24-28
24205341-8	2013	Overall, the environmental distribution of arsenic related genes suggests that the occurrence of different ArsC families provides different degrees of protection against arsenic as previously described in laboratory strains, and that the glutaredoxin (Grx)-linked arsenate reductases related to Enterobacteria do not confer enough arsenic resistance to live above certain levels of As concentrations.	Arsenic	43-50	steroid sulfatase	Homo sapiens	107-111
24205341-8	2013	Overall, the environmental distribution of arsenic related genes suggests that the occurrence of different ArsC families provides different degrees of protection against arsenic as previously described in laboratory strains, and that the glutaredoxin (Grx)-linked arsenate reductases related to Enterobacteria do not confer enough arsenic resistance to live above certain levels of As concentrations.	Arsenic	43-50	glutaredoxin	Homo sapiens	252-255
24205341-8	2013	Overall, the environmental distribution of arsenic related genes suggests that the occurrence of different ArsC families provides different degrees of protection against arsenic as previously described in laboratory strains, and that the glutaredoxin (Grx)-linked arsenate reductases related to Enterobacteria do not confer enough arsenic resistance to live above certain levels of As concentrations.	Arsenic	170-177	steroid sulfatase	Homo sapiens	107-111
24205341-8	2013	Overall, the environmental distribution of arsenic related genes suggests that the occurrence of different ArsC families provides different degrees of protection against arsenic as previously described in laboratory strains, and that the glutaredoxin (Grx)-linked arsenate reductases related to Enterobacteria do not confer enough arsenic resistance to live above certain levels of As concentrations.	Arsenic	170-177	glutaredoxin	Homo sapiens	252-255
24205341-8	2013	Overall, the environmental distribution of arsenic related genes suggests that the occurrence of different ArsC families provides different degrees of protection against arsenic as previously described in laboratory strains, and that the glutaredoxin (Grx)-linked arsenate reductases related to Enterobacteria do not confer enough arsenic resistance to live above certain levels of As concentrations.	Arsenic	170-177	steroid sulfatase	Homo sapiens	107-111
24205341-8	2013	Overall, the environmental distribution of arsenic related genes suggests that the occurrence of different ArsC families provides different degrees of protection against arsenic as previously described in laboratory strains, and that the glutaredoxin (Grx)-linked arsenate reductases related to Enterobacteria do not confer enough arsenic resistance to live above certain levels of As concentrations.	Arsenic	170-177	glutaredoxin	Homo sapiens	252-255
24255851-0	2013	Human GMDS gene fragment hypermethylation in chronic high level of arsenic exposure with and without arsenic induced cancer.	Arsenic	67-74	GDP-mannose 4,6-dehydratase	Homo sapiens	6-10
24255851-3	2013	We had earlier demonstrated the hypermethylation of promoter region of p53 and p16 genes in persons exposed to different doses of arsenic.	Arsenic	130-137	tumor protein p53	Homo sapiens	71-74
24255851-3	2013	We had earlier demonstrated the hypermethylation of promoter region of p53 and p16 genes in persons exposed to different doses of arsenic.	Arsenic	130-137	cyclin dependent kinase inhibitor 2A	Homo sapiens	79-82
24157516-7	2013	In the presence of cellular GSH, the cytotoxic trend was As &gt; Cd &gt; MIX &gt; Hg &gt; Pb, while in the absence of GSH, the cytotoxic trend was As &gt; Hg &gt; MIX &gt; Cd &gt; Pb.	Arsenic	57-59	Mix paired-like homeobox	Homo sapiens	73-76
24070218-4	2013	The change in the fluorescence and SERS intensities of a probe molecule (Rh6G) deposited on GNRAs and silica-coated GNRAs revealed that the as-fabricated silica layer does inhibit the quenching of molecular excited states and enhances photophysical/photochemical processes.	Arsenic	140-142	seryl-tRNA synthetase 1	Homo sapiens	35-39
23917332-0	2013	Preconcentration determination of arsenic species by sorption of As(V) on Amberlite IRA-410 coupled with fluorescence quenching of L-cysteine capped CdS nanoparticles.	Arsenic	34-41	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	65-70
23917332-1	2013	A simple and accurate method for arsenic speciation analysis in natural and drinking water samples is described in which preconcentration of arsenic as As(V) was coupled with spectrofluorometric determination.	Arsenic	33-40	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	152-157
23917332-1	2013	A simple and accurate method for arsenic speciation analysis in natural and drinking water samples is described in which preconcentration of arsenic as As(V) was coupled with spectrofluorometric determination.	Arsenic	141-148	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	152-157
23777639-5	2013	Increased tap water arsenic concentration and consumption were associated with significant upward trends for urinary speciated and total and toenail total arsenical concentrations.	Arsenic	20-27	nuclear RNA export factor 1	Homo sapiens	10-13
23770046-10	2013	Thus, the results showed that arsenic treatment enhanced EVI1 sumoylation, deregulated Bcl-xL, which eventually may induce apoptosis in EVI1 positive cancer cells.	Arsenic	30-37	MDS1 and EVI1 complex locus	Homo sapiens	57-61
23770046-10	2013	Thus, the results showed that arsenic treatment enhanced EVI1 sumoylation, deregulated Bcl-xL, which eventually may induce apoptosis in EVI1 positive cancer cells.	Arsenic	30-37	BCL2 like 1	Homo sapiens	87-93
23770046-10	2013	Thus, the results showed that arsenic treatment enhanced EVI1 sumoylation, deregulated Bcl-xL, which eventually may induce apoptosis in EVI1 positive cancer cells.	Arsenic	30-37	MDS1 and EVI1 complex locus	Homo sapiens	136-140
23870163-7	2013	In addition, we conducted a DNA sequence-based study on the gene codifying arsB, an As(III) efflux membrane protein pump related to arsenic resistance, for all the As-resistant bacterial isolates.	Arsenic	132-139	arylsulfatase B	Homo sapiens	75-79
23870163-7	2013	In addition, we conducted a DNA sequence-based study on the gene codifying arsB, an As(III) efflux membrane protein pump related to arsenic resistance, for all the As-resistant bacterial isolates.	Arsenic	84-86	arylsulfatase B	Homo sapiens	75-79
23872349-1	2013	BACKGROUND: Chronic high arsenic exposure is associated with squamous cell carcinoma (SCC) of the skin, and inorganic arsenic (iAs) metabolites may play an important role in this association.	Arsenic	25-32	serpin family B member 3	Homo sapiens	86-89
23830798-2	2013	A patient, with chemo- and trastuzumab-resistant HER2-overexpressing breast cancer, who presented concomitant acute promyelocytic leukemia, showed a response in her breast lesions to retinoic acid, arsenic, and aracytin.	Arsenic	198-205	erb-b2 receptor tyrosine kinase 2	Homo sapiens	49-53
23872349-3	2013	OBJECTIVE: We estimated associations between total urinary arsenic and arsenic species and SCC in a U.S. population.	Arsenic	59-66	serpin family B member 3	Homo sapiens	91-94
23872349-3	2013	OBJECTIVE: We estimated associations between total urinary arsenic and arsenic species and SCC in a U.S. population.	Arsenic	71-78	serpin family B member 3	Homo sapiens	91-94
23872349-11	2013	CONCLUSIONS: These results suggest that arsenic exposure at levels common in the United States relates to SCC and that arsenic metabolism ability does not modify the association.	Arsenic	40-47	serpin family B member 3	Homo sapiens	106-109
23777639-11	2013	These findings confirm the primacy of home tap water as a determinant of arsenic concentration in urine and toenails.	Arsenic	73-80	nuclear RNA export factor 1	Homo sapiens	43-46
23872714-0	2013	Epigenetic modifications of DAPK and p16 genes contribute to arsenic-induced skin lesions and nondermatological health effects.	Arsenic	61-68	death associated protein kinase 1	Homo sapiens	28-32
23727622-1	2013	Chronic exposure to arsenic can generate reactive oxidative species, which can induce certain proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8).	Arsenic	20-27	tumor necrosis factor	Homo sapiens	128-155
23727622-1	2013	Chronic exposure to arsenic can generate reactive oxidative species, which can induce certain proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8).	Arsenic	20-27	tumor necrosis factor	Homo sapiens	157-166
23727622-1	2013	Chronic exposure to arsenic can generate reactive oxidative species, which can induce certain proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8).	Arsenic	20-27	interleukin 6	Homo sapiens	169-182
23727622-1	2013	Chronic exposure to arsenic can generate reactive oxidative species, which can induce certain proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8).	Arsenic	20-27	interleukin 6	Homo sapiens	184-188
23727622-1	2013	Chronic exposure to arsenic can generate reactive oxidative species, which can induce certain proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8).	Arsenic	20-27	C-X-C motif chemokine ligand 8	Homo sapiens	194-207
23727622-1	2013	Chronic exposure to arsenic can generate reactive oxidative species, which can induce certain proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8).	Arsenic	20-27	C-X-C motif chemokine ligand 8	Homo sapiens	209-213
23727622-10	2013	The present results also showed a significant increase in UC risk in subjects with the IL-8 -251 T/T genotype for each SD increase in urinary total arsenic and MMA%.	Arsenic	148-155	C-X-C motif chemokine ligand 8	Homo sapiens	87-91
23794209-2	2013	We determined the effects of androgen, cadmium, and arsenic on MT1/2 and MT3 in prostate carcinoma cells, and evaluated the functional effects of MT3 on cell proliferation, invasion, and tumorigenesis.	Arsenic	52-59	metallothionein 1I, pseudogene	Homo sapiens	63-68
23794209-6	2013	RESULTS: Androgen, cadmium, and arsenic treatments enhanced gene expression of MT1/2 and MT3 in prostate carcinoma LNCaP cells.	Arsenic	32-39	metallothionein 1I, pseudogene	Homo sapiens	79-84
23794209-6	2013	RESULTS: Androgen, cadmium, and arsenic treatments enhanced gene expression of MT1/2 and MT3 in prostate carcinoma LNCaP cells.	Arsenic	32-39	metallothionein 3	Homo sapiens	89-92
23743303-5	2013	Therefore, identification of nutritional factors which are able to inhibit CXCR4 is important for protection from environmental arsenic-induced carcinogenesis and for abolishing metastasis of malignantly transformed cells.	Arsenic	128-135	C-X-C motif chemokine receptor 4	Homo sapiens	75-80
23872714-0	2013	Epigenetic modifications of DAPK and p16 genes contribute to arsenic-induced skin lesions and nondermatological health effects.	Arsenic	61-68	cyclin dependent kinase inhibitor 2A	Homo sapiens	37-40
23603037-7	2013	Nano-insulin being non-toxic and effective at a much lesser dose, therefore, has potential for therapeutic use in the management of arsenic induced diabetes.	Arsenic	132-139	insulin	Homo sapiens	5-12
23942117-5	2013	Arsenic treatment enhanced phosphorylation-dependent activation of LATS1 kinase and other Hippo signaling regulatory proteins Sav1 and MOB1.	Arsenic	0-7	multigenic obesity QTL 1	Mus musculus	135-139
23942117-8	2013	Thus, as expected, unphosphorylated-Yap was translocated to the nucleus in arsenic-treated epidermis.	Arsenic	75-82	yes-associated protein 1	Mus musculus	36-39
23942117-10	2013	Consistently, an up-regulation of Yap-dependent target genes Cyr61, Gli2, Ankrd1 and Ctgf was observed in the skin of arsenic-treated mice.	Arsenic	118-125	yes-associated protein 1	Mus musculus	34-37
23942117-10	2013	Consistently, an up-regulation of Yap-dependent target genes Cyr61, Gli2, Ankrd1 and Ctgf was observed in the skin of arsenic-treated mice.	Arsenic	118-125	cellular communication network factor 1	Mus musculus	61-66
23942117-10	2013	Consistently, an up-regulation of Yap-dependent target genes Cyr61, Gli2, Ankrd1 and Ctgf was observed in the skin of arsenic-treated mice.	Arsenic	118-125	GLI-Kruppel family member GLI2	Mus musculus	68-72
23942117-10	2013	Consistently, an up-regulation of Yap-dependent target genes Cyr61, Gli2, Ankrd1 and Ctgf was observed in the skin of arsenic-treated mice.	Arsenic	118-125	ankyrin repeat domain 1 (cardiac muscle)	Mus musculus	74-80
23942117-10	2013	Consistently, an up-regulation of Yap-dependent target genes Cyr61, Gli2, Ankrd1 and Ctgf was observed in the skin of arsenic-treated mice.	Arsenic	118-125	cellular communication network factor 2	Mus musculus	85-89
23942117-13	2013	These data provide evidence that arsenic-induced canonical Hippo signaling pathway and Yap-mediated disruption of tight and adherens junctions are independently regulated.	Arsenic	33-40	yes-associated protein 1	Mus musculus	87-90
23603037-0	2013	Relative efficacies of insulin and poly (lactic-co-glycolic) acid encapsulated nano-insulin in modulating certain significant biomarkers in arsenic intoxicated L6 cells.	Arsenic	140-147	insulin	Homo sapiens	84-91
23603037-1	2013	The present study evaluates relative efficacies of insulin and PLGA-loaded-nano-insulin (NIn) in combating arsenic-induced impairment of glucose uptake, insulin resistance and mitochondrial dysfunction in L6 skeletal muscle cells.	Arsenic	107-114	insulin	Homo sapiens	80-87
23603037-1	2013	The present study evaluates relative efficacies of insulin and PLGA-loaded-nano-insulin (NIn) in combating arsenic-induced impairment of glucose uptake, insulin resistance and mitochondrial dysfunction in L6 skeletal muscle cells.	Arsenic	107-114	insulin	Homo sapiens	80-87
23732083-0	2013	Disruption of canonical TGFbeta-signaling in murine coronary progenitor cells by low level arsenic.	Arsenic	91-98	transforming growth factor, beta 1	Mus musculus	24-31
23732083-12	2013	Overall these results show that arsenic exposure blocks developmental EMT gene programming in murine coronary progenitor cells by disrupting TGFbeta2 signals and Smad activation, and that smooth muscle cell differentiation is refractory to this arsenic toxicity.	Arsenic	32-39	transforming growth factor, beta 2	Mus musculus	141-149
23942117-0	2013	Arsenic-induced cutaneous hyperplastic lesions are associated with the dysregulation of Yap, a Hippo signaling-related protein.	Arsenic	0-7	yes-associated protein 1	Mus musculus	88-91
23942117-5	2013	Arsenic treatment enhanced phosphorylation-dependent activation of LATS1 kinase and other Hippo signaling regulatory proteins Sav1 and MOB1.	Arsenic	0-7	large tumor suppressor	Mus musculus	67-72
23942117-5	2013	Arsenic treatment enhanced phosphorylation-dependent activation of LATS1 kinase and other Hippo signaling regulatory proteins Sav1 and MOB1.	Arsenic	0-7	salvador family WW domain containing 1	Mus musculus	126-130
23608991-4	2013	In the case of oak ash, As(V) percentage adsorption becomes higher with increasing added arsenic concentrations, while this increase in added arsenic causes lower percentage adsorption in the case of slate fines.	Arsenic	89-96	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	24-29
23699174-5	2013	Arsenic exposure of human HaCaT keratinocytes induced nuclear accumulation of PRMT1 and PRMT4, histone H4R3 and H3R17 methylation proximal to the ARE, but not to the non-ARE regions of ferritin genes.	Arsenic	0-7	protein arginine methyltransferase 1	Homo sapiens	78-83
23699174-5	2013	Arsenic exposure of human HaCaT keratinocytes induced nuclear accumulation of PRMT1 and PRMT4, histone H4R3 and H3R17 methylation proximal to the ARE, but not to the non-ARE regions of ferritin genes.	Arsenic	0-7	coactivator associated arginine methyltransferase 1	Homo sapiens	88-93
23699174-8	2013	Collectively, PRMT1 and PRMT4 regulate the ARE and cellular antioxidant response to arsenic.	Arsenic	84-91	protein arginine methyltransferase 1	Homo sapiens	14-19
23699174-8	2013	Collectively, PRMT1 and PRMT4 regulate the ARE and cellular antioxidant response to arsenic.	Arsenic	84-91	coactivator associated arginine methyltransferase 1	Homo sapiens	24-29
23871787-8	2013	Our study confirmed the antagonistic roles of curcumin to counteract inorganic arsenic-induced hepatic toxicity in vivo, and suggested that the potent Nrf2 activation capability might be valuable for the protective effects of curcumin against arsenic intoxication.	Arsenic	79-86	nuclear factor, erythroid derived 2, like 2	Mus musculus	151-155
23871787-0	2013	Curcumin attenuates arsenic-induced hepatic injuries and oxidative stress in experimental mice through activation of Nrf2 pathway, promotion of arsenic methylation and urinary excretion.	Arsenic	20-27	nuclear factor, erythroid derived 2, like 2	Mus musculus	117-121
23871787-5	2013	Our results showed that arsenic-induced elevation of serum alanine amino transferase (ALT) and aspartate aminotransferase (AST) activities, augmentation of hepatic malonaldehyde (MDA), as well as the reduction of blood and hepatic glutathione (GSH) levels, were all consistently relieved by curcumin.	Arsenic	24-31	glutamic pyruvic transaminase, soluble	Mus musculus	59-84
23871787-5	2013	Our results showed that arsenic-induced elevation of serum alanine amino transferase (ALT) and aspartate aminotransferase (AST) activities, augmentation of hepatic malonaldehyde (MDA), as well as the reduction of blood and hepatic glutathione (GSH) levels, were all consistently relieved by curcumin.	Arsenic	24-31	glutamic pyruvic transaminase, soluble	Mus musculus	86-89
23871787-5	2013	Our results showed that arsenic-induced elevation of serum alanine amino transferase (ALT) and aspartate aminotransferase (AST) activities, augmentation of hepatic malonaldehyde (MDA), as well as the reduction of blood and hepatic glutathione (GSH) levels, were all consistently relieved by curcumin.	Arsenic	24-31	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	95-121
23871787-5	2013	Our results showed that arsenic-induced elevation of serum alanine amino transferase (ALT) and aspartate aminotransferase (AST) activities, augmentation of hepatic malonaldehyde (MDA), as well as the reduction of blood and hepatic glutathione (GSH) levels, were all consistently relieved by curcumin.	Arsenic	24-31	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	123-126
22733434-0	2013	Long-term arsenic exposure induces histone H3 Lys9 dimethylation without altering DNA methylation in the promoter region of p16(INK4a) and down-regulates its expression in the liver of mice.	Arsenic	10-17	cyclin dependent kinase inhibitor 2A	Mus musculus	128-133
22733434-9	2013	These findings suggest that long-term arsenic exposure may induce down-regulation of p16(INK4a) by targeting recruitment of G9a and H3K9 dimethylation without altering DNA methylation before tumorigenesis in the liver.	Arsenic	38-45	cyclin dependent kinase inhibitor 2A	Mus musculus	85-88
23962110-4	2013	RESULTS: Here we assessed Th1/Th2/T(reg) cytokine gene expression profiles in 16 ATL patients before and 30 days after treatment with arsenic/IFN/zidovudine, in comparison with HTLV-I healthy carriers and sero-negative blood donors.	Arsenic	134-141	negative elongation factor complex member C/D	Homo sapiens	26-29
22733434-9	2013	These findings suggest that long-term arsenic exposure may induce down-regulation of p16(INK4a) by targeting recruitment of G9a and H3K9 dimethylation without altering DNA methylation before tumorigenesis in the liver.	Arsenic	38-45	cyclin dependent kinase inhibitor 2A	Mus musculus	89-94
24351557-17	2013	CONCLUSIONS: Arsenic could induce the changes of ERK2 and JNK1mRNA expression in the MAPK path way in arseniasis patients.It suggests that the MAPK signaling pathway take part in the occurrence and development process of arseniasis caused by burning coal.	Arsenic	13-20	mitogen-activated protein kinase 1	Homo sapiens	49-53
24351557-17	2013	CONCLUSIONS: Arsenic could induce the changes of ERK2 and JNK1mRNA expression in the MAPK path way in arseniasis patients.It suggests that the MAPK signaling pathway take part in the occurrence and development process of arseniasis caused by burning coal.	Arsenic	13-20	mitogen-activated protein kinase 8	Homo sapiens	58-62
24351558-13	2013	CONCLUSION: The combined effects of fluoride and arsenic on the Runx2, MMP-9, RANKL, Osterix of bone metabolism showed antagonistic effects.	Arsenic	49-56	RUNX family transcription factor 2	Rattus norvegicus	64-69
24351558-13	2013	CONCLUSION: The combined effects of fluoride and arsenic on the Runx2, MMP-9, RANKL, Osterix of bone metabolism showed antagonistic effects.	Arsenic	49-56	matrix metallopeptidase 9	Rattus norvegicus	71-76
24351558-13	2013	CONCLUSION: The combined effects of fluoride and arsenic on the Runx2, MMP-9, RANKL, Osterix of bone metabolism showed antagonistic effects.	Arsenic	49-56	TNF superfamily member 11	Rattus norvegicus	78-83
24351558-13	2013	CONCLUSION: The combined effects of fluoride and arsenic on the Runx2, MMP-9, RANKL, Osterix of bone metabolism showed antagonistic effects.	Arsenic	49-56	Sp7 transcription factor	Rattus norvegicus	85-92
22733434-6	2013	We focused on the tumor-related genes, p16(INK4a) , RASSF1A, Ha-ras and ER-alpha as target genes, because their expression and promoter methylation status in mice have been reported to be affected by long-term arsenic exposure.	Arsenic	210-217	Harvey rat sarcoma virus oncogene	Mus musculus	61-67
22733434-6	2013	We focused on the tumor-related genes, p16(INK4a) , RASSF1A, Ha-ras and ER-alpha as target genes, because their expression and promoter methylation status in mice have been reported to be affected by long-term arsenic exposure.	Arsenic	210-217	estrogen receptor 1 (alpha)	Mus musculus	72-80
22733434-7	2013	The results showed that long-term arsenic exposure induced a significant decrease in expression of p16(INK4a) associated with an increase in level of dimethylated histone H3 lysine 9 (H3K9), a transcription-suppressive histone modification, in the promoter region, but that DNA methylation of the promoter region was unaffected.	Arsenic	34-41	cyclin dependent kinase inhibitor 2A	Mus musculus	99-102
22733434-7	2013	The results showed that long-term arsenic exposure induced a significant decrease in expression of p16(INK4a) associated with an increase in level of dimethylated histone H3 lysine 9 (H3K9), a transcription-suppressive histone modification, in the promoter region, but that DNA methylation of the promoter region was unaffected.	Arsenic	34-41	cyclin dependent kinase inhibitor 2A	Mus musculus	103-108
23761297-7	2013	Oxidized LDL (Ox-LDL), C-reactive protein (CRP), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) levels were significantly higher in arsenic-endemic subjects than those in nonendemic subjects.	Arsenic	176-183	intercellular adhesion molecule 1	Homo sapiens	49-82
23761297-7	2013	Oxidized LDL (Ox-LDL), C-reactive protein (CRP), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) levels were significantly higher in arsenic-endemic subjects than those in nonendemic subjects.	Arsenic	176-183	intercellular adhesion molecule 1	Homo sapiens	84-90
23761297-7	2013	Oxidized LDL (Ox-LDL), C-reactive protein (CRP), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) levels were significantly higher in arsenic-endemic subjects than those in nonendemic subjects.	Arsenic	176-183	vascular cell adhesion molecule 1	Homo sapiens	97-130
23761297-7	2013	Oxidized LDL (Ox-LDL), C-reactive protein (CRP), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) levels were significantly higher in arsenic-endemic subjects than those in nonendemic subjects.	Arsenic	176-183	vascular cell adhesion molecule 1	Homo sapiens	132-138
23761297-9	2013	Among the circulating molecules tested in this study, HDL, Ox-LDL, and CRP showed dose-response relationships with arsenic exposure.	Arsenic	115-122	C-reactive protein	Homo sapiens	71-74
23962110-7	2013	Importantly, arsenic/IFN/zidovudine therapy sharply diminished IL-10 transcript and serum levels concomittant with decrease in IL-4 and increases in IFN-gamma and IL-2 mRNA, whether or not values were adjusted to the percentage of CD4+CD25+ cells.	Arsenic	13-20	interferon alpha 1	Homo sapiens	21-24
23962110-7	2013	Importantly, arsenic/IFN/zidovudine therapy sharply diminished IL-10 transcript and serum levels concomittant with decrease in IL-4 and increases in IFN-gamma and IL-2 mRNA, whether or not values were adjusted to the percentage of CD4+CD25+ cells.	Arsenic	13-20	interleukin 10	Homo sapiens	63-68
23962110-7	2013	Importantly, arsenic/IFN/zidovudine therapy sharply diminished IL-10 transcript and serum levels concomittant with decrease in IL-4 and increases in IFN-gamma and IL-2 mRNA, whether or not values were adjusted to the percentage of CD4+CD25+ cells.	Arsenic	13-20	interleukin 4	Homo sapiens	127-131
23962110-7	2013	Importantly, arsenic/IFN/zidovudine therapy sharply diminished IL-10 transcript and serum levels concomittant with decrease in IL-4 and increases in IFN-gamma and IL-2 mRNA, whether or not values were adjusted to the percentage of CD4+CD25+ cells.	Arsenic	13-20	interferon gamma	Homo sapiens	149-158
23962110-7	2013	Importantly, arsenic/IFN/zidovudine therapy sharply diminished IL-10 transcript and serum levels concomittant with decrease in IL-4 and increases in IFN-gamma and IL-2 mRNA, whether or not values were adjusted to the percentage of CD4+CD25+ cells.	Arsenic	13-20	interleukin 2	Homo sapiens	163-167
23962110-7	2013	Importantly, arsenic/IFN/zidovudine therapy sharply diminished IL-10 transcript and serum levels concomittant with decrease in IL-4 and increases in IFN-gamma and IL-2 mRNA, whether or not values were adjusted to the percentage of CD4+CD25+ cells.	Arsenic	13-20	CD4 molecule	Homo sapiens	231-234
23962110-9	2013	CONCLUSIONS: The observed shift from a T(reg)/Th2 phenotype before treatment toward a Th1 phenotype after treatment with arsenic/IFN/zidovudine may play an important role in restoring an immuno-competent micro-environment, which enhances the eradication of ATL cells and the prevention of opportunistic infections.	Arsenic	121-128	negative elongation factor complex member C/D	Homo sapiens	86-89
23962110-9	2013	CONCLUSIONS: The observed shift from a T(reg)/Th2 phenotype before treatment toward a Th1 phenotype after treatment with arsenic/IFN/zidovudine may play an important role in restoring an immuno-competent micro-environment, which enhances the eradication of ATL cells and the prevention of opportunistic infections.	Arsenic	121-128	interferon alpha 1	Homo sapiens	129-132
23643801-0	2013	Epithelial to mesenchymal transition in arsenic-transformed cells promotes angiogenesis through activating beta-catenin-vascular endothelial growth factor pathway.	Arsenic	40-47	catenin beta 1	Homo sapiens	107-119
23643801-0	2013	Epithelial to mesenchymal transition in arsenic-transformed cells promotes angiogenesis through activating beta-catenin-vascular endothelial growth factor pathway.	Arsenic	40-47	vascular endothelial growth factor A	Homo sapiens	120-154
23643801-8	2013	Mechanistic studies revealed that beta-catenin was activated in arsenic-transformed cells up-regulating its target gene expression including angiogenic-stimulating vascular endothelial growth factor (VEGF).	Arsenic	64-71	catenin beta 1	Homo sapiens	34-46
23643801-8	2013	Mechanistic studies revealed that beta-catenin was activated in arsenic-transformed cells up-regulating its target gene expression including angiogenic-stimulating vascular endothelial growth factor (VEGF).	Arsenic	64-71	vascular endothelial growth factor A	Homo sapiens	164-198
23643801-8	2013	Mechanistic studies revealed that beta-catenin was activated in arsenic-transformed cells up-regulating its target gene expression including angiogenic-stimulating vascular endothelial growth factor (VEGF).	Arsenic	64-71	vascular endothelial growth factor A	Homo sapiens	200-204
23643801-9	2013	Stably expressing microRNA-200b in arsenic-transformed cells that reversed EMT inhibited beta-catenin activation, decreased VEGF expression and reduced tube formation by HUVECs.	Arsenic	35-42	catenin beta 1	Homo sapiens	89-101
23643801-9	2013	Stably expressing microRNA-200b in arsenic-transformed cells that reversed EMT inhibited beta-catenin activation, decreased VEGF expression and reduced tube formation by HUVECs.	Arsenic	35-42	vascular endothelial growth factor A	Homo sapiens	124-128
23643801-11	2013	Adding a VEGF neutralizing antibody into the conditioned medium from arsenic-transformed cells impaired tube formation by HUVECs.	Arsenic	69-76	vascular endothelial growth factor A	Homo sapiens	9-13
23643801-13	2013	These findings suggest that EMT in arsenic-transformed cells promotes angiogenesis through activating beta-catenin-VEGF pathway.	Arsenic	35-42	catenin beta 1	Homo sapiens	102-114
23643801-13	2013	These findings suggest that EMT in arsenic-transformed cells promotes angiogenesis through activating beta-catenin-VEGF pathway.	Arsenic	35-42	vascular endothelial growth factor A	Homo sapiens	115-119
23775713-4	2013	On exposure to arsenic, an oxidative stress inducer, USP10 is recruited into stress granules (SGs), and USP10-containing SGs reduce reactive oxygen species (ROS) production and inhibit ROS-dependent apoptosis.	Arsenic	15-22	ubiquitin specific peptidase 10	Homo sapiens	53-58
23967108-0	2013	Genetic susceptible locus in NOTCH2 interacts with arsenic in drinking water on risk of type 2 diabetes.	Arsenic	51-58	notch receptor 2	Homo sapiens	29-35
23967108-10	2013	A significant interaction between arsenic and NOTCH2 (rs699780) was observed which significantly increased the risk of T2DM (p for interaction = 0.003; q-value = 0.021).	Arsenic	34-41	notch receptor 2	Homo sapiens	46-52
23967108-11	2013	Further restricted analysis among participants exposed to water arsenic of less than 148 microg/L showed consistent results for interaction between the NOTCH2 variant and arsenic exposure on T2DM (p for interaction  = 0.048; q-value = 0.004).	Arsenic	171-178	notch receptor 2	Homo sapiens	152-158
23967108-12	2013	CONCLUSIONS: These findings suggest that genetic variation in NOTCH2 increased susceptibility to T2DM among people exposed to inorganic arsenic.	Arsenic	136-143	notch receptor 2	Homo sapiens	62-68
23775713-4	2013	On exposure to arsenic, an oxidative stress inducer, USP10 is recruited into stress granules (SGs), and USP10-containing SGs reduce reactive oxygen species (ROS) production and inhibit ROS-dependent apoptosis.	Arsenic	15-22	ubiquitin specific peptidase 10	Homo sapiens	104-109
23775713-5	2013	We found that interaction of Tax with USP10 inhibits arsenic-induced SG formation, stimulates ROS production, and augments ROS-dependent apoptosis in HTLV-1-infected T cells.	Arsenic	53-60	ubiquitin specific peptidase 10	Homo sapiens	38-43
23757598-7	2013	RESULTS: We found an association between urinary inorganic arsenic concentration and the estimated proportion of CD8+ T lymphocytes (1.18; 95% CI: 0.12, 2.23).	Arsenic	59-66	CD8a molecule	Homo sapiens	113-116
23788675-4	2013	Every 1-standard-deviation increase in urinary arsenic (357.9 microg/g creatinine) and well-water arsenic (102.0 microg/L) concentration was related to a 11.7-microm (95% confidence interval (CI): 1.8, 21.6) and 5.1-microm (95% CI: -0.2, 10.3) increase in cIMT, respectively.	Arsenic	47-54	CIMT	Homo sapiens	256-260
23788675-4	2013	Every 1-standard-deviation increase in urinary arsenic (357.9 microg/g creatinine) and well-water arsenic (102.0 microg/L) concentration was related to a 11.7-microm (95% confidence interval (CI): 1.8, 21.6) and 5.1-microm (95% CI: -0.2, 10.3) increase in cIMT, respectively.	Arsenic	98-105	CIMT	Homo sapiens	256-260
23788675-6	2013	Among participants with a higher urinary MMA percentage, a higher ratio of urinary MMA to inorganic arsenic, and a lower ratio of dimethylarsinic acid to MMA, the association between well-water arsenic and cIMT was stronger.	Arsenic	194-201	CIMT	Homo sapiens	206-210
23788675-7	2013	The findings indicate an effect of past long-term arsenic exposure on cIMT, which may be potentiated by suboptimal or incomplete arsenic methylation capacity.	Arsenic	50-57	CIMT	Homo sapiens	70-74
23788675-7	2013	The findings indicate an effect of past long-term arsenic exposure on cIMT, which may be potentiated by suboptimal or incomplete arsenic methylation capacity.	Arsenic	129-136	CIMT	Homo sapiens	70-74
23602911-3	2013	Although arsenic has been shown to generate reactive oxygen/nitrogen species (ROS/RNS), little is known about the role of arsenic-induced ROS/RNS in the mechanism underlying arsenic inhibition of DNA repair.	Arsenic	9-16	FAM20C golgi associated secretory pathway kinase	Homo sapiens	82-85
23602911-3	2013	Although arsenic has been shown to generate reactive oxygen/nitrogen species (ROS/RNS), little is known about the role of arsenic-induced ROS/RNS in the mechanism underlying arsenic inhibition of DNA repair.	Arsenic	122-129	FAM20C golgi associated secretory pathway kinase	Homo sapiens	142-145
23602911-3	2013	Although arsenic has been shown to generate reactive oxygen/nitrogen species (ROS/RNS), little is known about the role of arsenic-induced ROS/RNS in the mechanism underlying arsenic inhibition of DNA repair.	Arsenic	122-129	FAM20C golgi associated secretory pathway kinase	Homo sapiens	142-145
23708403-0	2013	Arsenic induces VL30 retrotransposition: the involvement of oxidative stress and heat-shock protein 70.	Arsenic	0-7	heat shock protein family A (Hsp70) member 4	Homo sapiens	81-102
24511153-0	2013	Influence of GSTT1 Genetic Polymorphisms on Arsenic Metabolism.	Arsenic	44-51	glutathione S-transferase theta 1	Homo sapiens	13-18
24511153-5	2013	A significant gene-environment interaction was observed between urinary arsenic exposure in drinking water GSTT1 but not GSTM1 where GSTT1 null individuals had a slightly higher excretion rate of arsenic compared to GSTT1 wildtypes after adjusting for other factors.	Arsenic	72-79	glutathione S-transferase theta 1	Homo sapiens	107-112
24511153-5	2013	A significant gene-environment interaction was observed between urinary arsenic exposure in drinking water GSTT1 but not GSTM1 where GSTT1 null individuals had a slightly higher excretion rate of arsenic compared to GSTT1 wildtypes after adjusting for other factors.	Arsenic	196-203	glutathione S-transferase theta 1	Homo sapiens	133-138
24511153-5	2013	A significant gene-environment interaction was observed between urinary arsenic exposure in drinking water GSTT1 but not GSTM1 where GSTT1 null individuals had a slightly higher excretion rate of arsenic compared to GSTT1 wildtypes after adjusting for other factors.	Arsenic	196-203	glutathione S-transferase theta 1	Homo sapiens	133-138
23650128-2	2013	Arsenic inhibits adipocyte differentiation and promotes insulin resistance; however, little is known of the impacts of and mechanisms for arsenic effects on adipose lipid storage and lipolysis.	Arsenic	0-7	insulin	Homo sapiens	56-63
23650128-4	2013	We first demonstrated that 5-week exposure of mice to 100 mug/l of arsenic in drinking water stimulated epididymal adipocyte hypertrophy, reduced the adipose tissue expression of perilipin (PLIN1, a lipid droplet coat protein), and increased perivascular ectopic fat deposition in skeletal muscle.	Arsenic	67-74	perilipin 1	Mus musculus	190-195
23650128-5	2013	Incubating adipocytes, differentiated from adipose-derived human mesenchymal stem cell, with arsenic stimulated lipolysis and decreased both Nile Red positive lipid droplets and PLIN1 expression.	Arsenic	93-100	perilipin 1	Homo sapiens	178-183
23650128-8	2013	Antagonizing Gi-coupled endothelin-1 type A and B receptors (EDNRA/EDNRB) also attenuated arsenic effects, but antagonizing other adipose Gi-coupled receptors that regulate fat metabolism was ineffective.	Arsenic	90-97	endothelin receptor type B	Homo sapiens	24-59
23650128-8	2013	Antagonizing Gi-coupled endothelin-1 type A and B receptors (EDNRA/EDNRB) also attenuated arsenic effects, but antagonizing other adipose Gi-coupled receptors that regulate fat metabolism was ineffective.	Arsenic	90-97	endothelin receptor type A	Homo sapiens	61-66
24511153-7	2013	This data suggests that GSTT1 contributes to the observed variability in arsenic metabolism.	Arsenic	73-80	glutathione S-transferase theta 1	Homo sapiens	24-29
24511153-8	2013	Since individuals with a higher primary methylation index and lower secondary methylation index are more susceptible to arsenic related disease, these results suggest that GSTT1 null individuals may be more susceptible to arsenic-related toxicity.	Arsenic	120-127	glutathione S-transferase theta 1	Homo sapiens	172-177
24511153-8	2013	Since individuals with a higher primary methylation index and lower secondary methylation index are more susceptible to arsenic related disease, these results suggest that GSTT1 null individuals may be more susceptible to arsenic-related toxicity.	Arsenic	222-229	glutathione S-transferase theta 1	Homo sapiens	172-177
23650128-8	2013	Antagonizing Gi-coupled endothelin-1 type A and B receptors (EDNRA/EDNRB) also attenuated arsenic effects, but antagonizing other adipose Gi-coupled receptors that regulate fat metabolism was ineffective.	Arsenic	90-97	endothelin receptor type B	Homo sapiens	67-72
23644288-0	2013	Association of NALP2 polymorphism with arsenic induced skin lesions and other health effects.	Arsenic	39-46	NLR family pyrin domain containing 2	Homo sapiens	15-20
23998577-0	2013	Expression of PML-RARalpha is up-regulated during ATRA and arsenics combined induction without influence on long-term prognosis of acute promyelocytic leukemia.	Arsenic	59-67	PML nuclear body scaffold	Homo sapiens	14-17
23998577-0	2013	Expression of PML-RARalpha is up-regulated during ATRA and arsenics combined induction without influence on long-term prognosis of acute promyelocytic leukemia.	Arsenic	59-67	retinoic acid receptor alpha	Homo sapiens	18-26
23998577-9	2013	It is concluded that up-regulation of PML-RARa expression is a common event during induction therapy with ATRA plus arsenics.	Arsenic	116-124	PML nuclear body scaffold	Homo sapiens	38-41
23998577-9	2013	It is concluded that up-regulation of PML-RARa expression is a common event during induction therapy with ATRA plus arsenics.	Arsenic	116-124	retinoic acid receptor alpha	Homo sapiens	42-46
23889914-8	2013	RESULTS: Arsenic exposure to mice caused a significant increase in the lipid peroxidation, ROS production and decreased cell viability, levels of reduced glutathione, the activity of superoxide dismutase, catalase, cytochrome c oxidase and mitochondrial membrane potential in the thymus as compared to controls.	Arsenic	9-16	catalase	Mus musculus	205-213
23889914-9	2013	Increased activity of caspase-3 linked with apoptosis assessed by the cell cycle analysis and annexin V/PI binding was also observed in mice exposed to arsenic as compared to controls.	Arsenic	152-159	caspase 3	Mus musculus	22-31
23889914-9	2013	Increased activity of caspase-3 linked with apoptosis assessed by the cell cycle analysis and annexin V/PI binding was also observed in mice exposed to arsenic as compared to controls.	Arsenic	152-159	annexin A5	Mus musculus	94-103
23889914-10	2013	Co-treatment with arsenic and amla decreased the levels of lipid peroxidation, ROS production, activity of caspase-3, apoptosis and increased cell viability, levels of antioxidant enzymes, cytochrome c oxidase and mitochondrial membrane potential as compared to mice treated with arsenic alone.	Arsenic	18-25	caspase 3	Mus musculus	107-116
23789648-10	2013	A monotonic increase in barriers is observed for pseudorotation with the successive replacement of phosphorus with arsenic in methyl-DHP.	Arsenic	115-122	dihydropyrimidinase	Homo sapiens	133-136
23866971-7	2013	RESULTS: Placental expression of the arsenic transporter AQP9 was positively associated with maternal urinary arsenic levels during pregnancy (coefficient estimate: 0.25; 95% confidence interval: 0.05 - 0.45).	Arsenic	37-44	aquaporin 9	Homo sapiens	57-61
23866971-10	2013	CONCLUSIONS: We identified the expression of AQP9 as a potential fetal biomarker for arsenic exposure.	Arsenic	85-92	aquaporin 9	Homo sapiens	45-49
23740867-0	2013	Arsa-diazonium salts with an arsenic-nitrogen triple bond.	Arsenic	29-36	arylsulfatase A	Homo sapiens	0-4
23644288-10	2013	These findings suggest that NALP2 A1052E SNP plays an important role toward development of arsenic-induced skin lesions, chromosomal damage and respiratory diseases.	Arsenic	91-98	NLR family pyrin domain containing 2	Homo sapiens	28-33
23619517-3	2013	A significant increase of acetylcholinesterase (AChE) activity was noted in both arsenic groups.	Arsenic	81-88	acetylcholinesterase	Rattus norvegicus	26-46
21809430-5	2013	Our results showed that intracellular ROS were both dose- and time-dependent induced by inorganic arsenic; Cellular Nrf2 protein levels increased rapidly after 2 h of exposure, elevated significantly at 6 h, and reached the maximum at 12 h. The endogenous Nrf2-regulated downstream HO-1 mRNA and protein were also induced dramatically and lasted for as long as 24 h. In addition, intracellular GSH levels elevated in consistent with Nrf2 activation.	Arsenic	98-105	NFE2 like bZIP transcription factor 2	Homo sapiens	116-120
27335833-8	2013	Keap1 protein as well as mRNA level decreased concomitantly in arsenic treated mice.	Arsenic	63-70	kelch-like ECH-associated protein 1	Mus musculus	0-5
27335833-9	2013	Our study clearly indicates the important role of Nrf2 in activating ARE driven genes related to GSH metabolic pathway and also the adaptive response mechanisms in arsenic induced hepatotoxicity.	Arsenic	164-171	nuclear factor, erythroid derived 2, like 2	Mus musculus	50-54
21809430-2	2013	Nuclear factor (erythroid-2 related) factor 2 (Nrf2) is a redox-sensitive transcription factor, regulating critically cellular defense responses against the toxic metallic arsenic in many cell types and tissues.	Arsenic	172-179	NFE2 like bZIP transcription factor 2	Homo sapiens	47-51
23619517-3	2013	A significant increase of acetylcholinesterase (AChE) activity was noted in both arsenic groups.	Arsenic	81-88	acetylcholinesterase	Rattus norvegicus	48-52
21809430-5	2013	Our results showed that intracellular ROS were both dose- and time-dependent induced by inorganic arsenic; Cellular Nrf2 protein levels increased rapidly after 2 h of exposure, elevated significantly at 6 h, and reached the maximum at 12 h. The endogenous Nrf2-regulated downstream HO-1 mRNA and protein were also induced dramatically and lasted for as long as 24 h. In addition, intracellular GSH levels elevated in consistent with Nrf2 activation.	Arsenic	98-105	NFE2 like bZIP transcription factor 2	Homo sapiens	256-260
23619517-5	2013	Catalase (CAT) activity in arsenic groups was increased, but no changes were found in the other groups.	Arsenic	27-34	catalase	Rattus norvegicus	0-8
21809430-5	2013	Our results showed that intracellular ROS were both dose- and time-dependent induced by inorganic arsenic; Cellular Nrf2 protein levels increased rapidly after 2 h of exposure, elevated significantly at 6 h, and reached the maximum at 12 h. The endogenous Nrf2-regulated downstream HO-1 mRNA and protein were also induced dramatically and lasted for as long as 24 h. In addition, intracellular GSH levels elevated in consistent with Nrf2 activation.	Arsenic	98-105	heme oxygenase 1	Homo sapiens	282-286
21809430-5	2013	Our results showed that intracellular ROS were both dose- and time-dependent induced by inorganic arsenic; Cellular Nrf2 protein levels increased rapidly after 2 h of exposure, elevated significantly at 6 h, and reached the maximum at 12 h. The endogenous Nrf2-regulated downstream HO-1 mRNA and protein were also induced dramatically and lasted for as long as 24 h. In addition, intracellular GSH levels elevated in consistent with Nrf2 activation.	Arsenic	98-105	NFE2 like bZIP transcription factor 2	Homo sapiens	256-260
23619517-5	2013	Catalase (CAT) activity in arsenic groups was increased, but no changes were found in the other groups.	Arsenic	27-34	catalase	Rattus norvegicus	10-13
21809430-6	2013	Our findings here suggest that inorganic arsenic alters cellular redox balance in hepatocytes to trigger Nrf2-regulated antioxidant responses promptly, which may represent an adaptive cell defense mechanism against inorganic arsenic induced liver injuries and hepatoxicity.	Arsenic	41-48	NFE2 like bZIP transcription factor 2	Homo sapiens	105-109
22727912-4	2013	We found a normocytic and normochromic anemia as well as a significant increase in hemolysis, TBARS production and catalase activity in the blood of arsenic intoxicated pups.	Arsenic	149-156	catalase	Rattus norvegicus	115-123
21809430-6	2013	Our findings here suggest that inorganic arsenic alters cellular redox balance in hepatocytes to trigger Nrf2-regulated antioxidant responses promptly, which may represent an adaptive cell defense mechanism against inorganic arsenic induced liver injuries and hepatoxicity.	Arsenic	225-232	NFE2 like bZIP transcription factor 2	Homo sapiens	105-109
23665909-1	2013	BACKGROUND: In humans, inorganic arsenic is metabolized to methylated metabolites mainly by arsenic (+3 oxidation state) methyltransferase (AS3MT).	Arsenic	33-40	arsenite methyltransferase	Homo sapiens	92-138
23665909-1	2013	BACKGROUND: In humans, inorganic arsenic is metabolized to methylated metabolites mainly by arsenic (+3 oxidation state) methyltransferase (AS3MT).	Arsenic	33-40	arsenite methyltransferase	Homo sapiens	140-145
23665909-3	2013	Recently, a putative N-6-adenine-specific DNA methyltransferase 1 (N6AMT1) was found to methylate arsenic in vitro.	Arsenic	98-105	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	21-65
23665909-3	2013	Recently, a putative N-6-adenine-specific DNA methyltransferase 1 (N6AMT1) was found to methylate arsenic in vitro.	Arsenic	98-105	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	67-73
23665909-4	2013	OBJECTIVE: We evaluated the role of N6AMT1 polymorphisms in arsenic methylation efficiency in humans.	Arsenic	60-67	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	36-42
23665909-12	2013	CONCLUSIONS: N6AMT1 polymorphisms were associated with arsenic methylation in Andean women, independent of AS3MT.	Arsenic	55-62	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	13-19
23665909-13	2013	N6AMT1 polymorphisms may be susceptibility markers for arsenic-related toxic effects.	Arsenic	55-62	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	0-6
24218851-4	2013	We investigated the functions of arsA, arsT, orf7 and orf8 in arsenic resistance using a plasmid-based gene knockout approach in the ars gene deficient Escherichia coli strain AW3110.	Arsenic	62-69	putative regulator	Escherichia coli	54-58
23321855-8	2013	In households with tap water As &lt;=10 p.p.b., over 93% of total arsenic exposure was attributable to diet.	Arsenic	66-73	nuclear RNA export factor 1	Homo sapiens	19-22
24218851-10	2013	The resulting abolishment of arsenate resistance suggests that the involvement of orf8 in arsenic resistance is not via reductase activity.	Arsenic	90-97	putative regulator	Escherichia coli	82-86
23339766-5	2013	TBARS production in both organs and liver glutathione peroxidase (GPx) activity also increased whereas catalase (CAT) activity in both organs decreased in arsenic-exposed pups; the antioxidant administration only recover TBARS concentration to control values.	Arsenic	155-162	catalase	Rattus norvegicus	103-111
23370535-3	2013	We reported that arsenic causes aberrant keratinocyte proliferation through mtTFA-mediated mitochondrial biogenesis in As-BD.	Arsenic	17-24	transcription factor A, mitochondrial	Homo sapiens	76-81
23339766-5	2013	TBARS production in both organs and liver glutathione peroxidase (GPx) activity also increased whereas catalase (CAT) activity in both organs decreased in arsenic-exposed pups; the antioxidant administration only recover TBARS concentration to control values.	Arsenic	155-162	catalase	Rattus norvegicus	113-116
23603059-7	2013	Taken together, our results indicate that arsenic indeed upregulates the AT1R expression, thus highlighting a role of arsenic-induced aberrant AT1R signaling in the pathogenesis of hypertension.	Arsenic	42-49	angiotensin II, type I receptor-associated protein	Mus musculus	73-77
23570992-10	2013	Of these 25, a single protein, hydroxysteroid dehydrogenase like 2, showed decreased expression in both males and females following arsenic exposure.	Arsenic	132-139	hydroxysteroid dehydrogenase like 2	Danio rerio	31-66
23603059-7	2013	Taken together, our results indicate that arsenic indeed upregulates the AT1R expression, thus highlighting a role of arsenic-induced aberrant AT1R signaling in the pathogenesis of hypertension.	Arsenic	118-125	angiotensin II, type I receptor-associated protein	Mus musculus	143-147
23603059-7	2013	Taken together, our results indicate that arsenic indeed upregulates the AT1R expression, thus highlighting a role of arsenic-induced aberrant AT1R signaling in the pathogenesis of hypertension.	Arsenic	118-125	angiotensin II, type I receptor-associated protein	Mus musculus	73-77
23562784-0	2013	Regulation of cellular Cyclin D1 gene by arsenic is mediated through miR-2909.	Arsenic	41-48	cyclin D1	Homo sapiens	23-32
23562784-0	2013	Regulation of cellular Cyclin D1 gene by arsenic is mediated through miR-2909.	Arsenic	41-48	microRNA 2909	Homo sapiens	69-77
23562784-3	2013	Here we provide reasonably good evidence to support the view that arsenic exposure to human PBMCs (peripheral blood mononuclear cells) at low concentrations results in the over-expression of miR-2909 within these cells.	Arsenic	66-73	microRNA 2909	Homo sapiens	191-199
23562784-5	2013	Arsenic dependent regulation of AATF (Apoptosis Antagonizing Transcription factor) and BCL3 (B-cell Lymphoma 3) were also found to be modulated through its capacity to induce miR-2909 expression.	Arsenic	0-7	apoptosis antagonizing transcription factor	Homo sapiens	32-36
23562784-5	2013	Arsenic dependent regulation of AATF (Apoptosis Antagonizing Transcription factor) and BCL3 (B-cell Lymphoma 3) were also found to be modulated through its capacity to induce miR-2909 expression.	Arsenic	0-7	apoptosis antagonizing transcription factor	Homo sapiens	38-81
23562784-5	2013	Arsenic dependent regulation of AATF (Apoptosis Antagonizing Transcription factor) and BCL3 (B-cell Lymphoma 3) were also found to be modulated through its capacity to induce miR-2909 expression.	Arsenic	0-7	BCL3 transcription coactivator	Homo sapiens	87-91
23562784-5	2013	Arsenic dependent regulation of AATF (Apoptosis Antagonizing Transcription factor) and BCL3 (B-cell Lymphoma 3) were also found to be modulated through its capacity to induce miR-2909 expression.	Arsenic	0-7	BCL3 transcription coactivator	Homo sapiens	93-110
23562784-5	2013	Arsenic dependent regulation of AATF (Apoptosis Antagonizing Transcription factor) and BCL3 (B-cell Lymphoma 3) were also found to be modulated through its capacity to induce miR-2909 expression.	Arsenic	0-7	microRNA 2909	Homo sapiens	175-183
23052202-0	2013	Multidrug resistance protein 1 (ABCC1) confers resistance to arsenic compounds in human myeloid leukemic HL-60 cells.	Arsenic	61-68	ATP binding cassette subfamily B member 1	Homo sapiens	0-30
23052202-0	2013	Multidrug resistance protein 1 (ABCC1) confers resistance to arsenic compounds in human myeloid leukemic HL-60 cells.	Arsenic	61-68	ATP binding cassette subfamily C member 1	Homo sapiens	32-37
23052202-5	2013	Moreover, we found that the multidrug resistance protein 1 (MRP1), but not MRP2, is expressed in HL-60 cells, which reduced the intracellular arsenic accumulation, and conferred resistance to inorganic iAs(III) and MMA(III).	Arsenic	142-149	ATP binding cassette subfamily B member 1	Homo sapiens	28-58
23591579-0	2013	Oxidative stress and MAPK involved into ATF2 expression in immortalized human urothelial cells treated by arsenic.	Arsenic	106-113	activating transcription factor 2	Homo sapiens	40-44
23052202-5	2013	Moreover, we found that the multidrug resistance protein 1 (MRP1), but not MRP2, is expressed in HL-60 cells, which reduced the intracellular arsenic accumulation, and conferred resistance to inorganic iAs(III) and MMA(III).	Arsenic	142-149	ATP binding cassette subfamily B member 1	Homo sapiens	60-64
23591579-3	2013	However, little is known about the effect of arsenic on expression of ATF2 and regulatory pathways in human urothelial cells.	Arsenic	45-52	activating transcription factor 2	Homo sapiens	70-74
23052202-6	2013	Pretreatment of HL-60 with MK571, an inhibitor of MRP1, significantly increased iAs(III) and MMA(III)-induced cytotoxicity and arsenic accumulations, suggesting that the expression of MRP1/4 may lead to HL-60 cells resistance to trivalent arsenic compounds.	Arsenic	127-134	ATP binding cassette subfamily B member 1	Homo sapiens	184-188
23591579-4	2013	In this study, ATF2 expression was measured in NaAsO(2)-treated human uroepithelial cell line (SV-HUC-1) with 1, 2, 4, 8 and 10 muM concentrations in order to provide some basis data for the study on mechanism of bladder cancer induced by arsenic.	Arsenic	239-246	activating transcription factor 2	Homo sapiens	15-19
23591579-5	2013	We found that ATF2 expression levels at 2, 4, 8 and 10 muM arsenic-treated cells were significantly higher than those of control cells, and the strongest expression occurred in 4 muM NaAsO(2)-treated cells.	Arsenic	59-66	activating transcription factor 2	Homo sapiens	14-18
23052202-6	2013	Pretreatment of HL-60 with MK571, an inhibitor of MRP1, significantly increased iAs(III) and MMA(III)-induced cytotoxicity and arsenic accumulations, suggesting that the expression of MRP1/4 may lead to HL-60 cells resistance to trivalent arsenic compounds.	Arsenic	239-246	ATP binding cassette subfamily B member 1	Homo sapiens	50-54
23591579-5	2013	We found that ATF2 expression levels at 2, 4, 8 and 10 muM arsenic-treated cells were significantly higher than those of control cells, and the strongest expression occurred in 4 muM NaAsO(2)-treated cells.	Arsenic	59-66	latexin	Homo sapiens	55-58
23052202-6	2013	Pretreatment of HL-60 with MK571, an inhibitor of MRP1, significantly increased iAs(III) and MMA(III)-induced cytotoxicity and arsenic accumulations, suggesting that the expression of MRP1/4 may lead to HL-60 cells resistance to trivalent arsenic compounds.	Arsenic	239-246	ATP binding cassette subfamily B member 1	Homo sapiens	184-188
23591579-6	2013	Antioxidants (melatonin) and JNK or p38 inhibitors decreased significantly arsenic-induced ATF2 expression.	Arsenic	75-82	mitogen-activated protein kinase 14	Homo sapiens	36-39
23591579-6	2013	Antioxidants (melatonin) and JNK or p38 inhibitors decreased significantly arsenic-induced ATF2 expression.	Arsenic	75-82	activating transcription factor 2	Homo sapiens	91-95
23640787-0	2013	Catalase has a key role in protecting cells from the genotoxic effects of monomethylarsonous acid: a highly active metabolite of arsenic.	Arsenic	129-136	catalase	Mus musculus	0-8
23591579-7	2013	Taken together, these data indicated that the increasing of ATF2 expression is mediated via oxidative stress induced by arsenic in SV-HUC-1 cells, and JNK or p38 rather than ERK is responsible for arsenic-induced ATF2 expression.	Arsenic	120-127	activating transcription factor 2	Homo sapiens	60-64
23591579-7	2013	Taken together, these data indicated that the increasing of ATF2 expression is mediated via oxidative stress induced by arsenic in SV-HUC-1 cells, and JNK or p38 rather than ERK is responsible for arsenic-induced ATF2 expression.	Arsenic	197-204	mitogen-activated protein kinase 14	Homo sapiens	158-161
23591579-7	2013	Taken together, these data indicated that the increasing of ATF2 expression is mediated via oxidative stress induced by arsenic in SV-HUC-1 cells, and JNK or p38 rather than ERK is responsible for arsenic-induced ATF2 expression.	Arsenic	197-204	activating transcription factor 2	Homo sapiens	213-217
23591579-8	2013	ROS were also involved in arsenic induced the activation of JNK and p38 MAPK signaling pathway.	Arsenic	26-33	mitogen-activated protein kinase 14	Homo sapiens	68-71
23401165-5	2013	Upgradient samples, unexposed to acetate, showed low levels of arsenic ( 1 muM), with greater than 90% as arsenate (As[V]) and a small amount of arsenite (As[III]).	Arsenic	63-70	latexin	Homo sapiens	75-78
23401165-6	2013	Downgradient acetate-stimulated water samples had much higher levels of arsenic (up to 8 muM), and 4 additional thioarsenic species were present under sulfate-reducing conditions.	Arsenic	72-79	latexin	Homo sapiens	89-92
23681673-6	2013	Later, MiADMSA pre-incubation for an hour preceded arsenic exposure (30 muM).	Arsenic	51-58	latexin	Homo sapiens	72-75
23681673-9	2013	Arsenic also caused a significant increase in lactate dehydrogenase accompanied by an elevated antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase and caspase activity).	Arsenic	0-7	caspase 9	Homo sapiens	175-182
23640787-3	2013	The authors" studies are centered on identifying a reactive species involved in the genotoxicity of arsenic using a catalase (CAT) knockout mouse model that is impaired in its ability to breakdown hydrogen peroxide (H2 O2 ).	Arsenic	100-107	catalase	Mus musculus	116-124
23640787-3	2013	The authors" studies are centered on identifying a reactive species involved in the genotoxicity of arsenic using a catalase (CAT) knockout mouse model that is impaired in its ability to breakdown hydrogen peroxide (H2 O2 ).	Arsenic	100-107	catalase	Mus musculus	126-129
23666632-6	2013	Investigation revealed that ArsC from C. sakazakii can play significant role during arsenic resistance and potential microorganism for bioremediation of arsenic toxicity.	Arsenic	84-91	ArsC family reductase	Cronobacter sakazakii	28-32
23772150-6	2013	Furthermore, the urinary total arsenic concentration was inversely associated with the insulin secretion index, HOMA2 %B (beta = -0.033, P = 0.032).	Arsenic	31-38	insulin	Homo sapiens	87-94
23530056-5	2013	While the SIMs of Arkadia are not essential for SnoN/Ski degradation in response to TGF-beta, we show that they are necessary for the interaction of Arkadia with polysumoylated PML in response to arsenic and its concomitant accumulation into PML nuclear bodies.	Arsenic	196-203	ring finger protein 111	Homo sapiens	18-25
23530056-5	2013	While the SIMs of Arkadia are not essential for SnoN/Ski degradation in response to TGF-beta, we show that they are necessary for the interaction of Arkadia with polysumoylated PML in response to arsenic and its concomitant accumulation into PML nuclear bodies.	Arsenic	196-203	PML nuclear body scaffold	Homo sapiens	177-180
23530056-5	2013	While the SIMs of Arkadia are not essential for SnoN/Ski degradation in response to TGF-beta, we show that they are necessary for the interaction of Arkadia with polysumoylated PML in response to arsenic and its concomitant accumulation into PML nuclear bodies.	Arsenic	196-203	PML nuclear body scaffold	Homo sapiens	242-245
23530056-5	2013	While the SIMs of Arkadia are not essential for SnoN/Ski degradation in response to TGF-beta, we show that they are necessary for the interaction of Arkadia with polysumoylated PML in response to arsenic and its concomitant accumulation into PML nuclear bodies.	Arsenic	196-203	ring finger protein 111	Homo sapiens	149-156
23530056-6	2013	Moreover, Arkadia depletion leads to accumulation of polysumoylated PML in response to arsenic, highlighting a requirement of Arkadia for arsenic-induced degradation of polysumoylated PML.	Arsenic	87-94	ring finger protein 111	Homo sapiens	10-17
23589329-0	2013	Arsenic inhibits autophagic flux, activating the Nrf2-Keap1 pathway in a p62-dependent manner.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	49-53
23589329-0	2013	Arsenic inhibits autophagic flux, activating the Nrf2-Keap1 pathway in a p62-dependent manner.	Arsenic	0-7	kelch like ECH associated protein 1	Homo sapiens	54-59
23530056-6	2013	Moreover, Arkadia depletion leads to accumulation of polysumoylated PML in response to arsenic, highlighting a requirement of Arkadia for arsenic-induced degradation of polysumoylated PML.	Arsenic	87-94	PML nuclear body scaffold	Homo sapiens	68-71
23589329-10	2013	Collectively, these findings provide evidence that arsenic causes prolonged activation of Nrf2 through autophagy dysfunction, possibly providing a scenario similar to that of constitutive activation of Nrf2 found in certain human cancers.	Arsenic	51-58	NFE2 like bZIP transcription factor 2	Homo sapiens	90-94
23530056-6	2013	Moreover, Arkadia depletion leads to accumulation of polysumoylated PML in response to arsenic, highlighting a requirement of Arkadia for arsenic-induced degradation of polysumoylated PML.	Arsenic	87-94	PML nuclear body scaffold	Homo sapiens	184-187
23530056-6	2013	Moreover, Arkadia depletion leads to accumulation of polysumoylated PML in response to arsenic, highlighting a requirement of Arkadia for arsenic-induced degradation of polysumoylated PML.	Arsenic	138-145	ring finger protein 111	Homo sapiens	10-17
23530056-6	2013	Moreover, Arkadia depletion leads to accumulation of polysumoylated PML in response to arsenic, highlighting a requirement of Arkadia for arsenic-induced degradation of polysumoylated PML.	Arsenic	138-145	PML nuclear body scaffold	Homo sapiens	68-71
23530056-6	2013	Moreover, Arkadia depletion leads to accumulation of polysumoylated PML in response to arsenic, highlighting a requirement of Arkadia for arsenic-induced degradation of polysumoylated PML.	Arsenic	138-145	ring finger protein 111	Homo sapiens	126-133
23530056-6	2013	Moreover, Arkadia depletion leads to accumulation of polysumoylated PML in response to arsenic, highlighting a requirement of Arkadia for arsenic-induced degradation of polysumoylated PML.	Arsenic	138-145	PML nuclear body scaffold	Homo sapiens	184-187
23589329-0	2013	Arsenic inhibits autophagic flux, activating the Nrf2-Keap1 pathway in a p62-dependent manner.	Arsenic	0-7	nucleoporin 62	Homo sapiens	73-76
23589329-4	2013	Here, we report a novel mechanism of Nrf2 activation by arsenic that is distinct from that of chemopreventive compounds.	Arsenic	56-63	NFE2 like bZIP transcription factor 2	Homo sapiens	37-41
23589329-5	2013	Arsenic deregulates the autophagic pathway through blockage of autophagic flux, resulting in accumulation of autophagosomes and sequestration of p62, Keap1, and LC3.	Arsenic	0-7	nucleoporin 62	Homo sapiens	145-148
23589329-5	2013	Arsenic deregulates the autophagic pathway through blockage of autophagic flux, resulting in accumulation of autophagosomes and sequestration of p62, Keap1, and LC3.	Arsenic	0-7	kelch like ECH associated protein 1	Homo sapiens	150-155
23589329-5	2013	Arsenic deregulates the autophagic pathway through blockage of autophagic flux, resulting in accumulation of autophagosomes and sequestration of p62, Keap1, and LC3.	Arsenic	0-7	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	161-164
23570516-12	2013	This study outlines a strategy for designing novel derivatives of 4APB with potentially better AChE inhibitory activities through interaction at the PAS and AS sites.	Arsenic	150-152	acetylcholinesterase (Cartwright blood group)	Homo sapiens	95-99
23589329-6	2013	Thus, arsenic activates Nrf2 through a noncanonical mechanism (p62 dependent), leading to a chronic, sustained activation of Nrf2.	Arsenic	6-13	NFE2 like bZIP transcription factor 2	Homo sapiens	24-28
23589329-6	2013	Thus, arsenic activates Nrf2 through a noncanonical mechanism (p62 dependent), leading to a chronic, sustained activation of Nrf2.	Arsenic	6-13	nucleoporin 62	Homo sapiens	63-66
23589329-6	2013	Thus, arsenic activates Nrf2 through a noncanonical mechanism (p62 dependent), leading to a chronic, sustained activation of Nrf2.	Arsenic	6-13	NFE2 like bZIP transcription factor 2	Homo sapiens	125-129
23563754-4	2013	In addition, markedly higher expression levels of AQP9, as assessed using flow cytometry, along with more intracellular arsenic accumulation, were observed in the NB4 cells.	Arsenic	120-127	aquaporin 9	Homo sapiens	50-54
23295455-3	2013	Here we report that arsenic activates the iron responsive transcription factor, Aft1, as a consequence of a defective high-affinity iron uptake mediated by Fet3 and Ftr1, whose mRNAs are drastically decreased upon arsenic exposure.	Arsenic	214-221	DNA-binding transcription factor AFT1	Saccharomyces cerevisiae S288C	80-84
23396038-1	2013	We describe a real-time PCR assay for the quantitative detection of arsB and ACR3(1) arsenite transporter gene families, two ubiquitous and key determinants of arsenic resistance in prokaryotes.	Arsenic	160-167	arylsulfatase B	Homo sapiens	68-72
23624839-0	2013	Arsenic reverses glioblastoma resistance to mTOR-targeted therapies.	Arsenic	0-7	mechanistic target of rapamycin kinase	Homo sapiens	44-48
23377826-3	2013	We provide evidence that a signaling cascade involving the kinase RSK1 is engaged in a negative feedback manner during arsenic-treatment of cells and exhibits regulatory effects on growth and survival of AML cells in response to treatment with As2O3.	Arsenic	119-126	ribosomal protein S6 kinase A1	Homo sapiens	66-70
23295455-3	2013	Here we report that arsenic activates the iron responsive transcription factor, Aft1, as a consequence of a defective high-affinity iron uptake mediated by Fet3 and Ftr1, whose mRNAs are drastically decreased upon arsenic exposure.	Arsenic	20-27	DNA-binding transcription factor AFT1	Saccharomyces cerevisiae S288C	80-84
23295455-3	2013	Here we report that arsenic activates the iron responsive transcription factor, Aft1, as a consequence of a defective high-affinity iron uptake mediated by Fet3 and Ftr1, whose mRNAs are drastically decreased upon arsenic exposure.	Arsenic	20-27	ferroxidase FET3	Saccharomyces cerevisiae S288C	156-160
23295455-3	2013	Here we report that arsenic activates the iron responsive transcription factor, Aft1, as a consequence of a defective high-affinity iron uptake mediated by Fet3 and Ftr1, whose mRNAs are drastically decreased upon arsenic exposure.	Arsenic	20-27	high-affinity iron permease FTR1	Saccharomyces cerevisiae S288C	165-169
23295455-4	2013	Moreover, arsenic causes the internalization and degradation of Fet3.	Arsenic	10-17	ferroxidase FET3	Saccharomyces cerevisiae S288C	64-68
23295455-5	2013	Most importantly, fet3ftr1 mutant exhibits increased arsenic resistance and decreased arsenic accumulation over the wild-type suggesting that Fet3 plays a role in arsenic toxicity.	Arsenic	53-60	ferroxidase FET3	Saccharomyces cerevisiae S288C	18-26
23295455-5	2013	Most importantly, fet3ftr1 mutant exhibits increased arsenic resistance and decreased arsenic accumulation over the wild-type suggesting that Fet3 plays a role in arsenic toxicity.	Arsenic	86-93	ferroxidase FET3	Saccharomyces cerevisiae S288C	18-26
23295455-6	2013	Finally we provide data suggesting that arsenic also disrupts iron uptake in mammals and the link between Fet3, arsenic and iron, can be relevant to clinical applications.	Arsenic	112-119	ferroxidase FET3	Saccharomyces cerevisiae S288C	106-110
22301814-2	2013	The treatment with arsenic exhibited a significant increase in some serum hepatic and renal biochemical parameters (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total protein, albumin, bilirubin, cholesterol, urea and creatinine).	Arsenic	19-26	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	142-168
23472850-0	2013	Nerve growth factor exhibits an antioxidant and an autocrine activity in mouse liver that is modulated by buthionine sulfoximine, arsenic, and acetaminophen.	Arsenic	130-137	nerve growth factor	Mus musculus	0-19
23265515-4	2013	Concentration of As(V) was deduced by the difference between total inorganic arsenic and As(III).	Arsenic	77-84	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	17-22
23940966-5	2013	The serum TNF-alpha levels of AS group and ASL group were significantly higher than those in control group, but the value of ASH and ASL was significantly lower than that in AS group.	Arsenic	30-32	tumor necrosis factor	Rattus norvegicus	10-19
24082510-1	2013	The effects of arsenic exposure during rapid brain growth period (RBGP) (postnatal period 4-11) on pyramidal neurons of cornu ammonis (specifically CA1 and CA3 regions) and granule cells of dentate gyrus (DG) of rat hippocampus were studied.	Arsenic	15-22	carbonic anhydrase 1	Rattus norvegicus	148-151
23940966-9	2013	(3) The value of p-AMPK protein of ASL and ASH groups was significantly higher than that of AS group, the value of p-AMPK protein of ASH group was significantly higher than that of the control group at the same time.	Arsenic	35-37	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	19-23
23579691-8	2013	Interestingly, we also find that Egfr signaling in the AS is required to repress zip expression in both the AS and the epidermis, and this may be generally restrictive to the progression of morphogenesis in these tissues.	Arsenic	55-57	Epidermal growth factor receptor	Drosophila melanogaster	33-37
23599296-0	2013	Draft Genome Sequence of Ochrobactrum pseudogrignonense Strain CDB2, a Highly Efficient Arsenate-Resistant Soil Bacterium from Arsenic-Contaminated Cattle Dip Sites.	Arsenic	127-134	GRAM domain containing 4	Bos taurus	155-158
23500428-1	2013	Arsenic is among the most toxic elements and it commonly exists in water as arsenite (As(III)) and arsenate (As(V)) ions.	Arsenic	0-7	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	108-114
23509325-3	2013	In contrast, arsenic, the other potent anti-APL therapy, only induces PML/RARA degradation by specifically targeting its PML moiety.	Arsenic	13-20	promyelocytic leukemia	Mus musculus	70-73
23509325-3	2013	In contrast, arsenic, the other potent anti-APL therapy, only induces PML/RARA degradation by specifically targeting its PML moiety.	Arsenic	13-20	retinoic acid receptor, alpha	Mus musculus	74-78
23509325-3	2013	In contrast, arsenic, the other potent anti-APL therapy, only induces PML/RARA degradation by specifically targeting its PML moiety.	Arsenic	13-20	promyelocytic leukemia	Mus musculus	121-124
23523789-6	2013	Importantly, we showed that the closely spaced N-terminal cysteine residues of Id3 interacted with the arsenic derivative phenylarsine oxide (PAO) and were essential for the arsenite-induced cytoplasmic accumulation, suggesting that arsenite induces the CRM1-dependent nuclear export of Id3 via binding to the N-terminal cysteines.	Arsenic	103-110	inhibitor of DNA binding 3, HLH protein	Homo sapiens	79-82
23579691-8	2013	Interestingly, we also find that Egfr signaling in the AS is required to repress zip expression in both the AS and the epidermis, and this may be generally restrictive to the progression of morphogenesis in these tissues.	Arsenic	55-57	unzipped	Drosophila melanogaster	81-84
23232865-5	2013	At 298.15 K, we estimate the asymptotic limits (infinite dilution) of the total standard enthalpies of hydration for Ca(II), oxalate ion and calcium oxalate as -480.78, -302.78 and -312.73 kcal mol(-1), resp.	Arsenic	29-31	carbonic anhydrase 2	Homo sapiens	117-123
23430410-6	2013	The ascorbate peroxidase and glutathione S-transferase activities consistently increased with an increase in the As concentration, while glutathione reductase (GR) activities increased only at 0.25 mM.	Arsenic	113-115	peroxidase-like	Triticum aestivum	14-24
23430410-6	2013	The ascorbate peroxidase and glutathione S-transferase activities consistently increased with an increase in the As concentration, while glutathione reductase (GR) activities increased only at 0.25 mM.	Arsenic	113-115	glutathione S-transferase	Triticum aestivum	29-54
23430410-8	2013	The activities of dehydroascorbate reductase (DHAR) and glyoxalase I (Gly I) decreased at any levels of As, while glutathione peroxidase (GPX) and glyoxalase II (Gly II) activities decreased only upon 0.5 mM As.	Arsenic	104-106	probable glutathione S-transferase DHAR1, cytosolic	Triticum aestivum	18-44
23430410-8	2013	The activities of dehydroascorbate reductase (DHAR) and glyoxalase I (Gly I) decreased at any levels of As, while glutathione peroxidase (GPX) and glyoxalase II (Gly II) activities decreased only upon 0.5 mM As.	Arsenic	104-106	probable glutathione S-transferase DHAR1, cytosolic	Triticum aestivum	46-50
23430410-8	2013	The activities of dehydroascorbate reductase (DHAR) and glyoxalase I (Gly I) decreased at any levels of As, while glutathione peroxidase (GPX) and glyoxalase II (Gly II) activities decreased only upon 0.5 mM As.	Arsenic	208-210	probable glutathione S-transferase DHAR1, cytosolic	Triticum aestivum	46-50
23376440-2	2013	Bladder is one of the major target organs of arsenic, and cyclooxygenase-2 (COX-2) may play an important role in arsenic-induced bladder cancer.	Arsenic	113-120	prostaglandin-endoperoxide synthase 2	Homo sapiens	58-74
23376440-2	2013	Bladder is one of the major target organs of arsenic, and cyclooxygenase-2 (COX-2) may play an important role in arsenic-induced bladder cancer.	Arsenic	113-120	prostaglandin-endoperoxide synthase 2	Homo sapiens	76-81
23376440-3	2013	However, the mechanism by which arsenic induces COX-2 in bladder cells remains unclear.	Arsenic	32-39	prostaglandin-endoperoxide synthase 2	Homo sapiens	48-53
23376440-4	2013	This study aimed at investigating arsenic-mediated intracellular redox status and signaling cascades leading to COX-2 induction in human uroepithelial cells (SV-HUC-1).	Arsenic	34-41	prostaglandin-endoperoxide synthase 2	Homo sapiens	112-117
23322787-1	2013	BACKGROUND: Arsenic (III) methyltransferase (AS3MT) has been related to urine arsenic metabolites in association studies.	Arsenic	78-85	arsenite methyltransferase	Homo sapiens	45-50
23246791-6	2013	PTH was given as injections (SC) at a dosage of 60mug/kg/d, and SrR as 900mg/kg/d in the diet.	Arsenic	5-7	parathyroid hormone	Rattus norvegicus	0-3
23093101-2	2013	We previously reported an association of diabetes and urinary concentration of dimethylarsinite (DMAs(III)), a toxic product of arsenic methylation by arsenic (+3 oxidation state) methyltransferase (AS3MT).	Arsenic	128-135	arsenite methyltransferase	Homo sapiens	199-204
23376179-3	2013	Our results indicated that RBS significantly suppressed the multivulva (Muv) phenotype of let-60 ras(gf) mutant that was positive correlated to arsenic concentrations in worms and also inhibited Muv phenotype of lin-15(lf) upstream of Ras/MAPK pathway, but did not affect the Muv phenotype resulting from loss-of-function mutations of lin-l(lf) downstream of Ras/MAPK pathway, which may be mechanism-based.	Arsenic	144-151	Ras protein let-60	Caenorhabditis elegans	90-96
24620584-8	2013	Arsenic induced hepatotoxicity was manifested by an increase (P &lt; 0.001) in serum ALT, AST and ALP.	Arsenic	0-7	PDZ and LIM domain 3	Rattus norvegicus	98-101
23458687-0	2013	Systems biology and birth defects prevention: blockade of the glucocorticoid receptor prevents arsenic-induced birth defects.	Arsenic	95-102	nuclear receptor subfamily 3 group C member 1	Gallus gallus	62-85
23232971-1	2013	The objective of this study was to evaluate the relationship between environmental arsenic exposure and serum matrix metalloproteinase (MMP)-9, a biomarker associated with cardiovascular disease and cancer.	Arsenic	83-90	matrix metallopeptidase 9	Homo sapiens	110-142
23232971-6	2013	Drinking water arsenic concentration and intake were positively associated with MMP-9, both in crude analysis and after adjustment for gender, country/ethnicity, age, body mass index, current smoking, and diabetes.	Arsenic	15-22	matrix metallopeptidase 9	Homo sapiens	80-85
23232971-7	2013	Urinary arsenic sum of species was positively associated with MMP-9 in multivariable analysis only.	Arsenic	8-15	matrix metallopeptidase 9	Homo sapiens	62-67
23232971-8	2013	Using Akaike"s Information Criterion, arsenic concentration in drinking water provided a better fitting model of MMP-9 than either urinary arsenic or drinking water arsenic intake.	Arsenic	38-45	matrix metallopeptidase 9	Homo sapiens	113-118
23093101-2	2013	We previously reported an association of diabetes and urinary concentration of dimethylarsinite (DMAs(III)), a toxic product of arsenic methylation by arsenic (+3 oxidation state) methyltransferase (AS3MT).	Arsenic	151-158	arsenite methyltransferase	Homo sapiens	199-204
23232971-9	2013	In conclusion, arsenic exposure evaluated using all three exposure metrics was positively associated with MMP-9.	Arsenic	15-22	matrix metallopeptidase 9	Homo sapiens	106-111
23229538-0	2013	Role of pigment epithelium-derived factor (PEDF) in arsenic-induced cell apoptosis of liver and brain in a rat model.	Arsenic	52-59	serpin family F member 1	Rattus norvegicus	8-41
23174854-0	2013	Low concentration of arsenic-induced aberrant mitosis in keratinocytes through E2F1 transcriptionally regulated Aurora-A.	Arsenic	21-28	E2F transcription factor 1	Homo sapiens	79-83
23174854-0	2013	Low concentration of arsenic-induced aberrant mitosis in keratinocytes through E2F1 transcriptionally regulated Aurora-A.	Arsenic	21-28	aurora kinase A	Homo sapiens	112-120
23174854-4	2013	Our previous study revealed that low-concentration arsenic induces Aurora-A overexpression in immortalized bladder cells.	Arsenic	51-58	aurora kinase A	Homo sapiens	67-75
23174854-5	2013	In this study, we hypothesized that low-concentration arsenic induces aberrant mitosis in keratinocytes due to Aurora-A overexpression.	Arsenic	54-61	aurora kinase A	Homo sapiens	111-119
23174854-7	2013	The mRNA/protein levels and kinase activity of Aurora-A were increased in immortalized keratinocyte HaCaT cells after arsenic treatment at low concentration (&lt; 1microM).	Arsenic	118-125	aurora kinase A	Homo sapiens	47-55
23174854-11	2013	Finally, in arsenic-treated HaCaT cells and in BD, a significant increase of dysfunctional p53 was found, and this event correlated with the increase in expression of Aurora-A.	Arsenic	12-19	tumor protein p53	Homo sapiens	91-94
23174854-11	2013	Finally, in arsenic-treated HaCaT cells and in BD, a significant increase of dysfunctional p53 was found, and this event correlated with the increase in expression of Aurora-A.	Arsenic	12-19	aurora kinase A	Homo sapiens	167-175
23174854-12	2013	Altogether, our data suggest that low concentration of arsenic induces activation of E2F1-Aurora-A axis and results in aberrant mitosis of keratinocytes.	Arsenic	55-62	E2F transcription factor 1	Homo sapiens	85-89
23174854-12	2013	Altogether, our data suggest that low concentration of arsenic induces activation of E2F1-Aurora-A axis and results in aberrant mitosis of keratinocytes.	Arsenic	55-62	aurora kinase A	Homo sapiens	90-98
23174854-14	2013	Our findings suggest that Aurora-A may be a potential target for the prevention and treatment of arsenic-related cancers.	Arsenic	97-104	aurora kinase A	Homo sapiens	26-34
22733250-1	2013	Arsenic (+3 oxidation state) methyltransferase (As3mt) plays a central role in the enzymatically catalyzed conversion of inorganic arsenic into methylated metabolites.	Arsenic	131-138	arsenite methyltransferase	Mus musculus	0-46
22733250-1	2013	Arsenic (+3 oxidation state) methyltransferase (As3mt) plays a central role in the enzymatically catalyzed conversion of inorganic arsenic into methylated metabolites.	Arsenic	131-138	arsenite methyltransferase	Mus musculus	48-53
22733250-4	2013	Here, we report on the presence of methylated oxy- and thioarsenicals in urine and liver from wild-type mice that efficiently methylate inorganic arsenic and from As3mt knockout mice that lack arsenic methyltransferase activity.	Arsenic	59-66	arsenite methyltransferase	Mus musculus	163-168
22914984-5	2013	This review has been framed on the lines of differential molecular responses of Nrf2 on arsenic exposure as well as the chemopreventive strategy which may be improvised to regulate Nrf2 in order to combat arsenic-induced oxidative stress and its long-term carcinogenic effect.	Arsenic	88-95	NFE2 like bZIP transcription factor 2	Homo sapiens	80-84
22914984-5	2013	This review has been framed on the lines of differential molecular responses of Nrf2 on arsenic exposure as well as the chemopreventive strategy which may be improvised to regulate Nrf2 in order to combat arsenic-induced oxidative stress and its long-term carcinogenic effect.	Arsenic	205-212	NFE2 like bZIP transcription factor 2	Homo sapiens	181-185
23408639-2	2013	Arsenic-containing compounds have been described to be efficacious in malignancies overexpressing EVI1.	Arsenic	0-7	MDS1 and EVI1 complex locus	Homo sapiens	98-102
23229538-0	2013	Role of pigment epithelium-derived factor (PEDF) in arsenic-induced cell apoptosis of liver and brain in a rat model.	Arsenic	52-59	serpin family F member 1	Rattus norvegicus	43-47
23229538-2	2013	Based on our previous study on human serum, the present study was to determine whether pigment epithelium-derived factor (PEDF) plays a role in the damage induced by chronic arsenic exposure in a rat model and to explore the possible signaling pathway involved.	Arsenic	174-181	serpin family F member 1	Rattus norvegicus	87-120
23229538-2	2013	Based on our previous study on human serum, the present study was to determine whether pigment epithelium-derived factor (PEDF) plays a role in the damage induced by chronic arsenic exposure in a rat model and to explore the possible signaling pathway involved.	Arsenic	174-181	serpin family F member 1	Rattus norvegicus	122-126
23229538-10	2013	The ratio of Bax/Bcl-2 in the high arsenic group (50 mg/L) was significantly higher than that in the control group.	Arsenic	35-42	BCL2 associated X, apoptosis regulator	Rattus norvegicus	13-16
23229538-10	2013	The ratio of Bax/Bcl-2 in the high arsenic group (50 mg/L) was significantly higher than that in the control group.	Arsenic	35-42	BCL2, apoptosis regulator	Rattus norvegicus	17-22
23221970-9	2013	Exposure to arsenic in utero up-regulated the expression of genes in the lung involved in mucus production (Clca3, Muc5b, Scgb3a1), innate immunity (Reg3gamma, Tff2, Dynlrb2, Lplunc1), and lung morphogenesis (Sox2).	Arsenic	12-19	chloride channel accessory 1	Mus musculus	108-113
22736102-7	2013	The effect biomonitoring by MEC assay confirmed that there is a genotoxic damage in local childhood population that could be associated with the arsenic exposure in the site.	Arsenic	145-152	C-C motif chemokine ligand 28	Homo sapiens	28-31
23221970-9	2013	Exposure to arsenic in utero up-regulated the expression of genes in the lung involved in mucus production (Clca3, Muc5b, Scgb3a1), innate immunity (Reg3gamma, Tff2, Dynlrb2, Lplunc1), and lung morphogenesis (Sox2).	Arsenic	12-19	mucin 5, subtype B, tracheobronchial	Mus musculus	115-120
23221970-9	2013	Exposure to arsenic in utero up-regulated the expression of genes in the lung involved in mucus production (Clca3, Muc5b, Scgb3a1), innate immunity (Reg3gamma, Tff2, Dynlrb2, Lplunc1), and lung morphogenesis (Sox2).	Arsenic	12-19	trefoil factor 2 (spasmolytic protein 1)	Mus musculus	160-164
23221970-9	2013	Exposure to arsenic in utero up-regulated the expression of genes in the lung involved in mucus production (Clca3, Muc5b, Scgb3a1), innate immunity (Reg3gamma, Tff2, Dynlrb2, Lplunc1), and lung morphogenesis (Sox2).	Arsenic	12-19	dynein light chain roadblock-type 2	Mus musculus	166-173
23221970-9	2013	Exposure to arsenic in utero up-regulated the expression of genes in the lung involved in mucus production (Clca3, Muc5b, Scgb3a1), innate immunity (Reg3gamma, Tff2, Dynlrb2, Lplunc1), and lung morphogenesis (Sox2).	Arsenic	12-19	secretoglobin, family 3A, member 1	Mus musculus	122-129
23221970-9	2013	Exposure to arsenic in utero up-regulated the expression of genes in the lung involved in mucus production (Clca3, Muc5b, Scgb3a1), innate immunity (Reg3gamma, Tff2, Dynlrb2, Lplunc1), and lung morphogenesis (Sox2).	Arsenic	12-19	BPI fold containing family B, member 1	Mus musculus	175-182
23221970-9	2013	Exposure to arsenic in utero up-regulated the expression of genes in the lung involved in mucus production (Clca3, Muc5b, Scgb3a1), innate immunity (Reg3gamma, Tff2, Dynlrb2, Lplunc1), and lung morphogenesis (Sox2).	Arsenic	12-19	SRY (sex determining region Y)-box 2	Mus musculus	209-213
23221970-10	2013	Arsenic exposure also induced mucous cell metaplasia and increased expression of CLCA3 protein in the large airways.	Arsenic	0-7	chloride channel accessory 1	Mus musculus	81-86
23221970-9	2013	Exposure to arsenic in utero up-regulated the expression of genes in the lung involved in mucus production (Clca3, Muc5b, Scgb3a1), innate immunity (Reg3gamma, Tff2, Dynlrb2, Lplunc1), and lung morphogenesis (Sox2).	Arsenic	12-19	regenerating islet-derived 3 gamma	Mus musculus	149-158
23221991-0	2013	Association between arsenic suppression of adipogenesis and induction of CHOP10 via the endoplasmic reticulum stress response.	Arsenic	20-27	DNA-damage inducible transcript 3	Mus musculus	73-79
23221991-8	2013	Time-course studies in 3T3-L1 cells revealed that inhibition of adipogenesis by arsenic occurred in the early stage of terminal adipogenic differentiation and was highly correlated with the induction of C/EBP homologous protein (CHOP10), an endoplasmic reticulum (ER) stress response protein.	Arsenic	80-87	DNA-damage inducible transcript 3	Mus musculus	229-235
23188707-0	2013	Arsenic-mediated activation of the Nrf2-Keap1 antioxidant pathway.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	35-39
23221991-9	2013	Induction of CHOP10 by arsenic is associated with reduced DNA-binding activity of CCAAT/enhancer-binding protein beta (C/EBPbeta), which regulates the transcription of peroxisome proliferator-activated receptor gamma and C/EBPalpha.	Arsenic	23-30	DNA-damage inducible transcript 3	Mus musculus	13-19
23221991-9	2013	Induction of CHOP10 by arsenic is associated with reduced DNA-binding activity of CCAAT/enhancer-binding protein beta (C/EBPbeta), which regulates the transcription of peroxisome proliferator-activated receptor gamma and C/EBPalpha.	Arsenic	23-30	CCAAT/enhancer binding protein (C/EBP), beta	Mus musculus	82-117
23221991-9	2013	Induction of CHOP10 by arsenic is associated with reduced DNA-binding activity of CCAAT/enhancer-binding protein beta (C/EBPbeta), which regulates the transcription of peroxisome proliferator-activated receptor gamma and C/EBPalpha.	Arsenic	23-30	CCAAT/enhancer binding protein (C/EBP), beta	Mus musculus	119-128
23221991-9	2013	Induction of CHOP10 by arsenic is associated with reduced DNA-binding activity of CCAAT/enhancer-binding protein beta (C/EBPbeta), which regulates the transcription of peroxisome proliferator-activated receptor gamma and C/EBPalpha.	Arsenic	23-30	peroxisome proliferator activated receptor gamma	Mus musculus	168-216
23221991-9	2013	Induction of CHOP10 by arsenic is associated with reduced DNA-binding activity of CCAAT/enhancer-binding protein beta (C/EBPbeta), which regulates the transcription of peroxisome proliferator-activated receptor gamma and C/EBPalpha.	Arsenic	23-30	CCAAT/enhancer binding protein (C/EBP), alpha	Mus musculus	221-231
23188707-5	2013	Evidence also suggests that arsenic prolongs Nrf2 activation and may mimic constitutive activation of Nrf2, which has been found in several human cancers due to disruption of the Nrf2-Keap1 axis.	Arsenic	28-35	NFE2 like bZIP transcription factor 2	Homo sapiens	45-49
23188707-0	2013	Arsenic-mediated activation of the Nrf2-Keap1 antioxidant pathway.	Arsenic	0-7	kelch like ECH associated protein 1	Homo sapiens	40-45
23188707-5	2013	Evidence also suggests that arsenic prolongs Nrf2 activation and may mimic constitutive activation of Nrf2, which has been found in several human cancers due to disruption of the Nrf2-Keap1 axis.	Arsenic	28-35	NFE2 like bZIP transcription factor 2	Homo sapiens	102-106
23188707-5	2013	Evidence also suggests that arsenic prolongs Nrf2 activation and may mimic constitutive activation of Nrf2, which has been found in several human cancers due to disruption of the Nrf2-Keap1 axis.	Arsenic	28-35	NFE2 like bZIP transcription factor 2	Homo sapiens	102-106
23188707-5	2013	Evidence also suggests that arsenic prolongs Nrf2 activation and may mimic constitutive activation of Nrf2, which has been found in several human cancers due to disruption of the Nrf2-Keap1 axis.	Arsenic	28-35	kelch like ECH associated protein 1	Homo sapiens	184-189
23188707-6	2013	The current literature strongly suggests that activation of Nrf2 by arsenic potentially contributes to, rather than protects against, arsenic toxicity and carcinogenicity.	Arsenic	68-75	NFE2 like bZIP transcription factor 2	Homo sapiens	60-64
23188707-8	2013	These findings will provide insight to further understand how arsenic promotes a prolonged Nrf2 response, which will lead to the identification of novel molecular markers and development of rational therapies for the prevention or intervention of arsenic-induced diseases.	Arsenic	62-69	NFE2 like bZIP transcription factor 2	Homo sapiens	91-95
23188707-8	2013	These findings will provide insight to further understand how arsenic promotes a prolonged Nrf2 response, which will lead to the identification of novel molecular markers and development of rational therapies for the prevention or intervention of arsenic-induced diseases.	Arsenic	247-254	NFE2 like bZIP transcription factor 2	Homo sapiens	91-95
23271742-0	2013	Arsenic suppresses cell survival via Pirh2-mediated proteasomal degradation of DeltaNp63 protein.	Arsenic	0-7	ring finger and CHY zinc finger domain containing 1	Homo sapiens	37-42
23271742-8	2013	Consistent with this, we found that knockdown of Pirh2 inhibits, whereas ectopic expression of Pirh2 enhances, arsenic-induced degradation of DeltaNp63 protein.	Arsenic	111-118	ring finger and CHY zinc finger domain containing 1	Homo sapiens	49-54
23271742-8	2013	Consistent with this, we found that knockdown of Pirh2 inhibits, whereas ectopic expression of Pirh2 enhances, arsenic-induced degradation of DeltaNp63 protein.	Arsenic	111-118	ring finger and CHY zinc finger domain containing 1	Homo sapiens	95-100
23271742-10	2013	Together, these data suggest that arsenic degrades DeltaNp63 protein at least in part via Pirh2-dependent proteolysis and that inhibition of DeltaNp63 expression facilitates tumor cells to arsenic-induced death.	Arsenic	34-41	ring finger and CHY zinc finger domain containing 1	Homo sapiens	90-95
23188707-4	2013	This review highlights studies demonstrating that arsenic activates the Nrf2-Keap1 antioxidant pathway by a distinct mechanism from that of natural compounds such as sulforaphane (SF) found in broccoli sprouts or tert-butylhyrdoquinone (tBHQ), a natural antioxidant commonly used as a food preservative.	Arsenic	50-57	NFE2 like bZIP transcription factor 2	Homo sapiens	72-76
23188707-4	2013	This review highlights studies demonstrating that arsenic activates the Nrf2-Keap1 antioxidant pathway by a distinct mechanism from that of natural compounds such as sulforaphane (SF) found in broccoli sprouts or tert-butylhyrdoquinone (tBHQ), a natural antioxidant commonly used as a food preservative.	Arsenic	50-57	kelch like ECH associated protein 1	Homo sapiens	77-82
23428130-6	2013	RESULTS: The Western blot showed that the expression of phosphor-dynamin-1 was significantly lower in the AS and CS groups than in the corresponding control groups (AC and CC groups) (P&lt;0.05).	Arsenic	106-108	dynamin 1	Homo sapiens	65-74
23596950-3	2013	The arsenic rejection of ESNA-1-LF was higher than those of the other membranes in all experiments (&gt; 94%), and the HODRA-CORE membrane gave the lowest removal of arsenic (&lt; 47%).	Arsenic	4-11	nuclear receptor coactivator 7	Homo sapiens	25-31
23108036-0	2013	Arsenic inhibits the adipogenic differentiation of mesenchymal stem cells by down-regulating peroxisome proliferator-activated receptor gamma and CCAAT enhancer-binding proteins.	Arsenic	0-7	peroxisome proliferator activated receptor gamma	Homo sapiens	93-141
23108036-4	2013	Arsenic reduced the formation of lipid droplets and the expression of adipogenesis-related proteins, such as CCAAT enhancer binding protein-(C/EBPs), peroxisome proliferator-activated receptor-gamma (PPAR-gamma), and adipocyte fatty acid-binding protein aP2 (aP2).	Arsenic	0-7	peroxisome proliferator activated receptor gamma	Homo sapiens	150-198
23108036-4	2013	Arsenic reduced the formation of lipid droplets and the expression of adipogenesis-related proteins, such as CCAAT enhancer binding protein-(C/EBPs), peroxisome proliferator-activated receptor-gamma (PPAR-gamma), and adipocyte fatty acid-binding protein aP2 (aP2).	Arsenic	0-7	peroxisome proliferator activated receptor gamma	Homo sapiens	200-210
23108036-4	2013	Arsenic reduced the formation of lipid droplets and the expression of adipogenesis-related proteins, such as CCAAT enhancer binding protein-(C/EBPs), peroxisome proliferator-activated receptor-gamma (PPAR-gamma), and adipocyte fatty acid-binding protein aP2 (aP2).	Arsenic	0-7	fatty acid binding protein 4	Homo sapiens	254-257
23108036-4	2013	Arsenic reduced the formation of lipid droplets and the expression of adipogenesis-related proteins, such as CCAAT enhancer binding protein-(C/EBPs), peroxisome proliferator-activated receptor-gamma (PPAR-gamma), and adipocyte fatty acid-binding protein aP2 (aP2).	Arsenic	0-7	fatty acid binding protein 4	Homo sapiens	259-262
23108036-5	2013	Arsenic mediates this process by sustaining PPAR-gamma activity.	Arsenic	0-7	peroxisome proliferator activated receptor gamma	Homo sapiens	44-54
23108036-6	2013	In addition, inhibition of PPAR-gamma activity with T0070907 and up-regulation with its agonist troglitazone, showed the direct association of PPAR-gamma and arsenic-mediated inhibition of differentiating hMSCs.	Arsenic	158-165	peroxisome proliferator activated receptor gamma	Homo sapiens	27-37
23108036-6	2013	In addition, inhibition of PPAR-gamma activity with T0070907 and up-regulation with its agonist troglitazone, showed the direct association of PPAR-gamma and arsenic-mediated inhibition of differentiating hMSCs.	Arsenic	158-165	peroxisome proliferator activated receptor gamma	Homo sapiens	143-153
23108036-7	2013	Taken together, these results indicate that arsenic inhibits adipogenic differentiation through PPAR-gamma pathway and suggest a novel inhibitory effect of arsenic on adipogenic differentiation in hMSCs.	Arsenic	44-51	peroxisome proliferator activated receptor gamma	Homo sapiens	96-106
23428130-9	2013	The immunohistochemical results showed that phosphor-dynamin-1 was highly expressed in the cytoplasm of hippocampal neurons of AC, CC and HC groups, but its expression was significantly reduced in the AS, CS and HM groups (P&lt;0.05).	Arsenic	201-203	dynamin 1	Homo sapiens	53-62
23200367-7	2013	As(V) concentration was calculated by the difference between As(III) and total arsenic.	Arsenic	79-86	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	0-5
23069314-7	2013	CONCLUSIONS: The integrated cellular-level TK/TD model presented here provides significant insight into the underlying regulatory mechanism of Nrf2-regulated antioxidant response due to arsenic exposure.	Arsenic	186-193	NFE2 like bZIP transcription factor 2	Homo sapiens	143-147
23122625-4	2013	The vertical profiles of As, Cd and Hg content in the cores retrieved from Qin and Nanliu River estuaries show increasing trends during 1985-2008 due to anthropogenic impact caused by local economic development.	Arsenic	25-27	forkhead box G1	Homo sapiens	75-78
23164666-1	2013	Experimental studies have demonstrated that the antileukemic trivalent inorganic arsenic prevents the development of severe pro-inflammatory diseases mediated by excessive Th1 and Th17 cell responses.	Arsenic	81-88	negative elongation factor complex member C/D	Homo sapiens	172-175
23164666-2	2013	Differentiation of Th1 and Th17 subsets is mainly regulated by interleukins (ILs) secreted from dendritic cells (DCs) and the ability of inorganic arsenic to impair interferon-gamma and IL-17 secretion by interfering with the physiology of DCs is unknown.	Arsenic	147-154	negative elongation factor complex member C/D	Homo sapiens	19-22
23164666-2	2013	Differentiation of Th1 and Th17 subsets is mainly regulated by interleukins (ILs) secreted from dendritic cells (DCs) and the ability of inorganic arsenic to impair interferon-gamma and IL-17 secretion by interfering with the physiology of DCs is unknown.	Arsenic	147-154	interferon gamma	Homo sapiens	165-181
23164666-2	2013	Differentiation of Th1 and Th17 subsets is mainly regulated by interleukins (ILs) secreted from dendritic cells (DCs) and the ability of inorganic arsenic to impair interferon-gamma and IL-17 secretion by interfering with the physiology of DCs is unknown.	Arsenic	147-154	interleukin 17A	Homo sapiens	186-191
23137061-8	2013	Compared to the passage-matched control, chronic arsenic exposure caused exposure-duration dependent increases in secreted MMP-2 and MMP-9 activity, Cox-2 expression, and more rapid proliferation (all &gt;2-fold), characteristics typical of cancer cells.	Arsenic	49-56	matrix metallopeptidase 2	Homo sapiens	123-128
23137061-8	2013	Compared to the passage-matched control, chronic arsenic exposure caused exposure-duration dependent increases in secreted MMP-2 and MMP-9 activity, Cox-2 expression, and more rapid proliferation (all &gt;2-fold), characteristics typical of cancer cells.	Arsenic	49-56	matrix metallopeptidase 9	Homo sapiens	133-138
23137061-8	2013	Compared to the passage-matched control, chronic arsenic exposure caused exposure-duration dependent increases in secreted MMP-2 and MMP-9 activity, Cox-2 expression, and more rapid proliferation (all &gt;2-fold), characteristics typical of cancer cells.	Arsenic	49-56	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	149-154
23252340-9	2013	It showed that more Fe atoms were coordinated with As atom in the monodentate complexes and the bidentate complexes of As(V)/As(III)-treated siderite under oxic conditions, in comparison with As(V)/As(III)-treated siderite under anoxic conditions and As(V)/As(III)-treated goethite.	Arsenic	51-53	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	119-124
23549458-2	2013	Chronic arsenic exposure results in various types of human skin lesions, including squamous cell carcinoma (SCC).	Arsenic	8-15	serpin family B member 3	Homo sapiens	108-111
23343988-4	2013	The detection limits under these conditions for As, Bi, Cd, Pb, Hg and Ti were 2.4, 4.08, 0.3, 2.1, 1.8, and 1.8 ng mL-1, respectively.	Arsenic	48-50	L1 cell adhesion molecule	Mus musculus	116-120
23549458-11	2013	Likewise, the expressions of activating transcription factor NF-kappaB and p53 genes in the arsenic-treated HaCaT cells were significantly higher than that in non-treated cells.	Arsenic	92-99	tumor protein p53	Homo sapiens	75-78
23051894-3	2013	Altogether, our studies have provided direct evidence that arsenic-induced, autophagy-mediated, degradation of BCR-ABL1 is an important mechanism for the generation of the effects of As 2O 3 on BCR-ABL1 transformed leukemic progenitors.	Arsenic	59-66	BCR activator of RhoGEF and GTPase	Homo sapiens	111-119
23108027-9	2013	Co-overexpression of the yeast ABC transporter YCF1 in combination with AtPht1;1 or AtPht1;7 suppresses the arsenate-sensitive phenotype while further enhancing arsenic uptake.	Arsenic	161-168	ATP-binding cassette glutathione S-conjugate transporter YCF1	Saccharomyces cerevisiae S288C	47-51
23108027-10	2013	Taken together, our results support an arsenic transport mechanism in which arsenate uptake is increased through Pi transporter overexpression, and arsenic tolerance is enhanced through YCF1-mediated vacuolar sequestration.	Arsenic	39-46	ATP-binding cassette glutathione S-conjugate transporter YCF1	Saccharomyces cerevisiae S288C	186-190
23108027-10	2013	Taken together, our results support an arsenic transport mechanism in which arsenate uptake is increased through Pi transporter overexpression, and arsenic tolerance is enhanced through YCF1-mediated vacuolar sequestration.	Arsenic	148-155	ATP-binding cassette glutathione S-conjugate transporter YCF1	Saccharomyces cerevisiae S288C	186-190
22826049-7	2013	In addition, in the subjects with AS the numbers of eosinophils (p=0.015) and the concentrations of IL-5 (p= 0.021) in IS samples were significantly higher than in the subjects without AS.	Arsenic	34-36	interleukin 5	Homo sapiens	100-104
23392890-11	2013	The results showed that the concentrations of NE, DA, and 5-HT; the number of synaptic vesicles; and the expressions of TH, TPH, and DBH genes in the brains of mice exposed to As alone were significantly decreased.	Arsenic	176-178	tyrosine hydroxylase	Mus musculus	120-122
23392890-11	2013	The results showed that the concentrations of NE, DA, and 5-HT; the number of synaptic vesicles; and the expressions of TH, TPH, and DBH genes in the brains of mice exposed to As alone were significantly decreased.	Arsenic	176-178	tryptophan hydroxylase 1	Mus musculus	124-127
23392890-11	2013	The results showed that the concentrations of NE, DA, and 5-HT; the number of synaptic vesicles; and the expressions of TH, TPH, and DBH genes in the brains of mice exposed to As alone were significantly decreased.	Arsenic	176-178	dopamine beta hydroxylase	Mus musculus	133-136
23392932-8	2013	Our results showed that the gene expression of TRbeta, a very important regulator of Camk4 transcription, was down-regulated in cerebral and cerebellar tissues of mice exposed to As.	Arsenic	179-181	apoptosis antagonizing transcription factor	Mus musculus	47-53
23392932-8	2013	Our results showed that the gene expression of TRbeta, a very important regulator of Camk4 transcription, was down-regulated in cerebral and cerebellar tissues of mice exposed to As.	Arsenic	179-181	calcium/calmodulin-dependent protein kinase IV	Mus musculus	85-90
23051894-3	2013	Altogether, our studies have provided direct evidence that arsenic-induced, autophagy-mediated, degradation of BCR-ABL1 is an important mechanism for the generation of the effects of As 2O 3 on BCR-ABL1 transformed leukemic progenitors.	Arsenic	59-66	BCR activator of RhoGEF and GTPase	Homo sapiens	194-202
23065225-6	2013	The expressions of caspase-7 protein and TUNEL positive cells were much higher for the rats treated by AS, compared with the untreated control group.	Arsenic	103-105	caspase 7	Rattus norvegicus	19-28
23358330-7	2013	Interestingly, the overexpression of MDR1 mRNA and P-glucoprotein (P-gp) in K562/ADM cells were down-regulated by RTS, where there are no obvious effects on ATO and realgar and arsenic can be subsequently accumulated in K562/ADM cells efficiently.	Arsenic	177-184	ATP binding cassette subfamily B member 1	Homo sapiens	37-41
23358330-9	2013	Meanwhile, Western blot analysis of AQP9, the main transporter of arsenic, was increased by RTS treatment particularly in K562/ADM.	Arsenic	66-73	aquaporin 9	Homo sapiens	36-40
24212999-6	2013	These results suggest that inorganic arsenic, but not inorganic mercury, may induce p53-dependent apoptotic pathways through downregulation of gene expression of Ube2d family in proximal tubular cells.	Arsenic	37-44	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	84-87
23103450-4	2013	Arsenic trioxide (As(2)O(3)), which is used to treat acute promyelocytic leukemia, can cause LQTS type 2 (LQT2) by reducing the hERG current through the diversion of hERG trafficking to the cytoplasmic membrane.	Arsenic	18-20	potassium voltage-gated channel subfamily H member 2	Homo sapiens	93-104
23103450-4	2013	Arsenic trioxide (As(2)O(3)), which is used to treat acute promyelocytic leukemia, can cause LQTS type 2 (LQT2) by reducing the hERG current through the diversion of hERG trafficking to the cytoplasmic membrane.	Arsenic	18-20	potassium voltage-gated channel subfamily H member 2	Homo sapiens	106-110
23103450-4	2013	Arsenic trioxide (As(2)O(3)), which is used to treat acute promyelocytic leukemia, can cause LQTS type 2 (LQT2) by reducing the hERG current through the diversion of hERG trafficking to the cytoplasmic membrane.	Arsenic	18-20	ETS transcription factor ERG	Homo sapiens	128-132
23103450-4	2013	Arsenic trioxide (As(2)O(3)), which is used to treat acute promyelocytic leukemia, can cause LQTS type 2 (LQT2) by reducing the hERG current through the diversion of hERG trafficking to the cytoplasmic membrane.	Arsenic	18-20	ETS transcription factor ERG	Homo sapiens	166-170
23255093-0	2013	JNK and STAT3 signaling pathways converge on Akt-mediated phosphorylation of EZH2 in bronchial epithelial cells induced by arsenic.	Arsenic	123-130	mitogen-activated protein kinase 8	Homo sapiens	0-3
23255093-0	2013	JNK and STAT3 signaling pathways converge on Akt-mediated phosphorylation of EZH2 in bronchial epithelial cells induced by arsenic.	Arsenic	123-130	signal transducer and activator of transcription 3	Homo sapiens	8-13
23255093-0	2013	JNK and STAT3 signaling pathways converge on Akt-mediated phosphorylation of EZH2 in bronchial epithelial cells induced by arsenic.	Arsenic	123-130	AKT serine/threonine kinase 1	Homo sapiens	45-48
23255093-0	2013	JNK and STAT3 signaling pathways converge on Akt-mediated phosphorylation of EZH2 in bronchial epithelial cells induced by arsenic.	Arsenic	123-130	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	77-81
23255093-4	2013	The involvement of kinases in As ( 3+) -induced EZH2 phosphorylation was validated by siRNA-based gene silencing.	Arsenic	30-32	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	48-52
23010019-7	2013	Maximum GOX adsorption capacity was found as 500 mg/g Fe(3+)-attached HPMC film.	Arsenic	33-35	hydroxyacid oxidase 1	Homo sapiens	8-11
23070617-3	2013	Inhabitants of San Antonio de los Cobres (SAC) in the Argentinean highlands generally carry an AS3MT (the major arsenic-metabolizing gene) haplotype associated with reduced health risks due to rapid arsenic excretion and lower urinary fraction of the monomethylated metabolite.	Arsenic	112-119	arsenite methyltransferase	Homo sapiens	95-100
24283477-6	2013	Cytochrome P-450 and cytochrome b 5 levels and activities of aniline p-hydroxylase (APH) and uridine diphosphate glucuronosyltransferase (UGT) were significantly decreased in groups treated with As, CPF, and As plus CPF, while glutathione S-transferase (GST) was not markedly altered.	Arsenic	195-197	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
24283477-6	2013	Cytochrome P-450 and cytochrome b 5 levels and activities of aniline p-hydroxylase (APH) and uridine diphosphate glucuronosyltransferase (UGT) were significantly decreased in groups treated with As, CPF, and As plus CPF, while glutathione S-transferase (GST) was not markedly altered.	Arsenic	195-197	cytochrome b5 type A	Rattus norvegicus	21-35
24283477-6	2013	Cytochrome P-450 and cytochrome b 5 levels and activities of aniline p-hydroxylase (APH) and uridine diphosphate glucuronosyltransferase (UGT) were significantly decreased in groups treated with As, CPF, and As plus CPF, while glutathione S-transferase (GST) was not markedly altered.	Arsenic	195-197	hematopoietic prostaglandin D synthase	Rattus norvegicus	227-252
24283477-6	2013	Cytochrome P-450 and cytochrome b 5 levels and activities of aniline p-hydroxylase (APH) and uridine diphosphate glucuronosyltransferase (UGT) were significantly decreased in groups treated with As, CPF, and As plus CPF, while glutathione S-transferase (GST) was not markedly altered.	Arsenic	195-197	hematopoietic prostaglandin D synthase	Rattus norvegicus	254-257
24283477-6	2013	Cytochrome P-450 and cytochrome b 5 levels and activities of aniline p-hydroxylase (APH) and uridine diphosphate glucuronosyltransferase (UGT) were significantly decreased in groups treated with As, CPF, and As plus CPF, while glutathione S-transferase (GST) was not markedly altered.	Arsenic	208-210	cytochrome b5 type A	Rattus norvegicus	21-35
23766851-4	2013	Nrf2 activation also offered moderate protection against liver injury produced by ethanol, arsenic, bromobenzene, and allyl alcohol but had no effects on the hepatotoxicity produced by D-galactosamine/endotoxin and the Fas ligand antibody Jo-2.	Arsenic	91-98	nuclear factor, erythroid derived 2, like 2	Mus musculus	0-4
23738048-0	2013	Activation of the Nrf2 pathway by inorganic arsenic in human hepatocytes and the role of transcriptional repressor Bach1.	Arsenic	44-51	NFE2 like bZIP transcription factor 2	Homo sapiens	18-22
23738048-1	2013	Previous studies have proved that the environmental toxicant, inorganic arsenic, activates nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in many different cell types.	Arsenic	72-79	NFE2 like bZIP transcription factor 2	Homo sapiens	91-134
23710286-8	2013	Our results provided a proof of the concept of using curcumin to activate the NRF2 pathway to alleviate arsenic-induced dermal damage.	Arsenic	104-111	NFE2 like bZIP transcription factor 2	Homo sapiens	78-82
23738048-1	2013	Previous studies have proved that the environmental toxicant, inorganic arsenic, activates nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in many different cell types.	Arsenic	72-79	NFE2 like bZIP transcription factor 2	Homo sapiens	136-140
23935510-7	2013	Arsenic-induced DSBs are processed by homologous recombination (HR), as shown by Rfa1 and Rad52 nuclear foci formation and requirement of HR proteins for cell survival during arsenic exposure.	Arsenic	0-7	replication factor A subunit protein RFA1	Saccharomyces cerevisiae S288C	81-85
23738048-2	2013	This study tried to explore the hepatic Nrf2 pathway upon arsenic treatment comprehensively, since liver is one of the major target organs of arsenical toxicity.	Arsenic	58-65	NFE2 like bZIP transcription factor 2	Homo sapiens	40-44
23738048-3	2013	Our results showed that inorganic arsenic significantly induced Nrf2 protein and mRNA expression in Chang human hepatocytes.	Arsenic	34-41	NFE2 like bZIP transcription factor 2	Homo sapiens	64-68
23738048-7	2013	Our results therefore confirmed the arsenic-induced Nrf2 pathway activation in hepatocytes and also suggested that the translocation of Bach1 was associated with the regulation of Nrf2 pathway by arsenic.	Arsenic	36-43	NFE2 like bZIP transcription factor 2	Homo sapiens	52-56
23738048-7	2013	Our results therefore confirmed the arsenic-induced Nrf2 pathway activation in hepatocytes and also suggested that the translocation of Bach1 was associated with the regulation of Nrf2 pathway by arsenic.	Arsenic	36-43	BTB domain and CNC homolog 1	Homo sapiens	136-141
23738048-7	2013	Our results therefore confirmed the arsenic-induced Nrf2 pathway activation in hepatocytes and also suggested that the translocation of Bach1 was associated with the regulation of Nrf2 pathway by arsenic.	Arsenic	36-43	NFE2 like bZIP transcription factor 2	Homo sapiens	180-184
23738048-7	2013	Our results therefore confirmed the arsenic-induced Nrf2 pathway activation in hepatocytes and also suggested that the translocation of Bach1 was associated with the regulation of Nrf2 pathway by arsenic.	Arsenic	196-203	BTB domain and CNC homolog 1	Homo sapiens	136-141
23738048-7	2013	Our results therefore confirmed the arsenic-induced Nrf2 pathway activation in hepatocytes and also suggested that the translocation of Bach1 was associated with the regulation of Nrf2 pathway by arsenic.	Arsenic	196-203	NFE2 like bZIP transcription factor 2	Homo sapiens	180-184
23935510-7	2013	Arsenic-induced DSBs are processed by homologous recombination (HR), as shown by Rfa1 and Rad52 nuclear foci formation and requirement of HR proteins for cell survival during arsenic exposure.	Arsenic	0-7	recombinase RAD52	Saccharomyces cerevisiae S288C	90-95
22612911-2	2013	XANES results for the composite after As(III) removal tests show that the As adsorbed is at the oxidized arsenic form, As(V).	Arsenic	105-112	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	119-124
23341986-0	2013	Efficient arsenic metabolism--the AS3MT haplotype is associated with DNA methylation and expression of multiple genes around AS3MT.	Arsenic	10-17	arsenite methyltransferase	Homo sapiens	34-39
23341986-0	2013	Efficient arsenic metabolism--the AS3MT haplotype is associated with DNA methylation and expression of multiple genes around AS3MT.	Arsenic	10-17	arsenite methyltransferase	Homo sapiens	125-130
23341986-5	2013	Here, we assessed the influence of genetic variation in AS3MT on DNA methylation and gene expression within 10q24, in people exposed to arsenic in drinking water.	Arsenic	136-143	arsenite methyltransferase	Homo sapiens	56-61
23600209-11	2013	The expression of NGF and GAP-43 mRNA were decreased as the dose of arsenic increasing (both P &lt; 0.05).	Arsenic	68-75	nerve growth factor	Rattus norvegicus	18-21
23600209-11	2013	The expression of NGF and GAP-43 mRNA were decreased as the dose of arsenic increasing (both P &lt; 0.05).	Arsenic	68-75	growth associated protein 43	Rattus norvegicus	26-32
23600209-12	2013	CONCLUSION: Rats exposure to arsenic during pregnancy and lactation, can damage hippocampus neuronal cell, and restrain the NGF and GAP-43 mRNA expression of F1 generation female rat, damaged the learning and memory ability at last.	Arsenic	29-36	nerve growth factor	Rattus norvegicus	124-127
23600209-12	2013	CONCLUSION: Rats exposure to arsenic during pregnancy and lactation, can damage hippocampus neuronal cell, and restrain the NGF and GAP-43 mRNA expression of F1 generation female rat, damaged the learning and memory ability at last.	Arsenic	29-36	growth associated protein 43	Rattus norvegicus	132-138
23600209-0	2013	[Effects of arsenic on nerve growth factor and nerve growth related mRNA expression in F1 hippocampal].	Arsenic	12-19	nerve growth factor	Rattus norvegicus	23-42
22956628-0	2013	Delayed temporal increase of hepatic Hsp70 in ApoE knockout mice after prenatal arsenic exposure.	Arsenic	80-87	heat shock protein 1B	Mus musculus	37-42
22956628-0	2013	Delayed temporal increase of hepatic Hsp70 in ApoE knockout mice after prenatal arsenic exposure.	Arsenic	80-87	apolipoprotein E	Mus musculus	46-50
22956628-1	2013	Prenatal arsenic exposure accelerates atherosclerosis in ApoE(-/-) mice by unknown mechanism.	Arsenic	9-16	apolipoprotein E	Mus musculus	57-61
22956628-4	2013	Earlier microarray analyses showed prenatal arsenic exposure increased Hsc70 (HspA8) and Hsp70 (HspA1a) mRNAs in livers of 10-week-old mice.	Arsenic	44-51	heat shock protein 8	Mus musculus	71-76
22956628-4	2013	Earlier microarray analyses showed prenatal arsenic exposure increased Hsc70 (HspA8) and Hsp70 (HspA1a) mRNAs in livers of 10-week-old mice.	Arsenic	44-51	heat shock protein 8	Mus musculus	78-83
22956628-4	2013	Earlier microarray analyses showed prenatal arsenic exposure increased Hsc70 (HspA8) and Hsp70 (HspA1a) mRNAs in livers of 10-week-old mice.	Arsenic	44-51	heat shock protein 1B	Mus musculus	89-94
22956628-4	2013	Earlier microarray analyses showed prenatal arsenic exposure increased Hsc70 (HspA8) and Hsp70 (HspA1a) mRNAs in livers of 10-week-old mice.	Arsenic	44-51	heat shock protein 1A	Mus musculus	96-102
22956628-5	2013	We determined effects of prenatal arsenic exposure on hepatic Hsp70 and Hsc70 expression by Western blot and on DNA methylation by methyl acceptance assay during prenatal and postnatal development.	Arsenic	34-41	heat shock protein 1B	Mus musculus	62-67
22956628-5	2013	We determined effects of prenatal arsenic exposure on hepatic Hsp70 and Hsc70 expression by Western blot and on DNA methylation by methyl acceptance assay during prenatal and postnatal development.	Arsenic	34-41	heat shock protein 8	Mus musculus	72-77
22956628-13	2013	Putative binding sites were identified in HSP70 for in utero arsenic exposure-suppressed microRNAs suggesting a possible mechanism.	Arsenic	61-68	heat shock protein 1B	Mus musculus	42-47
22956628-14	2013	Thus, prenatal arsenic exposure causes delayed temporal hepatic Hsp70 induction, suggesting a transient state of stress in livers which can predispose the mice to developing liver disease.	Arsenic	15-22	heat shock protein 1B	Mus musculus	64-69
22614922-4	2012	At day 14 following arsenic exposure (0.05 and 0.1 LD(50) dose), we observed a significant oxidative injury as evident from significant depletion of superoxide dismutase (SOD) and catalase activities in blood and tissues in addition to more pronounced accumulation of arsenic in blood and tissues.	Arsenic	20-27	catalase	Rattus norvegicus	180-188
23123153-0	2012	Arsenic urinary speciation in Mthfr deficient mice injected with sodium arsenate.	Arsenic	0-7	methylenetetrahydrofolate reductase	Mus musculus	30-35
22975029-0	2012	Sulforaphane prevents pulmonary damage in response to inhaled arsenic by activating the Nrf2-defense response.	Arsenic	62-69	NFE2 like bZIP transcription factor 2	Homo sapiens	88-92
22975029-4	2012	In this report, we tested whether Nrf2 activation protects mice from arsenic-induced toxicity.	Arsenic	69-76	nuclear factor, erythroid derived 2, like 2	Mus musculus	34-38
22975029-6	2012	Two-week exposure to arsenic-containing dust resulted in pathological alterations, oxidative DNA damage, and mild apoptotic cell death in the lung; all of which were blocked by sulforaphane (SF) in an Nrf2-dependent manner.	Arsenic	21-28	NFE2 like bZIP transcription factor 2	Homo sapiens	201-205
22975029-8	2012	This study provides strong evidence that dietary intervention targeting Nrf2 activation is a feasible approach to reduce adverse health effects associated with arsenic exposure.	Arsenic	160-167	NFE2 like bZIP transcription factor 2	Homo sapiens	72-76
23123153-7	2012	When fed a folate control diet, the Mthfr(-/-) mice excreted significantly less of the total arsenic in urine than did the Mthfr(+/+) and Mthfr(+/-) mice.	Arsenic	93-100	methylenetetrahydrofolate reductase	Mus musculus	36-41
23123153-8	2012	The Mthfr(-/-) had significantly lower levels of pentavalent arsenic in their urine than did the Mthfr(+/+)mice.	Arsenic	61-68	methylenetetrahydrofolate reductase	Mus musculus	4-9
22872060-0	2012	Ethanol enhances tumor angiogenesis in vitro induced by low-dose arsenic in colon cancer cells through hypoxia-inducible factor 1 alpha pathway.	Arsenic	65-72	hypoxia inducible factor 1 subunit alpha	Homo sapiens	103-135
22936492-4	2012	In this work, we analyzed the performance of the fluorescent compound APAO-FITC (synthesized from p-aminophenylarsenoxide, APAO, and fluorescein isothiocyanate, FITC) in arsenic/protein binding assays using thioredoxin 1 (Trx) as an arsenic-binding protein model.	Arsenic	170-177	thioredoxin	Homo sapiens	207-220
22936492-4	2012	In this work, we analyzed the performance of the fluorescent compound APAO-FITC (synthesized from p-aminophenylarsenoxide, APAO, and fluorescein isothiocyanate, FITC) in arsenic/protein binding assays using thioredoxin 1 (Trx) as an arsenic-binding protein model.	Arsenic	170-177	thioredoxin	Homo sapiens	222-225
23052575-0	2012	Effect of vitamin E supplementation on mRNA expression of superoxide dismutase and interleukin-2 in arsenic exposed goat leukocytes.	Arsenic	100-107	interleukin-2	Capra hircus	83-96
23379173-5	2012	Ca3 (AsO4)2 was the main compound, and the release of arsenic leaching was high.	Arsenic	54-61	carbonic anhydrase 3	Homo sapiens	0-3
22872060-8	2012	We have also found that ethanol increases the arsenic-induced expression and secretion of angiogenic signaling molecules such as vascular endothelial growth factor, which further confirmed the above observation.	Arsenic	46-53	vascular endothelial growth factor A	Homo sapiens	129-163
22872060-10	2012	We conclude that ethanol is able to enhance arsenic-induced tumor angiogenesis in colorectal cancer cells via the HIF-1alpha pathway.	Arsenic	44-51	hypoxia inducible factor 1 subunit alpha	Homo sapiens	114-124
23043314-9	2012	In similar geologic situations, rapid modern sea level rise will initiate this process globally, and may mobilize large accumulations of Hg and lesser amounts of As, and other redox sensitive metals to groundwater and surface water.	Arsenic	162-164	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	45-48
23257433-8	2012	The activity of NF-kappaB decreased significantly in As(2)O(3) or Bor group (P &lt; 0.05), this effect was most significant in the combination group (P &lt; 0.01).	Arsenic	53-55	nuclear factor kappa B subunit 1	Homo sapiens	16-25
23134409-6	2012	The heteroleptic 1:1 LP complexes 2-4 were also obtained by the one-pot reaction of Mes2Te, Ph3E (E = P, As, Sb) and HO3SCF3.	Arsenic	105-107	H3 histone pseudogene 26	Homo sapiens	92-96
23030510-6	2012	While 50 mg/L (0.81 mM) nitrate was completely removed at all EBCTs, more than 90% of 300 mug/L (4 muM) arsenic was removed with the total EBCT as low as 27 min.	Arsenic	104-111	latexin	Homo sapiens	99-102
22917110-9	2012	Similarly, carriers of the slow and more toxic metabolizing AS3MT haplotype showed stronger positive associations between arsenic exposure and telomere length, as compared to noncarriers (interaction urinary arsenic and haplotype p = 0.025).	Arsenic	122-129	arsenite methyltransferase	Homo sapiens	60-65
22917110-9	2012	Similarly, carriers of the slow and more toxic metabolizing AS3MT haplotype showed stronger positive associations between arsenic exposure and telomere length, as compared to noncarriers (interaction urinary arsenic and haplotype p = 0.025).	Arsenic	208-215	arsenite methyltransferase	Homo sapiens	60-65
22917110-10	2012	Urinary arsenic was positively correlated with the expression of telomerase reverse transcriptase (TERT, Spearman r = 0.22, p = 0.037), but no association was found between TERT expression and telomere length.	Arsenic	8-15	telomerase reverse transcriptase	Homo sapiens	65-97
22917110-10	2012	Urinary arsenic was positively correlated with the expression of telomerase reverse transcriptase (TERT, Spearman r = 0.22, p = 0.037), but no association was found between TERT expression and telomere length.	Arsenic	8-15	telomerase reverse transcriptase	Homo sapiens	99-103
22818949-9	2012	The performance of NF90 was tested with respect to the rejection of inorganic contaminants including boron (H(3)BO(3)) and arsenic (H(2)AsO(4)(-)).	Arsenic	123-130	interleukin enhancer binding factor 3	Homo sapiens	19-23
23073540-0	2012	Environmental arsenic exposure and DNA methylation of the tumor suppressor gene p16 and the DNA repair gene MLH1: effect of arsenic metabolism and genotype.	Arsenic	14-21	cyclin dependent kinase inhibitor 2A	Homo sapiens	80-83
23073540-7	2012	In linear regression analysis, log(2)-transformed urinary arsenic concentrations were positively associated with methylation of p16 (beta = 0.14, P = 0.0028) and MLH1 (beta = 0.28, P = 0.0011), but not with LINE1.	Arsenic	58-65	cyclin dependent kinase inhibitor 2A	Homo sapiens	128-131
23073540-7	2012	In linear regression analysis, log(2)-transformed urinary arsenic concentrations were positively associated with methylation of p16 (beta = 0.14, P = 0.0028) and MLH1 (beta = 0.28, P = 0.0011), but not with LINE1.	Arsenic	58-65	mutL homolog 1	Homo sapiens	162-166
23073540-8	2012	Arsenic concentrations were of borderline significance negatively correlated with expression of p16 (r(s) = -0.20; P = 0.066)), but not with MLH1.	Arsenic	0-7	cyclin dependent kinase inhibitor 2A	Homo sapiens	96-99
23073540-9	2012	The fraction of inorganic arsenic was positively (beta = 0.026; P = 0.010) and DMA was negatively (beta = -0.017, P = 0.043) associated with p16 methylation with no effect of MMA.	Arsenic	26-33	cyclin dependent kinase inhibitor 2A	Homo sapiens	141-144
22963862-3	2012	Moreover, we previously reported that arsenic enhanced caspase-3 activity coupled with progesterone production.	Arsenic	38-45	caspase 3	Homo sapiens	55-64
22963862-4	2012	Inhibition of caspase-3 activity can significantly inhibit progesterone production induced by arsenic or follicle-stimulating hormone (FSH).	Arsenic	94-101	caspase 3	Homo sapiens	14-23
23000044-8	2012	The present study demonstrates that Nrf2-mediated antioxidant response is critical in the pancreatic beta-cell defense mechanism against acute cytotoxicity by arsenic.	Arsenic	159-166	nuclear factor, erythroid derived 2, like 2	Mus musculus	36-40
22750630-8	2012	Immunohistochemical analysis revealed that telmisartan significantly decreased the arsenic-induced expression of inducible nitric oxide synthase, tumor necrosis factor-alpha, cyclooxygenase-2, nuclear factor-kappaB and caspase-3 in liver tissue.	Arsenic	83-90	prostaglandin-endoperoxide synthase 2	Mus musculus	175-228
23281543-0	2012	Exploring links between arsenic and diabetes, with Ana Navas-Acien.	Arsenic	24-31	BTG anti-proliferation factor 3	Homo sapiens	51-54
22825625-5	2012	Pretreatment with the PI3Kgamma inhibitor, AS 605240 decreased the LPS-induced increase of ROS generation, phosphorylation of Akt, and production of phosphatidyl 3,4,5-trisphosphate in A549 cells.	Arsenic	43-45	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Homo sapiens	22-31
22825625-5	2012	Pretreatment with the PI3Kgamma inhibitor, AS 605240 decreased the LPS-induced increase of ROS generation, phosphorylation of Akt, and production of phosphatidyl 3,4,5-trisphosphate in A549 cells.	Arsenic	43-45	AKT serine/threonine kinase 1	Homo sapiens	126-129
23175155-9	2012	Arsenic exposure significantly increased (p&lt;0.05) the activities of plasma alanine aminotransferase-glutamate pyruvate transaminase (ALT/GPT), and aspartate aminotransferase-glutamate oxaloacetate transaminase (AST/GOT), as well as the number of structural chromosomal aberrations (SCA) and frequency of micronuclei (MN) in the bone marrow cells.	Arsenic	0-7	glutamic--pyruvic transaminase	Rattus norvegicus	140-143
22940758-0	2012	Granulocyte colony-stimulating factor potentiates differentiation induction             by all-trans retinoic acid and arsenic trioxide and enhances arsenic uptake in             the acute promyelocytic leukemia cell line HT93A.	Arsenic	119-126	colony stimulating factor 3	Homo sapiens	0-37
22940758-8	2012	ATRA induced expression of aquaporin-9 (AQP9), a transmembrane transporter recognized as a major pathway of arsenic uptake, in a time- and dose-dependent manner.	Arsenic	108-115	aquaporin 9	Homo sapiens	27-38
22940758-8	2012	ATRA induced expression of aquaporin-9 (AQP9), a transmembrane transporter recognized as a major pathway of arsenic uptake, in a time- and dose-dependent manner.	Arsenic	108-115	aquaporin 9	Homo sapiens	40-44
22940758-12	2012	G-CSF not only promotes differentiation-inducing activities of both ATRA and ATO, but also makes APL cells vulnerable to increased arsenic uptake.	Arsenic	131-138	colony stimulating factor 3	Homo sapiens	0-5
22824674-3	2012	As a result, the adsorbent prepared at pH 4, which consists of schwertmannite, was selected because it exhibited the highest adsorption capacity of 13 mug As(V)/mg, while maintaining a residual arsenic concentration of 10 mug/L at an equilibrium pH 7.	Arsenic	194-201	prolyl 4-hydroxylase, transmembrane	Homo sapiens	39-43
22988968-11	2012	This FOXO3a accumulation may be well correlated with the As(2)O(3)-induced reduction of active IKKbeta, which may provide new insights into As(2)O(3)-related signaling activities.	Arsenic	57-59	forkhead box O3	Homo sapiens	5-11
22988968-11	2012	This FOXO3a accumulation may be well correlated with the As(2)O(3)-induced reduction of active IKKbeta, which may provide new insights into As(2)O(3)-related signaling activities.	Arsenic	57-59	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	95-102
22885595-3	2012	All heavy metals and arsenic display a V-shaped pH-dependent leaching pattern with important releases at pHs 2 and 11.	Arsenic	21-28	polyhomeotic homolog 2	Homo sapiens	105-117
22960421-6	2012	Compared to controls, we observed that the perinatal arsenic-exposed offspring exhibit an increase in hypothalamic CRF, altered CORT secretion both at baseline and in response to a stressor, decreased hippocampal 11beta-HSD 1 and altered subcellular GR distribution in the hypothalamus.	Arsenic	53-60	cortistatin	Mus musculus	128-132
22960421-6	2012	Compared to controls, we observed that the perinatal arsenic-exposed offspring exhibit an increase in hypothalamic CRF, altered CORT secretion both at baseline and in response to a stressor, decreased hippocampal 11beta-HSD 1 and altered subcellular GR distribution in the hypothalamus.	Arsenic	53-60	hydroxysteroid 11-beta dehydrogenase 1	Mus musculus	213-225
22824620-8	2012	The correlation observed between Caveolin-1 and downstream signaling molecule expression may be an important mechanism of arsenic-induced urothelial carcinogenesis.	Arsenic	122-129	caveolin 1	Homo sapiens	33-43
22700541-8	2012	Consistently, expression of an oxidative-stress-inducible gene heme oxygenase-1 (HO-1) was upregulated in the livers of the arsenic group.	Arsenic	124-131	heme oxygenase 1	Mus musculus	63-79
22700541-8	2012	Consistently, expression of an oxidative-stress-inducible gene heme oxygenase-1 (HO-1) was upregulated in the livers of the arsenic group.	Arsenic	124-131	heme oxygenase 1	Mus musculus	81-85
22696236-0	2012	JNK-dependent Stat3 phosphorylation contributes to Akt activation in response to arsenic exposure.	Arsenic	81-88	mitogen-activated protein kinase 8	Homo sapiens	0-3
22696236-0	2012	JNK-dependent Stat3 phosphorylation contributes to Akt activation in response to arsenic exposure.	Arsenic	81-88	signal transducer and activator of transcription 3	Homo sapiens	14-19
22696236-0	2012	JNK-dependent Stat3 phosphorylation contributes to Akt activation in response to arsenic exposure.	Arsenic	81-88	AKT serine/threonine kinase 1	Homo sapiens	51-54
22700541-0	2012	Late-onset increases in oxidative stress and other tumorigenic activities and tumors with a Ha-ras mutation in the liver of adult male C3H mice gestationally exposed to arsenic.	Arsenic	169-176	Harvey rat sarcoma virus oncogene	Mus musculus	92-98
22700541-2	2012	Gestational arsenic exposure has been shown to increase hepatic tumors in adult male offspring of C3H mice, which spontaneously develop hepatic tumors often harboring activating Ha-ras mutation.	Arsenic	12-19	Harvey rat sarcoma virus oncogene	Mus musculus	178-184
22700541-4	2012	The results of this study demonstrated that gestational arsenic exposure particularly increased hepatic tumors with a C61A Ha-ras mutation.	Arsenic	56-63	Harvey rat sarcoma virus oncogene	Mus musculus	123-129
22700541-10	2012	These results suggested that gestational arsenic exposure induces tumor-augmenting changes, including oxidative stress and L1 activation, in a late-onset manner, which would particularly promote tumorigenic expansion of cells with a C61A Ha-ras mutation.	Arsenic	41-48	Harvey rat sarcoma virus oncogene	Mus musculus	238-244
22827573-1	2012	CONTEXT: Arsenic, a toxic metalloid with major health concerns, elicits upregulation of heat shock protein 70 (HSP70) in rat hepatoma FGC4 cells, together with evidence of detachment of viable cells from the growth substratum.	Arsenic	9-16	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	88-109
22713597-9	2012	Arsenic was positively associated with 8-hydroxy-2"-deoxyguanosine in cord blood (B = 0.097; 95% CI 0.05 to 0.13), which was inversely associated with sjTRECs in CD4(+) and CD8(+) T cells.	Arsenic	0-7	CD4 molecule	Homo sapiens	162-165
22700541-5	2012	Real-time PCR analyses on the adult normal livers showed that two genes (Creld2, Slc25a30), whose expression are induced by endoplasmic reticulum stress and cellular oxidative stress, respectively, were significantly upregulated and two genes (Fabp4, Ell3), whose products are involved in lipid efflux and apoptosis, respectively, were significantly downregulated more than twofold by gestational arsenic exposure compared with control mice.	Arsenic	397-404	cysteine-rich with EGF-like domains 2	Mus musculus	73-79
22713597-9	2012	Arsenic was positively associated with 8-hydroxy-2"-deoxyguanosine in cord blood (B = 0.097; 95% CI 0.05 to 0.13), which was inversely associated with sjTRECs in CD4(+) and CD8(+) T cells.	Arsenic	0-7	CD8a molecule	Homo sapiens	173-176
22827573-1	2012	CONTEXT: Arsenic, a toxic metalloid with major health concerns, elicits upregulation of heat shock protein 70 (HSP70) in rat hepatoma FGC4 cells, together with evidence of detachment of viable cells from the growth substratum.	Arsenic	9-16	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	111-116
22843710-12	2012	Taken together, these results strongly suggest that the polycomb proteins, BMI1 and SUZ12 are required for cell transformation induced by organic arsenic exposure.	Arsenic	146-153	SUZ12 polycomb repressive complex 2 subunit	Mus musculus	84-89
22868225-0	2012	Methylation of arsenic by recombinant human wild-type arsenic (+3 oxidation state) methyltransferase and its methionine 287 threonine (M287T) polymorph: Role of glutathione.	Arsenic	15-22	arsenite methyltransferase	Homo sapiens	54-100
22868225-9	2012	AS3MT genotype exemplified by differences in regulation of wtAS3MT and AS3MT/M287T-catalyzed reactions by GSH may contribute to differences in the phenotype for arsenic methylation and, ultimately, to differences in the disease susceptibility in individuals chronically exposed to inorganic arsenic.	Arsenic	161-168	arsenite methyltransferase	Homo sapiens	0-5
22868225-9	2012	AS3MT genotype exemplified by differences in regulation of wtAS3MT and AS3MT/M287T-catalyzed reactions by GSH may contribute to differences in the phenotype for arsenic methylation and, ultimately, to differences in the disease susceptibility in individuals chronically exposed to inorganic arsenic.	Arsenic	161-168	arsenite methyltransferase	Homo sapiens	61-66
22771847-0	2012	Mechanisms underlying the inhibitory effects of arsenic compounds on protein tyrosine phosphatase (PTP).	Arsenic	48-55	protein tyrosine phosphatase non-receptor type 22	Homo sapiens	69-97
22771847-0	2012	Mechanisms underlying the inhibitory effects of arsenic compounds on protein tyrosine phosphatase (PTP).	Arsenic	48-55	protein tyrosine phosphatase non-receptor type 22	Homo sapiens	99-102
22771847-2	2012	At the same time, arsenic is also known to activate the phosphorylation-dependent signaling pathways including the epidermal growth factor receptor, the mitogen-activated protein kinase and insulin/insulin-like growth factor-1 pathways.	Arsenic	18-25	epidermal growth factor receptor	Homo sapiens	115-147
22771847-5	2012	In the present study, we have focused on the interaction of cellular PTPs with toxic trivalent arsenite (iAs(III)) and its intermediate metabolites such as monomethylarsonous acid (MMA(III)) and dimethylarsinous acid (DMA(III)) in vitro, and then determined the arsenic binding site in PTP by the use of recombinant PTPs (e.g., PTP1B and CD45).	Arsenic	262-269	protein tyrosine phosphatase non-receptor type 22	Homo sapiens	69-72
22771847-8	2012	These results suggest that arsenic exposure may disturb the cellular signaling pathways through PTP inactivation.	Arsenic	27-34	protein tyrosine phosphatase non-receptor type 22	Homo sapiens	96-99
22843710-0	2012	Polycomb (PcG) proteins, BMI1 and SUZ12, regulate arsenic-induced cell transformation.	Arsenic	50-57	Bmi1 polycomb ring finger oncogene	Mus musculus	25-29
22843710-0	2012	Polycomb (PcG) proteins, BMI1 and SUZ12, regulate arsenic-induced cell transformation.	Arsenic	50-57	SUZ12 polycomb repressive complex 2 subunit	Mus musculus	34-39
22843710-6	2012	In arsenic-induced transformed cells, polycomb group (PcG) proteins, including BMI1 and SUZ12, were activated resulting in enhanced histone H3K27 tri-methylation levels.	Arsenic	3-10	Bmi1 polycomb ring finger oncogene	Mus musculus	79-83
22843710-6	2012	In arsenic-induced transformed cells, polycomb group (PcG) proteins, including BMI1 and SUZ12, were activated resulting in enhanced histone H3K27 tri-methylation levels.	Arsenic	3-10	SUZ12 polycomb repressive complex 2 subunit	Mus musculus	88-93
22843710-8	2012	Introduction of small hairpin (sh) RNA-BMI1 or -SUZ12 into BALB/c 3T3 cells resulted in suppression of arsenic-induced transformation.	Arsenic	103-110	Bmi1 polycomb ring finger oncogene	Mus musculus	39-43
22843710-8	2012	Introduction of small hairpin (sh) RNA-BMI1 or -SUZ12 into BALB/c 3T3 cells resulted in suppression of arsenic-induced transformation.	Arsenic	103-110	SUZ12 polycomb repressive complex 2 subunit	Mus musculus	48-53
22843710-10	2012	As a consequence, the expression of p16(INK4a) and p19(ARF) was recovered in arsenic-treated BMI1- or SUZ12-knockdown cells.	Arsenic	77-84	cyclin dependent kinase inhibitor 2A	Mus musculus	36-39
22562211-1	2012	Previously, our in silico analyses identified four candidate genes that might be involved in uptake and/or accumulation of arsenics in plants: arsenate reductase 2 (ACR2), phytochelatin synthase 1 (PCS1) and two multi-drug resistant proteins (MRP1 and MRP2) [Lund et al.	Arsenic	123-131	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	198-202
22843710-10	2012	As a consequence, the expression of p16(INK4a) and p19(ARF) was recovered in arsenic-treated BMI1- or SUZ12-knockdown cells.	Arsenic	77-84	cyclin dependent kinase inhibitor 2A	Mus musculus	40-45
22843710-10	2012	As a consequence, the expression of p16(INK4a) and p19(ARF) was recovered in arsenic-treated BMI1- or SUZ12-knockdown cells.	Arsenic	77-84	cyclin dependent kinase inhibitor 2D	Mus musculus	51-54
22843710-10	2012	As a consequence, the expression of p16(INK4a) and p19(ARF) was recovered in arsenic-treated BMI1- or SUZ12-knockdown cells.	Arsenic	77-84	Bmi1 polycomb ring finger oncogene	Mus musculus	93-97
22843710-10	2012	As a consequence, the expression of p16(INK4a) and p19(ARF) was recovered in arsenic-treated BMI1- or SUZ12-knockdown cells.	Arsenic	77-84	SUZ12 polycomb repressive complex 2 subunit	Mus musculus	102-107
22843710-12	2012	Taken together, these results strongly suggest that the polycomb proteins, BMI1 and SUZ12 are required for cell transformation induced by organic arsenic exposure.	Arsenic	146-153	Bmi1 polycomb ring finger oncogene	Mus musculus	75-79
22562211-1	2012	Previously, our in silico analyses identified four candidate genes that might be involved in uptake and/or accumulation of arsenics in plants: arsenate reductase 2 (ACR2), phytochelatin synthase 1 (PCS1) and two multi-drug resistant proteins (MRP1 and MRP2) [Lund et al.	Arsenic	123-131	multidrug resistance-associated protein 1	Arabidopsis thaliana	243-247
22562211-0	2012	In silico and in vivo studies of an Arabidopsis thaliana gene, ACR2, putatively involved in arsenic accumulation in plants.	Arsenic	92-99	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	63-67
22562211-1	2012	Previously, our in silico analyses identified four candidate genes that might be involved in uptake and/or accumulation of arsenics in plants: arsenate reductase 2 (ACR2), phytochelatin synthase 1 (PCS1) and two multi-drug resistant proteins (MRP1 and MRP2) [Lund et al.	Arsenic	123-131	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	165-169
22562211-1	2012	Previously, our in silico analyses identified four candidate genes that might be involved in uptake and/or accumulation of arsenics in plants: arsenate reductase 2 (ACR2), phytochelatin synthase 1 (PCS1) and two multi-drug resistant proteins (MRP1 and MRP2) [Lund et al.	Arsenic	123-131	multidrug resistance-associated protein 2	Arabidopsis thaliana	252-256
22562211-1	2012	Previously, our in silico analyses identified four candidate genes that might be involved in uptake and/or accumulation of arsenics in plants: arsenate reductase 2 (ACR2), phytochelatin synthase 1 (PCS1) and two multi-drug resistant proteins (MRP1 and MRP2) [Lund et al.	Arsenic	123-131	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	172-196
22562211-7	2012	To validate the in silico results, we exposed a transfer-DNA (T-DNA)-tagged mutant of A. thaliana (mutation in the ACR2 gene) to various amounts of arsenic.	Arsenic	148-155	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	115-119
22641621-0	2012	Arsenic exposure inhibits myogenesis and neurogenesis in P19 stem cells through repression of the beta-catenin signaling pathway.	Arsenic	0-7	catenin (cadherin associated protein), beta 1	Mus musculus	98-110
22519831-5	2012	MDC-labeled autophagic vacuoles were observed by fluorescent inverted phase contrast microscopy and the enhanced MDC fluorescent staining was detected by flow cytometry in As(2)O(3)-treated cells.	Arsenic	172-174	C-C motif chemokine ligand 22	Homo sapiens	113-116
22519831-8	2012	Western blotting also showed that As(2)O(3) up-regulated Beclin-1.	Arsenic	34-36	beclin 1	Homo sapiens	57-65
22745270-0	2012	Arsenic stress elicits cytosolic Ca(2+) bursts and Crz1 activation in Saccharomyces cerevisiae.	Arsenic	0-7	DNA-binding transcription factor CRZ1	Saccharomyces cerevisiae S288C	51-55
22745270-3	2012	Here we show that Ca(2+) enhances the tolerance of the wild-type and arsenic-sensitive yap1 strains to arsenic stress in a Crz1-dependent manner, thus providing the first evidence that Ca(2+) signalling cascades are involved in arsenic stress responses.	Arsenic	69-76	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	87-91
22745270-3	2012	Here we show that Ca(2+) enhances the tolerance of the wild-type and arsenic-sensitive yap1 strains to arsenic stress in a Crz1-dependent manner, thus providing the first evidence that Ca(2+) signalling cascades are involved in arsenic stress responses.	Arsenic	69-76	DNA-binding transcription factor CRZ1	Saccharomyces cerevisiae S288C	123-127
22745270-3	2012	Here we show that Ca(2+) enhances the tolerance of the wild-type and arsenic-sensitive yap1 strains to arsenic stress in a Crz1-dependent manner, thus providing the first evidence that Ca(2+) signalling cascades are involved in arsenic stress responses.	Arsenic	103-110	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	87-91
22745270-3	2012	Here we show that Ca(2+) enhances the tolerance of the wild-type and arsenic-sensitive yap1 strains to arsenic stress in a Crz1-dependent manner, thus providing the first evidence that Ca(2+) signalling cascades are involved in arsenic stress responses.	Arsenic	103-110	DNA-binding transcription factor CRZ1	Saccharomyces cerevisiae S288C	123-127
22745270-3	2012	Here we show that Ca(2+) enhances the tolerance of the wild-type and arsenic-sensitive yap1 strains to arsenic stress in a Crz1-dependent manner, thus providing the first evidence that Ca(2+) signalling cascades are involved in arsenic stress responses.	Arsenic	103-110	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	87-91
22745270-3	2012	Here we show that Ca(2+) enhances the tolerance of the wild-type and arsenic-sensitive yap1 strains to arsenic stress in a Crz1-dependent manner, thus providing the first evidence that Ca(2+) signalling cascades are involved in arsenic stress responses.	Arsenic	103-110	DNA-binding transcription factor CRZ1	Saccharomyces cerevisiae S288C	123-127
22745270-7	2012	Taken together, these data establish that activation of Ca(2+) signalling pathways and the downstream activation of the Crz1 transcription factor contribute to arsenic tolerance in the eukaryotic model organism S. cerevisiae.	Arsenic	160-167	DNA-binding transcription factor CRZ1	Saccharomyces cerevisiae S288C	120-124
22673340-0	2012	Fate of As(V)-treated nano zero-valent iron: determination of arsenic desorption potential under varying environmental conditions by phosphate extraction.	Arsenic	62-69	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	8-13
22673340-5	2012	Less arsenic desorption was observed at lower pH or higher As(V)/NZVI mass ratio, where stronger complexes (bidentate) formed between As(V) and NZVI corrosion products as indicated by FTIR analysis.	Arsenic	5-12	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	59-64
22673340-5	2012	Less arsenic desorption was observed at lower pH or higher As(V)/NZVI mass ratio, where stronger complexes (bidentate) formed between As(V) and NZVI corrosion products as indicated by FTIR analysis.	Arsenic	5-12	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	134-139
22641621-9	2012	This study demonstrates that arsenic can perturb the embryonic differentiation process by repressing the Wnt/beta-catenin signaling pathway.	Arsenic	29-36	catenin (cadherin associated protein), beta 1	Mus musculus	109-121
22560974-4	2012	A marked bioaccumulation of Cd, As, Hg and Zn was observed in the strain over-expressing MBP-MT in the cytoplasm, whereas Cu was accumulated to higher levels when MBP-MT was over-expressed in the periplasm.	Arsenic	32-34	myelin basic protein	Ovis aries	89-92
22673528-0	2012	Spin crossover in phosphorus- and arsenic-bridged cyclopentadienyl-manganese(II) dimers.	Arsenic	34-41	spindlin 1	Homo sapiens	0-4
22841115-1	2012	This study describes the optimization and validation of a quick and simple method for the simultaneous determination of total content and available fractions of As, Cr, Cu, Ni, Pb and Tl in sediments by ET AAS, which has been proved to be useful for environmental research.	Arsenic	161-163	FYVE, RhoGEF and PH domain containing 1	Homo sapiens	206-209
22883023-8	2012	Serum levels of IL6 and IL8 also increased in the arsenic exposed group.	Arsenic	50-57	interleukin 6	Homo sapiens	16-19
22883023-8	2012	Serum levels of IL6 and IL8 also increased in the arsenic exposed group.	Arsenic	50-57	C-X-C motif chemokine ligand 8	Homo sapiens	24-27
22704994-6	2012	Arsenic significantly decreased blood delta-aminolevulinic acid dehydratase (delta-ALAD) activity, reduced glutathione (GSH) and increased blood reactive oxygen species (ROS).	Arsenic	0-7	aminolevulinate dehydratase	Rattus norvegicus	38-75
22695135-4	2012	We found that arsenic inhibited inositol trisphosphate receptor (IP3R) function in the endoplasmic reticulum by inducing phosphorylation, which led to decreased intracellular calcium levels.	Arsenic	14-21	inositol 1,4,5-trisphosphate receptor type 3	Homo sapiens	65-69
21394736-8	2012	Finally, trivalent arsenic is found to bind with freshly isolated Hb from arsenicosis patients, binding affinity constant being 0.256 muM-1.	Arsenic	19-26	PWWP domain containing 3A, DNA repair factor	Homo sapiens	134-139
23141015-4	2012	RESULTS: Degree of AS in ApoE(-/-) and LDLR(-/-) mice fed with high-fat diet were significantly severer than those fed with normal diet and AS was more significant in ApoE(-/-) mice than in LDLR(-/-) mice.	Arsenic	19-21	apolipoprotein E	Mus musculus	25-29
23141015-4	2012	RESULTS: Degree of AS in ApoE(-/-) and LDLR(-/-) mice fed with high-fat diet were significantly severer than those fed with normal diet and AS was more significant in ApoE(-/-) mice than in LDLR(-/-) mice.	Arsenic	19-21	low density lipoprotein receptor	Mus musculus	39-43
22581830-0	2012	Subchronic exposure to arsenic inhibits spermatogenesis and downregulates the expression of ddx3y in testis and epididymis of mice.	Arsenic	23-30	DEAD box helicase 3, Y-linked	Mus musculus	92-97
22581830-4	2012	The goal of this study is to determine whether subchronic As exposure inhibits Ddx3y expression, an Y-linked gene important in spermatogenesis and sperm maturation, and whether the inhibited expression of Ddx3y is closely associated with As-induced male reproductive toxicity Adult mice were given drinking water alone or water containing 1, 2, and 4mg/l arsenic trioxide (As(2)O(3)) for 60 days.	Arsenic	58-60	DEAD box helicase 3, Y-linked	Mus musculus	79-84
22581830-12	2012	Our results indicated that Ddx3y may be an important target gene of As and the downregulated expression of Ddx3y may be closely related to male reproductive toxicity induced by As.	Arsenic	68-70	DEAD box helicase 3, Y-linked	Mus musculus	27-32
22704994-6	2012	Arsenic significantly decreased blood delta-aminolevulinic acid dehydratase (delta-ALAD) activity, reduced glutathione (GSH) and increased blood reactive oxygen species (ROS).	Arsenic	0-7	aminolevulinate dehydratase	Rattus norvegicus	77-87
22704994-8	2012	By contrast, hepatic GSH, superoxide dismutase and catalase activities significantly decreased on arsenic exposure, indicative of oxidative stress.	Arsenic	98-105	catalase	Rattus norvegicus	51-59
22692509-0	2012	The arsenic-based cure of acute promyelocytic leukemia promotes cytoplasmic sequestration of PML and PML/RARA through inhibition of PML body recycling.	Arsenic	4-11	PML nuclear body scaffold	Homo sapiens	93-96
22692509-0	2012	The arsenic-based cure of acute promyelocytic leukemia promotes cytoplasmic sequestration of PML and PML/RARA through inhibition of PML body recycling.	Arsenic	4-11	PML nuclear body scaffold	Homo sapiens	101-104
22692509-0	2012	The arsenic-based cure of acute promyelocytic leukemia promotes cytoplasmic sequestration of PML and PML/RARA through inhibition of PML body recycling.	Arsenic	4-11	retinoic acid receptor alpha	Homo sapiens	105-109
22692509-0	2012	The arsenic-based cure of acute promyelocytic leukemia promotes cytoplasmic sequestration of PML and PML/RARA through inhibition of PML body recycling.	Arsenic	4-11	PML nuclear body scaffold	Homo sapiens	101-104
22466225-8	2012	Arsenic exposure was also associated with higher methylation of some of the tested CpG sites in the promoter region of p16 in umbilical cord and maternal leukocytes.	Arsenic	0-7	cyclin dependent kinase inhibitor 2A	Homo sapiens	119-122
22613031-0	2012	Arsenic impairs embryo development via down-regulating Dvr1 expression in zebrafish.	Arsenic	0-7	growth differentiation factor 3	Danio rerio	55-59
22613031-7	2012	Taken together, our results indicated for the first time that Dvr1 played an important role in the left-right asymmetry establishment of zebrafish embryo, and Dvr1 was involved in arsenic-mediated embryo toxicity, which gives novel insight into molecular mechanism of arsenic-mediated embryo toxicity.	Arsenic	180-187	growth differentiation factor 3	Danio rerio	159-163
22778276-3	2012	APL is remarkable because of the fortuitous identification of two clinically effective therapies, RA and arsenic, both of which degrade PML/RARA oncoprotein and, together, cure APL.	Arsenic	105-112	PML nuclear body scaffold	Homo sapiens	136-139
22778276-3	2012	APL is remarkable because of the fortuitous identification of two clinically effective therapies, RA and arsenic, both of which degrade PML/RARA oncoprotein and, together, cure APL.	Arsenic	105-112	retinoic acid receptor alpha	Homo sapiens	140-144
22778276-4	2012	Analysis of arsenic-induced PML or PML/RARA degradation has implicated oxidative stress in the biogenesis of nuclear bodies and SUMO in their degradation.	Arsenic	12-19	PML nuclear body scaffold	Homo sapiens	28-31
22778276-4	2012	Analysis of arsenic-induced PML or PML/RARA degradation has implicated oxidative stress in the biogenesis of nuclear bodies and SUMO in their degradation.	Arsenic	12-19	PML nuclear body scaffold	Homo sapiens	35-38
22778276-4	2012	Analysis of arsenic-induced PML or PML/RARA degradation has implicated oxidative stress in the biogenesis of nuclear bodies and SUMO in their degradation.	Arsenic	12-19	retinoic acid receptor alpha	Homo sapiens	39-43
22753750-0	2012	The organic arsenic derivative GMZ27 induces PML-RARalpha-independent apoptosis in myeloid leukemia cells.	Arsenic	12-19	PML nuclear body scaffold	Homo sapiens	45-48
22753750-0	2012	The organic arsenic derivative GMZ27 induces PML-RARalpha-independent apoptosis in myeloid leukemia cells.	Arsenic	12-19	retinoic acid receptor alpha	Homo sapiens	49-57
22322880-8	2012	We also found a significantly negative correlation between alpha-glucosidase activity and the levels of As (r = -0.367, P = 0.023).	Arsenic	104-106	sucrase-isomaltase	Homo sapiens	59-76
22440634-8	2012	Our results suggest that a low MMA% is associated with increased risk for MetS among As-exposed subjects and the genetic polymorphism of GSTO1, an enzyme responsible for the reduction of pentavalent arsenic species, may also play a modest modification role.	Arsenic	199-206	glutathione S-transferase omega 1	Homo sapiens	137-142
22575231-4	2012	In mammals, cellular inorganic arsenic is methylated by a SAM-dependent arsenic methyltransferase, AS3MT.	Arsenic	31-38	arsenite methyltransferase	Danio rerio	99-104
22405870-11	2012	Urinary arsenic and lead levels had a negative association with both miR-21 and miR-221.	Arsenic	8-15	microRNA 21	Homo sapiens	69-75
22405870-11	2012	Urinary arsenic and lead levels had a negative association with both miR-21 and miR-221.	Arsenic	8-15	microRNA 221	Homo sapiens	80-87
22405870-13	2012	CONCLUSION: The results of our study suggest an association between microalbuminuria, miR-21 and heavy metals (arsenic and lead).	Arsenic	111-118	microRNA 21	Homo sapiens	86-92
22466225-10	2012	CONCLUSIONS: Exposure to higher levels of arsenic was positively associated with DNA methylation in LINE-1 repeated elements, and to a lesser degree at CpG sites within the promoter region of the tumor suppressor gene p16.	Arsenic	42-49	cyclin dependent kinase inhibitor 2A	Homo sapiens	218-221
22552367-0	2012	Arsenic and chromium in drinking water promote tumorigenesis in a mouse colitis-associated colorectal cancer model and the potential mechanism is ROS-mediated Wnt/beta-catenin signaling pathway.	Arsenic	0-7	catenin (cadherin associated protein), beta 1	Mus musculus	163-175
22578268-7	2012	Pi and arsenic plant content analyses confirmed a role of Pht1;9 in Pi acquisition during Pi starvation and arsenate uptake at the root-soil interface.	Arsenic	7-14	phosphate transporter 1;9	Arabidopsis thaliana	58-64
22552367-11	2012	Our study provides a new animal model to study the carcinogenicity of As(III) and Cr(VI) and suggests that As(III) and Cr(VI) promote colorectal cancer tumorigenesis, at least partly, through ROS-mediated Wnt/beta-catenin signaling pathway.	Arsenic	107-109	catenin (cadherin associated protein), beta 1	Mus musculus	209-221
22634503-0	2012	Modulation of arsenic-induced epidermal growth factor receptor pathway signalling by resveratrol.	Arsenic	14-21	epidermal growth factor receptor	Homo sapiens	30-62
22747749-10	2012	CONCLUSIONS: Variation in As3MT and MTHFR is associated with bladder cancer among those exposed to relatively low concentrations of inorganic arsenic.	Arsenic	142-149	arsenite methyltransferase	Homo sapiens	26-31
22747749-10	2012	CONCLUSIONS: Variation in As3MT and MTHFR is associated with bladder cancer among those exposed to relatively low concentrations of inorganic arsenic.	Arsenic	142-149	methylenetetrahydrofolate reductase	Homo sapiens	36-41
22634503-6	2012	Arsenic-mediated ERK1/2 activation negatively regulated DNA polymerase beta expression and up regulated heme-oxygenase-1 at toxic concentrations.	Arsenic	0-7	mitogen-activated protein kinase 3	Homo sapiens	17-23
22634503-6	2012	Arsenic-mediated ERK1/2 activation negatively regulated DNA polymerase beta expression and up regulated heme-oxygenase-1 at toxic concentrations.	Arsenic	0-7	DNA polymerase beta	Homo sapiens	56-75
22634503-6	2012	Arsenic-mediated ERK1/2 activation negatively regulated DNA polymerase beta expression and up regulated heme-oxygenase-1 at toxic concentrations.	Arsenic	0-7	heme oxygenase 1	Homo sapiens	104-120
22634503-9	2012	Our research provides evidence that treatment with pharmacologically relevant doses of RVL influences cellular responses to As(III), largely due to RVL-mediated changes to Src and ERK1/2 activation.	Arsenic	124-126	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	172-175
22634503-9	2012	Our research provides evidence that treatment with pharmacologically relevant doses of RVL influences cellular responses to As(III), largely due to RVL-mediated changes to Src and ERK1/2 activation.	Arsenic	124-126	mitogen-activated protein kinase 3	Homo sapiens	180-186
22534204-2	2012	Both well water arsenic and urinary arsenic were positively associated with plasma levels of soluble VCAM-1.	Arsenic	16-23	vascular cell adhesion molecule 1	Homo sapiens	101-107
22193621-3	2012	Interestingly, whether there is an elevated risk of hypertension with arsenic or lead exposure in individuals with genetic variations in MnSOD or OGG1 has not yet been investigated.	Arsenic	70-77	superoxide dismutase 2	Homo sapiens	137-142
22575377-8	2012	The toxic and mobile species of arsenic (As III, As V) were detected.	Arsenic	32-39	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	49-53
22594554-7	2012	For TBAs/TBP, when the source gases were changed, the formed surface species showed a short diffusion length so as to reduce the As background after the InAsP growth.	Arsenic	6-8	TATA-box binding protein	Homo sapiens	9-12
22293942-0	2012	Association of glutathione S-transferase Omega 1-1 polymorphisms (A140D and E208K) with the expression of interleukin-8 (IL-8), transforming growth factor beta (TGF-beta), and apoptotic protease-activating factor 1 (Apaf-1) in humans chronically exposed to arsenic in drinking water.	Arsenic	257-264	glutathione S-transferase omega 1	Homo sapiens	15-50
22534204-2	2012	Both well water arsenic and urinary arsenic were positively associated with plasma levels of soluble VCAM-1.	Arsenic	36-43	vascular cell adhesion molecule 1	Homo sapiens	101-107
22534204-3	2012	For every 1-unit increase in log-transformed well water arsenic (ln mug/L) and urinary arsenic (ln mug/g creatinine), plasma soluble VCAM-1 was 1.02 (95% confidence interval: 1.01, 1.03) and 1.04 (95% confidence interval: 1.01, 1.07) times greater, respectively.	Arsenic	87-94	vascular cell adhesion molecule 1	Homo sapiens	133-139
22534204-4	2012	There was a significant interaction between arsenic exposure and higher body mass index, such that the increased levels of plasminogen activator inhibitor-1 and soluble VCAM-1 associated with arsenic exposure were stronger among people with higher body mass index.	Arsenic	44-51	serpin family E member 1	Homo sapiens	123-156
22534204-4	2012	There was a significant interaction between arsenic exposure and higher body mass index, such that the increased levels of plasminogen activator inhibitor-1 and soluble VCAM-1 associated with arsenic exposure were stronger among people with higher body mass index.	Arsenic	44-51	vascular cell adhesion molecule 1	Homo sapiens	169-175
22534204-4	2012	There was a significant interaction between arsenic exposure and higher body mass index, such that the increased levels of plasminogen activator inhibitor-1 and soluble VCAM-1 associated with arsenic exposure were stronger among people with higher body mass index.	Arsenic	192-199	serpin family E member 1	Homo sapiens	123-156
22534204-4	2012	There was a significant interaction between arsenic exposure and higher body mass index, such that the increased levels of plasminogen activator inhibitor-1 and soluble VCAM-1 associated with arsenic exposure were stronger among people with higher body mass index.	Arsenic	192-199	vascular cell adhesion molecule 1	Homo sapiens	169-175
22521605-4	2012	Inorganic arsenic has been shown to contribute to cardiac toxicities through production of reactive oxygen species (ROS) that result in the activation of NFkappaB.	Arsenic	10-17	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	154-162
22521605-10	2012	These data suggest that arsenic causes the expression and secretion of CRP and that CRP activates NFkappaB through activation of the Rho-kinase pathway, thereby providing a novel pathway by which arsenic can contribute to metabolic syndrome and cardiovascular disease.	Arsenic	24-31	C-reactive protein, pentraxin-related	Mus musculus	71-74
22521605-10	2012	These data suggest that arsenic causes the expression and secretion of CRP and that CRP activates NFkappaB through activation of the Rho-kinase pathway, thereby providing a novel pathway by which arsenic can contribute to metabolic syndrome and cardiovascular disease.	Arsenic	196-203	C-reactive protein, pentraxin-related	Mus musculus	84-87
22521605-10	2012	These data suggest that arsenic causes the expression and secretion of CRP and that CRP activates NFkappaB through activation of the Rho-kinase pathway, thereby providing a novel pathway by which arsenic can contribute to metabolic syndrome and cardiovascular disease.	Arsenic	196-203	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	98-106
22422340-5	2012	We found that fluoride and arsenic alone or combined increased the expression of VCAM-1, P-sel, MCP-1, IL-8, and IL-6 at the RNA and protein levels.	Arsenic	27-34	C-C motif chemokine 2	Oryctolagus cuniculus	96-101
22422340-5	2012	We found that fluoride and arsenic alone or combined increased the expression of VCAM-1, P-sel, MCP-1, IL-8, and IL-6 at the RNA and protein levels.	Arsenic	27-34	interleukin-8	Oryctolagus cuniculus	103-107
22422340-5	2012	We found that fluoride and arsenic alone or combined increased the expression of VCAM-1, P-sel, MCP-1, IL-8, and IL-6 at the RNA and protein levels.	Arsenic	27-34	interleukin-6	Oryctolagus cuniculus	113-117
22293942-4	2012	The polymorphism A140D of GSTO1-1 has been not only associated with distinct urinary profile of arsenic metabolites in populations chronically exposed to iAs in drinking water, but also with higher risk of childhood leukemia and lung disease in non-exposed populations, suggesting that GSTO1-1 involvement in other physiologic processes different from toxics metabolism could be more relevant than is thought.	Arsenic	96-103	glutathione S-transferase omega 1	Homo sapiens	26-33
22293942-4	2012	The polymorphism A140D of GSTO1-1 has been not only associated with distinct urinary profile of arsenic metabolites in populations chronically exposed to iAs in drinking water, but also with higher risk of childhood leukemia and lung disease in non-exposed populations, suggesting that GSTO1-1 involvement in other physiologic processes different from toxics metabolism could be more relevant than is thought.	Arsenic	96-103	glutathione S-transferase omega 1	Homo sapiens	286-293
22293942-7	2012	These results suggest an important role of GSTO1-1 in the inflammatory response and the apoptotic process and indicate that A140D and E208K polymorphisms could increase the risk of developing inflammatory and apoptosis-related diseases in As-exposed populations.	Arsenic	239-241	glutathione S-transferase omega 1	Homo sapiens	43-50
22422340-5	2012	We found that fluoride and arsenic alone or combined increased the expression of VCAM-1, P-sel, MCP-1, IL-8, and IL-6 at the RNA and protein levels.	Arsenic	27-34	vascular cell adhesion protein 1	Oryctolagus cuniculus	81-87
22422340-5	2012	We found that fluoride and arsenic alone or combined increased the expression of VCAM-1, P-sel, MCP-1, IL-8, and IL-6 at the RNA and protein levels.	Arsenic	27-34	P-selectin	Oryctolagus cuniculus	89-94
22193621-11	2012	Thus, both MnSOD and OGG1 genotypes may be prone to an increased risk of hypertension associated with arsenic exposure.	Arsenic	102-109	superoxide dismutase 2	Homo sapiens	11-16
22193621-11	2012	Thus, both MnSOD and OGG1 genotypes may be prone to an increased risk of hypertension associated with arsenic exposure.	Arsenic	102-109	8-oxoguanine DNA glycosylase	Homo sapiens	21-25
22526373-3	2012	We hypothesized that barium modulates arsenic-mediated biological effects, and we examined the effect of barium (1 muM) on arsenic (3 muM)-mediated apoptotic cell death of human HSC-5 and A431 SCC cells in vitro.	Arsenic	123-130	latexin	Homo sapiens	115-118
22488045-6	2012	HO-1 competitive inhibitor zinc protoporphyrin improved the cytotoxicity of arsenic in an inverted-U dose-response curve, indicating the biphasic hormetic effect of HO-1.	Arsenic	76-83	heme oxygenase 1	Mus musculus	0-4
22488045-6	2012	HO-1 competitive inhibitor zinc protoporphyrin improved the cytotoxicity of arsenic in an inverted-U dose-response curve, indicating the biphasic hormetic effect of HO-1.	Arsenic	76-83	heme oxygenase 1	Mus musculus	165-169
22488045-7	2012	HO-1 siRNA decreased VEGF expression in response to arsenic.	Arsenic	52-59	heme oxygenase 1	Mus musculus	0-4
22488045-7	2012	HO-1 siRNA decreased VEGF expression in response to arsenic.	Arsenic	52-59	vascular endothelial growth factor A	Mus musculus	21-25
22488045-8	2012	Arsenic exposure also enhanced NF-E2-related factor 2 (Nrf2) expression and increased activation of nuclear factor-kappaB (NF-kappaB).	Arsenic	0-7	nuclear factor, erythroid derived 2, like 2	Mus musculus	31-53
22488045-8	2012	Arsenic exposure also enhanced NF-E2-related factor 2 (Nrf2) expression and increased activation of nuclear factor-kappaB (NF-kappaB).	Arsenic	0-7	nuclear factor, erythroid derived 2, like 2	Mus musculus	55-59
22488045-9	2012	NF-kappaB inhibitor Bay 11-7082 reduced arsenic-mediated expression of HO-1 and IL-6.	Arsenic	40-47	heme oxygenase 1	Mus musculus	71-84
22488045-10	2012	Selective blocking of the MAPK pathways with p38 inhibitor SB203580 significantly decreased arsenic-induced HO-1 and VEGF expression, while JNKs inhibitor SP600125 increased IL-6 expression.	Arsenic	92-99	mitogen-activated protein kinase 14	Mus musculus	45-48
22488045-10	2012	Selective blocking of the MAPK pathways with p38 inhibitor SB203580 significantly decreased arsenic-induced HO-1 and VEGF expression, while JNKs inhibitor SP600125 increased IL-6 expression.	Arsenic	92-99	heme oxygenase 1	Mus musculus	108-112
22488045-10	2012	Selective blocking of the MAPK pathways with p38 inhibitor SB203580 significantly decreased arsenic-induced HO-1 and VEGF expression, while JNKs inhibitor SP600125 increased IL-6 expression.	Arsenic	92-99	vascular endothelial growth factor A	Mus musculus	117-121
22488045-11	2012	These results suggest that in arsenic-treated SVEC4-10 cells, HO-1 expression is mediated through Nrf2-, NF-kappaB-, and p38 MAPK-dependent signaling pathways and serves as an upstream regulator of VEGF.	Arsenic	30-37	heme oxygenase 1	Mus musculus	62-66
22488045-11	2012	These results suggest that in arsenic-treated SVEC4-10 cells, HO-1 expression is mediated through Nrf2-, NF-kappaB-, and p38 MAPK-dependent signaling pathways and serves as an upstream regulator of VEGF.	Arsenic	30-37	nuclear factor, erythroid derived 2, like 2	Mus musculus	98-102
22488045-11	2012	These results suggest that in arsenic-treated SVEC4-10 cells, HO-1 expression is mediated through Nrf2-, NF-kappaB-, and p38 MAPK-dependent signaling pathways and serves as an upstream regulator of VEGF.	Arsenic	30-37	mitogen-activated protein kinase 14	Mus musculus	121-129
22488045-11	2012	These results suggest that in arsenic-treated SVEC4-10 cells, HO-1 expression is mediated through Nrf2-, NF-kappaB-, and p38 MAPK-dependent signaling pathways and serves as an upstream regulator of VEGF.	Arsenic	30-37	vascular endothelial growth factor A	Mus musculus	198-202
22488045-0	2012	Arsenic modulates heme oxygenase-1, interleukin-6, and vascular endothelial growth factor expression in endothelial cells: roles of ROS, NF-kappaB, and MAPK pathways.	Arsenic	0-7	heme oxygenase 1	Mus musculus	18-34
22488045-0	2012	Arsenic modulates heme oxygenase-1, interleukin-6, and vascular endothelial growth factor expression in endothelial cells: roles of ROS, NF-kappaB, and MAPK pathways.	Arsenic	0-7	interleukin 6	Mus musculus	36-49
22488045-0	2012	Arsenic modulates heme oxygenase-1, interleukin-6, and vascular endothelial growth factor expression in endothelial cells: roles of ROS, NF-kappaB, and MAPK pathways.	Arsenic	0-7	vascular endothelial growth factor A	Mus musculus	55-89
22488045-4	2012	The mRNA levels of heme oxygenase-1 (HO-1), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and vascular endothelial growth factor (VEGF) were significantly increased by arsenic.	Arsenic	188-195	chemokine (C-C motif) ligand 2	Mus musculus	66-100
22488045-4	2012	The mRNA levels of heme oxygenase-1 (HO-1), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and vascular endothelial growth factor (VEGF) were significantly increased by arsenic.	Arsenic	188-195	vascular endothelial growth factor A	Mus musculus	114-148
22535251-1	2012	During the last couple of decades, efforts have been made to study the toxic effects of individual aryl hydrocarbon receptors (AhR) ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or heavy metals typified by arsenic As(III).	Arsenic	219-226	aryl-hydrocarbon receptor	Mus musculus	99-125
22535251-1	2012	During the last couple of decades, efforts have been made to study the toxic effects of individual aryl hydrocarbon receptors (AhR) ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or heavy metals typified by arsenic As(III).	Arsenic	219-226	aryl-hydrocarbon receptor	Mus musculus	127-130
22535251-8	2012	Upon co-exposure to As(III) and TCDD, As(III) inhibited the TCDD-mediated induction of Cyp1a1 in the kidney and heart, Cyp1a2 in the kidney and heart, while it potentiated TCDD-mediated induction of Cyp1a1 in the lung, and Nqo1 and Gsta1 in the kidney and lung.	Arsenic	20-22	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	87-93
22535251-8	2012	Upon co-exposure to As(III) and TCDD, As(III) inhibited the TCDD-mediated induction of Cyp1a1 in the kidney and heart, Cyp1a2 in the kidney and heart, while it potentiated TCDD-mediated induction of Cyp1a1 in the lung, and Nqo1 and Gsta1 in the kidney and lung.	Arsenic	20-22	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	119-125
22535251-8	2012	Upon co-exposure to As(III) and TCDD, As(III) inhibited the TCDD-mediated induction of Cyp1a1 in the kidney and heart, Cyp1a2 in the kidney and heart, while it potentiated TCDD-mediated induction of Cyp1a1 in the lung, and Nqo1 and Gsta1 in the kidney and lung.	Arsenic	20-22	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	199-205
22535251-8	2012	Upon co-exposure to As(III) and TCDD, As(III) inhibited the TCDD-mediated induction of Cyp1a1 in the kidney and heart, Cyp1a2 in the kidney and heart, while it potentiated TCDD-mediated induction of Cyp1a1 in the lung, and Nqo1 and Gsta1 in the kidney and lung.	Arsenic	20-22	NAD(P)H dehydrogenase, quinone 1	Mus musculus	223-227
22535251-8	2012	Upon co-exposure to As(III) and TCDD, As(III) inhibited the TCDD-mediated induction of Cyp1a1 in the kidney and heart, Cyp1a2 in the kidney and heart, while it potentiated TCDD-mediated induction of Cyp1a1 in the lung, and Nqo1 and Gsta1 in the kidney and lung.	Arsenic	20-22	glutathione S-transferase, alpha 1 (Ya)	Mus musculus	232-237
22330069-0	2012	Inhibition of small GTPase RalA regulates growth and arsenic-induced apoptosis in chronic myeloid leukemia (CML) cells.	Arsenic	53-60	RAS like proto-oncogene A	Homo sapiens	27-31
22526373-3	2012	We hypothesized that barium modulates arsenic-mediated biological effects, and we examined the effect of barium (1 muM) on arsenic (3 muM)-mediated apoptotic cell death of human HSC-5 and A431 SCC cells in vitro.	Arsenic	123-130	latexin	Homo sapiens	134-137
22526373-4	2012	Arsenic promoted SCC apoptosis with increased reactive oxygen species (ROS) production and JNK1/2 and caspase-3 activation (apoptotic pathway).	Arsenic	0-7	serpin family B member 3	Homo sapiens	17-20
22526373-4	2012	Arsenic promoted SCC apoptosis with increased reactive oxygen species (ROS) production and JNK1/2 and caspase-3 activation (apoptotic pathway).	Arsenic	0-7	mitogen-activated protein kinase 8	Homo sapiens	91-97
22526373-4	2012	Arsenic promoted SCC apoptosis with increased reactive oxygen species (ROS) production and JNK1/2 and caspase-3 activation (apoptotic pathway).	Arsenic	0-7	caspase 3	Homo sapiens	102-111
22526373-5	2012	In contrast, arsenic also inhibited SCC apoptosis with increased NF-kappaB activity and X-linked inhibitor of apoptosis protein (XIAP) expression level and decreased JNK activity (antiapoptotic pathway).	Arsenic	13-20	serpin family B member 3	Homo sapiens	36-39
22526373-5	2012	In contrast, arsenic also inhibited SCC apoptosis with increased NF-kappaB activity and X-linked inhibitor of apoptosis protein (XIAP) expression level and decreased JNK activity (antiapoptotic pathway).	Arsenic	13-20	X-linked inhibitor of apoptosis	Homo sapiens	88-127
22526373-5	2012	In contrast, arsenic also inhibited SCC apoptosis with increased NF-kappaB activity and X-linked inhibitor of apoptosis protein (XIAP) expression level and decreased JNK activity (antiapoptotic pathway).	Arsenic	13-20	X-linked inhibitor of apoptosis	Homo sapiens	129-133
22526373-5	2012	In contrast, arsenic also inhibited SCC apoptosis with increased NF-kappaB activity and X-linked inhibitor of apoptosis protein (XIAP) expression level and decreased JNK activity (antiapoptotic pathway).	Arsenic	13-20	mitogen-activated protein kinase 8	Homo sapiens	166-169
22526373-6	2012	These results suggest that arsenic bidirectionally promotes apoptotic and antiapoptotic pathways in SCC cells.	Arsenic	27-34	serpin family B member 3	Homo sapiens	100-103
22526373-7	2012	Interestingly, barium in the presence of arsenic increased NF-kappaB activity and XIAP expression and decreased JNK activity without affecting ROS production, resulting in the inhibition of the arsenic-mediated apoptotic pathway.	Arsenic	41-48	X-linked inhibitor of apoptosis	Homo sapiens	82-86
22526373-8	2012	Since the anticancer effect of arsenic is mainly dependent on cancer apoptosis, barium-mediated inhibition of arsenic-induced apoptosis may promote progression of SCC in patients in Bangladesh who keep drinking barium and arsenic-polluted water after the development of cancer.	Arsenic	110-117	serpin family B member 3	Homo sapiens	163-166
22526373-8	2012	Since the anticancer effect of arsenic is mainly dependent on cancer apoptosis, barium-mediated inhibition of arsenic-induced apoptosis may promote progression of SCC in patients in Bangladesh who keep drinking barium and arsenic-polluted water after the development of cancer.	Arsenic	110-117	serpin family B member 3	Homo sapiens	163-166
22866392-1	2012	Iron-impregnated granular activated carbons (Fe-GAC) can remove arsenic effectively from water.	Arsenic	64-71	glutaminase	Homo sapiens	48-51
21308489-7	2012	Furthermore, the activity and mRNA of catalase were decreased strikingly following arsenic exposure.	Arsenic	83-90	catalase	Homo sapiens	38-46
22339537-1	2012	We determined whether single nucleotide polymorphisms (SNPs) in the glutathione S-transferase omega (GSTO) and arsenic(III)methyltransferase (AS3MT) genes were associated with concentrations of urinary arsenic metabolites among 900 individuals without skin lesions in Bangladesh.	Arsenic	111-118	arsenite methyltransferase	Homo sapiens	142-147
22978106-9	2012	CONCLUSION: As2O3 could inhibit the expression of Notch1 and the cell proliferation and the migration force of SKBR-3 cells, which primarily revealed that As2O3 might affect the biological behavior of human breast cancer cells possibly through Notch1 signaling pathway, thus providing theoretical and experimental bases for treating breast cancer by arsenic.	Arsenic	350-357	notch receptor 1	Homo sapiens	244-250
22467879-0	2012	Arsenic promotes ubiquitinylation and lysosomal degradation of cystic fibrosis transmembrane conductance regulator (CFTR) chloride channels in human airway epithelial cells.	Arsenic	0-7	CF transmembrane conductance regulator	Homo sapiens	63-114
22467879-0	2012	Arsenic promotes ubiquitinylation and lysosomal degradation of cystic fibrosis transmembrane conductance regulator (CFTR) chloride channels in human airway epithelial cells.	Arsenic	0-7	CF transmembrane conductance regulator	Homo sapiens	116-120
22467879-2	2012	Recently, we observed in the gill of killifish, an environmental model organism, that arsenic exposure induced the ubiquitinylation and degradation of cystic fibrosis transmembrane conductance regulator (CFTR), a chloride channel that is essential for the mucociliary clearance of respiratory pathogens in humans.	Arsenic	86-93	cystic fibrosis transmembrane conductance regulator	Fundulus heteroclitus	151-202
22467879-2	2012	Recently, we observed in the gill of killifish, an environmental model organism, that arsenic exposure induced the ubiquitinylation and degradation of cystic fibrosis transmembrane conductance regulator (CFTR), a chloride channel that is essential for the mucociliary clearance of respiratory pathogens in humans.	Arsenic	86-93	cystic fibrosis transmembrane conductance regulator	Fundulus heteroclitus	204-208
22467879-3	2012	Accordingly, in this study, we tested the hypothesis that low dose arsenic exposure reduces the abundance and function of CFTR in human airway epithelial cells.	Arsenic	67-74	CF transmembrane conductance regulator	Homo sapiens	122-126
22467879-4	2012	Arsenic induced a time- and dose-dependent increase in multiubiquitinylated CFTR, which led to its lysosomal degradation, and a decrease in CFTR-mediated chloride secretion.	Arsenic	0-7	CF transmembrane conductance regulator	Homo sapiens	76-80
22467879-4	2012	Arsenic induced a time- and dose-dependent increase in multiubiquitinylated CFTR, which led to its lysosomal degradation, and a decrease in CFTR-mediated chloride secretion.	Arsenic	0-7	CF transmembrane conductance regulator	Homo sapiens	140-144
22467879-5	2012	Although arsenic had no effect on the abundance or activity of USP10, a deubiquitinylating enzyme, siRNA-mediated knockdown of c-Cbl, an E3 ubiquitin ligase, abolished the arsenic-stimulated degradation of CFTR.	Arsenic	172-179	Cbl proto-oncogene	Homo sapiens	127-132
22467879-5	2012	Although arsenic had no effect on the abundance or activity of USP10, a deubiquitinylating enzyme, siRNA-mediated knockdown of c-Cbl, an E3 ubiquitin ligase, abolished the arsenic-stimulated degradation of CFTR.	Arsenic	172-179	CF transmembrane conductance regulator	Homo sapiens	206-210
22467879-6	2012	Arsenic enhanced the degradation of CFTR by increasing phosphorylated c-Cbl, which increased its interaction with CFTR, and subsequent ubiquitinylation of CFTR.	Arsenic	0-7	CF transmembrane conductance regulator	Homo sapiens	36-40
22467879-6	2012	Arsenic enhanced the degradation of CFTR by increasing phosphorylated c-Cbl, which increased its interaction with CFTR, and subsequent ubiquitinylation of CFTR.	Arsenic	0-7	Cbl proto-oncogene	Homo sapiens	70-75
22467879-6	2012	Arsenic enhanced the degradation of CFTR by increasing phosphorylated c-Cbl, which increased its interaction with CFTR, and subsequent ubiquitinylation of CFTR.	Arsenic	0-7	CF transmembrane conductance regulator	Homo sapiens	114-118
22467879-6	2012	Arsenic enhanced the degradation of CFTR by increasing phosphorylated c-Cbl, which increased its interaction with CFTR, and subsequent ubiquitinylation of CFTR.	Arsenic	0-7	CF transmembrane conductance regulator	Homo sapiens	114-118
22467879-7	2012	Because epidemiological studies have shown that arsenic increases the incidence of respiratory infections, this study suggests that one potential mechanism of this effect involves arsenic-induced ubiquitinylation and degradation of CFTR, which decreases chloride secretion and airway surface liquid volume, effects that would be proposed to reduce mucociliary clearance of respiratory pathogens.	Arsenic	48-55	CF transmembrane conductance regulator	Homo sapiens	232-236
22467879-7	2012	Because epidemiological studies have shown that arsenic increases the incidence of respiratory infections, this study suggests that one potential mechanism of this effect involves arsenic-induced ubiquitinylation and degradation of CFTR, which decreases chloride secretion and airway surface liquid volume, effects that would be proposed to reduce mucociliary clearance of respiratory pathogens.	Arsenic	180-187	CF transmembrane conductance regulator	Homo sapiens	232-236
22483914-4	2012	2-Phospho-l-ascorbic acid was used as a novel substrate, in arsenic determination, which amperometric response decreased by the presence of As(V) ions.	Arsenic	60-67	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	140-145
22321510-0	2012	Arsenic mobilizes Langerhans cell migration and induces Th1 response in epicutaneous protein sensitization via CCL21: a plausible cause of decreased Langerhans cells in arsenic-induced intraepithelial carcinoma.	Arsenic	0-7	negative elongation factor complex member C/D, Th1l	Mus musculus	56-59
22551203-10	2012	RESULTS: Results showed that arsenic-exposed newborns had significantly higher levels of arsenic in cord blood, fingernails, toenails and hair than those of the unexposed subjects and a slight increase in promoter methylation of p53 in cord blood lymphocytes which significantly correlated with arsenic accumulation in nails (p &lt; 0.05) was observed, while LINE-1 methylation was unchanged.	Arsenic	29-36	tumor protein p53	Homo sapiens	229-232
22551203-13	2012	CONCLUSIONS: This study provides an important finding that in utero arsenic exposure affects DNA methylation, particularly at the p53 promoter region, which may be linked to the mechanism of arsenic carcinogenesis and the observed increased incidence of cancer later in life.	Arsenic	68-75	tumor protein p53	Homo sapiens	130-133
22321510-8	2012	Ninety-six hours after OVA sensitization, Langerin(+)EpCAM(+) cells in arsenic-treated WT mice were significantly increased in draining lymph nodes and decreased in epidermis without changes in the dermis.	Arsenic	71-78	CD207 antigen	Mus musculus	42-50
22321510-11	2012	However, cell proliferation and the induction of IFN-gamma by arsenic were found to be abolished in DT-treated Langerin-DTR mice.	Arsenic	62-69	interferon gamma	Mus musculus	49-58
22321510-11	2012	However, cell proliferation and the induction of IFN-gamma by arsenic were found to be abolished in DT-treated Langerin-DTR mice.	Arsenic	62-69	CD207 antigen	Mus musculus	111-119
22321510-12	2012	The expressions of CCL21 and CXCL12 were also increased in lymph nodes from arsenic-treated WT mice.	Arsenic	76-83	chemokine (C-X-C motif) ligand 12	Mus musculus	29-35
22321510-14	2012	The results of this study, the first to study oral arsenic polarization of Th1 responses in epicutaneous protein sensitization through CCL21-mediated LC migration, suggest the chronicity of As-BD without invasion might result from enhanced Th1 responses and altered LC migrations by arsenic.	Arsenic	51-58	negative elongation factor complex member C/D, Th1l	Mus musculus	75-78
22321510-14	2012	The results of this study, the first to study oral arsenic polarization of Th1 responses in epicutaneous protein sensitization through CCL21-mediated LC migration, suggest the chronicity of As-BD without invasion might result from enhanced Th1 responses and altered LC migrations by arsenic.	Arsenic	51-58	negative elongation factor complex member C/D, Th1l	Mus musculus	240-243
22321510-14	2012	The results of this study, the first to study oral arsenic polarization of Th1 responses in epicutaneous protein sensitization through CCL21-mediated LC migration, suggest the chronicity of As-BD without invasion might result from enhanced Th1 responses and altered LC migrations by arsenic.	Arsenic	283-290	negative elongation factor complex member C/D, Th1l	Mus musculus	75-78
22628173-7	2012	At high levels of arsenate, loss from the intact cells to the medium was observed with time; knockouts of two known arsenic extrusion genes, ACR3 and FPS1, did not prevent this loss.	Arsenic	116-123	Arr3p	Saccharomyces cerevisiae S288C	141-145
22339537-5	2012	Genetic polymorphisms GSTO and As3MT modify arsenic metabolism as evidenced by altered urinary arsenic excretion.	Arsenic	44-51	arsenite methyltransferase	Homo sapiens	31-36
22339537-5	2012	Genetic polymorphisms GSTO and As3MT modify arsenic metabolism as evidenced by altered urinary arsenic excretion.	Arsenic	95-102	arsenite methyltransferase	Homo sapiens	31-36
22509835-0	2012	Quercetin enhancement of arsenic-induced apoptosis via stimulating ROS-dependent p53 protein ubiquitination in human HaCaT keratinocytes.	Arsenic	25-32	tumor protein p53	Homo sapiens	81-84
22155346-2	2012	Arsenic has been reported to induce malignant transformation of human cells through Nrf2-dependent signaling pathway.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	84-88
22155346-4	2012	It is still unclear how Nrf2 may mediate cellular response of OSCC cells when treated with arsenic.	Arsenic	91-98	NFE2 like bZIP transcription factor 2	Homo sapiens	24-28
22330312-6	2012	As(V) accounted for 81-99% of the extractable species in the TSP samples which showed that As(V) was the major fraction of the extractable As.	Arsenic	0-2	thrombospondin 1	Homo sapiens	61-64
22330312-6	2012	As(V) accounted for 81-99% of the extractable species in the TSP samples which showed that As(V) was the major fraction of the extractable As.	Arsenic	0-2	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	91-96
22330312-8	2012	Higher values of enrichment factors demonstrated that arsenic in TSP mainly come from anthropogenic sources.	Arsenic	54-61	thrombospondin 1	Homo sapiens	65-68
22088973-9	2012	In nonsmokers, the adjusted odds of having dyspnoea were 1.36, 1.96, 2.34 and 1.80-fold greater for arsenic concentrations of 7-38, 39-90, 91-178 and 179-864 mug   L(-1), respectively, compared with the reference arsenic concentration of &lt;7 mug   L(-1) (p&lt;0.01; Chi-squared test for trend).	Arsenic	100-107	immunoglobulin kappa variable 1-16	Homo sapiens	164-169
22088973-9	2012	In nonsmokers, the adjusted odds of having dyspnoea were 1.36, 1.96, 2.34 and 1.80-fold greater for arsenic concentrations of 7-38, 39-90, 91-178 and 179-864 mug   L(-1), respectively, compared with the reference arsenic concentration of &lt;7 mug   L(-1) (p&lt;0.01; Chi-squared test for trend).	Arsenic	100-107	immunoglobulin kappa variable 1-16	Homo sapiens	250-255
22509835-8	2012	QUE plus As(+3) stimulation of apoptosis in human HaCaT keratinocytes via activating ROS-dependent p53 protein ubiquitination may offer a rationale for the use of QUE to improve the clinical efficacy of arsenics in treating psoriasis.	Arsenic	203-211	tumor protein p53	Homo sapiens	99-102
22664115-0	2012	Targeted inhibition of VEGF-modulated survival and arsenic sensitivity in acute myeloid leukemia (AML).	Arsenic	51-58	vascular endothelial growth factor A	Homo sapiens	23-27
22664115-12	2012	Therefore, targeted inhibition of VEGF suppressed survival and increased arsenic sensitivity in AML.	Arsenic	73-80	vascular endothelial growth factor A	Homo sapiens	34-38
22380876-0	2012	Heterologous expression of the yeast arsenite efflux system ACR3 improves Arabidopsis thaliana tolerance to arsenic stress.	Arsenic	108-115	Arr3p	Saccharomyces cerevisiae S288C	60-64
22380876-9	2012	The presence of ACR3 hardly affected tissue arsenic levels, but increased arsenic translocation to the shoot.	Arsenic	44-51	Arr3p	Saccharomyces cerevisiae S288C	16-20
22380876-9	2012	The presence of ACR3 hardly affected tissue arsenic levels, but increased arsenic translocation to the shoot.	Arsenic	74-81	Arr3p	Saccharomyces cerevisiae S288C	16-20
22380876-10	2012	Heterologous expression of yeast ACR3 endows plants with greater arsenic resistance, but does not lower significantly arsenic tissue levels.	Arsenic	65-72	Arr3p	Saccharomyces cerevisiae S288C	33-37
22446113-0	2012	Increased serum level of epidermal growth factor receptor in liver cancer patients and its association with exposure to arsenic.	Arsenic	120-127	epidermal growth factor receptor	Homo sapiens	25-57
23004905-4	2012	Here we present a complementary scheme that is based on the nudged-elastic-band method ordinarily used to find saddle points and we apply the scheme to find the most stable isomers of the phosphorus P(4), P(8) molecules and the corresponding molecules of As(n), Sb(n), and Bi(n) (n = 4,8) in the framework of the density functional theory.	Arsenic	255-257	solute carrier family 10 member 4	Homo sapiens	199-203
23004905-4	2012	Here we present a complementary scheme that is based on the nudged-elastic-band method ordinarily used to find saddle points and we apply the scheme to find the most stable isomers of the phosphorus P(4), P(8) molecules and the corresponding molecules of As(n), Sb(n), and Bi(n) (n = 4,8) in the framework of the density functional theory.	Arsenic	255-257	S100 calcium binding protein A8	Homo sapiens	205-209
21253733-2	2012	We perform this meta-analysis to collect all the relevant studies up to date to further clarify the association of IL-23R polymorphisms with AS.	Arsenic	141-143	interleukin 23 receptor	Homo sapiens	115-121
21253733-9	2012	We concluded that the genetic susceptibility for AS is associated with the IL-23R gene polymorphisms.	Arsenic	49-51	interleukin 23 receptor	Homo sapiens	75-81
22446113-1	2012	Arsenic is a human carcinogen and can activate epidermal growth factor receptor (EGFR) in human cell lines.	Arsenic	0-7	epidermal growth factor receptor	Homo sapiens	47-79
22446113-1	2012	Arsenic is a human carcinogen and can activate epidermal growth factor receptor (EGFR) in human cell lines.	Arsenic	0-7	epidermal growth factor receptor	Homo sapiens	81-85
22446113-2	2012	As EGFR is associated with the occurrence of cancers, we conducted a study to evaluate whether serum EGFR may increase in liver cancer patients, particularly in those with exposure to arsenic.	Arsenic	184-191	epidermal growth factor receptor	Homo sapiens	101-105
22446113-5	2012	When we compared 22 patients residing in an endemic area of arsenic intoxication to 22 age- and sex-matched patients residing outside the area, we found that patients from the endemic area had higher EGFR levels (882.8 vs. 511.6 fmol/mL, p = 0.04).	Arsenic	60-67	epidermal growth factor receptor	Homo sapiens	200-204
22446113-6	2012	We concluded that EGFR is over-expressed in patients of liver cancer, particularly in those with exposure to arsenic, and therefore, serum EGFR level is not only a potential biomarker of liver cancer, but also a potential biomarker of cancers associated with arsenic exposure.	Arsenic	109-116	epidermal growth factor receptor	Homo sapiens	18-22
22446113-6	2012	We concluded that EGFR is over-expressed in patients of liver cancer, particularly in those with exposure to arsenic, and therefore, serum EGFR level is not only a potential biomarker of liver cancer, but also a potential biomarker of cancers associated with arsenic exposure.	Arsenic	109-116	epidermal growth factor receptor	Homo sapiens	139-143
22446113-6	2012	We concluded that EGFR is over-expressed in patients of liver cancer, particularly in those with exposure to arsenic, and therefore, serum EGFR level is not only a potential biomarker of liver cancer, but also a potential biomarker of cancers associated with arsenic exposure.	Arsenic	259-266	epidermal growth factor receptor	Homo sapiens	18-22
22446113-6	2012	We concluded that EGFR is over-expressed in patients of liver cancer, particularly in those with exposure to arsenic, and therefore, serum EGFR level is not only a potential biomarker of liver cancer, but also a potential biomarker of cancers associated with arsenic exposure.	Arsenic	259-266	epidermal growth factor receptor	Homo sapiens	139-143
22425709-5	2012	Activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP) mRNA were induced by all three arsenic species, however, evidence suggested that they might be induced by different pathways in the case of iAsIII and MMAIII.	Arsenic	108-115	activating transcription factor 4	Rattus norvegicus	0-33
22425709-5	2012	Activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP) mRNA were induced by all three arsenic species, however, evidence suggested that they might be induced by different pathways in the case of iAsIII and MMAIII.	Arsenic	108-115	activating transcription factor 4	Rattus norvegicus	35-39
22425709-5	2012	Activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP) mRNA were induced by all three arsenic species, however, evidence suggested that they might be induced by different pathways in the case of iAsIII and MMAIII.	Arsenic	108-115	DNA-damage inducible transcript 3	Rattus norvegicus	45-69
22425709-5	2012	Activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP) mRNA were induced by all three arsenic species, however, evidence suggested that they might be induced by different pathways in the case of iAsIII and MMAIII.	Arsenic	108-115	DNA-damage inducible transcript 3	Rattus norvegicus	71-75
22387748-4	2012	Because overactivation of PARP-1 often leads to apoptotic cell death, and unrepaired DNA lesions promote genomic instability and carcinogenesis, we hypothesized that inhibition of PARP-1 by arsenic may promote the survival of potentially "initiated carcinogenic cells," i.e., cells with unrepaired DNA lesions.	Arsenic	190-197	poly(ADP-ribose) polymerase 1	Homo sapiens	180-186
25722672-4	2012	Results indicated that pine pollen suppressed cell apoptosis in the cerebral cortex of arsenic-poisoned mice by reducing Bax, Bcl-2 protein expression and increasing p53 protein expression.	Arsenic	87-94	BCL2-associated X protein	Mus musculus	121-124
22426358-3	2012	In this study, several mechanisms by which arsenic could alter myogenin expression were examined.	Arsenic	43-50	myogenin	Mus musculus	63-71
22426358-4	2012	Exposing differentiating C2C12 cells to 20 nM arsenic increased H3K9 dimethylation (H3K9me2) and H3K9 trimethylation (H3K9me3) by 3-fold near the transcription start site of myogenin, which is indicative of increased repressive marks, and reduced H3K9 acetylation (H3K9Ac) by 0.5-fold, indicative of reduced permissive marks.	Arsenic	46-53	myogenin	Mus musculus	174-182
22426358-5	2012	Protein expression of Glp or Ehmt1, a H3-K9 methyltransferase, was also increased by 1.6-fold in arsenic-exposed cells.	Arsenic	97-104	euchromatic histone methyltransferase 1	Mus musculus	22-25
22426358-5	2012	Protein expression of Glp or Ehmt1, a H3-K9 methyltransferase, was also increased by 1.6-fold in arsenic-exposed cells.	Arsenic	97-104	euchromatic histone methyltransferase 1	Mus musculus	29-34
22426358-6	2012	In addition to the altered histone remodeling status on the myogenin promoter, protein and mRNA levels of Igf-1, a myogenic growth factor, were significantly repressed by arsenic exposure.	Arsenic	171-178	myogenin	Mus musculus	60-68
22426358-6	2012	In addition to the altered histone remodeling status on the myogenin promoter, protein and mRNA levels of Igf-1, a myogenic growth factor, were significantly repressed by arsenic exposure.	Arsenic	171-178	insulin-like growth factor 1	Mus musculus	106-111
22426358-7	2012	Moreover, a 2-fold induction of Ezh2 expression, and an increased recruitment of Ezh2 (3.3-fold) and Dnmt3a (~2-fold) to the myogenin promoter at the transcription start site (-40 to +42), were detected in the arsenic-treated cells.	Arsenic	210-217	DNA methyltransferase 3A	Mus musculus	101-107
22426358-7	2012	Moreover, a 2-fold induction of Ezh2 expression, and an increased recruitment of Ezh2 (3.3-fold) and Dnmt3a (~2-fold) to the myogenin promoter at the transcription start site (-40 to +42), were detected in the arsenic-treated cells.	Arsenic	210-217	myogenin	Mus musculus	125-133
22426358-8	2012	Together, we conclude that the repressed myogenin expression in arsenic-exposed C2C12 cells was likely due to a combination of reduced expression of Igf-1, enhanced nuclear expression and promoter recruitment of Ezh2, and altered histone remodeling status on myogenin promoter (-40 to +42).	Arsenic	64-71	myogenin	Mus musculus	41-49
22426358-8	2012	Together, we conclude that the repressed myogenin expression in arsenic-exposed C2C12 cells was likely due to a combination of reduced expression of Igf-1, enhanced nuclear expression and promoter recruitment of Ezh2, and altered histone remodeling status on myogenin promoter (-40 to +42).	Arsenic	64-71	insulin-like growth factor 1	Mus musculus	149-154
22426358-8	2012	Together, we conclude that the repressed myogenin expression in arsenic-exposed C2C12 cells was likely due to a combination of reduced expression of Igf-1, enhanced nuclear expression and promoter recruitment of Ezh2, and altered histone remodeling status on myogenin promoter (-40 to +42).	Arsenic	64-71	enhancer of zeste 2 polycomb repressive complex 2 subunit	Mus musculus	212-216
22426358-8	2012	Together, we conclude that the repressed myogenin expression in arsenic-exposed C2C12 cells was likely due to a combination of reduced expression of Igf-1, enhanced nuclear expression and promoter recruitment of Ezh2, and altered histone remodeling status on myogenin promoter (-40 to +42).	Arsenic	64-71	myogenin	Mus musculus	259-267
25722672-4	2012	Results indicated that pine pollen suppressed cell apoptosis in the cerebral cortex of arsenic-poisoned mice by reducing Bax, Bcl-2 protein expression and increasing p53 protein expression.	Arsenic	87-94	B cell leukemia/lymphoma 2	Mus musculus	126-131
25722672-4	2012	Results indicated that pine pollen suppressed cell apoptosis in the cerebral cortex of arsenic-poisoned mice by reducing Bax, Bcl-2 protein expression and increasing p53 protein expression.	Arsenic	87-94	transformation related protein 53, pseudogene	Mus musculus	166-169
22469443-6	2012	RESULTS: Serum levels of IL-8, MCP-1, and CCL-20 were significantly higher in the AS group than in the AR and NA groups.	Arsenic	82-84	C-X-C motif chemokine ligand 8	Homo sapiens	25-29
23213425-5	2012	By selectively restoring Ush function in either the AS or the epidermis in ush mutants, we show that the AS makes a greater (Ush-dependent) contribution to closure than the epidermis.	Arsenic	52-54	u-shaped	Drosophila melanogaster	25-28
23213425-5	2012	By selectively restoring Ush function in either the AS or the epidermis in ush mutants, we show that the AS makes a greater (Ush-dependent) contribution to closure than the epidermis.	Arsenic	105-107	u-shaped	Drosophila melanogaster	25-28
23213425-5	2012	By selectively restoring Ush function in either the AS or the epidermis in ush mutants, we show that the AS makes a greater (Ush-dependent) contribution to closure than the epidermis.	Arsenic	105-107	u-shaped	Drosophila melanogaster	75-78
23213425-5	2012	By selectively restoring Ush function in either the AS or the epidermis in ush mutants, we show that the AS makes a greater (Ush-dependent) contribution to closure than the epidermis.	Arsenic	105-107	u-shaped	Drosophila melanogaster	125-128
23213425-6	2012	A signal from the AS induces epidermal cell elongation and JNK activation in the DME, while cable formation requires Ush on both sides of the leading edge, i.e. in both the AS and epidermis.	Arsenic	18-20	basket	Drosophila melanogaster	59-62
22306368-6	2012	We found evidence of genotype-arsenic interactions in the high exposure group; GSTP1 Ile105Val homozygous individuals had an odds ratio (OR) of 5.4 [95% confidence interval (CI): 1.5-20.2; P for interaction=0.03] and AQP3 Phe130Phe carriers had an OR=2.2 (95% CI: 0.8-6.1; P for interaction=0.10).	Arsenic	30-37	glutathione S-transferase pi 1	Homo sapiens	79-84
22469443-6	2012	RESULTS: Serum levels of IL-8, MCP-1, and CCL-20 were significantly higher in the AS group than in the AR and NA groups.	Arsenic	82-84	C-C motif chemokine ligand 2	Homo sapiens	31-36
22469443-6	2012	RESULTS: Serum levels of IL-8, MCP-1, and CCL-20 were significantly higher in the AS group than in the AR and NA groups.	Arsenic	82-84	C-C motif chemokine ligand 20	Homo sapiens	42-48
22492492-9	2012	These results suggest that arsenic-containing compounds are responsible for HO-1 induction by Lumbricus extract.	Arsenic	27-34	heme oxygenase 1	Homo sapiens	76-80
22492492-10	2012	Although the exact role of toxic arsenic compounds in the treatment of oxidative injury remains unclear, concomitant HO-1 induction may be a key mechanism to antagonize the cytotoxicity of arsenic compounds in human cells.	Arsenic	189-196	heme oxygenase 1	Homo sapiens	117-121
22492492-0	2012	Concomitant induction of heme oxygenase-1 attenuates the cytotoxicity of arsenic species from lumbricus extract in human liver HepG2 cells.	Arsenic	73-80	heme oxygenase 1	Homo sapiens	25-41
22342767-4	2012	Arsenic triggers sumoylation/ubiquitination and proteasomal degradation of PML-RARalpha via directly binding to the C3HC4 zinc finger motif in the RBCC domain of the PML moiety and induction of its homodimerization/multimerization and interaction with the SUMO E2 conjugase Ubc9.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	75-78
22342767-4	2012	Arsenic triggers sumoylation/ubiquitination and proteasomal degradation of PML-RARalpha via directly binding to the C3HC4 zinc finger motif in the RBCC domain of the PML moiety and induction of its homodimerization/multimerization and interaction with the SUMO E2 conjugase Ubc9.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	166-169
22342767-4	2012	Arsenic triggers sumoylation/ubiquitination and proteasomal degradation of PML-RARalpha via directly binding to the C3HC4 zinc finger motif in the RBCC domain of the PML moiety and induction of its homodimerization/multimerization and interaction with the SUMO E2 conjugase Ubc9.	Arsenic	0-7	ubiquitin conjugating enzyme E2 I	Homo sapiens	274-278
22138666-9	2012	Few studies have evaluated changes in systolic and diastolic BP (SBP and DBP, respectively) measurements by arsenic exposure levels, and those studies reported inconclusive findings.	Arsenic	108-115	selenium binding protein 1	Homo sapiens	65-68
22138666-9	2012	Few studies have evaluated changes in systolic and diastolic BP (SBP and DBP, respectively) measurements by arsenic exposure levels, and those studies reported inconclusive findings.	Arsenic	108-115	D-box binding PAR bZIP transcription factor	Homo sapiens	73-76
22236721-6	2012	Further, arsenic enhanced cyclooxygenase-1 and cyclooxygenase-2 activities and tumor necrosis factor-alpha, interleukin-1beta and prostaglandin-E(2) production in hind paw muscle.	Arsenic	9-16	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	26-42
22310326-0	2012	Arsenic decreases RXRalpha-dependent transcription of CYP3A and suppresses immune regulators in hepatocytes.	Arsenic	0-7	retinoid X receptor alpha	Homo sapiens	18-26
22310326-0	2012	Arsenic decreases RXRalpha-dependent transcription of CYP3A and suppresses immune regulators in hepatocytes.	Arsenic	0-7	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	54-59
22310326-3	2012	Previous studies have shown that arsenic decreases expression of CYP3A, a critical drug metabolizing enzyme in human and rat liver.	Arsenic	33-40	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	65-70
22310326-9	2012	Previous studies have shown that arsenic in the concentration range of 2-5 muM affects CYP3A mRNA.	Arsenic	33-40	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	87-92
22330421-0	2012	E-cadherin polymorphisms and susceptibility to arsenic-related skin lesions in West Bengal, India.	Arsenic	47-54	cadherin 1	Homo sapiens	0-10
22330421-11	2012	CONCLUSIONS: This is the first study that indicates that CDH1 polymorphisms can contribute to the etiology of premalignant skin lesions in people chronically exposed to arsenic in drinking water, and that this gene may be a factor in individual susceptibility to cutaneous diseases.	Arsenic	169-176	cadherin 1	Homo sapiens	57-61
22476201-3	2012	OBJECTIVE: We investigated the cross-regulations among NRF2, NRF1, and KEAP1, a cullin-3-adapter protein that allows NRF2 to be ubiquinated and degraded by the proteasome complex, in arsenic-induced antioxidant responses.	Arsenic	183-190	NFE2 like bZIP transcription factor 2	Homo sapiens	55-59
22476201-3	2012	OBJECTIVE: We investigated the cross-regulations among NRF2, NRF1, and KEAP1, a cullin-3-adapter protein that allows NRF2 to be ubiquinated and degraded by the proteasome complex, in arsenic-induced antioxidant responses.	Arsenic	183-190	kelch like ECH associated protein 1	Homo sapiens	71-76
22476201-3	2012	OBJECTIVE: We investigated the cross-regulations among NRF2, NRF1, and KEAP1, a cullin-3-adapter protein that allows NRF2 to be ubiquinated and degraded by the proteasome complex, in arsenic-induced antioxidant responses.	Arsenic	183-190	NFE2 like bZIP transcription factor 2	Homo sapiens	117-121
22720593-2	2012	The results show, the order of the radical concentration of the seven contaminations is Ni2+ &gt; Benzene &gt; Cd &gt; Pb &gt; Cr6+ &gt; As &gt; Hg.	Arsenic	137-139	teratocarcinoma-derived growth factor 1 pseudogene 6	Homo sapiens	127-130
22448968-6	2012	The arsenic atom of both compounds cross-links cysteine residues 57 and 257 of human ANT1.	Arsenic	4-11	solute carrier family 25 member 4	Homo sapiens	85-89
22383794-0	2012	CEBPE activation in PML-RARA cells by arsenic.	Arsenic	38-45	CCAAT enhancer binding protein epsilon	Homo sapiens	0-5
22236721-6	2012	Further, arsenic enhanced cyclooxygenase-1 and cyclooxygenase-2 activities and tumor necrosis factor-alpha, interleukin-1beta and prostaglandin-E(2) production in hind paw muscle.	Arsenic	9-16	tumor necrosis factor	Rattus norvegicus	47-106
22236721-6	2012	Further, arsenic enhanced cyclooxygenase-1 and cyclooxygenase-2 activities and tumor necrosis factor-alpha, interleukin-1beta and prostaglandin-E(2) production in hind paw muscle.	Arsenic	9-16	interleukin 1 beta	Rattus norvegicus	108-125
22236721-8	2012	This may relate to arsenic-mediated local release of tumor necrosis factor-alpha and interleukin-1beta, which causes cyclooxygenase induction and consequent prostaglandin-E(2) release.	Arsenic	19-26	interleukin 1 beta	Rattus norvegicus	85-102
21947419-0	2012	SLC39A2 and FSIP1 polymorphisms as potential modifiers of arsenic-related bladder cancer.	Arsenic	58-65	solute carrier family 39 member 2	Homo sapiens	0-7
20851583-7	2012	The activities of glutathione peroxidase (GPx) and glutathione-S-transferase (GST) of As-treated group were found lower compared to the control and the Se-treated group.	Arsenic	86-88	hematopoietic prostaglandin D synthase	Rattus norvegicus	51-76
20851583-7	2012	The activities of glutathione peroxidase (GPx) and glutathione-S-transferase (GST) of As-treated group were found lower compared to the control and the Se-treated group.	Arsenic	86-88	hematopoietic prostaglandin D synthase	Rattus norvegicus	78-81
21947419-0	2012	SLC39A2 and FSIP1 polymorphisms as potential modifiers of arsenic-related bladder cancer.	Arsenic	58-65	fibrous sheath interacting protein 1	Homo sapiens	12-17
21947419-7	2012	The adjusted odds ratio (OR) for the FSIP1 polymorphism was 2.57 [95% confidence interval (CI) 1.13, 5.85] for heterozygote variants (AG) and 12.20 (95% CI 2.51, 59.30) for homozygote variants (GG) compared to homozygote wild types (AA) in the high arsenic group (greater than the 90th percentile), and unrelated in the low arsenic group (equal to or below the 90th percentile) (P for interaction = 0.002).	Arsenic	249-256	fibrous sheath interacting protein 1	Homo sapiens	37-42
21947419-7	2012	The adjusted odds ratio (OR) for the FSIP1 polymorphism was 2.57 [95% confidence interval (CI) 1.13, 5.85] for heterozygote variants (AG) and 12.20 (95% CI 2.51, 59.30) for homozygote variants (GG) compared to homozygote wild types (AA) in the high arsenic group (greater than the 90th percentile), and unrelated in the low arsenic group (equal to or below the 90th percentile) (P for interaction = 0.002).	Arsenic	324-331	fibrous sheath interacting protein 1	Homo sapiens	37-42
21947419-8	2012	For the SLC39A2 polymorphism, the adjusted ORs were 2.96 (95% CI 1.23, 7.15) and 2.91 (95% CI 1.00, 8.52) for heterozygote (TC) and homozygote (CC) variants compared to homozygote wild types (TT), respectively, and close to one in the low arsenic group (P for interaction = 0.03).	Arsenic	239-246	solute carrier family 39 member 2	Homo sapiens	8-15
22197475-6	2012	The ATP-binding cassette (ABC) transporter proteins, multidrug resistance protein 1 (MRP1/ABCC1) and the related protein MRP2 (ABCC2), are thought to play an important role in arsenic detoxification through the cellular efflux of arsenic-GSH conjugates.	Arsenic	176-183	ATP binding cassette subfamily B member 1	Homo sapiens	53-83
22434702-7	2012	Arsenic significantly (p &lt; 0.01) reduced mRNA expression of the superoxide dismutase 2 (SOD2) gene with respect to the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) gene.	Arsenic	0-7	superoxide dismutase 2	Rattus norvegicus	67-89
22434702-7	2012	Arsenic significantly (p &lt; 0.01) reduced mRNA expression of the superoxide dismutase 2 (SOD2) gene with respect to the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) gene.	Arsenic	0-7	superoxide dismutase 2	Rattus norvegicus	91-95
22434702-7	2012	Arsenic significantly (p &lt; 0.01) reduced mRNA expression of the superoxide dismutase 2 (SOD2) gene with respect to the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) gene.	Arsenic	0-7	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	122-162
22197475-6	2012	The ATP-binding cassette (ABC) transporter proteins, multidrug resistance protein 1 (MRP1/ABCC1) and the related protein MRP2 (ABCC2), are thought to play an important role in arsenic detoxification through the cellular efflux of arsenic-GSH conjugates.	Arsenic	176-183	ATP binding cassette subfamily C member 1	Homo sapiens	85-89
22197475-6	2012	The ATP-binding cassette (ABC) transporter proteins, multidrug resistance protein 1 (MRP1/ABCC1) and the related protein MRP2 (ABCC2), are thought to play an important role in arsenic detoxification through the cellular efflux of arsenic-GSH conjugates.	Arsenic	176-183	ATP binding cassette subfamily C member 1	Homo sapiens	90-95
22197475-6	2012	The ATP-binding cassette (ABC) transporter proteins, multidrug resistance protein 1 (MRP1/ABCC1) and the related protein MRP2 (ABCC2), are thought to play an important role in arsenic detoxification through the cellular efflux of arsenic-GSH conjugates.	Arsenic	176-183	ATP binding cassette subfamily C member 2	Homo sapiens	121-125
22197475-6	2012	The ATP-binding cassette (ABC) transporter proteins, multidrug resistance protein 1 (MRP1/ABCC1) and the related protein MRP2 (ABCC2), are thought to play an important role in arsenic detoxification through the cellular efflux of arsenic-GSH conjugates.	Arsenic	176-183	ATP binding cassette subfamily C member 2	Homo sapiens	127-132
22197475-6	2012	The ATP-binding cassette (ABC) transporter proteins, multidrug resistance protein 1 (MRP1/ABCC1) and the related protein MRP2 (ABCC2), are thought to play an important role in arsenic detoxification through the cellular efflux of arsenic-GSH conjugates.	Arsenic	230-237	ATP binding cassette subfamily B member 1	Homo sapiens	53-83
22197475-6	2012	The ATP-binding cassette (ABC) transporter proteins, multidrug resistance protein 1 (MRP1/ABCC1) and the related protein MRP2 (ABCC2), are thought to play an important role in arsenic detoxification through the cellular efflux of arsenic-GSH conjugates.	Arsenic	230-237	ATP binding cassette subfamily C member 1	Homo sapiens	85-89
22197475-6	2012	The ATP-binding cassette (ABC) transporter proteins, multidrug resistance protein 1 (MRP1/ABCC1) and the related protein MRP2 (ABCC2), are thought to play an important role in arsenic detoxification through the cellular efflux of arsenic-GSH conjugates.	Arsenic	230-237	ATP binding cassette subfamily C member 1	Homo sapiens	90-95
22197475-6	2012	The ATP-binding cassette (ABC) transporter proteins, multidrug resistance protein 1 (MRP1/ABCC1) and the related protein MRP2 (ABCC2), are thought to play an important role in arsenic detoxification through the cellular efflux of arsenic-GSH conjugates.	Arsenic	230-237	ATP binding cassette subfamily C member 2	Homo sapiens	121-125
22197475-6	2012	The ATP-binding cassette (ABC) transporter proteins, multidrug resistance protein 1 (MRP1/ABCC1) and the related protein MRP2 (ABCC2), are thought to play an important role in arsenic detoxification through the cellular efflux of arsenic-GSH conjugates.	Arsenic	230-237	ATP binding cassette subfamily C member 2	Homo sapiens	127-132
22245594-0	2012	Elevated levels of plasma Big endothelin-1 and its relation to hypertension and skin lesions in individuals exposed to arsenic.	Arsenic	119-126	endothelin 1	Homo sapiens	30-42
22245594-8	2012	Significant increase in Big ET-1 levels were observed with the increasing concentrations of As in drinking water, hair and nails.	Arsenic	92-94	endothelin 1	Homo sapiens	28-32
22245594-12	2012	Thus, this study demonstrated a novel dose-response relationship between As exposure and plasma Big ET-1 levels indicating the possible involvement of plasma Big ET-1 levels in As-induced hypertension and skin lesions.	Arsenic	73-75	endothelin 1	Homo sapiens	100-104
22245594-12	2012	Thus, this study demonstrated a novel dose-response relationship between As exposure and plasma Big ET-1 levels indicating the possible involvement of plasma Big ET-1 levels in As-induced hypertension and skin lesions.	Arsenic	73-75	endothelin 1	Homo sapiens	162-166
22245594-12	2012	Thus, this study demonstrated a novel dose-response relationship between As exposure and plasma Big ET-1 levels indicating the possible involvement of plasma Big ET-1 levels in As-induced hypertension and skin lesions.	Arsenic	177-179	endothelin 1	Homo sapiens	100-104
22245594-12	2012	Thus, this study demonstrated a novel dose-response relationship between As exposure and plasma Big ET-1 levels indicating the possible involvement of plasma Big ET-1 levels in As-induced hypertension and skin lesions.	Arsenic	177-179	endothelin 1	Homo sapiens	162-166
22178741-7	2012	In addition, inorganic arsenic also increases the deoxyguanosine oxidation level, alters the cytosine methylation state, decreases the activities of glutathione reductase and glucose-6-phosphate dehydrogenase, decreases the protein expression of NAD(P)H quinone oxidoreductase-1 (NQO-1) and increases the protein expression of specific protein 1 (Sp1) in bladder tissues.	Arsenic	23-30	glutathione reductase	Mus musculus	149-170
22215663-0	2012	Functional RNA interference (RNAi) screen identifies system A neutral amino acid transporter 2 (SNAT2) as a mediator of arsenic-induced endoplasmic reticulum stress.	Arsenic	120-127	solute carrier family 38 member 2	Homo sapiens	53-94
22215663-0	2012	Functional RNA interference (RNAi) screen identifies system A neutral amino acid transporter 2 (SNAT2) as a mediator of arsenic-induced endoplasmic reticulum stress.	Arsenic	120-127	solute carrier family 38 member 2	Homo sapiens	96-101
22215663-10	2012	These findings reveal SNAT2 as an important and specific mediator of arsenic-induced ER stress, and suggest a role for aberrant mTOR activation in arsenic-related human diseases.	Arsenic	69-76	solute carrier family 38 member 2	Homo sapiens	22-27
22215663-10	2012	These findings reveal SNAT2 as an important and specific mediator of arsenic-induced ER stress, and suggest a role for aberrant mTOR activation in arsenic-related human diseases.	Arsenic	147-154	mechanistic target of rapamycin kinase	Homo sapiens	128-132
22202168-0	2012	Changes in serum thioredoxin among individuals chronically exposed to arsenic in drinking water.	Arsenic	70-77	thioredoxin	Homo sapiens	17-28
22202168-3	2012	In this study, we examined the differences in the levels of serum thioredoxin1 (TRX1) among individuals exposed to different levels of arsenic in drinking water and detected early biomarkers of arsenic poisoning before the appearance of skin lesions.	Arsenic	135-142	thioredoxin	Homo sapiens	66-78
22202168-3	2012	In this study, we examined the differences in the levels of serum thioredoxin1 (TRX1) among individuals exposed to different levels of arsenic in drinking water and detected early biomarkers of arsenic poisoning before the appearance of skin lesions.	Arsenic	135-142	thioredoxin	Homo sapiens	80-84
22202168-7	2012	Our results showed that the levels of serum TRX1 in arsenicosis patients were significantly higher than that of the subjects who were chronically exposed to arsenic, but without skin lesions.	Arsenic	52-59	thioredoxin	Homo sapiens	44-48
22178741-7	2012	In addition, inorganic arsenic also increases the deoxyguanosine oxidation level, alters the cytosine methylation state, decreases the activities of glutathione reductase and glucose-6-phosphate dehydrogenase, decreases the protein expression of NAD(P)H quinone oxidoreductase-1 (NQO-1) and increases the protein expression of specific protein 1 (Sp1) in bladder tissues.	Arsenic	23-30	NAD(P)H dehydrogenase, quinone 1	Mus musculus	246-278
22178533-14	2012	Subsequent pathway analysis further revealed a gene network involving interleukin 1-alpha (IL1A) in mediating the arsenic-resistant phenotype.	Arsenic	114-121	interleukin 1 alpha	Homo sapiens	70-89
22178533-14	2012	Subsequent pathway analysis further revealed a gene network involving interleukin 1-alpha (IL1A) in mediating the arsenic-resistant phenotype.	Arsenic	114-121	interleukin 1 alpha	Homo sapiens	91-95
22178741-7	2012	In addition, inorganic arsenic also increases the deoxyguanosine oxidation level, alters the cytosine methylation state, decreases the activities of glutathione reductase and glucose-6-phosphate dehydrogenase, decreases the protein expression of NAD(P)H quinone oxidoreductase-1 (NQO-1) and increases the protein expression of specific protein 1 (Sp1) in bladder tissues.	Arsenic	23-30	NAD(P)H dehydrogenase, quinone 1	Mus musculus	280-285
22178741-7	2012	In addition, inorganic arsenic also increases the deoxyguanosine oxidation level, alters the cytosine methylation state, decreases the activities of glutathione reductase and glucose-6-phosphate dehydrogenase, decreases the protein expression of NAD(P)H quinone oxidoreductase-1 (NQO-1) and increases the protein expression of specific protein 1 (Sp1) in bladder tissues.	Arsenic	23-30	trans-acting transcription factor 1	Mus musculus	327-345
22202168-8	2012	A positive correlation was seen between the levels of serum TRX1 and the total water arsenic intake or the levels of urinary arsenic species.	Arsenic	85-92	thioredoxin	Homo sapiens	60-64
22202168-8	2012	A positive correlation was seen between the levels of serum TRX1 and the total water arsenic intake or the levels of urinary arsenic species.	Arsenic	125-132	thioredoxin	Homo sapiens	60-64
22493600-1	2012	BACKGROUND/AIMS: Arsenic (As) is linked to insulin resistance in animal studies, but the effect of low-level As exposure on the prevalence of diabetes in humans is uncertain.	Arsenic	17-24	insulin	Homo sapiens	43-50
22202168-9	2012	The results of this study indicate that arsenic exposure could significantly change the levels of human serum TRX1, which can be detected before arsenic-specific dermatological symptoms occur.	Arsenic	40-47	thioredoxin	Homo sapiens	110-114
22202168-9	2012	The results of this study indicate that arsenic exposure could significantly change the levels of human serum TRX1, which can be detected before arsenic-specific dermatological symptoms occur.	Arsenic	145-152	thioredoxin	Homo sapiens	110-114
22131352-7	2012	In addition, NPR-C-, AT1, and M2 receptor-mediated inhibition of AC and Gialpha protein expression was enhanced in AS-treated cells, whereas NPR-A-mediated cyclic GMP (cGMP) formation and Gsalpha-mediated stimulation of AC were significantly reduced.	Arsenic	115-117	natriuretic peptide receptor 3	Mus musculus	13-18
22131352-7	2012	In addition, NPR-C-, AT1, and M2 receptor-mediated inhibition of AC and Gialpha protein expression was enhanced in AS-treated cells, whereas NPR-A-mediated cyclic GMP (cGMP) formation and Gsalpha-mediated stimulation of AC were significantly reduced.	Arsenic	115-117	angiotensin II receptor, type 1a	Mus musculus	21-24
22493600-1	2012	BACKGROUND/AIMS: Arsenic (As) is linked to insulin resistance in animal studies, but the effect of low-level As exposure on the prevalence of diabetes in humans is uncertain.	Arsenic	26-28	insulin	Homo sapiens	43-50
22281350-9	2012	We concluded that replacing AS with SS had negative effects on milk yield, whereas dry matter intake, energy-corrected milk, and milk efficiency were similar.	Arsenic	28-30	Weaning weight-maternal milk	Bos taurus	63-67
21670987-8	2012	Trace levels of As, Cd, Cr, Co, Cu, Fe, Pb, Mn, Mo, Ni, V, Zn, Sr, and Hg were detected in ground, spring, and tap water sources using inductively coupled plasma atomic emission spectrometry, and their levels were below WHO and Japanese water quality standard limits.	Arsenic	16-18	nuclear RNA export factor 1	Homo sapiens	111-114
21503876-0	2012	MicroRNA-181b and microRNA-9 mediate arsenic-induced angiogenesis via NRP1.	Arsenic	37-44	neuropilin 1	Homo sapiens	70-74
21503876-10	2012	Data from the transwell migration assay and the tube-formation assay indicated that miR-9 and mir-181b inhibited the arsenic-induced EA.hy926 cell migration and tube formation by targeting NRP1.	Arsenic	117-124	neuropilin 1	Homo sapiens	189-193
22801079-0	2012	[Changes of cdk5, p35 and p53 gene expression levels in arsenic-induced neural cell apoptosis].	Arsenic	56-63	cyclin-dependent kinase 5	Rattus norvegicus	12-16
22801079-0	2012	[Changes of cdk5, p35 and p53 gene expression levels in arsenic-induced neural cell apoptosis].	Arsenic	56-63	cyclin-dependent kinase 5 regulatory subunit 1	Rattus norvegicus	18-21
22801079-0	2012	[Changes of cdk5, p35 and p53 gene expression levels in arsenic-induced neural cell apoptosis].	Arsenic	56-63	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	26-29
22136492-3	2012	In addition, GST-T1 and GST-M1 null genotypes have been shown to be responsible for interindividual variations in the metabolism of arsenic, a known human carcinogen.	Arsenic	132-139	glutathione S-transferase theta 1	Homo sapiens	13-30
22272800-11	2012	Furthermore, the total arsenic concentrations of HMW-F in BM plasma were much higher than those in PB plasma.	Arsenic	23-30	cilia and flagella associated protein 97	Homo sapiens	49-52
22272800-13	2012	These results may further provide not only significance of clinical application of ATO, but also a new insight into host defense mechanisms in APL patients undergoing ATO treatment, since HMW proteins-bound arsenic complex could be thought to protect BM from the attack of free arsenic species.	Arsenic	207-214	cilia and flagella associated protein 97	Homo sapiens	188-191
22272800-13	2012	These results may further provide not only significance of clinical application of ATO, but also a new insight into host defense mechanisms in APL patients undergoing ATO treatment, since HMW proteins-bound arsenic complex could be thought to protect BM from the attack of free arsenic species.	Arsenic	278-285	cilia and flagella associated protein 97	Homo sapiens	188-191
22119299-3	2012	When grown on cadmium or arsenic (arsenite/arsenate), Dual-gene transgenic lines accumulated over 2-10 folds cadmium/arsenite and 2-3 folds arsenate than wild type or plants expressing AsPCS1 or YCF1 alone.	Arsenic	25-32	hypothetical protein	Arabidopsis thaliana	195-199
22123111-5	2012	Thereto Mn is added to excess (~1 muM Mn) to the water leading to a Mn coating during the deposition of As on the electrode at a deposition potential of -1.3 V. Deposition of As(0) from dissolved As(V) caused elemental Mn to be re-oxidised to Mn(II) in a 1:1 molar ratio providing evidence for the reaction mechanism.	Arsenic	175-177	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	196-201
22938487-6	2012	Results indicated that Th1 cytokines such as TNF-alpha, IFNgamma, IL12 and the Th2 cytokines such as IL4, IL6, IL10 which were respectively downregulated and upregulated following arsenic induction were more efficiently restored to their near normal levels by T11TS alone in comparison with the combined regimen.	Arsenic	180-187	negative elongation factor complex member C/D, Th1l	Mus musculus	23-26
22100662-9	2012	Specifically, three hypotheses may explain the role of GSTO1-1 in the pathophysiology of AD: the antioxidant activity of GSTO1-1 may protect brain tissue against oxidative stress; GSTO1-1 activity regulate interleukin-1beta activation and its genetic variation may act to modulate inflammation in AD; GSTO1-1 is involved in the arsenic biotransformation pathway and gene polymorphisms may be implicated in the modulation of arsenic neurotoxicity.	Arsenic	328-335	glutathione S-transferase omega 1	Homo sapiens	55-62
22938487-6	2012	Results indicated that Th1 cytokines such as TNF-alpha, IFNgamma, IL12 and the Th2 cytokines such as IL4, IL6, IL10 which were respectively downregulated and upregulated following arsenic induction were more efficiently restored to their near normal levels by T11TS alone in comparison with the combined regimen.	Arsenic	180-187	heart and neural crest derivatives expressed 2	Mus musculus	79-82
22100662-9	2012	Specifically, three hypotheses may explain the role of GSTO1-1 in the pathophysiology of AD: the antioxidant activity of GSTO1-1 may protect brain tissue against oxidative stress; GSTO1-1 activity regulate interleukin-1beta activation and its genetic variation may act to modulate inflammation in AD; GSTO1-1 is involved in the arsenic biotransformation pathway and gene polymorphisms may be implicated in the modulation of arsenic neurotoxicity.	Arsenic	328-335	glutathione S-transferase omega 1	Homo sapiens	121-128
22100662-9	2012	Specifically, three hypotheses may explain the role of GSTO1-1 in the pathophysiology of AD: the antioxidant activity of GSTO1-1 may protect brain tissue against oxidative stress; GSTO1-1 activity regulate interleukin-1beta activation and its genetic variation may act to modulate inflammation in AD; GSTO1-1 is involved in the arsenic biotransformation pathway and gene polymorphisms may be implicated in the modulation of arsenic neurotoxicity.	Arsenic	328-335	glutathione S-transferase omega 1	Homo sapiens	121-128
22100662-9	2012	Specifically, three hypotheses may explain the role of GSTO1-1 in the pathophysiology of AD: the antioxidant activity of GSTO1-1 may protect brain tissue against oxidative stress; GSTO1-1 activity regulate interleukin-1beta activation and its genetic variation may act to modulate inflammation in AD; GSTO1-1 is involved in the arsenic biotransformation pathway and gene polymorphisms may be implicated in the modulation of arsenic neurotoxicity.	Arsenic	328-335	glutathione S-transferase omega 1	Homo sapiens	121-128
22938487-6	2012	Results indicated that Th1 cytokines such as TNF-alpha, IFNgamma, IL12 and the Th2 cytokines such as IL4, IL6, IL10 which were respectively downregulated and upregulated following arsenic induction were more efficiently restored to their near normal levels by T11TS alone in comparison with the combined regimen.	Arsenic	180-187	interleukin 4	Mus musculus	101-104
23123458-3	2012	In 2002, arsenite (+3 oxidation state) methyltransferase (As3MT) was discovered to be an enzyme responsible for arsenic methylation.	Arsenic	112-119	arsenite methyltransferase	Homo sapiens	58-63
22938487-6	2012	Results indicated that Th1 cytokines such as TNF-alpha, IFNgamma, IL12 and the Th2 cytokines such as IL4, IL6, IL10 which were respectively downregulated and upregulated following arsenic induction were more efficiently restored to their near normal levels by T11TS alone in comparison with the combined regimen.	Arsenic	180-187	interleukin 6	Mus musculus	106-109
22938487-6	2012	Results indicated that Th1 cytokines such as TNF-alpha, IFNgamma, IL12 and the Th2 cytokines such as IL4, IL6, IL10 which were respectively downregulated and upregulated following arsenic induction were more efficiently restored to their near normal levels by T11TS alone in comparison with the combined regimen.	Arsenic	180-187	interleukin 10	Mus musculus	111-115
23123458-4	2012	This review focuses on current information on the function, genetic polymorphism, and alternative splicing of As3MT, all of which contribute to arsenic metabolism and toxicity.	Arsenic	144-151	arsenite methyltransferase	Homo sapiens	110-115
23115478-5	2012	Molecular network construction for arsenic upregulated genes TNFSF18 (tumor necrosis factor [ligand] superfamily member 18) and IL1R2 (interleukin 1 Receptor, type 2) revealed subnetwork interconnections to E2F4, an oncogenic transcription factor, predominantly expressed at the onset of keratinocyte differentiation.	Arsenic	35-42	TNF superfamily member 18	Homo sapiens	61-68
23115478-5	2012	Molecular network construction for arsenic upregulated genes TNFSF18 (tumor necrosis factor [ligand] superfamily member 18) and IL1R2 (interleukin 1 Receptor, type 2) revealed subnetwork interconnections to E2F4, an oncogenic transcription factor, predominantly expressed at the onset of keratinocyte differentiation.	Arsenic	35-42	TNF superfamily member 18	Homo sapiens	70-122
23115478-5	2012	Molecular network construction for arsenic upregulated genes TNFSF18 (tumor necrosis factor [ligand] superfamily member 18) and IL1R2 (interleukin 1 Receptor, type 2) revealed subnetwork interconnections to E2F4, an oncogenic transcription factor, predominantly expressed at the onset of keratinocyte differentiation.	Arsenic	35-42	interleukin 1 receptor type 2	Homo sapiens	128-133
23115478-5	2012	Molecular network construction for arsenic upregulated genes TNFSF18 (tumor necrosis factor [ligand] superfamily member 18) and IL1R2 (interleukin 1 Receptor, type 2) revealed subnetwork interconnections to E2F4, an oncogenic transcription factor, predominantly expressed at the onset of keratinocyte differentiation.	Arsenic	35-42	interleukin 1 receptor type 2	Homo sapiens	135-165
23115478-5	2012	Molecular network construction for arsenic upregulated genes TNFSF18 (tumor necrosis factor [ligand] superfamily member 18) and IL1R2 (interleukin 1 Receptor, type 2) revealed subnetwork interconnections to E2F4, an oncogenic transcription factor, predominantly expressed at the onset of keratinocyte differentiation.	Arsenic	35-42	E2F transcription factor 4	Homo sapiens	207-211
21848401-4	2012	Arsenic only exposure decreased hepatic superoxide dismutase (SOD), catalase activities, and the level of nonprotein-soluble thiol (NPSH), with a concomitant increase in thiobarbituric acid reactive substances (TBARS) and conjugated dienes (CDs) in the liver.	Arsenic	0-7	catalase	Rattus norvegicus	68-76
21954225-0	2012	Akt activation is responsible for enhanced migratory and invasive behavior of arsenic-transformed human bronchial epithelial cells.	Arsenic	78-85	AKT serine/threonine kinase 1	Homo sapiens	0-3
21919981-4	2012	Two ABCC-type transporters, AtABCC1 and AtABCC2, that play a key role in arsenic detoxification, have recently been identified in Arabidopsis thaliana.	Arsenic	73-80	multidrug resistance-associated protein 1	Arabidopsis thaliana	28-35
21898718-1	2012	The objective of this study was to determine the effect of fluoride (F) and arsenic (As) on the activity of acetylcholinesterase (AChE), a critically important nervous system enzyme, and to test the protective role of buffalo epiphyseal (pineal) proteins (BEP) in rats.	Arsenic	76-83	acetylcholinesterase	Rattus norvegicus	108-128
21898718-1	2012	The objective of this study was to determine the effect of fluoride (F) and arsenic (As) on the activity of acetylcholinesterase (AChE), a critically important nervous system enzyme, and to test the protective role of buffalo epiphyseal (pineal) proteins (BEP) in rats.	Arsenic	76-83	acetylcholinesterase	Rattus norvegicus	130-134
21898718-1	2012	The objective of this study was to determine the effect of fluoride (F) and arsenic (As) on the activity of acetylcholinesterase (AChE), a critically important nervous system enzyme, and to test the protective role of buffalo epiphyseal (pineal) proteins (BEP) in rats.	Arsenic	85-87	acetylcholinesterase	Rattus norvegicus	108-128
21898718-1	2012	The objective of this study was to determine the effect of fluoride (F) and arsenic (As) on the activity of acetylcholinesterase (AChE), a critically important nervous system enzyme, and to test the protective role of buffalo epiphyseal (pineal) proteins (BEP) in rats.	Arsenic	85-87	acetylcholinesterase	Rattus norvegicus	130-134
22591283-3	2012	Results of the present study suggested that arsenic administration in rats caused apoptosis by elevating morphologic alterations, TUNEL-positive nuclei, caspase-3 activity, and DNA damage and by reducing cell adhesion and cell proliferation in a time-dependent manner.	Arsenic	44-51	caspase 3	Rattus norvegicus	153-162
22028001-0	2012	Individual variations in arsenic metabolism in Vietnamese: the association with arsenic exposure and GSTP1 genetic polymorphism.	Arsenic	25-32	glutathione S-transferase pi 1	Homo sapiens	101-106
22028001-1	2012	We investigated the association of As exposure and genetic polymorphism in glutathione S-transferase pi1 (GSTP1) with As metabolism in 190 local residents from the As contaminated groundwater areas in the Red River Delta, Vietnam.	Arsenic	118-120	glutathione S-transferase pi 1	Homo sapiens	75-104
22028001-1	2012	We investigated the association of As exposure and genetic polymorphism in glutathione S-transferase pi1 (GSTP1) with As metabolism in 190 local residents from the As contaminated groundwater areas in the Red River Delta, Vietnam.	Arsenic	118-120	glutathione S-transferase pi 1	Homo sapiens	106-111
22028001-6	2012	In the high As exposure group, As(III)/As(V) ratios in the urine of wild type of GSTP1 Ile105Val were significantly higher than those of the hetero type, while the opposite trend was observed for M/I.	Arsenic	12-14	glutathione S-transferase pi 1	Homo sapiens	81-86
22362285-2	2012	Arsenic trioxide (As(2)O(3)) is known to degrade PML protein and has been used for the treatment of patients with acute PML.	Arsenic	18-20	PML nuclear body scaffold	Homo sapiens	49-52
22362285-2	2012	Arsenic trioxide (As(2)O(3)) is known to degrade PML protein and has been used for the treatment of patients with acute PML.	Arsenic	18-20	PML nuclear body scaffold	Homo sapiens	120-123
22120617-7	2012	Collectively, the present study reveals that a mechanism underlying arsenic-induced cell proliferation may be through induction and activation of VEGF signaling, and this may subsequently contribute to tumor formation.	Arsenic	68-75	vascular endothelial growth factor A	Homo sapiens	146-150
22489166-5	2012	Here, we review the recent advances in understanding of arsenic and antimony transport pathways in eukaryotes, including a dual role of aquaglyceroporins in uptake and efflux of metalloids, elucidation of arsenic transport mechanism by the yeast Acr3 transporter and its role in arsenic hyperaccumulation in ferns, identification of vacuolar transporters of arsenic-phytochelatin complexes in plants and forms of arsenic substrates recognized by mammalian ABC transporters.	Arsenic	56-63	Arr3p	Saccharomyces cerevisiae S288C	246-250
21391215-0	2012	Arsenic induced progesterone production in a caspase-3-dependent manner and changed redox status in preovulatory granulosa cells.	Arsenic	0-7	caspase 3	Rattus norvegicus	45-54
22429367-9	2012	The frequency of the PTGS2 G765C mutation was significantly higher in the AR/ASR groups versus the AS group.	Arsenic	77-79	prostaglandin-endoperoxide synthase 2	Homo sapiens	21-26
21919981-4	2012	Two ABCC-type transporters, AtABCC1 and AtABCC2, that play a key role in arsenic detoxification, have recently been identified in Arabidopsis thaliana.	Arsenic	73-80	multidrug resistance-associated protein 2	Arabidopsis thaliana	40-47
22719926-2	2012	Transplacental arsenic exposure promotes atherogenesis in apolipoprotein E-knockout (ApoE(-/-)) mice.	Arsenic	15-22	apolipoprotein E	Mus musculus	85-89
22719926-8	2012	We identified an arsenic exposure related 51-gene signature at PND1 and PND70 with several hubs of interaction (Hspa8, IgM and Hnf4a).	Arsenic	17-24	heat shock protein 8	Mus musculus	112-117
22719926-8	2012	We identified an arsenic exposure related 51-gene signature at PND1 and PND70 with several hubs of interaction (Hspa8, IgM and Hnf4a).	Arsenic	17-24	immunoglobulin heavy constant mu	Mus musculus	119-122
22719926-8	2012	We identified an arsenic exposure related 51-gene signature at PND1 and PND70 with several hubs of interaction (Hspa8, IgM and Hnf4a).	Arsenic	17-24	hepatic nuclear factor 4, alpha	Mus musculus	127-132
22736905-5	2012	Distribution of arsenic in animal body indicates that major portion of arsenic was eliminated through feces, urine, and milk.	Arsenic	16-23	Weaning weight-maternal milk	Bos taurus	120-124
22056243-6	2012	As discussed below, arsenic binding, oxidation, sumoylation on PML nuclear bodies, and RNF4-mediated ubiquitination all contribute to the As(2)O(3)-triggered catabolism of PML/RARA.	Arsenic	20-27	PML nuclear body scaffold	Homo sapiens	172-175
22056243-6	2012	As discussed below, arsenic binding, oxidation, sumoylation on PML nuclear bodies, and RNF4-mediated ubiquitination all contribute to the As(2)O(3)-triggered catabolism of PML/RARA.	Arsenic	20-27	retinoic acid receptor alpha	Homo sapiens	176-180
22558281-0	2012	Arsenic induces functional re-expression of estrogen receptor alpha by demethylation of DNA in estrogen receptor-negative human breast cancer.	Arsenic	0-7	estrogen receptor 1	Homo sapiens	44-67
22488606-7	2012	The distribution of As levels detected, based on the NIS guideline, and expressed as a percentage thereof, was highest in the tubewells of the Bara district (3.8%), followed by the Kailali district (3.4%).	Arsenic	20-22	lin-9 DREAM MuvB core complex component	Homo sapiens	143-147
22104380-0	2012	The relationship between obesity, insulin and arsenic methylation capability in Taiwan adolescents.	Arsenic	46-53	insulin	Homo sapiens	34-41
22104380-5	2012	Participants with obesity accompanied by high insulin levels had higher inorganic arsenic, significantly higher MMA percentage and significantly lower DMA percentage than those with obesity and low insulin levels.	Arsenic	82-89	insulin	Homo sapiens	46-53
22104380-6	2012	It seems children with obesity and high insulin levels had lower arsenic methylation capacity than those with obesity and low insulin.	Arsenic	65-72	insulin	Homo sapiens	40-47
22736905-5	2012	Distribution of arsenic in animal body indicates that major portion of arsenic was eliminated through feces, urine, and milk.	Arsenic	71-78	Weaning weight-maternal milk	Bos taurus	120-124
22736905-8	2012	Consumption of egg, agricultural produces grown in contaminated soil, and milk might have produced arsenicosis and may be considered as alternative source of arsenic contamination.	Arsenic	99-106	Weaning weight-maternal milk	Bos taurus	74-78
22018869-3	2011	Microcosm experiments using sediments from arsenic contaminated shallow alluvial aquifers in the blackfoot disease endemic area showed simultaneous microbial reduction of Fe(III) and As(V).	Arsenic	43-50	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	183-188
22678215-1	2012	Subsurface arsenic and iron removal (SAR/SIR) is a novel technology to remove arsenic, iron and other groundwater components by using the subsoil.	Arsenic	11-18	sarcosine dehydrogenase	Homo sapiens	37-40
22678215-1	2012	Subsurface arsenic and iron removal (SAR/SIR) is a novel technology to remove arsenic, iron and other groundwater components by using the subsoil.	Arsenic	78-85	sarcosine dehydrogenase	Homo sapiens	37-40
21982800-0	2011	The polymorphisms of P53 codon 72 and MDM2 SNP309 and renal cell carcinoma risk in a low arsenic exposure area.	Arsenic	89-96	tumor protein p53	Homo sapiens	21-24
21982800-5	2011	RCC patients with the p53Arg/Arg genotype had a signicantly low percentage of inorganic arsenic, a low percentage of monomethylarsonic acid (MMA), and a high percentage of dimethylarsinic acid (DMA), which indicates efcient arsenic methylation capacity.	Arsenic	88-95	tumor protein p53	Homo sapiens	22-25
22391311-5	2012	Recent evidence has shown that arsenic can inhibit the Hedgehog pathway by inhibiting GLI proteins.	Arsenic	31-38	GLI family zinc finger 1	Homo sapiens	86-89
21982800-6	2011	Subjects with the p53 Arg/Pro + Pro/Pro genotype or MDM2 SNP309 TG+GG genotype, in conjunction with high urinary total arsenic (&gt;=14.02mug/L), had a signicantly higher RCC risk than those with the p53 Arg/Arg or MDM2 SNP309 TT genotypes and low urinary total arsenic.	Arsenic	119-126	MDM2 proto-oncogene	Homo sapiens	52-56
21982800-7	2011	Taken together, this is the first study to show that a variant genotype of p53 Arg(72)Pro or MDM2 SNP309 may modify the arsenic-related RCC risk even in a non-obvious arsenic exposure area.	Arsenic	120-127	tumor protein p53	Homo sapiens	75-78
21982800-7	2011	Taken together, this is the first study to show that a variant genotype of p53 Arg(72)Pro or MDM2 SNP309 may modify the arsenic-related RCC risk even in a non-obvious arsenic exposure area.	Arsenic	120-127	MDM2 proto-oncogene	Homo sapiens	93-97
21982800-7	2011	Taken together, this is the first study to show that a variant genotype of p53 Arg(72)Pro or MDM2 SNP309 may modify the arsenic-related RCC risk even in a non-obvious arsenic exposure area.	Arsenic	167-174	tumor protein p53	Homo sapiens	75-78
22199276-8	2011	As(2)O(3) and arsenic acid induced apoptotic cell morphology and increased caspase-3/7 activity in the leukemia cells.	Arsenic	0-2	caspase 3	Homo sapiens	75-84
21945498-0	2011	Association of heme oxygenase-1 GT-repeat polymorphism with blood pressure phenotypes and its relevance to future cardiovascular mortality risk: an observation based on arsenic-exposed individuals.	Arsenic	169-176	heme oxygenase 1	Homo sapiens	15-31
22199276-4	2011	Cellular caspase-3/7 activities were measured after arsenic treatment.	Arsenic	52-59	caspase 3	Homo sapiens	9-18
21839772-5	2011	Simultaneous treatment with arsenic and curcumin (100mg/kg body weight, p.o., 28 days) increased learning and memory performance associated with increased binding of (3)H-QNB in hippocampus (54%), frontal cortex (25%) and activity of acetylcholinesterase in hippocampus (41%) and frontal cortex (29%) as compared to arsenic treated rats.	Arsenic	28-35	acetylcholinesterase	Rattus norvegicus	234-254
21918036-12	2011	These results suggest that MRP1 is an important cellular protective pathway for the highly toxic MMA(III) and have implications for environmental and clinical exposure to arsenic.	Arsenic	171-178	ATP binding cassette subfamily C member 1	Homo sapiens	27-31
22198754-2	2011	This study presents an overview of the arsenic contamination problems in Vietnam, Cambodia, Lao People"s Democratic Republic and Thailand.	Arsenic	39-46	interleukin 4 induced 1	Homo sapiens	92-95
21622483-0	2011	Effects of low-level arsenic exposure on urinary N-acetyl-beta-D-glucosaminidase activity.	Arsenic	21-28	O-GlcNAcase	Homo sapiens	49-80
21622483-3	2011	The study subjects were divided into 4 groups according to urinary NAG activity and seafood consumption prior to urine sampling, and the correlation between arsenic concentration and urinary NAG activity was tested for each group.	Arsenic	157-164	O-GlcNAcase	Homo sapiens	191-194
21622483-6	2011	The correlation between urinary arsenic concentration and NAG activity in urine was significant only in subjects who did not consume seafood within 3 days prior to urine sampling and whose urinary NAG activity was 7.44 U/g creatinine (75th percentile) or higher.	Arsenic	32-39	O-GlcNAcase	Homo sapiens	58-61
21622483-6	2011	The correlation between urinary arsenic concentration and NAG activity in urine was significant only in subjects who did not consume seafood within 3 days prior to urine sampling and whose urinary NAG activity was 7.44 U/g creatinine (75th percentile) or higher.	Arsenic	32-39	O-GlcNAcase	Homo sapiens	197-200
21622483-7	2011	The urinary arsenic concentration was a significant determinant of urinary NAG activity in subjects with NAG activity higher than 7.44 U/g creatinine and especially in those who had not consumed seafood recently.	Arsenic	12-19	O-GlcNAcase	Homo sapiens	75-78
21622483-7	2011	The urinary arsenic concentration was a significant determinant of urinary NAG activity in subjects with NAG activity higher than 7.44 U/g creatinine and especially in those who had not consumed seafood recently.	Arsenic	12-19	O-GlcNAcase	Homo sapiens	105-108
21911445-4	2011	In this study, we showed that subchronic arsenic exposure to SKH-1 mice induced unfolded protein response (UPR) signaling regulated by proteins, inositol-requiring enzyme-1 (IRE1), PKR-like endoplasmic reticulum kinase (PERK) and activating transcription factor 6 (ATF6).	Arsenic	41-48	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	145-172
21911445-4	2011	In this study, we showed that subchronic arsenic exposure to SKH-1 mice induced unfolded protein response (UPR) signaling regulated by proteins, inositol-requiring enzyme-1 (IRE1), PKR-like endoplasmic reticulum kinase (PERK) and activating transcription factor 6 (ATF6).	Arsenic	41-48	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	174-178
21911445-4	2011	In this study, we showed that subchronic arsenic exposure to SKH-1 mice induced unfolded protein response (UPR) signaling regulated by proteins, inositol-requiring enzyme-1 (IRE1), PKR-like endoplasmic reticulum kinase (PERK) and activating transcription factor 6 (ATF6).	Arsenic	41-48	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	181-218
21911445-4	2011	In this study, we showed that subchronic arsenic exposure to SKH-1 mice induced unfolded protein response (UPR) signaling regulated by proteins, inositol-requiring enzyme-1 (IRE1), PKR-like endoplasmic reticulum kinase (PERK) and activating transcription factor 6 (ATF6).	Arsenic	41-48	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	220-224
21911445-4	2011	In this study, we showed that subchronic arsenic exposure to SKH-1 mice induced unfolded protein response (UPR) signaling regulated by proteins, inositol-requiring enzyme-1 (IRE1), PKR-like endoplasmic reticulum kinase (PERK) and activating transcription factor 6 (ATF6).	Arsenic	41-48	activating transcription factor 6	Mus musculus	230-263
21911445-4	2011	In this study, we showed that subchronic arsenic exposure to SKH-1 mice induced unfolded protein response (UPR) signaling regulated by proteins, inositol-requiring enzyme-1 (IRE1), PKR-like endoplasmic reticulum kinase (PERK) and activating transcription factor 6 (ATF6).	Arsenic	41-48	activating transcription factor 6	Mus musculus	265-269
21911445-6	2011	Arsenic induced IRE1 phosphorylation which resulted in augmented splicing of X-box binding protein 1 (XBP-1) leading to its migration to the nucleus, and also enhanced transcriptional activation of downstream target proteins.	Arsenic	0-7	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	16-20
21911445-6	2011	Arsenic induced IRE1 phosphorylation which resulted in augmented splicing of X-box binding protein 1 (XBP-1) leading to its migration to the nucleus, and also enhanced transcriptional activation of downstream target proteins.	Arsenic	0-7	X-box binding protein 1	Homo sapiens	77-100
21911445-6	2011	Arsenic induced IRE1 phosphorylation which resulted in augmented splicing of X-box binding protein 1 (XBP-1) leading to its migration to the nucleus, and also enhanced transcriptional activation of downstream target proteins.	Arsenic	0-7	X-box binding protein 1	Homo sapiens	102-107
21911445-7	2011	Hyperphosphorylation of PERK which induces eukaryotic translation initial factor 2alpha (eIF2alpha) in a phosphorylation-dependent manner enhanced translation of ATF4, in addition to augmenting proteolytic activation of ATF6 in arsenic-treated skin.	Arsenic	228-235	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	24-28
21911445-7	2011	Hyperphosphorylation of PERK which induces eukaryotic translation initial factor 2alpha (eIF2alpha) in a phosphorylation-dependent manner enhanced translation of ATF4, in addition to augmenting proteolytic activation of ATF6 in arsenic-treated skin.	Arsenic	228-235	eukaryotic translation initiation factor 2A	Homo sapiens	89-98
21911445-7	2011	Hyperphosphorylation of PERK which induces eukaryotic translation initial factor 2alpha (eIF2alpha) in a phosphorylation-dependent manner enhanced translation of ATF4, in addition to augmenting proteolytic activation of ATF6 in arsenic-treated skin.	Arsenic	228-235	activating transcription factor 4	Homo sapiens	162-166
21911445-7	2011	Hyperphosphorylation of PERK which induces eukaryotic translation initial factor 2alpha (eIF2alpha) in a phosphorylation-dependent manner enhanced translation of ATF4, in addition to augmenting proteolytic activation of ATF6 in arsenic-treated skin.	Arsenic	228-235	activating transcription factor 6	Homo sapiens	220-224
21911445-10	2011	In addition, arsenic induced inflammation-related p38/MAPKAPK-2 MAPK signaling and alterations in Th-1/Th-2/Th-17 cytokines/chemokines and their receptors.	Arsenic	13-20	mitogen-activated protein kinase 14	Homo sapiens	50-53
21911445-10	2011	In addition, arsenic induced inflammation-related p38/MAPKAPK-2 MAPK signaling and alterations in Th-1/Th-2/Th-17 cytokines/chemokines and their receptors.	Arsenic	13-20	MAPK activated protein kinase 2	Homo sapiens	54-63
21911445-10	2011	In addition, arsenic induced inflammation-related p38/MAPKAPK-2 MAPK signaling and alterations in Th-1/Th-2/Th-17 cytokines/chemokines and their receptors.	Arsenic	13-20	negative elongation factor complex member C/D	Homo sapiens	98-102
21945491-7	2011	Both intracellular arsenic accumulation and its cytotoxicity in the C-cells were significantly abrogated by sorbitol, a competitive AQP9 inhibitor, in a dose-dependent manner.	Arsenic	19-26	aquaporin 9	Homo sapiens	132-136
21945126-2	2011	Fluorescence quenching was used to study the interaction of these Amantadine Schiff-Bases (AS, AS-5-C and AS-o-V) with bovine serum albumin (BSA).	Arsenic	91-93	albumin	Homo sapiens	126-139
21945491-12	2011	These results suggest that AQP9 and MRP2 are involved in controlling arsenic accumulation in these normal cells, which then contribute to differential sensitivity to As(III) cytotoxicity between these cells.	Arsenic	69-76	aquaporin 9	Homo sapiens	27-31
21945491-12	2011	These results suggest that AQP9 and MRP2 are involved in controlling arsenic accumulation in these normal cells, which then contribute to differential sensitivity to As(III) cytotoxicity between these cells.	Arsenic	69-76	ATP binding cassette subfamily C member 2	Homo sapiens	36-40
21934131-1	2011	Arsenic (+3 oxidation state) methyltransferase (As3mt) catalyzes methylation of inorganic arsenic (iAs) producing a number of methylated arsenic metabolites.	Arsenic	90-97	arsenite methyltransferase	Mus musculus	0-46
21934131-1	2011	Arsenic (+3 oxidation state) methyltransferase (As3mt) catalyzes methylation of inorganic arsenic (iAs) producing a number of methylated arsenic metabolites.	Arsenic	90-97	arsenite methyltransferase	Mus musculus	48-53
21978585-0	2011	Reduction of As(V) to As(III) by commercial ZVI or As(0) with acid-treated ZVI.	Arsenic	22-24	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	13-18
21723934-8	2011	Furthermore, a significant decrease in DNA methyltransferase (DNMT) 1 and 3a expression was observed following arsenic exposure.	Arsenic	111-118	DNA methyltransferase 1	Gallus gallus	39-75
21963172-0	2011	Co2+-exchange mechanism of birnessite and its application for the removal of Pb2+ and As(III).	Arsenic	86-88	mitochondrially encoded cytochrome c oxidase III	Homo sapiens	89-92
21921037-3	2011	Arsenic treatment, which induces Pml degradation, caused Setdb1 signals to disappear.	Arsenic	0-7	promyelocytic leukemia	Mus musculus	33-36
21921037-3	2011	Arsenic treatment, which induces Pml degradation, caused Setdb1 signals to disappear.	Arsenic	0-7	SET domain, bifurcated 1	Mus musculus	57-63
22005461-1	2011	Arsenic (+3 oxidation state) methyltransferase (As3MT) catalyzes the methylation of trivalent arsenic (As(III)) to monomethylarsonate (MMA(V)) and dimethylarsinic acid (DMA(V)), and plays an important role in the detoxification of arsenicals.	Arsenic	94-101	arsenite methyltransferase	Homo sapiens	0-46
22005461-1	2011	Arsenic (+3 oxidation state) methyltransferase (As3MT) catalyzes the methylation of trivalent arsenic (As(III)) to monomethylarsonate (MMA(V)) and dimethylarsinic acid (DMA(V)), and plays an important role in the detoxification of arsenicals.	Arsenic	94-101	arsenite methyltransferase	Homo sapiens	48-53
22005461-9	2011	These data suggest that the expression pattern of splicing variants of the As3MT gene may affect the capacity for arsenic methylation in cells.	Arsenic	114-121	arsenite methyltransferase	Homo sapiens	75-80
21846841-7	2011	Moreover, the CYP2J2-specific inhibitor compound 26 enhanced arsenic cytotoxicity to a clinically relevant concentration of ATO (1-2 muM).	Arsenic	61-68	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	14-20
21971544-11	2011	These results indicate cell transformation induced by chronic arsenic exposure is mediated by increased cellular levels of ROS, which mediates activation of AKT, ERK1/2, and p70S6K1.	Arsenic	62-69	AKT serine/threonine kinase 1	Homo sapiens	157-160
21865284-9	2011	CONCLUSIONS: These results suggest that the ERAP1 gene is associated with genetic predisposition to AS and influences the functional severity of the disease in a Spanish population.	Arsenic	100-102	endoplasmic reticulum aminopeptidase 1	Homo sapiens	44-49
21971544-11	2011	These results indicate cell transformation induced by chronic arsenic exposure is mediated by increased cellular levels of ROS, which mediates activation of AKT, ERK1/2, and p70S6K1.	Arsenic	62-69	mitogen-activated protein kinase 3	Homo sapiens	162-168
21854796-0	2011	Reactive oxygen species mediate arsenic induced cell transformation and tumorigenesis through Wnt/beta-catenin pathway in human colorectal adenocarcinoma DLD1 cells.	Arsenic	32-39	catenin beta 1	Homo sapiens	98-110
21864513-9	2011	The toxic effect of arsenic was also indicated by significantly decreased activities of enzymatic antioxidants like superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and glucose-6-phosphate dehydrogenase along with non-enzymatic antioxidant like reduced glutathione.	Arsenic	20-27	catalase	Rattus norvegicus	138-146
21864513-9	2011	The toxic effect of arsenic was also indicated by significantly decreased activities of enzymatic antioxidants like superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and glucose-6-phosphate dehydrogenase along with non-enzymatic antioxidant like reduced glutathione.	Arsenic	20-27	hematopoietic prostaglandin D synthase	Rattus norvegicus	172-197
21864513-9	2011	The toxic effect of arsenic was also indicated by significantly decreased activities of enzymatic antioxidants like superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and glucose-6-phosphate dehydrogenase along with non-enzymatic antioxidant like reduced glutathione.	Arsenic	20-27	glutathione-disulfide reductase	Rattus norvegicus	199-220
21864513-9	2011	The toxic effect of arsenic was also indicated by significantly decreased activities of enzymatic antioxidants like superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and glucose-6-phosphate dehydrogenase along with non-enzymatic antioxidant like reduced glutathione.	Arsenic	20-27	glucose-6-phosphate dehydrogenase	Rattus norvegicus	225-258
21871723-7	2011	Correlation between the properties of the media and arsenic and methylene blue removal suggested that surface area and GAC type may be the dominant factors controlling the arsenic and organic co-contaminant removal performance of the fabricated Zr-GAC media.	Arsenic	52-59	glutaminase	Homo sapiens	245-251
21871723-7	2011	Correlation between the properties of the media and arsenic and methylene blue removal suggested that surface area and GAC type may be the dominant factors controlling the arsenic and organic co-contaminant removal performance of the fabricated Zr-GAC media.	Arsenic	172-179	glutaminase	Homo sapiens	119-122
21871723-7	2011	Correlation between the properties of the media and arsenic and methylene blue removal suggested that surface area and GAC type may be the dominant factors controlling the arsenic and organic co-contaminant removal performance of the fabricated Zr-GAC media.	Arsenic	172-179	glutaminase	Homo sapiens	245-251
21851829-6	2011	After 20 weeks, we found arsenic, alone or combined with HCD, may promote atherosclerosis formation with transient increases in HSP 70 and hs-CRP.	Arsenic	25-32	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	128-134
21851829-9	2011	In conclusion, arsenic exposure may induce atherosclerosis through modifying reverse cholesterol transport in cholesterol metabolism and suppressing LXRbeta and CEPT-1 expressions.	Arsenic	15-22	choline/ethanolamine phosphotransferase 1	Rattus norvegicus	161-167
21854796-5	2011	Our results show that arsenic was able to activate p47(phox) and p67(phox), two key proteins for activation of NADPH oxidase.	Arsenic	22-29	pleckstrin	Homo sapiens	51-54
21854796-5	2011	Our results show that arsenic was able to activate p47(phox) and p67(phox), two key proteins for activation of NADPH oxidase.	Arsenic	22-29	CD33 molecule	Homo sapiens	65-68
21854796-7	2011	Arsenic increased beta-catenin expression level and its promoter activity.	Arsenic	0-7	catenin beta 1	Homo sapiens	18-30
21854796-8	2011	ROS played a major role in arsenic-induced beta-catenin activation.	Arsenic	27-34	catenin beta 1	Homo sapiens	43-55
21854796-12	2011	The results indicate that ROS are involved in arsenic induced cell transformation and tumor formation possible through Wnt/beta-catenin pathway in human colorectal adenocarcinoma cell line DLD1 cells.	Arsenic	46-53	catenin beta 1	Homo sapiens	123-135
21327618-5	2011	We injected TF antisense oligonucleotide (TF-AS) intravenously (i.v) in mice prior to LPS treatment, to block TF, and measured their blood urea nitrogen (BUN), creatinine (CRE), alkaline phosphatase (ALP), and potassium.	Arsenic	45-47	coagulation factor III	Mus musculus	12-14
21962096-7	2011	RESULTS: Expression of TIMP-1 was significantly reduced in the AS group when compared with both the AT and CRSsNP (control) groups (P &lt; .001).	Arsenic	63-65	TIMP metallopeptidase inhibitor 1	Homo sapiens	23-29
21962096-8	2011	The MMP-9/TIMP-1 ratio was significantly increased in the AS group when compared with other patient groups (P &lt; .001).	Arsenic	58-60	matrix metallopeptidase 9	Homo sapiens	4-9
21962096-8	2011	The MMP-9/TIMP-1 ratio was significantly increased in the AS group when compared with other patient groups (P &lt; .001).	Arsenic	58-60	TIMP metallopeptidase inhibitor 1	Homo sapiens	10-16
23724280-6	2011	The expressions of arsenic-sensitive stress gene metallothionein-1 were increased 3-7-folds after arsenite or arsenate, but were unaltered after NHJD and realgar.	Arsenic	19-26	metallothionein 1	Mus musculus	49-66
21327618-5	2011	We injected TF antisense oligonucleotide (TF-AS) intravenously (i.v) in mice prior to LPS treatment, to block TF, and measured their blood urea nitrogen (BUN), creatinine (CRE), alkaline phosphatase (ALP), and potassium.	Arsenic	45-47	coagulation factor III	Mus musculus	42-44
21327618-5	2011	We injected TF antisense oligonucleotide (TF-AS) intravenously (i.v) in mice prior to LPS treatment, to block TF, and measured their blood urea nitrogen (BUN), creatinine (CRE), alkaline phosphatase (ALP), and potassium.	Arsenic	45-47	coagulation factor III	Mus musculus	42-44
21567414-5	2011	Pure AS with &gt; 96% purity was prepared by enzymatic hydrolysis of TSE using Mash, and the chemical structure of AS was confirmed by (1)H- and (13)C-nuclear magnetic resonance analyses.	Arsenic	5-7	spermatogenesis associated 6	Mus musculus	79-83
21683489-3	2011	Our results show a large net export of both lead and arsenic via runoff (282 +- 21.3 gPb ha(-1) y(-1) and 60.4 +- 10.5 gAs ha(-1) y(-1)), but contrasting controls on this release.	Arsenic	53-60	glycophorin B (MNS blood group)	Homo sapiens	85-88
21782832-8	2011	Thus, cellular OGG activity was most sensitively affected by dimethylarsinic acid (DMA(V)), DNA ligase IIIalpha (LIGIIIalpha) protein level by arsenite and X-ray cross complementing protein 1 (XRCC1 protein) content by monomethylarsonic acid (MMA(V)), with significant effects starting at &gt;=3.2muM cellular arsenic.	Arsenic	310-317	X-ray repair cross complementing 1	Homo sapiens	193-198
21549764-8	2011	(3) Microinjection of Arc/Arg3.1 antisense oligodeoxynucleotide (AS) into the NAc core inhibited the acquisition, expression and reinstatement of morphine CPP; however, intra-NAc shell infusions of the AS only blocked the expression of CPP.	Arsenic	65-67	activity-regulated cytoskeleton-associated protein	Rattus norvegicus	22-32
21750348-0	2011	miR-190-mediated downregulation of PHLPP contributes to arsenic-induced Akt activation and carcinogenesis.	Arsenic	56-63	microRNA 190a	Homo sapiens	0-7
21750348-0	2011	miR-190-mediated downregulation of PHLPP contributes to arsenic-induced Akt activation and carcinogenesis.	Arsenic	56-63	PH domain and leucine rich repeat protein phosphatase 1	Homo sapiens	35-40
21750348-0	2011	miR-190-mediated downregulation of PHLPP contributes to arsenic-induced Akt activation and carcinogenesis.	Arsenic	56-63	AKT serine/threonine kinase 1	Homo sapiens	72-75
21750349-6	2011	Metabolism of arsenic, catalyzed by arsenic (+3 oxidation state) methyltransferase, is a sequential process of reduction from pentavalency to trivalency followed by oxidative methylation back to pentavalency.	Arsenic	14-21	arsenite methyltransferase	Homo sapiens	36-82
21914522-11	2011	The results of the study in West Bengal suggest that deficiency in DNA repair capacity, perturbation of methylation of promoter region of p53 and p16 genes, and genomic methylation alteration may be involved in arsenic-induced disease manifestation in humans.	Arsenic	211-218	tumor protein p53	Homo sapiens	138-141
22026679-1	2011	Experimental data from the Trident Laser facility is presented showing quasimonoenergetic carbon ions from nm-scaled foil targets with an energy spread of as low as +-15% at 35 MeV.	Arsenic	36-38	forkhead box M1	Homo sapiens	27-34
21812391-4	2011	Comparison of CD spectra of aR-7 to HMP-Y6 leads to the assignment of HMP-Y6 and hibarimicin B atropoisomers as aR and aS, respectively.	Arsenic	119-121	thyroid hormone receptor alpha	Homo sapiens	28-32
21809819-9	2011	These results provide some of the fundamental knowledge about As(V)-magnetite interactions that is essential for developing effective water treatment technologies for arsenic.	Arsenic	167-174	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	62-67
21884364-7	2011	Gibbs energies of the arsenic redox reactions generally correlate linearly with pH, increasing with increasing pH for As(III) oxidation and decreasing with increasing pH for As(V) reduction.	Arsenic	22-29	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	174-179
21844220-2	2011	Previous work showed that protonated aminosulfonates (AS), notably taurine, directly and reversibly inhibit homomeric and heteromeric channels that contain Cx26, a widely distributed connexin, but not homomeric Cx32 channels.	Arsenic	54-56	gap junction protein beta 2	Homo sapiens	156-160
21844220-2	2011	Previous work showed that protonated aminosulfonates (AS), notably taurine, directly and reversibly inhibit homomeric and heteromeric channels that contain Cx26, a widely distributed connexin, but not homomeric Cx32 channels.	Arsenic	54-56	gap junction protein beta 1	Homo sapiens	211-215
21827493-7	2011	Arsenate or As(2) O(3) at 0.2-10microg/ml significantly inhibited the amount of active MMP-2 and pro-MMP-2 secreted into the A375 cell culture supernatant (P&lt;0.05).	Arsenic	12-14	matrix metallopeptidase 2	Mus musculus	87-92
21827493-7	2011	Arsenate or As(2) O(3) at 0.2-10microg/ml significantly inhibited the amount of active MMP-2 and pro-MMP-2 secreted into the A375 cell culture supernatant (P&lt;0.05).	Arsenic	12-14	matrix metallopeptidase 2	Mus musculus	101-106
21914522-11	2011	The results of the study in West Bengal suggest that deficiency in DNA repair capacity, perturbation of methylation of promoter region of p53 and p16 genes, and genomic methylation alteration may be involved in arsenic-induced disease manifestation in humans.	Arsenic	211-218	cyclin dependent kinase inhibitor 2A	Homo sapiens	146-149
21914522-12	2011	P53 polymorphism has been found to be associated with increased occurrence of arsenic-induced keratosis.	Arsenic	78-85	tumor protein p53	Homo sapiens	0-3
21914527-5	2011	In patients with arsenic-induced Bowen"s disease, there is a selective CD4 T-cell apoptosis through tumor necrosis factor-alpha pathway, decrease in macrophage differentiation and phagocytosis, reduced Langerhans cell numbers and dendrites, altered regulatory T-cell distribution, and other immune alterations.	Arsenic	17-24	CD4 molecule	Homo sapiens	71-74
21703283-0	2011	Vascular hyperpermeability in response to inflammatory mustard oil is mediated by Rho kinase in mice systemically exposed to arsenic.	Arsenic	125-132	Rho-associated coiled-coil containing protein kinase 2	Mus musculus	82-92
21914527-5	2011	In patients with arsenic-induced Bowen"s disease, there is a selective CD4 T-cell apoptosis through tumor necrosis factor-alpha pathway, decrease in macrophage differentiation and phagocytosis, reduced Langerhans cell numbers and dendrites, altered regulatory T-cell distribution, and other immune alterations.	Arsenic	17-24	tumor necrosis factor	Homo sapiens	100-127
21703283-3	2011	The aim of this study was to investigate whether RhoA/Rho kinase (ROCK)-mediated vascular leakage (hyperpermeability) is induced by mustard oil in mice systemically exposed to arsenic.	Arsenic	176-183	ras homolog family member A	Mus musculus	49-53
21914528-10	2011	Moreover, although the precise mechanisms for the arsenic-induced diabetogenic effect are still largely undefined, recent in vitro experimental studies indicated that inorganic arsenic or its metabolites impair insulin-dependent glucose uptake or glucose-stimulated insulin secretion.	Arsenic	177-184	insulin	Homo sapiens	211-218
21703283-3	2011	The aim of this study was to investigate whether RhoA/Rho kinase (ROCK)-mediated vascular leakage (hyperpermeability) is induced by mustard oil in mice systemically exposed to arsenic.	Arsenic	176-183	Rho-associated coiled-coil containing protein kinase 2	Mus musculus	54-64
21703283-11	2011	ROCK2 levels in mouse ears treated with mustard oil were higher in the arsenic group as compared with the control group.	Arsenic	71-78	Rho-associated coiled-coil containing protein kinase 2	Mus musculus	0-5
21703283-13	2011	These findings indicate that increased ROCK2 levels and enhanced ROCK activity are responsible for mustard oil-induced vascular hyperpermeability in arsenic-fed mice.	Arsenic	149-156	Rho-associated coiled-coil containing protein kinase 2	Mus musculus	39-44
21914528-10	2011	Moreover, although the precise mechanisms for the arsenic-induced diabetogenic effect are still largely undefined, recent in vitro experimental studies indicated that inorganic arsenic or its metabolites impair insulin-dependent glucose uptake or glucose-stimulated insulin secretion.	Arsenic	177-184	insulin	Homo sapiens	266-273
21784148-0	2011	Reduced expression of MAPK/ERK genes in perinatal arsenic-exposed offspring induced by glucocorticoid receptor deficits.	Arsenic	50-57	mitogen-activated protein kinase 1	Mus musculus	27-30
21777978-0	2011	Arsenic increases lipopolysaccharide-dependent expression of interleukin-8 gene by stimulating a redox-sensitive pathway that strengthens p38-kinase activation.	Arsenic	0-7	C-X-C motif chemokine ligand 8	Homo sapiens	61-74
21777978-0	2011	Arsenic increases lipopolysaccharide-dependent expression of interleukin-8 gene by stimulating a redox-sensitive pathway that strengthens p38-kinase activation.	Arsenic	0-7	mitogen-activated protein kinase 14	Homo sapiens	138-141
21784148-0	2011	Reduced expression of MAPK/ERK genes in perinatal arsenic-exposed offspring induced by glucocorticoid receptor deficits.	Arsenic	50-57	nuclear receptor subfamily 3, group C, member 1	Mus musculus	87-110
21784148-1	2011	Changes within the glucocorticoid receptor (GR) cellular signaling pathway were evaluated in adolescent mice exposed to 50 ppb arsenic during gestation.	Arsenic	127-134	nuclear receptor subfamily 3, group C, member 1	Mus musculus	19-42
21784148-1	2011	Changes within the glucocorticoid receptor (GR) cellular signaling pathway were evaluated in adolescent mice exposed to 50 ppb arsenic during gestation.	Arsenic	127-134	nuclear receptor subfamily 3, group C, member 1	Mus musculus	44-46
21784148-2	2011	Previously, we reported increased basal plasma corticosterone levels, decreased hippocampal GR levels and deficits in learning and memory performance in perinatal arsenic-exposed mice.	Arsenic	163-170	nuclear receptor subfamily 3, group C, member 1	Mus musculus	92-94
21784148-7	2011	The decreased in vivo GR binding coincides with significantly decreased mRNA levels and slight reductions of protein of both H-Ras and Raf-1 in perinatally arsenic-exposed mice.	Arsenic	156-163	nuclear receptor subfamily 3, group C, member 1	Mus musculus	22-24
21784148-7	2011	The decreased in vivo GR binding coincides with significantly decreased mRNA levels and slight reductions of protein of both H-Ras and Raf-1 in perinatally arsenic-exposed mice.	Arsenic	156-163	Harvey rat sarcoma virus oncogene	Mus musculus	125-130
21784148-7	2011	The decreased in vivo GR binding coincides with significantly decreased mRNA levels and slight reductions of protein of both H-Ras and Raf-1 in perinatally arsenic-exposed mice.	Arsenic	156-163	v-raf-leukemia viral oncogene 1	Mus musculus	135-140
21784148-8	2011	Nuclear activated extracellular-signal regulated kinase (ERK), a downstream target of Ras and Raf, whose transcriptional targets also play an important role in learning and memory, was decreased in the hippocampus of arsenic-exposed animals when compared to controls.	Arsenic	217-224	mitogen-activated protein kinase 1	Mus musculus	18-55
21784148-8	2011	Nuclear activated extracellular-signal regulated kinase (ERK), a downstream target of Ras and Raf, whose transcriptional targets also play an important role in learning and memory, was decreased in the hippocampus of arsenic-exposed animals when compared to controls.	Arsenic	217-224	mitogen-activated protein kinase 1	Mus musculus	57-60
21784148-8	2011	Nuclear activated extracellular-signal regulated kinase (ERK), a downstream target of Ras and Raf, whose transcriptional targets also play an important role in learning and memory, was decreased in the hippocampus of arsenic-exposed animals when compared to controls.	Arsenic	217-224	zinc fingers and homeoboxes 2	Mus musculus	94-97
21784148-9	2011	GR-mediated transcriptional deficits in the MAPK/ERK pathway could be an underlying cause of previously reported learning deficits and provide the link to arsenic-induced deficiencies in cognitive development.	Arsenic	155-162	nuclear receptor subfamily 3, group C, member 1	Mus musculus	0-2
21784148-9	2011	GR-mediated transcriptional deficits in the MAPK/ERK pathway could be an underlying cause of previously reported learning deficits and provide the link to arsenic-induced deficiencies in cognitive development.	Arsenic	155-162	mitogen-activated protein kinase 1	Mus musculus	49-52
21854209-10	2011	Consistent with these in vitro studies, significant arsenate accumulation is observed in all examined zebrafish tissues where NaPi-IIb1 is expressed, particularly intestine, kidney, and eye, indicating that zebrafish NaPi-IIb1 is likely the transport protein that is responsible for arsenic accumulation in vivo.	Arsenic	283-290	solute carrier family 34 member 2a	Danio rerio	126-135
21854209-10	2011	Consistent with these in vitro studies, significant arsenate accumulation is observed in all examined zebrafish tissues where NaPi-IIb1 is expressed, particularly intestine, kidney, and eye, indicating that zebrafish NaPi-IIb1 is likely the transport protein that is responsible for arsenic accumulation in vivo.	Arsenic	283-290	solute carrier family 34 member 2a	Danio rerio	217-226
21621526-6	2011	Cyp1a1 expression was directly related to the level of NO production and to reduced arsenic cytotoxicity.	Arsenic	84-91	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	0-6
21684075-4	2011	The arsenic adsorption experiment results demonstrated that they were effective, especially at low equilibrium arsenic concentrations, in removing both As(III) and As(V) from lab-prepared and natural water samples.	Arsenic	4-11	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	164-169
21596116-1	2011	Galectin-1 (GAL1) is known as a beta-galactoside-binding protein that also can bind with arsenic to regulate cell functions.	Arsenic	89-96	lectin, galactose binding, soluble 1	Mus musculus	0-10
21726739-0	2011	Determination of arsenic based on quenching of CdS quantum dots fluorescence using the gas-diffusion flow injection method.	Arsenic	17-24	CDP-diacylglycerol synthase 1	Homo sapiens	47-50
21596116-1	2011	Galectin-1 (GAL1) is known as a beta-galactoside-binding protein that also can bind with arsenic to regulate cell functions.	Arsenic	89-96	lectin, galactose binding, soluble 1	Mus musculus	12-16
21596116-7	2011	Moreover, atomic absorption spectrophotometric results showed that GAL1 gene knockdown reduced the total arsenic accumulation of both cells after the NaAsO(2) and As(2)O(3) treatment.	Arsenic	105-112	lectin, galactose binding, soluble 1	Mus musculus	67-71
21596116-8	2011	These results suggested that GAL1 gene knockdown mediates the apoptotic effects of arsenic in 3T3 and KB cells via regulation of the cellular arsenic levels.	Arsenic	83-90	lectin, galactose binding, soluble 1	Mus musculus	29-33
21596116-8	2011	These results suggested that GAL1 gene knockdown mediates the apoptotic effects of arsenic in 3T3 and KB cells via regulation of the cellular arsenic levels.	Arsenic	142-149	lectin, galactose binding, soluble 1	Mus musculus	29-33
21596116-9	2011	We propose that down-regulation of GAL1 expression may be a useful and specific biomarker in assessing the toxicity of arsenic exposure.	Arsenic	119-126	lectin, galactose binding, soluble 1	Mus musculus	35-39
20859623-5	2011	Arsenic oxidation and reduction capacity was assayed with high-performance liquid chromatography coupled to gaseous formation performing the detection by atomic absortion in a quartz bucket (HPLC/HG/QAAS), and polymerase chain reaction was used to detect aox and ars genes.	Arsenic	0-7	acyl-CoA oxidase 1	Homo sapiens	255-258
21806879-8	2011	RESULTS: The level of serum IFN-gamma at the AS group and the VAP group, compared with the control group, was significantly increased(all P&lt;0.01), at the same time, the level of serum IFN-gamma in the VAP group was significantly higher than in the AS group(P&lt;0.01).	Arsenic	45-47	interferon gamma	Oryctolagus cuniculus	28-37
21972493-0	2011	Enhanced arsenic tolerance of transgenic eastern cottonwood plants expressing gamma-glutamylcysteine synthetase.	Arsenic	9-16	glutamate-cysteine ligase catalytic subunit	Homo sapiens	78-111
21972493-4	2011	Recent studies demonstrate that increasing thiol-sinks in transgenic plants by overexpressing the bacterial gamma-glutamylcysteine synthetase (ECS) gene results in a higher tolerance and accumulation of metals and metalloids such as cadmium, mercury, and arsenic.	Arsenic	255-262	glutamate-cysteine ligase catalytic subunit	Homo sapiens	108-141
21605584-0	2011	Inhibition of arsenic-induced rat liver injury by grape seed exact through suppression of NADPH oxidase and TGF-beta/Smad activation.	Arsenic	14-21	transforming growth factor, beta 1	Rattus norvegicus	108-116
21605584-5	2011	Moreover, GSE reduced arsenic-stimulated Smad2/3 phosphorylation and protein levels of NADPH oxidase subunits (Nox2, Nox4 and p47phox).	Arsenic	22-29	SMAD family member 2	Rattus norvegicus	41-48
21605584-5	2011	Moreover, GSE reduced arsenic-stimulated Smad2/3 phosphorylation and protein levels of NADPH oxidase subunits (Nox2, Nox4 and p47phox).	Arsenic	22-29	cytochrome b-245 beta chain	Rattus norvegicus	111-115
21605584-5	2011	Moreover, GSE reduced arsenic-stimulated Smad2/3 phosphorylation and protein levels of NADPH oxidase subunits (Nox2, Nox4 and p47phox).	Arsenic	22-29	NADPH oxidase 4	Rattus norvegicus	117-121
21605584-5	2011	Moreover, GSE reduced arsenic-stimulated Smad2/3 phosphorylation and protein levels of NADPH oxidase subunits (Nox2, Nox4 and p47phox).	Arsenic	22-29	neutrophil cytosolic factor 1	Rattus norvegicus	126-133
21605584-8	2011	Both NADPH oxidases flavoprotein inhibitor DPI and Nox4 siRNA blocked arsenic-induced ROS production, whereas Nox4 overexpression suppressed the inhibitory effects of GSE on arsenic-induced ROS production and NADPH oxidase activities, as well as expression of TGF-beta1, type I procollagen (Coll-I) and alpha-smooth muscle actin (alpha-SMA) mRNA.	Arsenic	70-77	NADPH oxidase 4	Rattus norvegicus	51-55
21605584-8	2011	Both NADPH oxidases flavoprotein inhibitor DPI and Nox4 siRNA blocked arsenic-induced ROS production, whereas Nox4 overexpression suppressed the inhibitory effects of GSE on arsenic-induced ROS production and NADPH oxidase activities, as well as expression of TGF-beta1, type I procollagen (Coll-I) and alpha-smooth muscle actin (alpha-SMA) mRNA.	Arsenic	174-181	NADPH oxidase 4	Rattus norvegicus	110-114
21605584-8	2011	Both NADPH oxidases flavoprotein inhibitor DPI and Nox4 siRNA blocked arsenic-induced ROS production, whereas Nox4 overexpression suppressed the inhibitory effects of GSE on arsenic-induced ROS production and NADPH oxidase activities, as well as expression of TGF-beta1, type I procollagen (Coll-I) and alpha-smooth muscle actin (alpha-SMA) mRNA.	Arsenic	174-181	transforming growth factor, beta 1	Rattus norvegicus	260-269
21605584-8	2011	Both NADPH oxidases flavoprotein inhibitor DPI and Nox4 siRNA blocked arsenic-induced ROS production, whereas Nox4 overexpression suppressed the inhibitory effects of GSE on arsenic-induced ROS production and NADPH oxidase activities, as well as expression of TGF-beta1, type I procollagen (Coll-I) and alpha-smooth muscle actin (alpha-SMA) mRNA.	Arsenic	174-181	actin gamma 2, smooth muscle	Rattus norvegicus	303-328
21605584-8	2011	Both NADPH oxidases flavoprotein inhibitor DPI and Nox4 siRNA blocked arsenic-induced ROS production, whereas Nox4 overexpression suppressed the inhibitory effects of GSE on arsenic-induced ROS production and NADPH oxidase activities, as well as expression of TGF-beta1, type I procollagen (Coll-I) and alpha-smooth muscle actin (alpha-SMA) mRNA.	Arsenic	174-181	actin gamma 2, smooth muscle	Rattus norvegicus	330-339
21605584-10	2011	Collectively, GSE could be a potential dietary therapeutic agent for arsenic-induced liver injury through suppression of NADPH oxidase and TGF-beta/Smad activation.	Arsenic	69-76	transforming growth factor, beta 1	Rattus norvegicus	139-147
21605854-2	2011	The purpose of this study is to explore the interaction effect on risk of carotid atherosclerosis between arsenic exposure and risk genotypes of purine nucleoside phosphorylase (PNP), arsenic (+3) methyltransferase (As3MT), and glutathione S-transferase omega 1 (GSTO1) and omega 2 (GSTO2).	Arsenic	106-113	purine nucleoside phosphorylase	Homo sapiens	178-181
21605854-2	2011	The purpose of this study is to explore the interaction effect on risk of carotid atherosclerosis between arsenic exposure and risk genotypes of purine nucleoside phosphorylase (PNP), arsenic (+3) methyltransferase (As3MT), and glutathione S-transferase omega 1 (GSTO1) and omega 2 (GSTO2).	Arsenic	106-113	arsenite methyltransferase	Homo sapiens	216-221
21605854-2	2011	The purpose of this study is to explore the interaction effect on risk of carotid atherosclerosis between arsenic exposure and risk genotypes of purine nucleoside phosphorylase (PNP), arsenic (+3) methyltransferase (As3MT), and glutathione S-transferase omega 1 (GSTO1) and omega 2 (GSTO2).	Arsenic	106-113	glutathione S-transferase omega 1	Homo sapiens	228-261
21605854-2	2011	The purpose of this study is to explore the interaction effect on risk of carotid atherosclerosis between arsenic exposure and risk genotypes of purine nucleoside phosphorylase (PNP), arsenic (+3) methyltransferase (As3MT), and glutathione S-transferase omega 1 (GSTO1) and omega 2 (GSTO2).	Arsenic	106-113	glutathione S-transferase omega 1	Homo sapiens	263-268
21605854-2	2011	The purpose of this study is to explore the interaction effect on risk of carotid atherosclerosis between arsenic exposure and risk genotypes of purine nucleoside phosphorylase (PNP), arsenic (+3) methyltransferase (As3MT), and glutathione S-transferase omega 1 (GSTO1) and omega 2 (GSTO2).	Arsenic	106-113	glutathione S-transferase omega 2	Homo sapiens	283-288
21605854-10	2011	In conclusion, arsenic metabolic genes, PNP, As3MT, and GSTO, may exacerbate the formation of atherosclerosis in individuals with high levels of arsenic concentration in well water (&gt;50mug/l).	Arsenic	145-152	purine nucleoside phosphorylase	Homo sapiens	40-43
21605854-10	2011	In conclusion, arsenic metabolic genes, PNP, As3MT, and GSTO, may exacerbate the formation of atherosclerosis in individuals with high levels of arsenic concentration in well water (&gt;50mug/l).	Arsenic	145-152	arsenite methyltransferase	Homo sapiens	45-50
21110054-9	2011	Decomposition of the binding energy into ligand-residue pair interactions shows that two residues (Tyr175 and Tyr177) have nearly-zero interactions with AMP in the scFv:AMP-H2O complex, whereas their interactions with METH in the scFv:METH complex are as large as -0.8 and -0.74 kcal mol(-1).	Arsenic	191-193	immunglobulin heavy chain variable region	Homo sapiens	164-168
21806879-8	2011	RESULTS: The level of serum IFN-gamma at the AS group and the VAP group, compared with the control group, was significantly increased(all P&lt;0.01), at the same time, the level of serum IFN-gamma in the VAP group was significantly higher than in the AS group(P&lt;0.01).	Arsenic	45-47	interferon gamma	Oryctolagus cuniculus	187-196
21806879-8	2011	RESULTS: The level of serum IFN-gamma at the AS group and the VAP group, compared with the control group, was significantly increased(all P&lt;0.01), at the same time, the level of serum IFN-gamma in the VAP group was significantly higher than in the AS group(P&lt;0.01).	Arsenic	251-253	interferon gamma	Oryctolagus cuniculus	28-37
21806879-8	2011	RESULTS: The level of serum IFN-gamma at the AS group and the VAP group, compared with the control group, was significantly increased(all P&lt;0.01), at the same time, the level of serum IFN-gamma in the VAP group was significantly higher than in the AS group(P&lt;0.01).	Arsenic	251-253	interferon gamma	Oryctolagus cuniculus	187-196
21447319-2	2011	In yeast cells, it has been clearly shown that Acr3p is localized to the plasma membrane and facilitates efflux of trivalent arsenic and antimony.	Arsenic	125-132	Arr3p	Saccharomyces cerevisiae S288C	47-52
21554949-8	2011	The carcinogenic potential of arsenic may be attributed to activation of redox-sensitive transcription factors and other signaling pathways involving nuclear factor kappaB, activator protein-1, and p53.	Arsenic	30-37	tumor protein p53	Homo sapiens	198-201
21740555-9	2011	As regards the exposure-response relationship with arsenic in the drinking water, the respective activities of ALP, AST and ALT were found to be significantly increased in the high-exposure groups compared to the lowest-exposure groups before and after adjustments were made for different covariates.	Arsenic	51-58	alkaline phosphatase, placental	Homo sapiens	111-114
21740555-9	2011	As regards the exposure-response relationship with arsenic in the drinking water, the respective activities of ALP, AST and ALT were found to be significantly increased in the high-exposure groups compared to the lowest-exposure groups before and after adjustments were made for different covariates.	Arsenic	51-58	solute carrier family 17 member 5	Homo sapiens	116-119
21798077-0	2011	Genetic polymorphisms in glutathione S-transferase (GST) superfamily and risk of arsenic-induced urothelial carcinoma in residents of southwestern Taiwan.	Arsenic	81-88	glutathione S-transferase kappa 1	Homo sapiens	25-50
21798077-0	2011	Genetic polymorphisms in glutathione S-transferase (GST) superfamily and risk of arsenic-induced urothelial carcinoma in residents of southwestern Taiwan.	Arsenic	81-88	glutathione S-transferase kappa 1	Homo sapiens	52-55
21798077-7	2011	Among the subjects with cumulative arsenic exposure (CAE) &gt;= 20 mg/L*year, the GSTT1 null genotype conferred a significantly increased cancer risk (RR, 3.25, 95% CI, 1.20-8.80).	Arsenic	35-42	glutathione S-transferase theta 1	Homo sapiens	82-87
21798077-8	2011	The gene-environment interaction between the GSTT1 and high arsenic exposure with respect to cancer risk was statistically significant (multiplicative model, p = 0.0151) and etiologic fraction was as high as 0.86 (95% CI, 0.51-1.22).	Arsenic	60-67	glutathione S-transferase theta 1	Homo sapiens	45-50
21798077-9	2011	The genetic effects of GSTO1/GSTO2 were largely confined to high arsenic level (CAE &gt;= 20).	Arsenic	65-72	glutathione S-transferase omega 1	Homo sapiens	23-28
21798077-9	2011	The genetic effects of GSTO1/GSTO2 were largely confined to high arsenic level (CAE &gt;= 20).	Arsenic	65-72	glutathione S-transferase omega 2	Homo sapiens	29-34
21798077-12	2011	The genetic effects of GSTT1 and GSTO1 on arsenic-induced urothelial carcinogenesis are largely confined to very high exposure level.	Arsenic	42-49	glutathione S-transferase theta 1	Homo sapiens	23-28
21798077-12	2011	The genetic effects of GSTT1 and GSTO1 on arsenic-induced urothelial carcinogenesis are largely confined to very high exposure level.	Arsenic	42-49	glutathione S-transferase omega 1	Homo sapiens	33-38
21605886-0	2011	Arsenic mediated disruption of promyelocytic leukemia protein nuclear bodies induces ganciclovir susceptibility in Epstein-Barr positive epithelial cells.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	31-61
21370284-0	2011	Role of DNA polymerase beta in the genotoxicity of arsenic.	Arsenic	51-58	DNA polymerase beta	Homo sapiens	8-27
22586354-4	2011	In acute promyelocytic leukemia, the cooperative degradation of PML/RARA by arsenic and retinoic acid cures most patients.	Arsenic	76-83	PML nuclear body scaffold	Homo sapiens	64-67
22586354-4	2011	In acute promyelocytic leukemia, the cooperative degradation of PML/RARA by arsenic and retinoic acid cures most patients.	Arsenic	76-83	retinoic acid receptor alpha	Homo sapiens	68-72
21549690-3	2011	RESULTS: Fe/As promoted the production of lipid peroxidation as reflected by the formation of malondialdehyde and H(2)O(2) along with reduced PUFA levels and elevated glutathione disulfide/total glutathione ratio, a reliable index of cellular redox status.	Arsenic	12-14	pumilio RNA binding family member 3	Homo sapiens	142-146
21370284-10	2011	In contrast, cells harboring overexpressed Pol beta resulted in a lower level of DNA damage and MN than Pol beta wild-type cells, indicating overexpression of the enzyme can combat arsenic-induced genotoxic effects.	Arsenic	181-188	DNA polymerase beta	Homo sapiens	43-51
21669332-4	2011	Arsenic concentrations in the leach solution of non-glazed potteries varied from 30.9 to 800 mug L-1, while the glazed potteries varied generally from below the limit of detection (0.5 mug L-1) to 30.6 mug L-1, but in one poorly glazed series it reached to 110 mug L-1.	Arsenic	0-7	immunoglobulin kappa variable 1-16	Homo sapiens	97-100
21712587-3	2011	All geochemical parameters measured point to a condition in which the mobilization of As becomes more favorable moving down the topographic gradient, likely resulting through competition (Meh-P, SOM), neutral or slightly basic pH, and redox conditions that are favorable for As mobilization (higher Fe(II) and total-Fe concentrations in water extracts).	Arsenic	86-88	grainyhead like transcription factor 3	Homo sapiens	195-198
21268130-6	2011	Knockdown of eIF4B expression resulted in inhibition of arsenic-induced cell proliferation, transformation, and translation.	Arsenic	56-63	eukaryotic translation initiation factor 4B	Homo sapiens	13-18
21268130-8	2011	Taken together, these results indicate that activation and up-regulation of eIF4B contributes to arsenic-induced transformation in JB6 cells.	Arsenic	97-104	eukaryotic translation initiation factor 4B	Homo sapiens	76-81
21861350-0	2011	[Effects of inorganic arsenic on mRNA expression of Nrf2 and Nrf2-regulated downstream anti-oxidant enzymes in Chang hepatocytes].	Arsenic	22-29	NFE2 like bZIP transcription factor 2	Homo sapiens	52-56
21512104-0	2011	Exposure to moderate arsenic concentrations increases atherosclerosis in ApoE-/- mouse model.	Arsenic	21-28	apolipoprotein E	Mus musculus	73-77
21512104-8	2011	Arsenic-enhanced lesions correlated with several proatherogenic molecular changes, including decreased liver X receptor (LXR) target gene expression and increased proinflammatory cytokines.	Arsenic	0-7	nuclear receptor subfamily 1, group H, member 3	Mus musculus	103-119
21512104-8	2011	Arsenic-enhanced lesions correlated with several proatherogenic molecular changes, including decreased liver X receptor (LXR) target gene expression and increased proinflammatory cytokines.	Arsenic	0-7	nuclear receptor subfamily 1, group H, member 3	Mus musculus	121-124
21550362-0	2011	Metabolites of arsenic and increased DNA damage of p53 gene in arsenic plant workers.	Arsenic	63-70	tumor protein p53	Homo sapiens	51-54
21550362-6	2011	Those findings suggested that DNA damage of exon 5 and 8 of p53 gene existed in the population occupationally exposed to arsenic.	Arsenic	121-128	tumor protein p53	Homo sapiens	60-63
21861350-6	2011	CONCLUSION: No elevation of Nrf2 transcription was found, while inorganic arsenic could increase the Nrf2-regulated NQO1 and HO-1 mRNA expression in human hepatocytes.	Arsenic	74-81	NFE2 like bZIP transcription factor 2	Homo sapiens	101-105
21861350-6	2011	CONCLUSION: No elevation of Nrf2 transcription was found, while inorganic arsenic could increase the Nrf2-regulated NQO1 and HO-1 mRNA expression in human hepatocytes.	Arsenic	74-81	NAD(P)H quinone dehydrogenase 1	Homo sapiens	116-120
21861350-0	2011	[Effects of inorganic arsenic on mRNA expression of Nrf2 and Nrf2-regulated downstream anti-oxidant enzymes in Chang hepatocytes].	Arsenic	22-29	NFE2 like bZIP transcription factor 2	Homo sapiens	61-65
21861350-6	2011	CONCLUSION: No elevation of Nrf2 transcription was found, while inorganic arsenic could increase the Nrf2-regulated NQO1 and HO-1 mRNA expression in human hepatocytes.	Arsenic	74-81	heme oxygenase 1	Homo sapiens	125-129
21422471-2	2011	In the past 3 decades, arsenic was revived and shown to be able to induce complete remission and to achieve, when combined with all-trans retinoic acid and chemotherapy, a 5-year overall survival of 90% in patients with acute promyelocytic leukemia driven by the t(15;17) translocation-generated promyelocytic leukemia-retinoic acid receptor alpha (PML-RARalpha) fusion.	Arsenic	23-30	PML nuclear body scaffold	Homo sapiens	349-352
21422471-2	2011	In the past 3 decades, arsenic was revived and shown to be able to induce complete remission and to achieve, when combined with all-trans retinoic acid and chemotherapy, a 5-year overall survival of 90% in patients with acute promyelocytic leukemia driven by the t(15;17) translocation-generated promyelocytic leukemia-retinoic acid receptor alpha (PML-RARalpha) fusion.	Arsenic	23-30	retinoic acid receptor alpha	Homo sapiens	353-361
21422471-4	2011	Interestingly, arsenic directly binds the C3HC4 zinc finger motif in the RBCC domain of PML and PML-RARalpha, induces their homodimerization and multimerization, and enhances their interaction with the SUMO E2 conjugase Ubc9, facilitating subsequent sumoylation/ubiquitination and proteasomal degradation.	Arsenic	15-22	PML nuclear body scaffold	Homo sapiens	88-91
21422471-4	2011	Interestingly, arsenic directly binds the C3HC4 zinc finger motif in the RBCC domain of PML and PML-RARalpha, induces their homodimerization and multimerization, and enhances their interaction with the SUMO E2 conjugase Ubc9, facilitating subsequent sumoylation/ubiquitination and proteasomal degradation.	Arsenic	15-22	PML nuclear body scaffold	Homo sapiens	96-99
21422471-4	2011	Interestingly, arsenic directly binds the C3HC4 zinc finger motif in the RBCC domain of PML and PML-RARalpha, induces their homodimerization and multimerization, and enhances their interaction with the SUMO E2 conjugase Ubc9, facilitating subsequent sumoylation/ubiquitination and proteasomal degradation.	Arsenic	15-22	retinoic acid receptor alpha	Homo sapiens	100-108
21422471-4	2011	Interestingly, arsenic directly binds the C3HC4 zinc finger motif in the RBCC domain of PML and PML-RARalpha, induces their homodimerization and multimerization, and enhances their interaction with the SUMO E2 conjugase Ubc9, facilitating subsequent sumoylation/ubiquitination and proteasomal degradation.	Arsenic	15-22	ubiquitin conjugating enzyme E2 I	Homo sapiens	220-224
21422471-5	2011	Arsenic-caused intermolecular disulfide formation in PML also contributes to PML-multimerization.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	53-56
21422471-5	2011	Arsenic-caused intermolecular disulfide formation in PML also contributes to PML-multimerization.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	77-80
21422471-6	2011	All-trans retinoic acid, which targets PML-RARalpha for degradation through its RARalpha moiety, synergizes with arsenic in eliminating leukemia-initiating cells.	Arsenic	113-120	PML nuclear body scaffold	Homo sapiens	39-42
21422471-6	2011	All-trans retinoic acid, which targets PML-RARalpha for degradation through its RARalpha moiety, synergizes with arsenic in eliminating leukemia-initiating cells.	Arsenic	113-120	retinoic acid receptor alpha	Homo sapiens	43-51
21422471-6	2011	All-trans retinoic acid, which targets PML-RARalpha for degradation through its RARalpha moiety, synergizes with arsenic in eliminating leukemia-initiating cells.	Arsenic	113-120	retinoic acid receptor alpha	Homo sapiens	80-88
21537954-1	2011	It has been suggested that arsenic (+3 oxidation state) methyltransferase (AS3MT) plays a critical role in methylation of arsenic, and that arsenic-glutathione conjugate is a substrate for AS3MT-catalyzed methylation of arsenic.	Arsenic	27-34	arsenite methyltransferase	Homo sapiens	75-80
20978746-7	2011	The MDD and MDD + arsenic suppressed DNMT1 expression only in the male mice livers.	Arsenic	18-25	DNA methyltransferase (cytosine-5) 1	Mus musculus	37-42
21537954-1	2011	It has been suggested that arsenic (+3 oxidation state) methyltransferase (AS3MT) plays a critical role in methylation of arsenic, and that arsenic-glutathione conjugate is a substrate for AS3MT-catalyzed methylation of arsenic.	Arsenic	27-34	arsenite methyltransferase	Homo sapiens	189-194
21537954-1	2011	It has been suggested that arsenic (+3 oxidation state) methyltransferase (AS3MT) plays a critical role in methylation of arsenic, and that arsenic-glutathione conjugate is a substrate for AS3MT-catalyzed methylation of arsenic.	Arsenic	122-129	arsenite methyltransferase	Homo sapiens	27-73
21537954-1	2011	It has been suggested that arsenic (+3 oxidation state) methyltransferase (AS3MT) plays a critical role in methylation of arsenic, and that arsenic-glutathione conjugate is a substrate for AS3MT-catalyzed methylation of arsenic.	Arsenic	122-129	arsenite methyltransferase	Homo sapiens	75-80
21537954-1	2011	It has been suggested that arsenic (+3 oxidation state) methyltransferase (AS3MT) plays a critical role in methylation of arsenic, and that arsenic-glutathione conjugate is a substrate for AS3MT-catalyzed methylation of arsenic.	Arsenic	122-129	arsenite methyltransferase	Homo sapiens	27-73
21537954-1	2011	It has been suggested that arsenic (+3 oxidation state) methyltransferase (AS3MT) plays a critical role in methylation of arsenic, and that arsenic-glutathione conjugate is a substrate for AS3MT-catalyzed methylation of arsenic.	Arsenic	122-129	arsenite methyltransferase	Homo sapiens	75-80
21537954-11	2011	These findings indicated that AS3MT expression enhanced the cytotoxic effect of arsenite in tet(+) cells because these cells accumulated more arsenic metabolites than did the tet(-) cells, and accordingly, the tet(+) cells were more susceptible to arsenic than were the tet(-) cells.	Arsenic	142-149	arsenite methyltransferase	Homo sapiens	30-35
21537954-11	2011	These findings indicated that AS3MT expression enhanced the cytotoxic effect of arsenite in tet(+) cells because these cells accumulated more arsenic metabolites than did the tet(-) cells, and accordingly, the tet(+) cells were more susceptible to arsenic than were the tet(-) cells.	Arsenic	248-255	arsenite methyltransferase	Homo sapiens	30-35
21188475-3	2011	ArsD transfers As(III) to ArsA and increases the affinity of ArsA for As(III), allowing resistance to environmental concentrations of arsenic.	Arsenic	134-141	ArsD	Escherichia coli	0-4
21776218-3	2011	We found that expression of tumor necrosis factor-alpha (TNF-alpha), which activates both inflammation and NF-kappaB-dependent survival pathways, was strongly associated with water and urinary arsenic levels.	Arsenic	193-200	tumor necrosis factor	Homo sapiens	28-55
21440049-0	2011	Arsenic affects expression and processing of amyloid precursor protein (APP) in primary neuronal cells overexpressing the Swedish mutation of human APP.	Arsenic	0-7	amyloid beta precursor protein	Homo sapiens	45-70
21193388-0	2011	Involvement of N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) in arsenic biomethylation and its role in arsenic-induced toxicity.	Arsenic	72-79	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	15-59
21193388-0	2011	Involvement of N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) in arsenic biomethylation and its role in arsenic-induced toxicity.	Arsenic	72-79	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	61-67
21193388-0	2011	Involvement of N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) in arsenic biomethylation and its role in arsenic-induced toxicity.	Arsenic	111-118	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	15-59
21193388-0	2011	Involvement of N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) in arsenic biomethylation and its role in arsenic-induced toxicity.	Arsenic	111-118	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	61-67
21193388-6	2011	OBJECTIVE: We investigated the potential role of N6AMT1 in arsenic-induced toxicity.	Arsenic	59-66	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	49-55
21193388-10	2011	Moreover, N6AMT1 is expressed in many human tissues at variable levels, although at levels lower than those of AS3MT, supporting a potential participation in arsenic metabolism in vivo.	Arsenic	158-165	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	10-16
21776218-3	2011	We found that expression of tumor necrosis factor-alpha (TNF-alpha), which activates both inflammation and NF-kappaB-dependent survival pathways, was strongly associated with water and urinary arsenic levels.	Arsenic	193-200	tumor necrosis factor	Homo sapiens	57-66
21776218-3	2011	We found that expression of tumor necrosis factor-alpha (TNF-alpha), which activates both inflammation and NF-kappaB-dependent survival pathways, was strongly associated with water and urinary arsenic levels.	Arsenic	193-200	nuclear factor kappa B subunit 1	Homo sapiens	107-116
21776218-4	2011	Expression of KCNA5, which encodes a potassium ion channel protein, was positively associated with water and toe nail arsenic levels.	Arsenic	118-125	potassium voltage-gated channel subfamily A member 5	Homo sapiens	14-19
21776218-7	2011	Expression of the ion-channel genes CACNA1, KCNH2, KCNQ1 and KCNE1 were down-regulated by 1-muM arsenic.	Arsenic	96-103	potassium voltage-gated channel subfamily H member 2	Homo sapiens	44-49
21776218-7	2011	Expression of the ion-channel genes CACNA1, KCNH2, KCNQ1 and KCNE1 were down-regulated by 1-muM arsenic.	Arsenic	96-103	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	51-56
21776218-7	2011	Expression of the ion-channel genes CACNA1, KCNH2, KCNQ1 and KCNE1 were down-regulated by 1-muM arsenic.	Arsenic	96-103	potassium voltage-gated channel subfamily E regulatory subunit 1	Homo sapiens	61-66
21624607-3	2011	METHODS: A combination of real-time polymerase chain reaction, Western analysis, and immunohistochemistry was used to characterize Kindlin-2 expression in arsenite (As(+3))- and cadmium (Cd(+2))-transformed human cell lines, their tumor transplants in immunocompromised mice, and in archival specimens of human bladder and bladder cancer.	Arsenic	165-167	FERM domain containing kindlin 2	Homo sapiens	131-140
21385732-1	2011	The enzyme arsenic (+3 oxidation state) methyltransferase (As3mt) catalyzes reactions converting inorganic arsenic to methylated metabolites, some of which are highly cytotoxic.	Arsenic	11-18	arsenite methyltransferase	Mus musculus	59-64
21385732-2	2011	In a previous study, female As3mt knockout (KO) mice treated with diet containing 100 or 150 ppm arsenic as arsenite showed systemic toxicity and significant effects on the urothelium.	Arsenic	97-104	arsenite methyltransferase	Mus musculus	28-33
21942197-7	2011	Chemical processes that may influence AIRP performance are also discussed herein, including iron and arsenic oxidation, arsenic co-precipitation with iron, multiple iron additions, interference by organics, and iron crystallization.	Arsenic	101-108	5'-nucleotidase, cytosolic IB	Homo sapiens	38-42
21524100-3	2011	This produces a ringlike feature in STM images, whose diameter depends on the tunneling conditions and distance to charged arsenic vacancies.	Arsenic	123-130	sulfotransferase family 1A member 3	Homo sapiens	36-39
21942197-7	2011	Chemical processes that may influence AIRP performance are also discussed herein, including iron and arsenic oxidation, arsenic co-precipitation with iron, multiple iron additions, interference by organics, and iron crystallization.	Arsenic	120-127	5'-nucleotidase, cytosolic IB	Homo sapiens	38-42
21454520-0	2011	Mutant p53 protein is targeted by arsenic for degradation and plays a role in arsenic-mediated growth suppression.	Arsenic	34-41	tumor protein p53	Homo sapiens	7-10
21454520-0	2011	Mutant p53 protein is targeted by arsenic for degradation and plays a role in arsenic-mediated growth suppression.	Arsenic	78-85	tumor protein p53	Homo sapiens	7-10
21454520-4	2011	Interestingly, wild type p53 is accumulated in cells treated with arsenic compounds, presumably due to arsenic-induced oxidative stresses.	Arsenic	66-73	tumor protein p53	Homo sapiens	25-28
21454520-4	2011	Interestingly, wild type p53 is accumulated in cells treated with arsenic compounds, presumably due to arsenic-induced oxidative stresses.	Arsenic	103-110	tumor protein p53	Homo sapiens	25-28
21454520-6	2011	In contrast, we found that arsenic compounds degrade both endogenous and ectopically expressed mutant p53 in time- and dose-dependent manners.	Arsenic	27-34	tumor protein p53	Homo sapiens	102-105
21454520-7	2011	We also found that arsenic trioxide decreases the stability of mutant p53 protein through a proteasomal pathway, and blockage of mutant p53 nuclear export can alleviate the arsenic-induced mutant p53 degradation.	Arsenic	19-26	tumor protein p53	Homo sapiens	70-73
21454520-9	2011	Taken together, we found that mutant p53 is a target of arsenic compounds, which provides an insight into exploring arsenic compound-based therapy for tumors harboring a mutant p53.	Arsenic	56-63	tumor protein p53	Homo sapiens	37-40
21454520-9	2011	Taken together, we found that mutant p53 is a target of arsenic compounds, which provides an insight into exploring arsenic compound-based therapy for tumors harboring a mutant p53.	Arsenic	56-63	tumor protein p53	Homo sapiens	177-180
21454520-9	2011	Taken together, we found that mutant p53 is a target of arsenic compounds, which provides an insight into exploring arsenic compound-based therapy for tumors harboring a mutant p53.	Arsenic	116-123	tumor protein p53	Homo sapiens	37-40
21454520-9	2011	Taken together, we found that mutant p53 is a target of arsenic compounds, which provides an insight into exploring arsenic compound-based therapy for tumors harboring a mutant p53.	Arsenic	116-123	tumor protein p53	Homo sapiens	177-180
21669162-3	2011	OBJECTIVE: This study examines whether Ars Alb LM 0/3 could provide some degree of amelioration for the victims living in an arsenic-affected village where no arsenic-free drinking water is available.	Arsenic	125-132	RIEG2	Homo sapiens	39-42
21669162-12	2011	CONCLUSION: Ars Alb LM 0/3 shows potential for use in high-risk arsenic villages as an interim treatment for amelioration of arsenic toxicity until more extensive medical treatment and facilities can be provided to the numerous victims of arsenic poisoning.	Arsenic	64-71	RIEG2	Homo sapiens	12-15
21514422-8	2011	Blocking of mitochondrial function by oligomycin A (Complex V inhibitor) or knockdown of mtTFA by RNA interference abrogated arsenic-induced cell proliferation without affecting cyclin D1 expression.	Arsenic	125-132	transcription factor A, mitochondrial	Homo sapiens	89-94
21543848-4	2011	The structure was solved by molecular replacement (MR) using Na-ASP-2, a one-CAP-domain ASP, as the search model.	Arsenic	15-17	beta-secretase 1	Homo sapiens	64-69
21356263-0	2011	Relation between occupational exposure to lead, cadmium, arsenic and concentration of cystatin C.	Arsenic	57-64	cystatin C	Homo sapiens	86-96
21356263-7	2011	Concentration of cystatin C was found to be significantly higher in Pb group than in Cd and As groups, also in Pb/Cd group higher than in Cd group and in Pb/As group than in As group.	Arsenic	92-94	cystatin C	Homo sapiens	17-27
21356263-7	2011	Concentration of cystatin C was found to be significantly higher in Pb group than in Cd and As groups, also in Pb/Cd group higher than in Cd group and in Pb/As group than in As group.	Arsenic	157-159	cystatin C	Homo sapiens	17-27
21356263-7	2011	Concentration of cystatin C was found to be significantly higher in Pb group than in Cd and As groups, also in Pb/Cd group higher than in Cd group and in Pb/As group than in As group.	Arsenic	157-159	cystatin C	Homo sapiens	17-27
21356263-9	2011	Regression analysis demonstrated that higher blood level of lead, higher urinary level of arsenic, more advanced age and higher body mass index represented independent risk factors of an increased serum concentration of cystatin C in the group of persons exposed to lead, cadmium and arsenic.	Arsenic	90-97	cystatin C	Homo sapiens	220-230
21356263-9	2011	Regression analysis demonstrated that higher blood level of lead, higher urinary level of arsenic, more advanced age and higher body mass index represented independent risk factors of an increased serum concentration of cystatin C in the group of persons exposed to lead, cadmium and arsenic.	Arsenic	284-291	cystatin C	Homo sapiens	220-230
21356263-10	2011	CONCLUSIONS: Higher blood level of lead and higher urinary level of arsenic represented independent risk factors of an increased serum concentration of cystatin C in the group of persons occupationally exposed to lead, cadmium and arsenic.	Arsenic	68-75	cystatin C	Homo sapiens	152-162
21356263-10	2011	CONCLUSIONS: Higher blood level of lead and higher urinary level of arsenic represented independent risk factors of an increased serum concentration of cystatin C in the group of persons occupationally exposed to lead, cadmium and arsenic.	Arsenic	231-238	cystatin C	Homo sapiens	152-162
21514422-9	2011	We concluded that mtTFA up-regulation, augmented mitochondrial biogenesis, and enhanced mitochondrial functions may contribute to arsenic-induced cell proliferation.	Arsenic	130-137	transcription factor A, mitochondrial	Homo sapiens	18-23
21349312-3	2011	Co-exposure to DDVP, MCP or arsenic produced significant inhibition of brain and serum AChE levels suggesting synergism.	Arsenic	28-35	acetylcholinesterase	Rattus norvegicus	87-91
21240543-8	2011	We docked PPP2CA with okadaic acid and calculated the value of affinity energy as -8.8 kcal/mol.	Arsenic	79-81	serine/threonine-protein phosphatase 2A catalytic subunit alpha isoform	Canis lupus familiaris	10-16
21272920-10	2011	By blocking PS, lactadherin was able to inhibit over 90% of the intrinsic tenase/prothrombinase activity of As(2)O(3)-treated HUVECs, and restored coagulation times of As(2)O(3)-treated cells and microparticles to control levels.	Arsenic	108-110	milk fat globule EGF and factor V/VIII domain containing	Homo sapiens	16-27
21272920-10	2011	By blocking PS, lactadherin was able to inhibit over 90% of the intrinsic tenase/prothrombinase activity of As(2)O(3)-treated HUVECs, and restored coagulation times of As(2)O(3)-treated cells and microparticles to control levels.	Arsenic	168-170	milk fat globule EGF and factor V/VIII domain containing	Homo sapiens	16-27
21292642-9	2011	These findings establish for the first time a causal role for depletion of miR-200b expression in human cell malignant transformation and tumor formation resulting from arsenic exposure.	Arsenic	169-176	microRNA 200b	Homo sapiens	75-83
21357384-0	2011	Polymorphisms in the TNF-alpha and IL10 gene promoters and risk of arsenic-induced skin lesions and other nondermatological health effects.	Arsenic	67-74	tumor necrosis factor	Homo sapiens	21-30
21320519-6	2011	Multivariate regression models showed that higher BMI, arsenic (+3 oxidation state) methyltransferase (AS3MT) genetic variant 7388, and higher total urinary arsenic were significantly associated with low percentage of urinary arsenic excreted as monomethylarsonic acid (%uMMA) or high ratio between urinary dimethylarsinic acid and uMMA (uDMA/uMMA), while AS3MT genetic variant M287T was associated with high %uMMA and low uDMA/uMMA.	Arsenic	55-62	arsenite methyltransferase	Homo sapiens	103-108
21357384-0	2011	Polymorphisms in the TNF-alpha and IL10 gene promoters and risk of arsenic-induced skin lesions and other nondermatological health effects.	Arsenic	67-74	interleukin 10	Homo sapiens	35-39
21357384-5	2011	The aim of the present work was to investigate the association between the TNF-alpha-308G&gt;A (rs1800629) and IL10 -3575T&gt;A (rs1800890) polymorphisms and arsenic-induced dermatological and nondermatological health outcomes.	Arsenic	158-165	tumor necrosis factor	Homo sapiens	75-84
21357384-5	2011	The aim of the present work was to investigate the association between the TNF-alpha-308G&gt;A (rs1800629) and IL10 -3575T&gt;A (rs1800890) polymorphisms and arsenic-induced dermatological and nondermatological health outcomes.	Arsenic	158-165	interleukin 10	Homo sapiens	111-115
21357384-10	2011	Individuals with GA/AA (-308 TNF-alpha) and TA/AA (-3575 IL10) genotypes were at higher risk of developing arsenic-induced skin lesions, ocular, and respiratory diseases.	Arsenic	107-114	tumor necrosis factor	Homo sapiens	29-38
21357384-10	2011	Individuals with GA/AA (-308 TNF-alpha) and TA/AA (-3575 IL10) genotypes were at higher risk of developing arsenic-induced skin lesions, ocular, and respiratory diseases.	Arsenic	107-114	interleukin 10	Homo sapiens	57-61
21357385-5	2011	We examined the effects of acute (24 h) exposure with environmentally relevant levels of arsenic (i.e., &lt; 4 muM as Na-arsenite) on wound-induced Ca2+ signaling pathways in human bronchial epithelial cell line (16HBE14o-).	Arsenic	89-96	latexin	Homo sapiens	111-114
21756780-1	2011	OBJECTIVE: To explore the influence of arsenic pollution caused by coal-burning on methylation (promoter and exon 5) and mutation (exon 5) of human p53 gene, and to analyze the relationship between methylation, mutation and arsenism.	Arsenic	39-46	tumor protein p53	Homo sapiens	148-151
21756780-14	2011	CONCLUSION: Arsenic pollution caused by coal-burning can cause the hypermethylation of p53 gene in promoter region, hypomethylation and mutation of p53 gene (exon 5), and the changes of methylation of p53 gene are related with its mutation and might be one of the important etiological factors of arsenic pathogenicity or carcinogenesis.	Arsenic	12-19	tumor protein p53	Homo sapiens	87-90
21756780-14	2011	CONCLUSION: Arsenic pollution caused by coal-burning can cause the hypermethylation of p53 gene in promoter region, hypomethylation and mutation of p53 gene (exon 5), and the changes of methylation of p53 gene are related with its mutation and might be one of the important etiological factors of arsenic pathogenicity or carcinogenesis.	Arsenic	12-19	tumor protein p53	Homo sapiens	148-151
21756780-14	2011	CONCLUSION: Arsenic pollution caused by coal-burning can cause the hypermethylation of p53 gene in promoter region, hypomethylation and mutation of p53 gene (exon 5), and the changes of methylation of p53 gene are related with its mutation and might be one of the important etiological factors of arsenic pathogenicity or carcinogenesis.	Arsenic	12-19	tumor protein p53	Homo sapiens	148-151
21315065-3	2011	We found that a non-lethal concentration of arsenic trioxide (1 muM) significantly induced the expression of heme oxygenase-1 (HO-1), a response biomarker to arsenic, without stimulating measurable superoxide production.	Arsenic	44-51	latexin	Homo sapiens	64-67
21315065-3	2011	We found that a non-lethal concentration of arsenic trioxide (1 muM) significantly induced the expression of heme oxygenase-1 (HO-1), a response biomarker to arsenic, without stimulating measurable superoxide production.	Arsenic	44-51	heme oxygenase 1	Homo sapiens	109-125
21315065-3	2011	We found that a non-lethal concentration of arsenic trioxide (1 muM) significantly induced the expression of heme oxygenase-1 (HO-1), a response biomarker to arsenic, without stimulating measurable superoxide production.	Arsenic	44-51	heme oxygenase 1	Homo sapiens	127-131
21315065-4	2011	Co-treatment of cells with the HO-1 competitive inhibitor zinc protoporphyrin (Znpp) potentiated arsenic-induced cytotoxicity, indicating that HO-1 confers a cytoprotective effect against arsenic toxicity.	Arsenic	97-104	heme oxygenase 1	Homo sapiens	31-35
21315065-4	2011	Co-treatment of cells with the HO-1 competitive inhibitor zinc protoporphyrin (Znpp) potentiated arsenic-induced cytotoxicity, indicating that HO-1 confers a cytoprotective effect against arsenic toxicity.	Arsenic	97-104	heme oxygenase 1	Homo sapiens	143-147
21345585-6	2011	The concentration of As(V) was calculated by difference between the total soluble inorganic arsenic and As(III) concentrations.	Arsenic	92-99	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	21-26
21376942-4	2011	Nowadays, more arsenic species is detected and analyzed in different kind of water (mineral, tap, waste), mainly owing to great possibilities resulting from coupling high performance liquid chromatography (HPLC) with inductively coupled plasma mass spectrometry (ICP-MS).	Arsenic	15-22	nuclear RNA export factor 1	Homo sapiens	93-96
21320519-6	2011	Multivariate regression models showed that higher BMI, arsenic (+3 oxidation state) methyltransferase (AS3MT) genetic variant 7388, and higher total urinary arsenic were significantly associated with low percentage of urinary arsenic excreted as monomethylarsonic acid (%uMMA) or high ratio between urinary dimethylarsinic acid and uMMA (uDMA/uMMA), while AS3MT genetic variant M287T was associated with high %uMMA and low uDMA/uMMA.	Arsenic	157-164	arsenite methyltransferase	Homo sapiens	356-361
21396911-5	2011	This study proposes that in response to arsenic exposure, the NRF2-mediated adaptive induction of endogenous antioxidant enzymes blunts insulin-stimulated ROS signaling and thus impairs ISGU.	Arsenic	40-47	NFE2 like bZIP transcription factor 2	Homo sapiens	62-66
21396911-5	2011	This study proposes that in response to arsenic exposure, the NRF2-mediated adaptive induction of endogenous antioxidant enzymes blunts insulin-stimulated ROS signaling and thus impairs ISGU.	Arsenic	40-47	insulin	Homo sapiens	136-143
21333531-6	2011	The results indicate that the oxidation of As(III) to less mobile As(V) utilizing ClO(3)(-) as a terminal electron acceptor provides a sustainable bioremediation strategy for arsenic contamination in anaerobic environments.	Arsenic	175-182	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	66-71
21378128-8	2011	This novel analysis confirmed that persons who excrete a higher proportion of MMA have a greater risk of skin lesions after data are adequately controlled for urinary arsenic metabolites, current arsenic exposure, and other risk factors.	Arsenic	167-174	monocyte to macrophage differentiation associated	Homo sapiens	78-81
21378128-8	2011	This novel analysis confirmed that persons who excrete a higher proportion of MMA have a greater risk of skin lesions after data are adequately controlled for urinary arsenic metabolites, current arsenic exposure, and other risk factors.	Arsenic	196-203	monocyte to macrophage differentiation associated	Homo sapiens	78-81
20842677-2	2011	Arsenic is a potent endocrine disruptor, including of the estrogen receptor.	Arsenic	0-7	estrogen receptor 1	Homo sapiens	58-75
21045647-3	2011	All patients underwent serial central graft thickness measurements with AS-OCT.	Arsenic	72-74	plexin A2	Homo sapiens	75-78
21219961-6	2011	Arsenic decreased cNOS-mediated NO release and eNOS expression in Phase-II.	Arsenic	0-7	nitric oxide synthase 3	Rattus norvegicus	18-22
21518486-3	2011	The results showed that the bortezomib combined with As(2)O(3) could induce significant apoptosis of NB4 cells and activation of caspase 3 and caspase 9, but As(2)O(3) (0.5 micromol/L) alone could not cause marked activation of caspase cascade and apoptosis of NB4 cells.	Arsenic	53-55	caspase 3	Homo sapiens	129-138
21266531-0	2011	The ATP-binding cassette transporter ABCB6 is induced by arsenic and protects against arsenic cytotoxicity.	Arsenic	57-64	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	37-42
21266531-0	2011	The ATP-binding cassette transporter ABCB6 is induced by arsenic and protects against arsenic cytotoxicity.	Arsenic	86-93	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	37-42
21266531-3	2011	ABCB6 is an ATP-binding cassette transporter that is highly expressed in cells resistant to arsenic.	Arsenic	92-99	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	0-5
21461218-2	2011	METHODS: Forty-five eyes (45 patients) underwent AS-OCT imaging to evaluate anterior chamber configuration before and 2 days after phacoemulsification and IOL implantation.	Arsenic	49-51	plexin A2	Homo sapiens	52-55
21518486-3	2011	The results showed that the bortezomib combined with As(2)O(3) could induce significant apoptosis of NB4 cells and activation of caspase 3 and caspase 9, but As(2)O(3) (0.5 micromol/L) alone could not cause marked activation of caspase cascade and apoptosis of NB4 cells.	Arsenic	53-55	caspase 9	Homo sapiens	143-152
21262220-8	2011	Immunohistochemical analysis revealed that coenzyme Q10 significantly decreased the arsenic-induced expression of inducible nitric oxide synthase, nuclear factor-kappaB, Fas ligand and caspase-3 in testicular tissue.	Arsenic	84-91	Fas ligand	Rattus norvegicus	170-180
21262220-8	2011	Immunohistochemical analysis revealed that coenzyme Q10 significantly decreased the arsenic-induced expression of inducible nitric oxide synthase, nuclear factor-kappaB, Fas ligand and caspase-3 in testicular tissue.	Arsenic	84-91	caspase 3	Rattus norvegicus	185-194
21129479-10	2011	The expressions of arsenic-sensitive stress genes, namely metallothionein-1 and heme oxygenase-1, were increased after arsenite or arsenate by 3-10-folds, but were unaltered after LWS and realgar.	Arsenic	19-26	metallothionein 1	Mus musculus	58-75
21235219-0	2011	Chronic exposure to arsenic causes increased cell survival, DNA damage, and increased expression of mitochondrial transcription factor A (mtTFA) in human prostate epithelial cells.	Arsenic	20-27	transcription factor A, mitochondrial	Homo sapiens	100-136
21235219-0	2011	Chronic exposure to arsenic causes increased cell survival, DNA damage, and increased expression of mitochondrial transcription factor A (mtTFA) in human prostate epithelial cells.	Arsenic	20-27	transcription factor A, mitochondrial	Homo sapiens	138-143
21235219-5	2011	Therefore, the objectives of this study were to investigate the effect of arsenic on cell proliferation/survival and genotoxicity, and to determine the effect of arsenic on the expression of mitochondrial transcription factor A (mtTFA) in human prostate epithelial cells, RWPE-1.	Arsenic	162-169	transcription factor A, mitochondrial	Homo sapiens	191-227
21235219-5	2011	Therefore, the objectives of this study were to investigate the effect of arsenic on cell proliferation/survival and genotoxicity, and to determine the effect of arsenic on the expression of mitochondrial transcription factor A (mtTFA) in human prostate epithelial cells, RWPE-1.	Arsenic	162-169	transcription factor A, mitochondrial	Homo sapiens	229-234
21235219-8	2011	Expressions of DNA repair genes ERCC6, XPC, OGG1, and reactive oxygen species (ROS) scavenger MnSOD was also altered in arsenic-exposed cells.	Arsenic	120-127	ERCC excision repair 6, chromatin remodeling factor	Homo sapiens	32-37
21235219-8	2011	Expressions of DNA repair genes ERCC6, XPC, OGG1, and reactive oxygen species (ROS) scavenger MnSOD was also altered in arsenic-exposed cells.	Arsenic	120-127	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	39-42
21235219-8	2011	Expressions of DNA repair genes ERCC6, XPC, OGG1, and reactive oxygen species (ROS) scavenger MnSOD was also altered in arsenic-exposed cells.	Arsenic	120-127	8-oxoguanine DNA glycosylase	Homo sapiens	44-48
21235219-8	2011	Expressions of DNA repair genes ERCC6, XPC, OGG1, and reactive oxygen species (ROS) scavenger MnSOD was also altered in arsenic-exposed cells.	Arsenic	120-127	superoxide dismutase 2	Homo sapiens	94-99
21235219-9	2011	Arsenic concentration-dependent increased expression of mtTFA and its regulator NRF-1 was observed in arsenic-exposed cells, suggesting that arsenic regulates mitochondrial activity through an NRF-1-dependent pathway.	Arsenic	0-7	transcription factor A, mitochondrial	Homo sapiens	56-61
21235219-9	2011	Arsenic concentration-dependent increased expression of mtTFA and its regulator NRF-1 was observed in arsenic-exposed cells, suggesting that arsenic regulates mitochondrial activity through an NRF-1-dependent pathway.	Arsenic	0-7	nuclear respiratory factor 1	Homo sapiens	80-85
21235219-9	2011	Arsenic concentration-dependent increased expression of mtTFA and its regulator NRF-1 was observed in arsenic-exposed cells, suggesting that arsenic regulates mitochondrial activity through an NRF-1-dependent pathway.	Arsenic	0-7	nuclear respiratory factor 1	Homo sapiens	193-198
21235219-9	2011	Arsenic concentration-dependent increased expression of mtTFA and its regulator NRF-1 was observed in arsenic-exposed cells, suggesting that arsenic regulates mitochondrial activity through an NRF-1-dependent pathway.	Arsenic	102-109	transcription factor A, mitochondrial	Homo sapiens	56-61
21235219-9	2011	Arsenic concentration-dependent increased expression of mtTFA and its regulator NRF-1 was observed in arsenic-exposed cells, suggesting that arsenic regulates mitochondrial activity through an NRF-1-dependent pathway.	Arsenic	102-109	nuclear respiratory factor 1	Homo sapiens	80-85
21235219-9	2011	Arsenic concentration-dependent increased expression of mtTFA and its regulator NRF-1 was observed in arsenic-exposed cells, suggesting that arsenic regulates mitochondrial activity through an NRF-1-dependent pathway.	Arsenic	102-109	nuclear respiratory factor 1	Homo sapiens	193-198
21235219-9	2011	Arsenic concentration-dependent increased expression of mtTFA and its regulator NRF-1 was observed in arsenic-exposed cells, suggesting that arsenic regulates mitochondrial activity through an NRF-1-dependent pathway.	Arsenic	141-148	transcription factor A, mitochondrial	Homo sapiens	56-61
21235219-9	2011	Arsenic concentration-dependent increased expression of mtTFA and its regulator NRF-1 was observed in arsenic-exposed cells, suggesting that arsenic regulates mitochondrial activity through an NRF-1-dependent pathway.	Arsenic	141-148	nuclear respiratory factor 1	Homo sapiens	80-85
21235219-9	2011	Arsenic concentration-dependent increased expression of mtTFA and its regulator NRF-1 was observed in arsenic-exposed cells, suggesting that arsenic regulates mitochondrial activity through an NRF-1-dependent pathway.	Arsenic	141-148	nuclear respiratory factor 1	Homo sapiens	193-198
21235219-11	2011	Additionally, this study also provides evidence that arsenic controls mitochondrial function by regulating mtTFA expression.	Arsenic	53-60	transcription factor A, mitochondrial	Homo sapiens	107-112
21129479-10	2011	The expressions of arsenic-sensitive stress genes, namely metallothionein-1 and heme oxygenase-1, were increased after arsenite or arsenate by 3-10-folds, but were unaltered after LWS and realgar.	Arsenic	19-26	heme oxygenase 1	Mus musculus	80-96
20842442-12	2011	Furthermore, overexpression of abcc1 improved the survival rates of embryos exposed to Cd, Hg or As, while overexpression of a abcc1 mutant (ABCC1-G1420D) sensitized zebrafish embryos to toxic metals.	Arsenic	97-99	ATP-binding cassette, sub-family C (CFTR/MRP), member 1	Danio rerio	31-36
21321608-5	2011	The mammalian STUbL RNF4 associates with Promyelocytic leukaemia (PML) nuclear bodies and regulates PML/PML-fusion protein stability in response to arsenic-induced stress.	Arsenic	148-155	ring finger protein 4	Homo sapiens	20-24
21321608-5	2011	The mammalian STUbL RNF4 associates with Promyelocytic leukaemia (PML) nuclear bodies and regulates PML/PML-fusion protein stability in response to arsenic-induced stress.	Arsenic	148-155	PML nuclear body scaffold	Homo sapiens	41-64
21321608-5	2011	The mammalian STUbL RNF4 associates with Promyelocytic leukaemia (PML) nuclear bodies and regulates PML/PML-fusion protein stability in response to arsenic-induced stress.	Arsenic	148-155	PML nuclear body scaffold	Homo sapiens	66-69
21321608-5	2011	The mammalian STUbL RNF4 associates with Promyelocytic leukaemia (PML) nuclear bodies and regulates PML/PML-fusion protein stability in response to arsenic-induced stress.	Arsenic	148-155	PML nuclear body scaffold	Homo sapiens	100-103
21321608-5	2011	The mammalian STUbL RNF4 associates with Promyelocytic leukaemia (PML) nuclear bodies and regulates PML/PML-fusion protein stability in response to arsenic-induced stress.	Arsenic	148-155	PML nuclear body scaffold	Homo sapiens	100-103
20143188-0	2011	miRNA-21 regulates arsenic-induced anti-leukemia activity in myelogenous cell lines.	Arsenic	19-26	microRNA 21	Homo sapiens	0-8
21195159-4	2011	Arsenic promoted not only c-RET tyrosine kinase activity but also genetically activated RET-MEN2A kinase activity with promotion of dimer formation of RET proteins.	Arsenic	0-7	ret proto-oncogene	Mus musculus	26-31
21195159-4	2011	Arsenic promoted not only c-RET tyrosine kinase activity but also genetically activated RET-MEN2A kinase activity with promotion of dimer formation of RET proteins.	Arsenic	0-7	ret proto-oncogene	Mus musculus	28-31
21195159-4	2011	Arsenic promoted not only c-RET tyrosine kinase activity but also genetically activated RET-MEN2A kinase activity with promotion of dimer formation of RET proteins.	Arsenic	0-7	ret proto-oncogene	Mus musculus	88-91
21195159-5	2011	Arsenic also increased secretion of the active form of MMP-2 in both RET-MEN2A-transfectants and c-RET-transfectants.	Arsenic	0-7	matrix metallopeptidase 2	Mus musculus	55-60
21195159-5	2011	Arsenic also increased secretion of the active form of MMP-2 in both RET-MEN2A-transfectants and c-RET-transfectants.	Arsenic	0-7	ret proto-oncogene	Mus musculus	69-72
21195159-5	2011	Arsenic also increased secretion of the active form of MMP-2 in both RET-MEN2A-transfectants and c-RET-transfectants.	Arsenic	0-7	ret proto-oncogene	Mus musculus	97-102
21195159-6	2011	On the other hand, arsenic promoted poly-(ADP-ribose) polymerase (PARP) degradation and cell death in both malignant and non-malignant cells.	Arsenic	19-26	poly (ADP-ribose) polymerase family, member 1	Mus musculus	36-64
21195159-6	2011	On the other hand, arsenic promoted poly-(ADP-ribose) polymerase (PARP) degradation and cell death in both malignant and non-malignant cells.	Arsenic	19-26	poly (ADP-ribose) polymerase family, member 1	Mus musculus	66-70
21195159-7	2011	Interestingly, l-cysteine inhibited the arsenic-mediated tumor-promoting effects (activation of kinases and MMP-2 secretion) but not arsenic-mediated anti-cancer effects (PARP degradation and cell death).	Arsenic	40-47	matrix metallopeptidase 2	Mus musculus	108-113
21195159-8	2011	Our results suggest redox-linked regulation of arsenic-mediated activities of kinases and MMP-2 secretion but not arsenic-mediated cell death.	Arsenic	47-54	matrix metallopeptidase 2	Mus musculus	90-95
21332098-6	2011	Our results indicated that curcumin suppressed the 8-hydroxy-20-deoxyguanosine level and OGG1 expression, which were increased by arsenic.	Arsenic	130-137	8-oxoguanine DNA glycosylase	Homo sapiens	89-93
21560304-6	2011	FSH and PRL level increased in low arsenic group and decreased in high arsenic groups (P &gt; 0.05).	Arsenic	35-42	prolactin	Rattus norvegicus	8-11
21281968-2	2011	In particular, interleukin-2 (IL2) secretion and T cell proliferation are reduced when peripheral blood mononuclear cells (PBMC) from individuals chronically exposed to arsenic are stimulated ex vivo with lectins such as phytohemaglutinin (PHA).	Arsenic	169-176	interleukin 2	Homo sapiens	15-28
21281968-2	2011	In particular, interleukin-2 (IL2) secretion and T cell proliferation are reduced when peripheral blood mononuclear cells (PBMC) from individuals chronically exposed to arsenic are stimulated ex vivo with lectins such as phytohemaglutinin (PHA).	Arsenic	169-176	interleukin 2	Homo sapiens	30-33
21281968-11	2011	Our findings demonstrate that, at least in vitro, inorganic arsenic acts directly on human T cells and impairs their activity, probably independently of HO-1 expression and monocyte-related accessory signals.	Arsenic	60-67	heme oxygenase 1	Homo sapiens	153-157
21560304-7	2011	GnRH and Cort level increased in arsenic groups, and GnRH level obviously increased in 0.4 microg/ml group and Cort level obviously increased in 0.1 and 0.4 microg/ml groups (P &lt; 0.05).	Arsenic	33-40	cortistatin	Rattus norvegicus	9-13
21560304-6	2011	FSH and PRL level increased in low arsenic group and decreased in high arsenic groups (P &gt; 0.05).	Arsenic	71-78	prolactin	Rattus norvegicus	8-11
21560304-7	2011	GnRH and Cort level increased in arsenic groups, and GnRH level obviously increased in 0.4 microg/ml group and Cort level obviously increased in 0.1 and 0.4 microg/ml groups (P &lt; 0.05).	Arsenic	33-40	gonadotropin releasing hormone 1	Rattus norvegicus	0-4
21406910-6	2011	We have performed a systematic study of the effect of local distortions around an arsenic atom on nu(Q) and eta.	Arsenic	82-89	endothelin receptor type A	Homo sapiens	108-111
21461292-9	2011	The observed over expression of TNFSF18 (167 fold) coupled with moderate expression of IGFL1 (3.1 fold), IL1R2 (5.9 fold) and AKR1C3 (9.2 fold) with a decreased RGS2 (2.0 fold) suggests that chronic arsenic exposure could produce sustained levels of TNF with modulation by an IL-1 analogue resulting in chronic immunologic insult.	Arsenic	199-206	TNF superfamily member 18	Homo sapiens	32-39
21461292-9	2011	The observed over expression of TNFSF18 (167 fold) coupled with moderate expression of IGFL1 (3.1 fold), IL1R2 (5.9 fold) and AKR1C3 (9.2 fold) with a decreased RGS2 (2.0 fold) suggests that chronic arsenic exposure could produce sustained levels of TNF with modulation by an IL-1 analogue resulting in chronic immunologic insult.	Arsenic	199-206	regulator of G protein signaling 2	Homo sapiens	161-165
21461292-9	2011	The observed over expression of TNFSF18 (167 fold) coupled with moderate expression of IGFL1 (3.1 fold), IL1R2 (5.9 fold) and AKR1C3 (9.2 fold) with a decreased RGS2 (2.0 fold) suggests that chronic arsenic exposure could produce sustained levels of TNF with modulation by an IL-1 analogue resulting in chronic immunologic insult.	Arsenic	199-206	tumor necrosis factor	Homo sapiens	32-35
21283237-1	2011	A wavelength-encoded interferometric high-temperature sensor based on an all-solid photonic bandgap fiber (AS-PBF) is reported.	Arsenic	107-109	zinc finger protein 395	Homo sapiens	110-113
21094969-4	2011	Analyses of downstream sediments reveal that a portion of the arsenic is retained as a mixed As(III)/As(V) solid-phase, though not at levels considered to be environmentally deleterious.	Arsenic	62-69	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	101-106
20571777-0	2011	Genetic variants associated with arsenic metabolism within human arsenic (+3 oxidation state) methyltransferase show wide variation across multiple populations.	Arsenic	33-40	arsenite methyltransferase	Homo sapiens	65-111
21253702-0	2011	Dietary intake of total and inorganic arsenic by adults in arsenic-contaminated Dan Chang district, Thailand, using duplicate food approach.	Arsenic	59-66	NBL1, DAN family BMP antagonist	Homo sapiens	80-83
21109336-0	2011	Contamination by arsenic and other trace elements of tube-well water along the Mekong River in Lao PDR.	Arsenic	17-24	interleukin 4 induced 1	Homo sapiens	95-98
21194611-2	2011	Previous studies have demonstrated that arsenic and chromium complexes are able to activate p53, but there is a dearth of data investigating whether uranium complexes exhibit similar effects.	Arsenic	40-47	tumor protein p53	Homo sapiens	92-95
21247820-0	2011	Polymorphisms in arsenic(+III oxidation state) methyltransferase (AS3MT) predict gene expression of AS3MT as well as arsenic metabolism.	Arsenic	17-24	arsenite methyltransferase	Homo sapiens	66-71
21247820-0	2011	Polymorphisms in arsenic(+III oxidation state) methyltransferase (AS3MT) predict gene expression of AS3MT as well as arsenic metabolism.	Arsenic	17-24	arsenite methyltransferase	Homo sapiens	100-105
21247820-0	2011	Polymorphisms in arsenic(+III oxidation state) methyltransferase (AS3MT) predict gene expression of AS3MT as well as arsenic metabolism.	Arsenic	117-124	arsenite methyltransferase	Homo sapiens	66-71
21199900-7	2011	Attenuating cPLA(2)alpha activation by AS or diphenylene iodonium prevented the induction of cyclooxygenase-2 and the production of PGE(2) that were essential for ICAM-1 upregulation.	Arsenic	39-41	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	12-24
21199900-7	2011	Attenuating cPLA(2)alpha activation by AS or diphenylene iodonium prevented the induction of cyclooxygenase-2 and the production of PGE(2) that were essential for ICAM-1 upregulation.	Arsenic	39-41	prostaglandin-endoperoxide synthase 2	Mus musculus	93-109
21199900-7	2011	Attenuating cPLA(2)alpha activation by AS or diphenylene iodonium prevented the induction of cyclooxygenase-2 and the production of PGE(2) that were essential for ICAM-1 upregulation.	Arsenic	39-41	intercellular adhesion molecule 1	Mus musculus	163-169
21780702-8	2011	The column capacities of 1.32 mg As(III)/g sorbent and 1.21 mg As(V)/g sorbent were found for initial concentration of 1.00 mg/L arsenic.	Arsenic	129-136	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	63-68
21299644-2	2011	Transfer of As(III) increases the affinity of ArsA for As(III), allowing resistance to environmental arsenic concentrations.	Arsenic	101-108	arylsulfatase A	Homo sapiens	46-50
20805060-11	2011	CONCLUSIONS: Here, we demonstrate for the first time that long isoforms of NRF1 contribute to arsenic-induced antioxidant response in human keratinocytes and protect the cells from acute arsenic cytotoxicity.	Arsenic	94-101	NFE2 like bZIP transcription factor 1	Homo sapiens	75-79
21074318-5	2011	The recombinant E. coli expressing the GST fused trimeric hMT-1A protein exhibited the highest Cd(II) and As(III) bioaccumulation ability, 6.36 mg Cd/g dry cells and 7.59 mg As/g dry cells, respectively.	Arsenic	106-108	metallothionein 1A	Homo sapiens	58-64
21040761-0	2011	Effects of MEK and DNMT inhibitors on arsenic-treated human uroepithelial cells in relation to Cyclin-D1 and p16.	Arsenic	38-45	mitogen-activated protein kinase kinase 7	Homo sapiens	11-14
21040761-0	2011	Effects of MEK and DNMT inhibitors on arsenic-treated human uroepithelial cells in relation to Cyclin-D1 and p16.	Arsenic	38-45	DNA methyltransferase 1	Homo sapiens	19-23
21040761-0	2011	Effects of MEK and DNMT inhibitors on arsenic-treated human uroepithelial cells in relation to Cyclin-D1 and p16.	Arsenic	38-45	cyclin D1	Homo sapiens	95-104
21040761-0	2011	Effects of MEK and DNMT inhibitors on arsenic-treated human uroepithelial cells in relation to Cyclin-D1 and p16.	Arsenic	38-45	cyclin dependent kinase inhibitor 2A	Homo sapiens	109-112
21040761-12	2011	Finally, these results indicated that Cyclin-D1 and p16 both might play important roles in carcinogenesis as a result of arsenic.	Arsenic	121-128	cyclin D1	Homo sapiens	38-47
21040761-12	2011	Finally, these results indicated that Cyclin-D1 and p16 both might play important roles in carcinogenesis as a result of arsenic.	Arsenic	121-128	cyclin dependent kinase inhibitor 2A	Homo sapiens	52-55
21176837-4	2011	Arsenic binding studies were undertaken under conditions optimized with respect to the crucial separation factor of the nonapeptides vasotocin (Vtc) and vasopressin (Vpr) in a shortened gradient time of 7.5 min.	Arsenic	0-7	arginine vasopressin	Homo sapiens	153-164
20238242-8	2011	Arsenic concentration in water was &gt; 10 mug L-1 (maximum limit permitted by Brazilian environmental regulations for water destined for human consumption) at all sampling sites, varying between 36.7 and 68.3 mug L-1.	Arsenic	0-7	immunoglobulin kappa variable 1-16	Homo sapiens	47-50
21226115-2	2011	Specifically, 4-acetoxystyrene (AS) has been chosen as a monomer for ATRP due to its ability to provide acetoxyl groups, which can be converted into phenolic hydroxyl groups for electrochemical detection in the presence of tyrosinase.	Arsenic	32-34	tyrosinase	Oryctolagus cuniculus	223-233
20883709-6	2011	Our observations also correlate well with previously identified impacts of As and Cd on specific genes associated with metal-induced toxicity (Cdkn1a, Mt1).	Arsenic	75-77	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	143-149
20883709-6	2011	Our observations also correlate well with previously identified impacts of As and Cd on specific genes associated with metal-induced toxicity (Cdkn1a, Mt1).	Arsenic	75-77	metallothionein 1	Mus musculus	151-154
21035470-0	2011	Precancerous and non-cancer disease endpoints of chronic arsenic exposure: the level of chromosomal damage and XRCC3 T241M polymorphism.	Arsenic	57-64	X-ray repair cross complementing 3	Homo sapiens	111-116
21035470-4	2011	We have investigated the association of XRCC3 T241M polymorphism with arsenic-induced precancerous and non-cancer disease outcomes.	Arsenic	70-77	X-ray repair cross complementing 3	Homo sapiens	40-45
20869459-8	2011	In addition, expression of abcc5 in ZF4 cells and zebrafish embryos was significantly induced by cadmium (Cd), lead (Pb), mercury (Hg) or arsenic (As).	Arsenic	138-145	ATP-binding cassette, sub-family C (CFTR/MRP), member 5	Danio rerio	27-32
20869459-8	2011	In addition, expression of abcc5 in ZF4 cells and zebrafish embryos was significantly induced by cadmium (Cd), lead (Pb), mercury (Hg) or arsenic (As).	Arsenic	147-149	ATP-binding cassette, sub-family C (CFTR/MRP), member 5	Danio rerio	27-32
21787675-4	2011	These effects of arsenic were coupled with enhanced mitochondrial swelling, inhibition of cytochrome c oxidase, Ca(2+)-ATPase, a decrease in mitochondrial calcium content, changes in indices of hepatic mitochondrial oxidative stress and iNOS expression.	Arsenic	17-24	nitric oxide synthase 2	Rattus norvegicus	237-241
21787675-5	2011	Arsenic also increased hepatic caspase 3 activity and DNA fragmentation.	Arsenic	0-7	caspase 3	Rattus norvegicus	31-40
20238242-8	2011	Arsenic concentration in water was &gt; 10 mug L-1 (maximum limit permitted by Brazilian environmental regulations for water destined for human consumption) at all sampling sites, varying between 36.7 and 68.3 mug L-1.	Arsenic	0-7	immunoglobulin kappa variable 1-16	Homo sapiens	214-217
20805060-0	2011	Long isoforms of NRF1 contribute to arsenic-induced antioxidant response in human keratinocytes.	Arsenic	36-43	NFE2 like bZIP transcription factor 1	Homo sapiens	17-21
20805060-11	2011	CONCLUSIONS: Here, we demonstrate for the first time that long isoforms of NRF1 contribute to arsenic-induced antioxidant response in human keratinocytes and protect the cells from acute arsenic cytotoxicity.	Arsenic	187-194	NFE2 like bZIP transcription factor 1	Homo sapiens	75-79
20805060-3	2011	OBJECTIVES: We investigated the role of NRF1 in arsenic-induced antioxidant response and cytotoxicity in human keratinocytes.	Arsenic	48-55	NFE2 like bZIP transcription factor 1	Homo sapiens	40-44
21731446-0	2011	Individual variations in inorganic arsenic metabolism associated with AS3MT genetic polymorphisms.	Arsenic	35-42	arsenite methyltransferase	Homo sapiens	70-75
21173536-7	2011	The expressions of SOD1 and Prdx2 were down-regulated in the brain of mice exposed to As, but iNOS expression was not disturbed by As exposure.	Arsenic	86-88	superoxide dismutase 1, soluble	Mus musculus	19-23
21173536-7	2011	The expressions of SOD1 and Prdx2 were down-regulated in the brain of mice exposed to As, but iNOS expression was not disturbed by As exposure.	Arsenic	86-88	peroxiredoxin 2	Mus musculus	28-33
21731446-2	2011	Arsenic (+3 oxidation state) methyltransferase (AS3MT) that can catalyze the transfer of a methyl group from S-adenosyl-l-methionine (AdoMet) to trivalent arsenical, may play a role in arsenic metabolism in humans.	Arsenic	155-162	arsenite methyltransferase	Homo sapiens	0-46
21731446-2	2011	Arsenic (+3 oxidation state) methyltransferase (AS3MT) that can catalyze the transfer of a methyl group from S-adenosyl-l-methionine (AdoMet) to trivalent arsenical, may play a role in arsenic metabolism in humans.	Arsenic	155-162	arsenite methyltransferase	Homo sapiens	48-53
21731446-3	2011	Since the genetic polymorphisms of AS3MT gene may be associated with the susceptibility to inorganic arsenic toxicity, relationships of several single nucleotide polymorphisms (SNPs) in AS3MT with inorganic arsenic metabolism have been investigated.	Arsenic	101-108	arsenite methyltransferase	Homo sapiens	35-40
21731446-5	2011	Results of genotype dependent differences in arsenic metabolism for most of SNPs in AS3MT were Inconsistent throughout the studies.	Arsenic	45-52	arsenite methyltransferase	Homo sapiens	84-89
21731446-6	2011	Nevertheless, two SNPs, AS3MT 12390 (rs3740393) and 14458 (rs11191439) were consistently related to arsenic methylation regardless of the populations examined for the analysis.	Arsenic	100-107	arsenite methyltransferase	Homo sapiens	24-29
21687637-8	2011	HIF-1 and VEGF are downstream effectors of AKT and ERK1/2 that are required for arsenic-inducing angiogenesis.	Arsenic	80-87	vascular endothelial growth factor A	Homo sapiens	10-14
22181980-6	2011	This study aimed to elucidate the role of tea against arsenic-induced formation of 8-hydroxy-2"-deoxyguanosine (8OHdG) and arsenic-suppressed DNA repair in Swiss albino mice.	Arsenic	54-61	solute carrier family 7 (cationic amino acid transporter, y+ system), member 2	Mus musculus	42-45
22181980-6	2011	This study aimed to elucidate the role of tea against arsenic-induced formation of 8-hydroxy-2"-deoxyguanosine (8OHdG) and arsenic-suppressed DNA repair in Swiss albino mice.	Arsenic	123-130	solute carrier family 7 (cationic amino acid transporter, y+ system), member 2	Mus musculus	42-45
22181980-9	2011	Thus, tea polyphenols may prove effective in treating arsenic-induced carcinogenesis.	Arsenic	54-61	solute carrier family 7 (cationic amino acid transporter, y+ system), member 2	Mus musculus	6-9
22432323-1	2011	A highly selective ligand exchange type adsorbent was developed for the removal of trace arsenic(V) (As(V)) and phosphate from water.	Arsenic	89-96	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	101-106
21822400-4	2011	A method was developed in this study for the on-site speciation of the most toxic dissolved arsenic species: As (III), As (V), monomethylarsonic acid (MMA) and dimethylarsenic acid (DMA).	Arsenic	92-99	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	119-125
21829673-8	2011	RESULTS: The alleles HLA-A*68, C*08 and DQB*05 were more frequently associated with severe outcomes (ND vs. AS, P(A*68) = 0.013/Pc = 0.26, P(C*08) = 0.0075/Pc = 0.064, and P(DQB1*05) = 0.029/Pc = 0.68), However the apparent DQB1*05 association was driven by age.	Arsenic	108-110	major histocompatibility complex, class I, A	Homo sapiens	21-26
21687637-5	2011	To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF).	Arsenic	36-43	AKT serine/threonine kinase 1	Homo sapiens	154-157
21687637-5	2011	To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF).	Arsenic	36-43	mitogen-activated protein kinase 3	Homo sapiens	162-168
21687637-5	2011	To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF).	Arsenic	36-43	hypoxia inducible factor 1 subunit alpha	Homo sapiens	220-246
21687637-5	2011	To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF).	Arsenic	36-43	hypoxia inducible factor 1 subunit alpha	Homo sapiens	248-253
22102309-3	2011	Both epidemiological and experimental evidence indicates that arsenic and ultraviolet radiation act on signaling pathways that effect the expression of cyclin D1.	Arsenic	62-69	cyclin D1	Homo sapiens	152-161
21912678-1	2011	The crystal structures of two proteins, a putative pyrazinamidase/nicotinamidase from the dental pathogen Streptococcus mutans (SmPncA) and the human caspase-6 (Casp6), were solved by de novo arsenic single-wavelength anomalous diffraction (As-SAD) phasing method.	Arsenic	192-199	caspase 6	Homo sapiens	150-159
21912678-1	2011	The crystal structures of two proteins, a putative pyrazinamidase/nicotinamidase from the dental pathogen Streptococcus mutans (SmPncA) and the human caspase-6 (Casp6), were solved by de novo arsenic single-wavelength anomalous diffraction (As-SAD) phasing method.	Arsenic	192-199	caspase 6	Homo sapiens	161-166
21912678-6	2011	In Casp6, four cysteines were found to bind cacodyl, a trivalent arsenic group (As (III)), in the presence of the reducing agent, dithiothreitol (DTT), and arsenic atoms were the only anomalous scatterers for SAD phasing.	Arsenic	65-72	caspase 6	Homo sapiens	3-8
21695274-3	2011	Arabidopsis SAP10 showed differential regulation by various abiotic stresses such as heavy metals and metalloids (Ni, Cd, Mn, Zn, and As), high and low temperatures, cold, and ABA.	Arsenic	134-136	stress-associated protein 10	Arabidopsis thaliana	12-17
21687637-5	2011	To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF).	Arsenic	36-43	vascular endothelial growth factor A	Homo sapiens	259-293
21687637-5	2011	To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF).	Arsenic	36-43	vascular endothelial growth factor A	Homo sapiens	295-299
21687637-8	2011	HIF-1 and VEGF are downstream effectors of AKT and ERK1/2 that are required for arsenic-inducing angiogenesis.	Arsenic	80-87	AKT serine/threonine kinase 1	Homo sapiens	43-46
21687637-5	2011	To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF).	Arsenic	80-87	AKT serine/threonine kinase 1	Homo sapiens	154-157
21687637-5	2011	To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF).	Arsenic	80-87	mitogen-activated protein kinase 3	Homo sapiens	162-168
21687637-5	2011	To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF).	Arsenic	80-87	hypoxia inducible factor 1 subunit alpha	Homo sapiens	220-246
21687637-5	2011	To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF).	Arsenic	80-87	hypoxia inducible factor 1 subunit alpha	Homo sapiens	248-253
21687637-8	2011	HIF-1 and VEGF are downstream effectors of AKT and ERK1/2 that are required for arsenic-inducing angiogenesis.	Arsenic	80-87	mitogen-activated protein kinase 3	Homo sapiens	51-57
21118980-4	2010	Interestingly, arsenic directly bound the RING finger domain of c-CBL to inhibit its self-ubiquitination/degradation without interfering with the enhancement of ubiquitination and subsequent proteolysis of its substrate BCR-ABL.	Arsenic	15-22	Casitas B-lineage lymphoma	Mus musculus	64-69
21687637-5	2011	To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF).	Arsenic	80-87	vascular endothelial growth factor A	Homo sapiens	259-293
21687637-5	2011	To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF).	Arsenic	80-87	vascular endothelial growth factor A	Homo sapiens	295-299
21687637-7	2011	Inhibition of ROS, AKT and ERK1/2 signaling pathways is sufficient to attenuate arsenic-inducing angiogenesis.	Arsenic	80-87	AKT serine/threonine kinase 1	Homo sapiens	19-22
21687637-7	2011	Inhibition of ROS, AKT and ERK1/2 signaling pathways is sufficient to attenuate arsenic-inducing angiogenesis.	Arsenic	80-87	mitogen-activated protein kinase 3	Homo sapiens	27-33
21687637-8	2011	HIF-1 and VEGF are downstream effectors of AKT and ERK1/2 that are required for arsenic-inducing angiogenesis.	Arsenic	80-87	hypoxia inducible factor 1 subunit alpha	Homo sapiens	0-5
21059470-5	2010	It was observed that high amount of arsenic was present in milk, feces, hair of cattle and water and straw samples in arsenic prone village.	Arsenic	36-43	Weaning weight-maternal milk	Bos taurus	59-63
21059470-6	2010	Milk product also contained significant amount of arsenic than that of milk product of control village.	Arsenic	50-57	Weaning weight-maternal milk	Bos taurus	0-4
20937726-0	2011	Carcinogenic effects of "whole-life" exposure to inorganic arsenic in CD1 mice.	Arsenic	59-66	CD1 antigen complex	Mus musculus	70-73
20937726-4	2011	CD1 mice were exposed to 0, 6, 12, or 24 ppm arsenic in the drinking water 2 weeks prior to breeding, during pregnancy, lactation, and after weaning through adulthood.	Arsenic	45-52	CD1 antigen complex	Mus musculus	0-3
20946910-5	2011	Arsenic-induced activation of caspase 3 was associated with phosphatidylserine exposure on the cell surface and microvesiculation of erythrocyte membrane.	Arsenic	0-7	caspase 3	Rattus norvegicus	30-39
20887743-0	2010	Arsenic (+3 oxidation state) methyltransferase genotype affects steady-state distribution and clearance of arsenic in arsenate-treated mice.	Arsenic	107-114	arsenite methyltransferase	Mus musculus	0-46
20887743-1	2010	Arsenic (+3 oxidation state) methyltransferase (As3mt) catalyzes formation of mono-, di-, and tri-methylated metabolites of inorganic arsenic.	Arsenic	134-141	arsenite methyltransferase	Mus musculus	0-46
20887743-1	2010	Arsenic (+3 oxidation state) methyltransferase (As3mt) catalyzes formation of mono-, di-, and tri-methylated metabolites of inorganic arsenic.	Arsenic	134-141	arsenite methyltransferase	Mus musculus	48-53
20887743-4	2010	At steady state, arsenic body burdens in As3mt knockout mice were 16 to 20 times greater than in wild-type mice.	Arsenic	17-24	arsenite methyltransferase	Mus musculus	41-46
20887743-5	2010	During the post dosing clearance period, arsenic body burdens declined in As3mt knockout mice to ~35% and in wild-type mice to ~10% of steady-state levels.	Arsenic	41-48	arsenite methyltransferase	Mus musculus	74-79
20887743-6	2010	Urinary concentration of arsenic was significantly lower in As3mt knockout mice than in wild-type mice.	Arsenic	25-32	arsenite methyltransferase	Mus musculus	60-65
20887743-7	2010	At steady state, As3mt knockout mice had significantly higher fractions of the body burden of arsenic in liver, kidney, and urinary bladder than did wild-type mice.	Arsenic	94-101	PDS5 cohesin associated factor B	Mus musculus	17-20
20887743-9	2010	Inorganic arsenic was the predominant species in tissues of As3mt knockout mice; tissues from wild-type mice contained mixtures of inorganic arsenic and its methylated metabolites.	Arsenic	10-17	arsenite methyltransferase	Mus musculus	60-65
20887743-10	2010	Diminished capacity for arsenic methylation in As3mt knockout mice prolongs retention of inorganic arsenic in tissues and affects whole body clearance of arsenic.	Arsenic	24-31	arsenite methyltransferase	Mus musculus	47-52
20887743-10	2010	Diminished capacity for arsenic methylation in As3mt knockout mice prolongs retention of inorganic arsenic in tissues and affects whole body clearance of arsenic.	Arsenic	99-106	arsenite methyltransferase	Mus musculus	47-52
20887743-10	2010	Diminished capacity for arsenic methylation in As3mt knockout mice prolongs retention of inorganic arsenic in tissues and affects whole body clearance of arsenic.	Arsenic	99-106	arsenite methyltransferase	Mus musculus	47-52
21118980-5	2010	Degradation of BCR-ABL due to c-CBL induction as a result of arsenic treatment was also observed in vivo in CML mice.	Arsenic	61-68	Casitas B-lineage lymphoma	Mus musculus	30-35
20887743-11	2010	Altered retention and tissue tropism of arsenic in As3mt knockout mice could affect the toxic or carcinogenic effects associated with exposure to this metalloid or its methylated metabolites.	Arsenic	40-47	arsenite methyltransferase	Mus musculus	51-56
21078981-7	2010	Here we show that in the absence of two ABCC-type transporters, AtABCC1 and AtABCC2, Arabidopsis thaliana is extremely sensitive to arsenic and arsenic-based herbicides.	Arsenic	132-139	multidrug resistance-associated protein 1	Arabidopsis thaliana	64-71
21078981-7	2010	Here we show that in the absence of two ABCC-type transporters, AtABCC1 and AtABCC2, Arabidopsis thaliana is extremely sensitive to arsenic and arsenic-based herbicides.	Arsenic	132-139	multidrug resistance-associated protein 2	Arabidopsis thaliana	76-83
21078981-7	2010	Here we show that in the absence of two ABCC-type transporters, AtABCC1 and AtABCC2, Arabidopsis thaliana is extremely sensitive to arsenic and arsenic-based herbicides.	Arsenic	144-151	multidrug resistance-associated protein 1	Arabidopsis thaliana	64-71
21078981-7	2010	Here we show that in the absence of two ABCC-type transporters, AtABCC1 and AtABCC2, Arabidopsis thaliana is extremely sensitive to arsenic and arsenic-based herbicides.	Arsenic	144-151	multidrug resistance-associated protein 2	Arabidopsis thaliana	76-83
21078981-11	2010	Overexpression of AtPCS1 and AtABCC1 resulted in plants exhibiting increased arsenic tolerance.	Arsenic	77-84	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	18-24
21078981-11	2010	Overexpression of AtPCS1 and AtABCC1 resulted in plants exhibiting increased arsenic tolerance.	Arsenic	77-84	multidrug resistance-associated protein 1	Arabidopsis thaliana	29-36
20735377-8	2010	Arsenic induced cytoplasmic microfilament rearrangement (tight perinuclear distribution with projections, stress fibres and pseudopodia) which was reversed by S. Also, activated JNK showed a similar distribution to actin.	Arsenic	0-7	mitogen-activated protein kinase 8	Homo sapiens	178-181
20943951-0	2010	Arsenic-induced SUMO-dependent recruitment of RNF4 into PML nuclear bodies.	Arsenic	0-7	ring finger protein 4	Homo sapiens	46-50
20480386-17	2010	Detectable levels of MA(V) were reported in both provinces up to a concentration of 79 mug l(-1) (equating to up to 33% of the total arsenic).	Arsenic	133-140	kelch like family member 2	Homo sapiens	21-26
20943951-0	2010	Arsenic-induced SUMO-dependent recruitment of RNF4 into PML nuclear bodies.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	56-59
20943951-2	2010	Arsenic is an effective treatment for this disease as it induces SUMO-dependent ubiquitin-mediated proteasomal degradation of the PML-RAR fusion protein.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	130-133
20943951-2	2010	Arsenic is an effective treatment for this disease as it induces SUMO-dependent ubiquitin-mediated proteasomal degradation of the PML-RAR fusion protein.	Arsenic	0-7	retinoic acid receptor alpha	Homo sapiens	134-137
20943951-3	2010	Here we analyze the nuclear trafficking dynamics of PML and its SUMO-dependent ubiquitin E3 ligase, RNF4 in response to arsenic.	Arsenic	120-127	PML nuclear body scaffold	Homo sapiens	52-55
20943951-3	2010	Here we analyze the nuclear trafficking dynamics of PML and its SUMO-dependent ubiquitin E3 ligase, RNF4 in response to arsenic.	Arsenic	120-127	ring finger protein 4	Homo sapiens	100-104
20943951-4	2010	After administration of arsenic, PML immediately transits into nuclear bodies where it undergoes SUMO modification.	Arsenic	24-31	PML nuclear body scaffold	Homo sapiens	33-36
20943951-8	2010	These studies indicate that arsenic induces the rapid reorganization of the cell nucleus by SUMO modification of nuclear body-associated PML and uptake of the ubiquitin E3 ligase RNF4 leading to the ubiquitin-mediated degradation of PML.	Arsenic	28-35	PML nuclear body scaffold	Homo sapiens	137-140
20943951-8	2010	These studies indicate that arsenic induces the rapid reorganization of the cell nucleus by SUMO modification of nuclear body-associated PML and uptake of the ubiquitin E3 ligase RNF4 leading to the ubiquitin-mediated degradation of PML.	Arsenic	28-35	ring finger protein 4	Homo sapiens	179-183
20943951-8	2010	These studies indicate that arsenic induces the rapid reorganization of the cell nucleus by SUMO modification of nuclear body-associated PML and uptake of the ubiquitin E3 ligase RNF4 leading to the ubiquitin-mediated degradation of PML.	Arsenic	28-35	PML nuclear body scaffold	Homo sapiens	233-236
20688429-5	2010	Pore surface diffusion model calculations predicted that lignite Fe-GAC could remove ~6.3 L g(-1) dry media and ~4 L g(-1) dry media of water contaminated with 30 mug L(-1) TCE and arsenic, respectively.	Arsenic	181-188	glutaminase	Homo sapiens	68-71
24278533-0	2010	Inhalation toxicity of particulate matters doped with arsenic induced genotoxicity and altered akt signaling pathway in lungs of mice.	Arsenic	54-61	thymoma viral proto-oncogene 1	Mus musculus	95-98
24278533-10	2010	Taken together, inhaled PMs-Arsenic caused genotoxicity and altered Akt signaling pathway in the lung.	Arsenic	28-35	thymoma viral proto-oncogene 1	Mus musculus	68-71
20816728-6	2010	Gene expression analysis revealed that arsenic exposure increased global lysosomal gene expression, which was associated with increased functional activity of the lysosome protease, cathepsin D.	Arsenic	39-46	cathepsin D	Homo sapiens	182-193
20212062-2	2010	The study revealed that arsenic increased the activity of superoxide dismutase (SOD) and catalase (CAT) and the level of lipid peroxidation (LPO), protein carbonyl (PC) and nitric oxide (NO) at 1 hour, 1.5 hours and 2 hours of incubation.	Arsenic	24-31	catalase	Rattus norvegicus	89-97
20732340-0	2010	Evaluation of the serum catalase and myeloperoxidase activities in chronic arsenic-exposed individuals and concomitant cytogenetic damage.	Arsenic	75-82	catalase	Homo sapiens	24-32
20732340-0	2010	Evaluation of the serum catalase and myeloperoxidase activities in chronic arsenic-exposed individuals and concomitant cytogenetic damage.	Arsenic	75-82	myeloperoxidase	Homo sapiens	37-52
20740275-0	2010	Non-enzymatic roles for the URE2 glutathione S-transferase in the response of Saccharomyces cerevisiae to arsenic.	Arsenic	106-113	glutathione peroxidase	Saccharomyces cerevisiae S288C	28-32
21146138-6	2010	An increase in the concentration of As increased APX activity in leaves and roots, except As(V) at pH 4 and pH 9 in the leaves and As(III) at pH 9 in the roots, when there was a significant decrease in APX activity at low As concentrations.	Arsenic	36-38	ascorbate peroxidase 2	Zea mays	49-52
21146138-6	2010	An increase in the concentration of As increased APX activity in leaves and roots, except As(V) at pH 4 and pH 9 in the leaves and As(III) at pH 9 in the roots, when there was a significant decrease in APX activity at low As concentrations.	Arsenic	36-38	ascorbate peroxidase 2	Zea mays	202-205
20924919-5	2010	Arsenic concentrations reached values up to 964 mu g L-1 and exceeded the current WHO provisional guideline value of 10 mu g L-1 in more than 50% of the sampled wells.	Arsenic	0-7	immunoglobulin kappa variable 1-16	Homo sapiens	53-56
20924919-5	2010	Arsenic concentrations reached values up to 964 mu g L-1 and exceeded the current WHO provisional guideline value of 10 mu g L-1 in more than 50% of the sampled wells.	Arsenic	0-7	immunoglobulin kappa variable 1-16	Homo sapiens	125-128
20732340-7	2010	Our results show that individuals chronically exposed to arsenic have significantly higher CAT and MPO activities and higher incidence of CA.	Arsenic	57-64	catalase	Homo sapiens	91-94
20732340-7	2010	Our results show that individuals chronically exposed to arsenic have significantly higher CAT and MPO activities and higher incidence of CA.	Arsenic	57-64	myeloperoxidase	Homo sapiens	99-102
20732340-9	2010	These results indicate that chronic arsenic exposure causes higher CAT and MPO activities in serum that correlates with induction of genetic damage.	Arsenic	36-43	catalase	Homo sapiens	67-70
20732340-9	2010	These results indicate that chronic arsenic exposure causes higher CAT and MPO activities in serum that correlates with induction of genetic damage.	Arsenic	36-43	myeloperoxidase	Homo sapiens	75-78
20212062-2	2010	The study revealed that arsenic increased the activity of superoxide dismutase (SOD) and catalase (CAT) and the level of lipid peroxidation (LPO), protein carbonyl (PC) and nitric oxide (NO) at 1 hour, 1.5 hours and 2 hours of incubation.	Arsenic	24-31	catalase	Rattus norvegicus	99-102
20621591-6	2010	RESULTS: Compared with the patient controls and healthy controls, serum CXCL16 concentration was significantly increased in the AS group (P&lt;0.05, and 0.01).	Arsenic	128-130	C-X-C motif chemokine ligand 16	Homo sapiens	72-78
20947858-8	2010	In zip code-level analysis, arsenic was associated with an increased risk of stroke admission (relative risk, 1.03; 95% CI, 1.01 to 1.05 per mug/L increase in arsenic) after adjustment for confounders, and null or negative associations were found between arsenic and nonvascular outcomes.	Arsenic	28-35	death associated protein kinase 3	Homo sapiens	3-6
20946641-8	2010	Among the bona fide NMD targets, we identified a highly conserved AS-NMD event within the 3" UTR of the HNRNPA2B1 gene.	Arsenic	66-68	heterogeneous nuclear ribonucleoprotein A2/B1	Homo sapiens	104-113
20981267-6	2010	In addition to the identified candidate nsSNPs for increased or reduced arsenic responsiveness, we observed i) a nsSNP that results in the breakage of a disulfide bond, as candidate marker for reduced arsenic responsiveness of KLK7, a secreted serine protease participate in normal shedding of the skin; and ii) 6 pairs of vicinal cysteines in KLK7 protein that could be binding sites for arsenic.	Arsenic	201-208	kallikrein related peptidase 7	Homo sapiens	227-231
20981267-6	2010	In addition to the identified candidate nsSNPs for increased or reduced arsenic responsiveness, we observed i) a nsSNP that results in the breakage of a disulfide bond, as candidate marker for reduced arsenic responsiveness of KLK7, a secreted serine protease participate in normal shedding of the skin; and ii) 6 pairs of vicinal cysteines in KLK7 protein that could be binding sites for arsenic.	Arsenic	201-208	coagulation factor II, thrombin	Homo sapiens	244-259
20981267-6	2010	In addition to the identified candidate nsSNPs for increased or reduced arsenic responsiveness, we observed i) a nsSNP that results in the breakage of a disulfide bond, as candidate marker for reduced arsenic responsiveness of KLK7, a secreted serine protease participate in normal shedding of the skin; and ii) 6 pairs of vicinal cysteines in KLK7 protein that could be binding sites for arsenic.	Arsenic	201-208	kallikrein related peptidase 7	Homo sapiens	344-348
20981267-6	2010	In addition to the identified candidate nsSNPs for increased or reduced arsenic responsiveness, we observed i) a nsSNP that results in the breakage of a disulfide bond, as candidate marker for reduced arsenic responsiveness of KLK7, a secreted serine protease participate in normal shedding of the skin; and ii) 6 pairs of vicinal cysteines in KLK7 protein that could be binding sites for arsenic.	Arsenic	201-208	kallikrein related peptidase 7	Homo sapiens	227-231
20981267-6	2010	In addition to the identified candidate nsSNPs for increased or reduced arsenic responsiveness, we observed i) a nsSNP that results in the breakage of a disulfide bond, as candidate marker for reduced arsenic responsiveness of KLK7, a secreted serine protease participate in normal shedding of the skin; and ii) 6 pairs of vicinal cysteines in KLK7 protein that could be binding sites for arsenic.	Arsenic	201-208	coagulation factor II, thrombin	Homo sapiens	244-259
20981267-6	2010	In addition to the identified candidate nsSNPs for increased or reduced arsenic responsiveness, we observed i) a nsSNP that results in the breakage of a disulfide bond, as candidate marker for reduced arsenic responsiveness of KLK7, a secreted serine protease participate in normal shedding of the skin; and ii) 6 pairs of vicinal cysteines in KLK7 protein that could be binding sites for arsenic.	Arsenic	201-208	kallikrein related peptidase 7	Homo sapiens	344-348
20981267-8	2010	In particular, an epidermal expressed serine protease with crucial function in normal skin physiology was prioritized on the basis of abundance of vicinal cysteines for further research on arsenic-induced keratinocyte carcinogenesis.	Arsenic	189-196	coagulation factor II, thrombin	Homo sapiens	38-53
20708634-0	2010	GT-repeat polymorphism in the heme oxygenase-1 gene promoter is associated with cardiovascular mortality risk in an arsenic-exposed population in northeastern Taiwan.	Arsenic	116-123	heme oxygenase 1	Homo sapiens	30-46
20708634-3	2010	The relationship of HO-1 genotype with arsenic-associated cardiovascular disease has not been studied.	Arsenic	39-46	heme oxygenase 1	Homo sapiens	20-24
20708634-4	2010	In this study, we evaluated the relationship between the HO-1 GT-repeat polymorphism and cardiovascular mortality in an arsenic-exposed population.	Arsenic	120-127	heme oxygenase 1	Homo sapiens	57-61
20708634-12	2010	Shorter (GT)n repeats in the HO-1 gene promoter may confer protective effects against cardiovascular mortality related to arsenic exposure.	Arsenic	122-129	heme oxygenase 1	Homo sapiens	29-33
20580158-2	2010	Since most existing arsenic removal technologies are effective in removing As(V) (arsenate), this study focused on As(III).	Arsenic	20-27	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	75-80
20473132-3	2010	Arsenic toxicity induces hyperphosphorylation of protein tau and overtranscription of the amyloid precursor protein, which are involved in the formation of neurofibrillary tangles and brain amyloid plaques, consistent with the amyloid hypothesis of AD.	Arsenic	0-7	microtubule associated protein tau	Homo sapiens	57-60
20654705-0	2010	Arsenic-induced cell proliferation is associated with enhanced ROS generation, Erk signaling and CyclinA expression.	Arsenic	0-7	mitogen-activated protein kinase 1	Homo sapiens	79-82
20654705-0	2010	Arsenic-induced cell proliferation is associated with enhanced ROS generation, Erk signaling and CyclinA expression.	Arsenic	0-7	cyclin A2	Homo sapiens	97-104
20654705-4	2010	A novel, un-documented biomarker of arsenic exposure, CyclinA was identified by microarray analysis from the study.	Arsenic	36-43	cyclin A2	Homo sapiens	54-61
20654705-5	2010	Non-transformed cell lines HaCat and Int407 when exposed to clinically achievable arsenic concentration showed significant increase of CyclinA substantiating the clinical data.	Arsenic	82-89	cyclin A2	Homo sapiens	135-142
20654705-7	2010	On further investigation of the pathway to arsenic-induced proliferation, we observed that arsenic resulted: ROS generation; activated Erk signaling; stimulated AP-1 activity, including immediate early genes, c-Jun and c-Fos.	Arsenic	43-50	mitogen-activated protein kinase 1	Homo sapiens	135-138
20654705-7	2010	On further investigation of the pathway to arsenic-induced proliferation, we observed that arsenic resulted: ROS generation; activated Erk signaling; stimulated AP-1 activity, including immediate early genes, c-Jun and c-Fos.	Arsenic	43-50	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	209-214
20654705-7	2010	On further investigation of the pathway to arsenic-induced proliferation, we observed that arsenic resulted: ROS generation; activated Erk signaling; stimulated AP-1 activity, including immediate early genes, c-Jun and c-Fos.	Arsenic	43-50	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	219-224
20654705-7	2010	On further investigation of the pathway to arsenic-induced proliferation, we observed that arsenic resulted: ROS generation; activated Erk signaling; stimulated AP-1 activity, including immediate early genes, c-Jun and c-Fos.	Arsenic	91-98	mitogen-activated protein kinase 1	Homo sapiens	135-138
20654705-7	2010	On further investigation of the pathway to arsenic-induced proliferation, we observed that arsenic resulted: ROS generation; activated Erk signaling; stimulated AP-1 activity, including immediate early genes, c-Jun and c-Fos.	Arsenic	91-98	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	209-214
20654705-7	2010	On further investigation of the pathway to arsenic-induced proliferation, we observed that arsenic resulted: ROS generation; activated Erk signaling; stimulated AP-1 activity, including immediate early genes, c-Jun and c-Fos.	Arsenic	91-98	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	219-224
20473132-3	2010	Arsenic toxicity induces hyperphosphorylation of protein tau and overtranscription of the amyloid precursor protein, which are involved in the formation of neurofibrillary tangles and brain amyloid plaques, consistent with the amyloid hypothesis of AD.	Arsenic	0-7	amyloid beta precursor protein	Homo sapiens	90-115
20655937-4	2010	Heavy metals such as As(3+), Cr(6+), Pb(2+) and Cd(2+) substituted for Ca(2+) in the ssDNA binding and annealing activities of annexin A1.	Arsenic	21-23	annexin A1	Mus musculus	127-137
21335294-7	2010	Quantitative data indicated that, in these elderly patients (generally defined as &gt;=65 years of age) with type 2 DM, DPP-4 inhibitors were associated with significant HbA(1c) reductions that ranged from ~0.7% (baseline HbA(1c) = 7.8%; P &lt; 0.001) to 1.2% (baseline HbA(1c) = 8.3%; P &lt; 0.05).	Arsenic	79-81	dipeptidyl peptidase 4	Homo sapiens	120-125
20699661-2	2010	Arsenic trioxide (As(2)O(3)), used in the treatment of promyelocytic leukemia (PML), triggers cell death in several solid tumor cell lines including ovarian carcinomas.	Arsenic	18-20	PML nuclear body scaffold	Homo sapiens	79-82
20660648-2	2010	Using an unbiased chemogenomics approach in Saccharomyces cerevisiae, we found that mutants of the chaperonin complex TRiC and the functionally related prefoldin complex are all hypersensitive to arsenic compared to a wild-type strain.	Arsenic	196-203	t-complex 1	Bos taurus	118-122
20660648-4	2010	These observations led us to hypothesize that arsenic might inhibit TRiC function, required for folding of actin, tubulin, and other proteins postsynthesis.	Arsenic	46-53	t-complex 1	Bos taurus	68-72
20660648-4	2010	These observations led us to hypothesize that arsenic might inhibit TRiC function, required for folding of actin, tubulin, and other proteins postsynthesis.	Arsenic	46-53	actin epsilon 1	Bos taurus	107-112
20660648-5	2010	Consistent with this hypothesis, we found that arsenic treatment distorted morphology of both actin and microtubule filaments.	Arsenic	47-54	actin epsilon 1	Bos taurus	94-99
20660648-6	2010	Moreover, arsenic impaired substrate folding by both bovine and archaeal TRiC complexes in vitro.	Arsenic	10-17	t-complex 1	Bos taurus	73-77
20660648-7	2010	These results together indicate that TRiC is a conserved target of arsenic inhibition in various biological systems.	Arsenic	67-74	t-complex 1	Bos taurus	37-41
20818482-4	2010	Cells underwent induction of heat shock protein 70 only at the highest doses of inorganic arsenic (30 and 60 microM), suggesting a high threshold to respond to stress.	Arsenic	90-97	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	29-50
20638426-0	2010	Enhanced arsenic accumulation in Saccharomyces cerevisiae overexpressing transporters Fps1p or Hxt7p.	Arsenic	9-16	Fps1p	Saccharomyces cerevisiae S288C	86-91
20638426-0	2010	Enhanced arsenic accumulation in Saccharomyces cerevisiae overexpressing transporters Fps1p or Hxt7p.	Arsenic	9-16	hexose transporter HXT7	Saccharomyces cerevisiae S288C	95-100
19826909-0	2010	Stress inducible heat shock protein 70: a potent molecular and toxicological signature in arsenic exposed broiler chickens.	Arsenic	90-97	heat shock protein family A (Hsp70) member 2	Gallus gallus	17-38
20627814-1	2010	JAK2 and STAT3 polymorphisms have been implicated to be associated with inflammatory bowel disease, which might share common immunogenesis and genetic factors with AS.	Arsenic	164-166	Janus kinase 2	Homo sapiens	0-4
20656687-4	2010	In efforts to understand the functional relevance of arsenic-induced autophagy, we found that pharmacological inhibitors of autophagy or molecular targeting of beclin 1 or Atg7 results in reversal of the suppressive effects of As(2)O(3) on leukemic cell lines and primary leukemic progenitors from acute myelogenous leukemia patients.	Arsenic	53-60	beclin 1	Homo sapiens	160-168
20656687-4	2010	In efforts to understand the functional relevance of arsenic-induced autophagy, we found that pharmacological inhibitors of autophagy or molecular targeting of beclin 1 or Atg7 results in reversal of the suppressive effects of As(2)O(3) on leukemic cell lines and primary leukemic progenitors from acute myelogenous leukemia patients.	Arsenic	53-60	autophagy related 7	Homo sapiens	172-176
20478284-0	2010	High selenium status in individuals exposed to arsenic through coal-burning in Shaanxi (PR of China) modulates antioxidant enzymes, heme oxygenase-1 and DNA damage.	Arsenic	47-54	heme oxygenase 1	Homo sapiens	132-148
20478284-4	2010	RESULTS: High selenium status was correlated with elevated activities of serum superoxide dismutase, glutathione peroxidase, catalase, and reduced levels of malondialdehyde, and increased RNA and protein expression of heme oxygenase-1 in peripheral blood mononuclear cells (PBMC) of individuals in the high arsenic group.	Arsenic	307-314	heme oxygenase 1	Homo sapiens	218-234
20830294-0	2010	Protective role of taurine against arsenic-induced mitochondria-dependent hepatic apoptosis via the inhibition of PKCdelta-JNK pathway.	Arsenic	35-42	mitogen-activated protein kinase 8	Rattus norvegicus	123-126
20473585-4	2010	The arsenic-induced cell apoptosis and intracellular ROS were blocked by the addition of the antioxidant N-acetyl-L-cysteine (NAC).	Arsenic	4-11	X-linked Kx blood group	Homo sapiens	126-129
20473585-5	2010	The mRNAs of superoxide dismutase 2 (SOD2) and NAD(P)H:quinone oxidoreductase 1 (NQO1) increased strikingly when cells were treated with a low concentration of NaAsO(2) (5 microM) and the level of induction was decreased with higher concentrations of arsenic treatment.	Arsenic	251-258	superoxide dismutase 2	Homo sapiens	13-35
20473585-5	2010	The mRNAs of superoxide dismutase 2 (SOD2) and NAD(P)H:quinone oxidoreductase 1 (NQO1) increased strikingly when cells were treated with a low concentration of NaAsO(2) (5 microM) and the level of induction was decreased with higher concentrations of arsenic treatment.	Arsenic	251-258	superoxide dismutase 2	Homo sapiens	37-41
20473585-5	2010	The mRNAs of superoxide dismutase 2 (SOD2) and NAD(P)H:quinone oxidoreductase 1 (NQO1) increased strikingly when cells were treated with a low concentration of NaAsO(2) (5 microM) and the level of induction was decreased with higher concentrations of arsenic treatment.	Arsenic	251-258	NAD(P)H quinone dehydrogenase 1	Homo sapiens	47-79
20473585-5	2010	The mRNAs of superoxide dismutase 2 (SOD2) and NAD(P)H:quinone oxidoreductase 1 (NQO1) increased strikingly when cells were treated with a low concentration of NaAsO(2) (5 microM) and the level of induction was decreased with higher concentrations of arsenic treatment.	Arsenic	251-258	NAD(P)H quinone dehydrogenase 1	Homo sapiens	81-85
20473585-7	2010	The decrease in intracellular ROS and the increase in SOD2 and NQO1 expressions observed when HUVECs were treated with low concentration of NaAsO(2), suggest the role of the two enzymes in protecting HUVECs from injuries of arsenic exposure.	Arsenic	224-231	NAD(P)H quinone dehydrogenase 1	Homo sapiens	63-67
20627814-1	2010	JAK2 and STAT3 polymorphisms have been implicated to be associated with inflammatory bowel disease, which might share common immunogenesis and genetic factors with AS.	Arsenic	164-166	signal transducer and activator of transcription 3	Homo sapiens	9-14
20627814-5	2010	Haplotype analysis revealed an association of haplotype rs1536798/rs10119004/rs7857730-CGT in JAK2 locus with AS.	Arsenic	110-112	UDP glycosyltransferase 8	Homo sapiens	87-90
20627814-5	2010	Haplotype analysis revealed an association of haplotype rs1536798/rs10119004/rs7857730-CGT in JAK2 locus with AS.	Arsenic	110-112	Janus kinase 2	Homo sapiens	94-98
20627814-6	2010	In conclusion, we first demonstrated the association of JAK2 polymorphisms with the susceptibility of AS, which indicated that IL-23 pathway also was an important etiological factor in AS in Chinese population.	Arsenic	102-104	Janus kinase 2	Homo sapiens	56-60
20627814-6	2010	In conclusion, we first demonstrated the association of JAK2 polymorphisms with the susceptibility of AS, which indicated that IL-23 pathway also was an important etiological factor in AS in Chinese population.	Arsenic	102-104	interleukin 23 subunit alpha	Homo sapiens	127-132
20456704-4	2010	RESULTS: Twenty-eight of 47 respondents (60%) accept the use of at least one AS (AS-1, AS-3, or AS-5).	Arsenic	77-79	PDS5 cohesin associated factor B	Homo sapiens	87-91
20510259-7	2010	The NaPiIIb isoform showed the highest affinity for As(V) in mouse (57 microM), rat (51 microM), and human (9.7 microM), which are very similar to the affinities for Pi.	Arsenic	52-54	solute carrier family 34 (sodium phosphate), member 2	Mus musculus	4-11
20600216-2	2010	Previous studies have identified associations between the proportion of urinary MMA (%MMA) and increased risks of several arsenic-related diseases, although none of these reported on lung cancer.	Arsenic	122-129	monocyte to macrophage differentiation associated	Homo sapiens	85-89
20456704-4	2010	RESULTS: Twenty-eight of 47 respondents (60%) accept the use of at least one AS (AS-1, AS-3, or AS-5).	Arsenic	77-79	prostaglandin D2 receptor	Homo sapiens	81-85
20796278-0	2010	GT-repeat polymorphism in the heme oxygenase-1 gene promoter and the risk of carotid atherosclerosis related to arsenic exposure.	Arsenic	112-119	heme oxygenase 1	Homo sapiens	30-46
20796278-1	2010	BACKGROUND: Arsenic is a strong stimulus of heme oxygenase (HO)-1 expression in experimental studies in response to oxidative stress caused by a stimulus.	Arsenic	12-19	heme oxygenase 1	Homo sapiens	44-65
20796278-5	2010	In this study, we investigated the relationship between HO-1 genetic polymorphism and the risk of atherosclerosis related to arsenic.	Arsenic	125-132	heme oxygenase 1	Homo sapiens	56-60
20796278-13	2010	CONCLUSIONS: This exploratory study suggests that at a relatively high level of arsenic exposure, carriers of the short (GT)n allele (&lt; 27 repeats) in the HO-1 gene promoter had a lower probability of developing carotid atherosclerosis than non-carriers of the allele after long-term arsenic exposure via ground water.	Arsenic	80-87	heme oxygenase 1	Homo sapiens	158-162
20796278-13	2010	CONCLUSIONS: This exploratory study suggests that at a relatively high level of arsenic exposure, carriers of the short (GT)n allele (&lt; 27 repeats) in the HO-1 gene promoter had a lower probability of developing carotid atherosclerosis than non-carriers of the allele after long-term arsenic exposure via ground water.	Arsenic	287-294	heme oxygenase 1	Homo sapiens	158-162
20796278-14	2010	The short (GT)n repeat in the HO-1 gene promoter may provide protective effects against carotid atherosclerosis in individuals with a high level of arsenic exposure.	Arsenic	148-155	heme oxygenase 1	Homo sapiens	30-34
20510259-8	2010	Therefore, NaPiIIb can have a prominent role in the toxicokinetics of arsenic following oral exposure to freshwater or food contaminated with As(V).	Arsenic	70-77	solute carrier family 34 member 2	Homo sapiens	11-18
20707922-10	2010	The role of the NRF2 pathway in protecting cells against arsenic-induced cell killing was validated in tumor cells using shRNA-mediated knock-down.	Arsenic	57-64	NFE2 like bZIP transcription factor 2	Homo sapiens	16-20
20598115-13	2010	Downregulation of the estrogen receptor and estrogen-responsive genes in response to arsenic indicates a mechanism of suppression of female reproductive functions by an environmental toxicant that is contra-mechanistic to that of estrogen.	Arsenic	85-92	estrogen receptor 1	Rattus norvegicus	22-39
20670920-0	2010	Association of genetic variation in cystathionine-beta-synthase and arsenic metabolism.	Arsenic	68-75	cystathionine beta-synthase	Homo sapiens	36-63
20670920-4	2010	In 142 subjects in Cordoba Province, Argentina, variant genotypes for CBS rs234709 and rs4920037 SNPs compared with wild-type homozygotes were associated with 24% and 26% increases, respectively, in the mean proportion of arsenic excreted as monomethylarsonic acid (%MMA).	Arsenic	222-229	cystathionine beta-synthase	Homo sapiens	70-73
20670920-6	2010	Small inverse associations with CBS rs234709 and rs4920037 variants were also found for the mean levels of the proportion of arsenic excreted as dimethylarsinous acid (%DMA).	Arsenic	125-132	cystathionine beta-synthase	Homo sapiens	32-35
20670920-8	2010	These findings are the first to suggest that CBS polymorphisms may influence arsenic metabolism in humans and susceptibility to arsenic-related disease.	Arsenic	77-84	cystathionine beta-synthase	Homo sapiens	45-48
20670920-8	2010	These findings are the first to suggest that CBS polymorphisms may influence arsenic metabolism in humans and susceptibility to arsenic-related disease.	Arsenic	128-135	cystathionine beta-synthase	Homo sapiens	45-48
20609355-4	2010	We demonstrate that upon As(2)O(3) exposure, PML undergoes ROS-initiated intermolecular disulfide formation and binds arsenic directly.	Arsenic	118-125	PML nuclear body scaffold	Homo sapiens	45-48
20618979-0	2010	Association between arsenic exposure and plasma cholinesterase activity: a population based study in Bangladesh.	Arsenic	20-27	butyrylcholinesterase	Homo sapiens	48-62
20618979-3	2010	The relationship between plasma cholinesterase (PChE) activity and arsenic exposure has not yet been clearly documented.	Arsenic	67-74	butyrylcholinesterase	Homo sapiens	32-46
20584751-0	2010	Selenium-dependent and -independent transport of arsenic by the human multidrug resistance protein 2 (MRP2/ABCC2): implications for the mutual detoxification of arsenic and selenium.	Arsenic	49-56	ATP binding cassette subfamily C member 2	Homo sapiens	102-106
20584751-0	2010	Selenium-dependent and -independent transport of arsenic by the human multidrug resistance protein 2 (MRP2/ABCC2): implications for the mutual detoxification of arsenic and selenium.	Arsenic	49-56	ATP binding cassette subfamily C member 2	Homo sapiens	107-112
20584751-0	2010	Selenium-dependent and -independent transport of arsenic by the human multidrug resistance protein 2 (MRP2/ABCC2): implications for the mutual detoxification of arsenic and selenium.	Arsenic	161-168	ATP binding cassette subfamily C member 2	Homo sapiens	102-106
20584751-0	2010	Selenium-dependent and -independent transport of arsenic by the human multidrug resistance protein 2 (MRP2/ABCC2): implications for the mutual detoxification of arsenic and selenium.	Arsenic	161-168	ATP binding cassette subfamily C member 2	Homo sapiens	107-112
19468689-0	2010	MER1, a novel organic arsenic derivative, has potent PML-RARalpha-independent cytotoxic activity against leukemia cells.	Arsenic	22-29	retinoic acid receptor alpha	Homo sapiens	57-65
20624968-0	2010	Arsenic antagonizes the Hedgehog pathway by preventing ciliary accumulation and reducing stability of the Gli2 transcriptional effector.	Arsenic	0-7	GLI family zinc finger 2	Homo sapiens	106-110
20624968-3	2010	We report here that arsenicals, in contrast, antagonize the Hh pathway by targeting Gli transcriptional effectors; in the short term, arsenic blocks Hh-induced ciliary accumulation of Gli2, the primary activator of Hh-dependent transcription, and with prolonged incubation arsenic reduces steady-state levels of Gli2.	Arsenic	20-27	GLI family zinc finger 1	Homo sapiens	84-87
20624968-3	2010	We report here that arsenicals, in contrast, antagonize the Hh pathway by targeting Gli transcriptional effectors; in the short term, arsenic blocks Hh-induced ciliary accumulation of Gli2, the primary activator of Hh-dependent transcription, and with prolonged incubation arsenic reduces steady-state levels of Gli2.	Arsenic	134-141	GLI family zinc finger 2	Homo sapiens	184-188
20624968-3	2010	We report here that arsenicals, in contrast, antagonize the Hh pathway by targeting Gli transcriptional effectors; in the short term, arsenic blocks Hh-induced ciliary accumulation of Gli2, the primary activator of Hh-dependent transcription, and with prolonged incubation arsenic reduces steady-state levels of Gli2.	Arsenic	134-141	GLI family zinc finger 2	Homo sapiens	312-316
20382397-8	2010	Cl(-) (at concentrations &gt;10 mg/L) formed silver chloride with the adsorbed Ag(+) and decreased the SERS detection limits for arsenic species.	Arsenic	129-136	seryl-tRNA synthetase 2, mitochondrial	Homo sapiens	103-107
20705574-0	2010	Polymorphism of glutathione S-transferase (GST) variants and its effect on distribution of urinary arsenic species in people exposed to low inorganic arsenic in tap water: an exploratory study.	Arsenic	99-106	glutathione S-transferase kappa 1	Homo sapiens	16-41
20705574-0	2010	Polymorphism of glutathione S-transferase (GST) variants and its effect on distribution of urinary arsenic species in people exposed to low inorganic arsenic in tap water: an exploratory study.	Arsenic	99-106	glutathione S-transferase kappa 1	Homo sapiens	43-46
20705574-0	2010	Polymorphism of glutathione S-transferase (GST) variants and its effect on distribution of urinary arsenic species in people exposed to low inorganic arsenic in tap water: an exploratory study.	Arsenic	99-106	nuclear RNA export factor 1	Homo sapiens	161-164
20705574-0	2010	Polymorphism of glutathione S-transferase (GST) variants and its effect on distribution of urinary arsenic species in people exposed to low inorganic arsenic in tap water: an exploratory study.	Arsenic	150-157	glutathione S-transferase kappa 1	Homo sapiens	16-41
20705574-0	2010	Polymorphism of glutathione S-transferase (GST) variants and its effect on distribution of urinary arsenic species in people exposed to low inorganic arsenic in tap water: an exploratory study.	Arsenic	150-157	glutathione S-transferase kappa 1	Homo sapiens	43-46
20705574-0	2010	Polymorphism of glutathione S-transferase (GST) variants and its effect on distribution of urinary arsenic species in people exposed to low inorganic arsenic in tap water: an exploratory study.	Arsenic	150-157	nuclear RNA export factor 1	Homo sapiens	161-164
20705574-1	2010	Glutathione S-tranferases (GST) are multigenic enzymes that have been associated with arsenic metabolism.	Arsenic	86-93	glutathione S-transferase kappa 1	Homo sapiens	0-25
20705574-1	2010	Glutathione S-tranferases (GST) are multigenic enzymes that have been associated with arsenic metabolism.	Arsenic	86-93	glutathione S-transferase kappa 1	Homo sapiens	27-30
20705574-2	2010	The objective of this study was to evaluate the relationship between polymorphic variants of GST and urinary concentration of arsenic species in people exposed to low levels of arsenic.	Arsenic	126-133	glutathione S-transferase kappa 1	Homo sapiens	93-96
20705574-2	2010	The objective of this study was to evaluate the relationship between polymorphic variants of GST and urinary concentration of arsenic species in people exposed to low levels of arsenic.	Arsenic	177-184	glutathione S-transferase kappa 1	Homo sapiens	93-96
20705574-5	2010	The effect of GST variants on arsenic concentration was evaluated using univariate and covariate-adjusted regressions.	Arsenic	30-37	glutathione S-transferase kappa 1	Homo sapiens	14-17
20705574-7	2010	There was nondefinitive evidence that polymorphic variants of GST play a role in arsenic metabolism in sample of the Chilean subjects studied.	Arsenic	81-88	glutathione S-transferase kappa 1	Homo sapiens	62-65
19733843-4	2010	We investigated here if the dose-related accumulation of arsenic in the liver was related to the expression of aquaglyceroporin 9 (AQP9) in the same organ.	Arsenic	57-64	aquaporin 9	Mus musculus	111-129
19733843-4	2010	We investigated here if the dose-related accumulation of arsenic in the liver was related to the expression of aquaglyceroporin 9 (AQP9) in the same organ.	Arsenic	57-64	aquaporin 9	Mus musculus	131-135
19733843-7	2010	The increased transcription of AQP9 has been observed in fasting and diabetic rats, suggesting that this channel could play a role in the diabetogenic effect of arsenic.	Arsenic	161-168	aquaporin 9	Rattus norvegicus	31-35
20045512-0	2010	Association between GSTO2 polymorphism and the urinary arsenic profile in copper industry workers.	Arsenic	55-62	glutathione S-transferase omega 2	Homo sapiens	20-25
20045512-1	2010	Two members of the recently identified Omega class glutathione S-transferase enzymes (GSTO1 and GSTO2) have been proposed to play a role in the response to arsenic exposure.	Arsenic	156-163	glutathione S-transferase omega 1	Homo sapiens	86-91
20045512-1	2010	Two members of the recently identified Omega class glutathione S-transferase enzymes (GSTO1 and GSTO2) have been proposed to play a role in the response to arsenic exposure.	Arsenic	156-163	glutathione S-transferase omega 2	Homo sapiens	96-101
20630234-10	2010	Observed 4% fat-corrected milk was greatest for WDGS-AS, followed by WDGS-CS, and then CONT-CS and CONT-AS (30.7, 29.7, 28.3, and 27.2 kg/d, respectively).	Arsenic	53-55	Weaning weight-maternal milk	Bos taurus	26-30
20382397-12	2010	The fundamental findings obtained in this research are especially valuable for the development of sensitive and reliable SERS methods for rapid analysis of arsenic in contaminated water.	Arsenic	156-163	seryl-tRNA synthetase 2, mitochondrial	Homo sapiens	121-125
20507177-2	2010	Bacterial resistance to arsenic is facilitated by ArsD, which delivers As(III) to the ArsA ATPase, the catalytic subunit of the ArsAB pump.	Arsenic	24-31	arylsulfatase D	Homo sapiens	50-54
20488895-5	2010	The ptlpd1-1 plants accumulated the same amount of arsenic as wild-type plants, indicating that the aos phenotype was not due to increased arsenate in the tissues but to an increase in the innate sensitivity to the poison.	Arsenic	51-58	lipoamide dehydrogenase 1	Arabidopsis thaliana	4-10
20423714-2	2010	Arsenic (+3 oxidation state) methyltransferase (As3mt) catalyzes reactions which convert inorganic arsenic to methylated metabolites.	Arsenic	99-106	arsenite methyltransferase	Mus musculus	0-46
20423714-2	2010	Arsenic (+3 oxidation state) methyltransferase (As3mt) catalyzes reactions which convert inorganic arsenic to methylated metabolites.	Arsenic	99-106	arsenite methyltransferase	Mus musculus	48-53
20423714-3	2010	This study determined whether the As3mt null genotype in the mouse modifies cytotoxic and proliferative effects seen in urinary bladders of wild type mice after exposure to inorganic arsenic.	Arsenic	183-190	arsenite methyltransferase	Mus musculus	34-39
20423714-11	2010	Thus, diminished arsenic methylation in As3mt KO mice exacerbates systemic toxicity and the effects of As(III) on the bladder epithelium, showing that altered kinetic and dynamic behavior of arsenic can affect its toxicity.	Arsenic	17-24	arsenite methyltransferase	Mus musculus	40-45
20423714-11	2010	Thus, diminished arsenic methylation in As3mt KO mice exacerbates systemic toxicity and the effects of As(III) on the bladder epithelium, showing that altered kinetic and dynamic behavior of arsenic can affect its toxicity.	Arsenic	191-198	arsenite methyltransferase	Mus musculus	40-45
20138707-0	2010	Molecular interaction between arsenic hydrate microcrystals and the cell-surface endopeptidase CD10 (neprilysin) - a possible link to the development of renal and cutaneous malignancies upon occupational exposure to arsenic compounds?	Arsenic	30-37	membrane metalloendopeptidase	Homo sapiens	95-99
20138707-0	2010	Molecular interaction between arsenic hydrate microcrystals and the cell-surface endopeptidase CD10 (neprilysin) - a possible link to the development of renal and cutaneous malignancies upon occupational exposure to arsenic compounds?	Arsenic	30-37	membrane metalloendopeptidase	Homo sapiens	101-111
20138707-0	2010	Molecular interaction between arsenic hydrate microcrystals and the cell-surface endopeptidase CD10 (neprilysin) - a possible link to the development of renal and cutaneous malignancies upon occupational exposure to arsenic compounds?	Arsenic	216-223	membrane metalloendopeptidase	Homo sapiens	95-99
20138707-0	2010	Molecular interaction between arsenic hydrate microcrystals and the cell-surface endopeptidase CD10 (neprilysin) - a possible link to the development of renal and cutaneous malignancies upon occupational exposure to arsenic compounds?	Arsenic	216-223	membrane metalloendopeptidase	Homo sapiens	101-111
20138707-3	2010	The cell-surface endopeptidase CD10 is variably expressed in cutaneous and renal malignancies, and due to this expression profile, might theoretically be implicated in arsenic-induced skin and renal neoplasias.	Arsenic	168-175	membrane metalloendopeptidase	Homo sapiens	31-35
20138707-5	2010	Placing the focus on the structural composition of arsenic hydrate microcrystals encountered in the cellular microenvironment, the present hypothesis suggests so far neglected molecular interactions between arsenic microcrystals and membrane-bound CD10 to be implicated in arsenic-induced carcinogenesis.	Arsenic	51-58	membrane metalloendopeptidase	Homo sapiens	248-252
20138707-5	2010	Placing the focus on the structural composition of arsenic hydrate microcrystals encountered in the cellular microenvironment, the present hypothesis suggests so far neglected molecular interactions between arsenic microcrystals and membrane-bound CD10 to be implicated in arsenic-induced carcinogenesis.	Arsenic	207-214	membrane metalloendopeptidase	Homo sapiens	248-252
20138707-5	2010	Placing the focus on the structural composition of arsenic hydrate microcrystals encountered in the cellular microenvironment, the present hypothesis suggests so far neglected molecular interactions between arsenic microcrystals and membrane-bound CD10 to be implicated in arsenic-induced carcinogenesis.	Arsenic	207-214	membrane metalloendopeptidase	Homo sapiens	248-252
20507177-2	2010	Bacterial resistance to arsenic is facilitated by ArsD, which delivers As(III) to the ArsA ATPase, the catalytic subunit of the ArsAB pump.	Arsenic	24-31	arylsulfatase A	Homo sapiens	86-90
20507177-7	2010	ArsD binds one arsenic per monomer coordinated with the three sulfur atoms of Cys12, Cys13, and Cys18.	Arsenic	15-22	arylsulfatase D	Homo sapiens	0-4
20339114-0	2010	Inhibition of liver x receptor/retinoid X receptor-mediated transcription contributes to the proatherogenic effects of arsenic in macrophages in vitro.	Arsenic	119-126	retinoid X receptor alpha	Homo sapiens	31-50
20576154-4	2010	Abnormal findings were assessed in candidates and donors and oocyte yields in the latter were statistically associated with abnormal FSH and AMH (&gt;or&lt; 95% CI of as-levels) and with normal/abnormal numbers of CGG repeats (normal range 26-32).	Arsenic	23-25	anti-Mullerian hormone	Homo sapiens	141-144
20516118-9	2010	Taken together, the transformed cells induced by arsenic exhibited a decrease in ROS generation, which is responsible for the enhanced cell growth and colony formation of the transformed cells, most likely through a sustained alternative activation of the NF-kappaB transcription factor.	Arsenic	49-56	nuclear factor kappa B subunit 1	Homo sapiens	256-265
20207026-0	2010	Arsenic inhibits SGK1 activation of CFTR Cl- channels in the gill of killifish, Fundulus heteroclitus.	Arsenic	0-7	serine/threonine-protein kinase Sgk1	Fundulus heteroclitus	17-21
20207026-0	2010	Arsenic inhibits SGK1 activation of CFTR Cl- channels in the gill of killifish, Fundulus heteroclitus.	Arsenic	0-7	cystic fibrosis transmembrane conductance regulator	Fundulus heteroclitus	36-40
20207026-3	2010	Since arsenic exposure prevents acclimation to seawater by decreasing CFTR protein levels we tested the hypothesis that arsenic (as sodium arsenite) blocks acclimation to seawater by down regulating SGK1 expression.	Arsenic	6-13	cystic fibrosis transmembrane conductance regulator	Fundulus heteroclitus	70-74
20207026-3	2010	Since arsenic exposure prevents acclimation to seawater by decreasing CFTR protein levels we tested the hypothesis that arsenic (as sodium arsenite) blocks acclimation to seawater by down regulating SGK1 expression.	Arsenic	120-127	cystic fibrosis transmembrane conductance regulator	Fundulus heteroclitus	70-74
20466452-7	2010	It is also inferred that NO3 contamination from agricultural activities disturbs arsenic remobilization--by consuming available electron donors (e.g. organic matter), NO3 limits the reduction of iron oxides and consequently the release of arsenic.	Arsenic	81-88	NBL1, DAN family BMP antagonist	Homo sapiens	25-28
20466452-7	2010	It is also inferred that NO3 contamination from agricultural activities disturbs arsenic remobilization--by consuming available electron donors (e.g. organic matter), NO3 limits the reduction of iron oxides and consequently the release of arsenic.	Arsenic	81-88	NBL1, DAN family BMP antagonist	Homo sapiens	167-170
20466452-7	2010	It is also inferred that NO3 contamination from agricultural activities disturbs arsenic remobilization--by consuming available electron donors (e.g. organic matter), NO3 limits the reduction of iron oxides and consequently the release of arsenic.	Arsenic	239-246	NBL1, DAN family BMP antagonist	Homo sapiens	25-28
20466452-7	2010	It is also inferred that NO3 contamination from agricultural activities disturbs arsenic remobilization--by consuming available electron donors (e.g. organic matter), NO3 limits the reduction of iron oxides and consequently the release of arsenic.	Arsenic	239-246	NBL1, DAN family BMP antagonist	Homo sapiens	167-170
20207026-3	2010	Since arsenic exposure prevents acclimation to seawater by decreasing CFTR protein levels we tested the hypothesis that arsenic (as sodium arsenite) blocks acclimation to seawater by down regulating SGK1 expression.	Arsenic	120-127	serine/threonine-protein kinase Sgk1	Fundulus heteroclitus	199-203
20207026-5	2010	Arsenic reduced the seawater induced increase in SGK1 mRNA and protein abundance, and reduced both the total amount of CFTR and the amount of CFTR in the plasma membrane.	Arsenic	0-7	serine/threonine-protein kinase Sgk1	Fundulus heteroclitus	49-53
20207026-5	2010	Arsenic reduced the seawater induced increase in SGK1 mRNA and protein abundance, and reduced both the total amount of CFTR and the amount of CFTR in the plasma membrane.	Arsenic	0-7	cystic fibrosis transmembrane conductance regulator	Fundulus heteroclitus	119-123
20207026-5	2010	Arsenic reduced the seawater induced increase in SGK1 mRNA and protein abundance, and reduced both the total amount of CFTR and the amount of CFTR in the plasma membrane.	Arsenic	0-7	cystic fibrosis transmembrane conductance regulator	Fundulus heteroclitus	142-146
20207026-7	2010	Arsenic also increased the amount of ubiquitinated CFTR and its degradation by the lysosome.	Arsenic	0-7	cystic fibrosis transmembrane conductance regulator	Fundulus heteroclitus	51-55
20207026-8	2010	Thus, we propose a model whereby arsenic reduces the ability of killifish to acclimate to seawater by blocking the seawater induced increase in SGK1, which results in increased ubiquitination and degradation of CFTR.	Arsenic	33-40	serine/threonine-protein kinase Sgk1	Fundulus heteroclitus	144-148
20207026-8	2010	Thus, we propose a model whereby arsenic reduces the ability of killifish to acclimate to seawater by blocking the seawater induced increase in SGK1, which results in increased ubiquitination and degradation of CFTR.	Arsenic	33-40	cystic fibrosis transmembrane conductance regulator	Fundulus heteroclitus	211-215
20587388-5	2010	Selenium was the most effective in reducing arsenic-induced inhibition of blood delta-aminolevulinic acid dehydratase (ALAD) activity and liver oxidative stress.	Arsenic	44-51	aminolevulinate dehydratase	Homo sapiens	80-117
20587388-5	2010	Selenium was the most effective in reducing arsenic-induced inhibition of blood delta-aminolevulinic acid dehydratase (ALAD) activity and liver oxidative stress.	Arsenic	44-51	aminolevulinate dehydratase	Homo sapiens	119-123
20339114-1	2010	OBJECTIVE: To determine whether arsenic inhibits transcriptional activation of the liver X receptor (LXR)/retinoid X receptor (RXR) heterodimers, thereby impairing cholesterol efflux from macrophages and potentially contributing to a proatherogenic phenotype.	Arsenic	32-39	retinoid X receptor alpha	Homo sapiens	106-125
20339114-1	2010	OBJECTIVE: To determine whether arsenic inhibits transcriptional activation of the liver X receptor (LXR)/retinoid X receptor (RXR) heterodimers, thereby impairing cholesterol efflux from macrophages and potentially contributing to a proatherogenic phenotype.	Arsenic	32-39	retinoid X receptor alpha	Homo sapiens	127-130
20339114-3	2010	Previous findings showed that arsenic inhibits transcriptional activation of type 2 nuclear receptors, known to heterodimerize with RXR.	Arsenic	30-37	retinoid X receptor alpha	Homo sapiens	132-135
20339114-4	2010	Environmentally relevant arsenic doses decrease the LXR/RXR ligand-induced expression of the LXR target genes (ABCA1 and SREBP-1c).	Arsenic	25-32	retinoid X receptor alpha	Homo sapiens	56-59
20339114-4	2010	Environmentally relevant arsenic doses decrease the LXR/RXR ligand-induced expression of the LXR target genes (ABCA1 and SREBP-1c).	Arsenic	25-32	ATP binding cassette subfamily A member 1	Homo sapiens	111-116
20339114-4	2010	Environmentally relevant arsenic doses decrease the LXR/RXR ligand-induced expression of the LXR target genes (ABCA1 and SREBP-1c).	Arsenic	25-32	sterol regulatory element binding transcription factor 1	Homo sapiens	121-129
20339114-6	2010	This selectivity correlated with the ability of arsenic to decrease LXR/RXR ligand-induced, but not cAMP-induced, cholesterol efflux.	Arsenic	48-55	retinoid X receptor alpha	Homo sapiens	72-75
20339114-7	2010	By using chromatin immunoprecipitation assays, we found that arsenic inhibits the ability of LXR/RXR ligands to induce activation markers on the ABCA1 and SREBP-1c promoters and blocks ligand-induced release of the nuclear receptor coexpressor (NCoR) from the promoter.	Arsenic	61-68	retinoid X receptor alpha	Homo sapiens	97-100
20339114-7	2010	By using chromatin immunoprecipitation assays, we found that arsenic inhibits the ability of LXR/RXR ligands to induce activation markers on the ABCA1 and SREBP-1c promoters and blocks ligand-induced release of the nuclear receptor coexpressor (NCoR) from the promoter.	Arsenic	61-68	ATP binding cassette subfamily A member 1	Homo sapiens	145-150
20339114-7	2010	By using chromatin immunoprecipitation assays, we found that arsenic inhibits the ability of LXR/RXR ligands to induce activation markers on the ABCA1 and SREBP-1c promoters and blocks ligand-induced release of the nuclear receptor coexpressor (NCoR) from the promoter.	Arsenic	61-68	sterol regulatory element binding transcription factor 1	Homo sapiens	155-163
20339114-7	2010	By using chromatin immunoprecipitation assays, we found that arsenic inhibits the ability of LXR/RXR ligands to induce activation markers on the ABCA1 and SREBP-1c promoters and blocks ligand-induced release of the nuclear receptor coexpressor (NCoR) from the promoter.	Arsenic	61-68	nuclear receptor corepressor 1	Homo sapiens	245-249
20339114-8	2010	Arsenic did not alter the ability of LXR to transrepress inflammatory gene transcription, further supporting our hypothesis that RXR is the target for arsenic inhibition.	Arsenic	151-158	retinoid X receptor alpha	Homo sapiens	129-132
20206246-4	2010	The level of beclin-1 expression underwent only modest alterations when the UROtsa cells were malignantly transformed by Cd(2+) or As(3+) or when the parental cells were exposed acutely to Cd(2+) or As(3+).	Arsenic	131-133	beclin 1	Homo sapiens	13-21
20100676-5	2010	OBJECTIVES: We tested the hypothesis that activation of Nrf2 and induction of antioxidant enzymes in response to arsenic exposure impedes glucose-triggered ROS signaling and thus GSIS.	Arsenic	113-120	NFE2 like bZIP transcription factor 2	Homo sapiens	56-60
20519851-0	2010	Reduction of arsenic-induced cytotoxicity through Nrf2/HO-1 signaling in HepG2 cells.	Arsenic	13-20	NFE2 like bZIP transcription factor 2	Homo sapiens	50-54
20519851-0	2010	Reduction of arsenic-induced cytotoxicity through Nrf2/HO-1 signaling in HepG2 cells.	Arsenic	13-20	heme oxygenase 1	Homo sapiens	55-59
20532380-0	2010	Genetic polymorphism of As3MT and delayed urinary DMA excretion after organic arsenic intake from oyster ingestion.	Arsenic	78-85	arsenite methyltransferase	Homo sapiens	24-29
20532380-3	2010	The goal of this study was to explore the effects of genetic polymorphisms of human PNP, As3MT and GSTO1 on organic arsenic metabolism among study subjects after oyster ingestion.	Arsenic	116-123	arsenite methyltransferase	Homo sapiens	89-94
20532380-10	2010	As3MT was suggested to be one of the major factors affecting the metabolism of dietary organic arsenic in terms of urinary DMA level.	Arsenic	95-102	arsenite methyltransferase	Homo sapiens	0-5
20530755-4	2010	Pv ACR3 is able to rescue the arsenic-sensitive phenotypes of yeast deficient for ACR3.	Arsenic	30-37	Arr3p	Saccharomyces cerevisiae S288C	3-7
20530755-4	2010	Pv ACR3 is able to rescue the arsenic-sensitive phenotypes of yeast deficient for ACR3.	Arsenic	30-37	Arr3p	Saccharomyces cerevisiae S288C	82-86
20530755-5	2010	ACR3 transcripts are upregulated by arsenic in sporophyte roots and gametophytes, tissues that directly contact soil, whereas ACR3;1 expression is unaffected by arsenic.	Arsenic	36-43	Arr3p	Saccharomyces cerevisiae S288C	0-4
20530755-9	2010	The duplication of ACR3 in P. vittata and the loss of ACR3 in angiosperms may explain arsenic tolerance in this unusual group of ferns while precluding the same trait in angiosperms.	Arsenic	86-93	Arr3p	Saccharomyces cerevisiae S288C	19-23
20530755-9	2010	The duplication of ACR3 in P. vittata and the loss of ACR3 in angiosperms may explain arsenic tolerance in this unusual group of ferns while precluding the same trait in angiosperms.	Arsenic	86-93	Arr3p	Saccharomyces cerevisiae S288C	54-58
20371279-11	2010	The major compounds of AS, ferulic acid and Z-ligustilide, also significantly decreased NF-kappaB luciferase activity, which may contribute to the anti-inflammatory activity of AS.	Arsenic	23-25	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	88-97
20371279-11	2010	The major compounds of AS, ferulic acid and Z-ligustilide, also significantly decreased NF-kappaB luciferase activity, which may contribute to the anti-inflammatory activity of AS.	Arsenic	177-179	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	88-97
20138079-12	2010	Immunoblot analyses indicate that the superior arsenic methylation capacities of dog, rat and monkey hepatocytes examined in this study may be associated with a higher As3mt expression.	Arsenic	47-54	arsenite methyltransferase	Rattus norvegicus	168-173
20235151-4	2010	Arsenic also increased extracellular domain-deleted RET-PTC1 kinase activity with promotion of disulfide bond-mediated dimerization of RET-PTC1 protein.	Arsenic	0-7	ret proto-oncogene	Homo sapiens	52-55
20235151-4	2010	Arsenic also increased extracellular domain-deleted RET-PTC1 kinase activity with promotion of disulfide bond-mediated dimerization of RET-PTC1 protein.	Arsenic	0-7	patched 1	Homo sapiens	56-60
20235151-4	2010	Arsenic also increased extracellular domain-deleted RET-PTC1 kinase activity with promotion of disulfide bond-mediated dimerization of RET-PTC1 protein.	Arsenic	0-7	ret proto-oncogene	Homo sapiens	135-138
20235151-4	2010	Arsenic also increased extracellular domain-deleted RET-PTC1 kinase activity with promotion of disulfide bond-mediated dimerization of RET-PTC1 protein.	Arsenic	0-7	patched 1	Homo sapiens	139-143
20235151-5	2010	Arsenic increased RET-PTC1 kinase activity with cysteine 365 (C365) replaced by alanine with promotion of dimer formation but not with cysteine 376 (C376) replaced by alanine.	Arsenic	0-7	ret proto-oncogene	Homo sapiens	18-21
20235151-5	2010	Arsenic increased RET-PTC1 kinase activity with cysteine 365 (C365) replaced by alanine with promotion of dimer formation but not with cysteine 376 (C376) replaced by alanine.	Arsenic	0-7	patched 1	Homo sapiens	22-26
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Arsenic	25-32	ret proto-oncogene	Homo sapiens	56-59
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Arsenic	25-32	ret proto-oncogene	Homo sapiens	117-120
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Arsenic	25-32	ret proto-oncogene	Homo sapiens	117-120
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Arsenic	25-32	ret proto-oncogene	Homo sapiens	117-120
20235151-0	2010	A redox-linked novel pathway for arsenic-mediated RET tyrosine kinase activation.	Arsenic	33-40	ret proto-oncogene	Homo sapiens	50-53
20235151-1	2010	We examined the biochemical effects of arsenic on the activities of RET proto-oncogene (c-RET protein tyrosine kinases) and RET oncogene (RET-MEN2A and RET-PTC1 protein tyrosine kinases) products.	Arsenic	39-46	ret proto-oncogene	Homo sapiens	68-71
20235151-2	2010	Arsenic activated c-RET kinase with promotion of disulfide bond-mediated dimerization of c-RET protein.	Arsenic	0-7	ret proto-oncogene	Homo sapiens	20-23
20235151-2	2010	Arsenic activated c-RET kinase with promotion of disulfide bond-mediated dimerization of c-RET protein.	Arsenic	0-7	ret proto-oncogene	Homo sapiens	91-94
20235151-3	2010	Arsenic further activated RET-MEN2A kinase, which was already 3- to 10-fold augmented by genetic mutation compared with c-RET kinase activity, with promotion of disulfide bond-mediated dimerization of RET-MEN2A protein (superactivation).	Arsenic	0-7	ret proto-oncogene	Homo sapiens	26-29
20235151-3	2010	Arsenic further activated RET-MEN2A kinase, which was already 3- to 10-fold augmented by genetic mutation compared with c-RET kinase activity, with promotion of disulfide bond-mediated dimerization of RET-MEN2A protein (superactivation).	Arsenic	0-7	ret proto-oncogene	Homo sapiens	30-35
20235151-3	2010	Arsenic further activated RET-MEN2A kinase, which was already 3- to 10-fold augmented by genetic mutation compared with c-RET kinase activity, with promotion of disulfide bond-mediated dimerization of RET-MEN2A protein (superactivation).	Arsenic	0-7	ret proto-oncogene	Homo sapiens	205-210
20361763-0	2010	Arsenic binding and transfer by the ArsD As(III) metallochaperone.	Arsenic	0-7	ArsD	Escherichia coli	36-40
20235151-6	2010	Our results suggest that arsenic-mediated regulation of RET kinase activity is dependent on conformational change of RET protein through modulation of a special cysteine sited at the intracellular domain in RET protein (relevant cysteine of C376 in RET-PTC1 protein).	Arsenic	25-32	patched 1	Homo sapiens	253-257
20235151-7	2010	Moreover, arsenic enhanced the activity of immunoprecipitated RET protein with increase in thiol-dependent dimer formation.	Arsenic	10-17	ret proto-oncogene	Homo sapiens	62-65
20235151-8	2010	As arsenic (14.2 microM) was detected in the cells cultured with arsenic (100 microM), direct association between arsenic and RET in the cells might modulate dimer formation.	Arsenic	3-10	ret proto-oncogene	Homo sapiens	126-129
20235151-8	2010	As arsenic (14.2 microM) was detected in the cells cultured with arsenic (100 microM), direct association between arsenic and RET in the cells might modulate dimer formation.	Arsenic	65-72	ret proto-oncogene	Homo sapiens	126-129
20235151-8	2010	As arsenic (14.2 microM) was detected in the cells cultured with arsenic (100 microM), direct association between arsenic and RET in the cells might modulate dimer formation.	Arsenic	65-72	ret proto-oncogene	Homo sapiens	126-129
20235151-9	2010	Thus, we demonstrated a novel redox-linked mechanism of activation of arsenic-mediated RET proto-oncogene and oncogene products.	Arsenic	70-77	ret proto-oncogene	Homo sapiens	87-90
20361763-2	2010	Interaction with ArsD increases the affinity of ArsA for As(III), conferring resistance to environmental concentrations of arsenic.	Arsenic	123-130	ArsD	Escherichia coli	17-21
20629307-11	2010	Interestingly, compared with the rats in the OB group, the serum concentrations of TNF-alpha and CRP decreased significantly in the rats in the OB-AS group, to which high dose aspirin was given (P &lt; 0.05).	Arsenic	147-149	tumor necrosis factor	Rattus norvegicus	83-92
20439172-0	2010	Arsenic inhibits neurite outgrowth by inhibiting the LKB1-AMPK signaling pathway.	Arsenic	0-7	serine/threonine kinase 11	Mus musculus	53-57
20439172-0	2010	Arsenic inhibits neurite outgrowth by inhibiting the LKB1-AMPK signaling pathway.	Arsenic	0-7	protein kinase, AMP-activated, alpha 1 catalytic subunit	Mus musculus	58-62
20439172-2	2010	OBJECTIVES AND METHODS: We evaluated the role of the LKB1-AMPK pathway in As-induced developmental neurotoxicity using Neuro-2a (N2a) neuroblastoma cells as a model of developing neurons.	Arsenic	74-76	serine/threonine kinase 11	Mus musculus	53-57
20439172-2	2010	OBJECTIVES AND METHODS: We evaluated the role of the LKB1-AMPK pathway in As-induced developmental neurotoxicity using Neuro-2a (N2a) neuroblastoma cells as a model of developing neurons.	Arsenic	74-76	protein kinase, AMP-activated, alpha 1 catalytic subunit	Mus musculus	58-62
20439172-4	2010	Activation of adenosine monophosphate-activated kinase (AMPK) induced by retinoic acid in differentiating cells was blocked by As.	Arsenic	127-129	protein kinase, AMP-activated, alpha 1 catalytic subunit	Mus musculus	56-60
20204330-1	2010	Arsenate [As(V)] solution reference material, National Metrology Institute of Japan (NMIJ) certified reference material (CRM) 7912-a, for speciation of arsenic species was developed and certified by NMIJ, the National Institute of Advanced Industrial Science and Technology.	Arsenic	152-159	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	9-15
20439172-7	2010	Antioxidants, such as N-acetyl cysteine and superoxide dismutase, but not catalase, protected against As-induced inactivation of the LKB1-AMPK pathway and reversed the inhibitory effect of As on neurite outgrowth.	Arsenic	102-104	serine/threonine kinase 11	Mus musculus	133-137
20439172-7	2010	Antioxidants, such as N-acetyl cysteine and superoxide dismutase, but not catalase, protected against As-induced inactivation of the LKB1-AMPK pathway and reversed the inhibitory effect of As on neurite outgrowth.	Arsenic	102-104	protein kinase, AMP-activated, alpha 1 catalytic subunit	Mus musculus	138-142
20439172-9	2010	Oxidative stress induced by As, especially excessive superoxide, plays a critical role in blocking the LKB1-AMPK pathway.	Arsenic	28-30	serine/threonine kinase 11	Mus musculus	103-107
20439172-9	2010	Oxidative stress induced by As, especially excessive superoxide, plays a critical role in blocking the LKB1-AMPK pathway.	Arsenic	28-30	protein kinase, AMP-activated, alpha 1 catalytic subunit	Mus musculus	108-112
20083128-0	2010	Arsenic promotes angiogenesis in vitro via a heme oxygenase-1-dependent mechanism.	Arsenic	0-7	heme oxygenase 1	Homo sapiens	45-61
20114059-0	2010	Reduced cellular redox status induces 4-hydroxynonenal-mediated caspase 3 activation leading to erythrocyte death during chronic arsenic exposure in rats.	Arsenic	129-136	caspase 3	Rattus norvegicus	64-73
20114059-6	2010	Suppression of antioxidant system coupled with increased generation of ROS eventually led to activation of caspase 3 during arsenic exposure.	Arsenic	124-131	caspase 3	Rattus norvegicus	107-116
20045430-7	2010	At 3 mo exposure the sustained production of cytokines like IL-1, IL-6, IL-8 and TNF is coincident with the appearance of characteristics associated with cell transformation seen in other arsenic-UROtsa studies.	Arsenic	188-195	tumor necrosis factor	Homo sapiens	81-84
20378816-4	2010	Here we show that arsenic binds directly to cysteine residues in zinc fingers located within the RBCC domain of PML-RARalpha and PML.	Arsenic	18-25	PML nuclear body scaffold	Homo sapiens	112-115
20378816-4	2010	Here we show that arsenic binds directly to cysteine residues in zinc fingers located within the RBCC domain of PML-RARalpha and PML.	Arsenic	18-25	retinoic acid receptor alpha	Homo sapiens	116-124
20378816-4	2010	Here we show that arsenic binds directly to cysteine residues in zinc fingers located within the RBCC domain of PML-RARalpha and PML.	Arsenic	18-25	PML nuclear body scaffold	Homo sapiens	129-132
20378816-5	2010	Arsenic binding induces PML oligomerization, which increases its interaction with the small ubiquitin-like protein modifier (SUMO)-conjugating enzyme UBC9, resulting in enhanced SUMOylation and degradation.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	24-27
20378816-5	2010	Arsenic binding induces PML oligomerization, which increases its interaction with the small ubiquitin-like protein modifier (SUMO)-conjugating enzyme UBC9, resulting in enhanced SUMOylation and degradation.	Arsenic	0-7	ubiquitin conjugating enzyme E2 I	Homo sapiens	150-154
20389564-0	2010	Influence of annealing conditions on the optical and structural properties of spin-coated As(2)S(3) chalcogenide glass thin films.	Arsenic	90-92	spindlin 1	Homo sapiens	78-82
20122981-5	2010	Interestingly, ascorbic acid markedly upregulated lymphocytes relative mRNA expression of lymphocytes SOD2 gene corresponding to GAPDH, house keeping candidate gene in arsenic-treated rat, which might provide anti-oxidative activity in the blood.	Arsenic	168-175	superoxide dismutase 2	Rattus norvegicus	102-106
20014157-0	2010	Genetic association between intronic variants in AS3MT and arsenic methylation efficiency is focused on a large linkage disequilibrium cluster in chromosome 10.	Arsenic	59-66	arsenite methyltransferase	Homo sapiens	49-54
20014157-3	2010	Specifically, variants in arsenic (3+ oxidation state) methyltransferase (AS3MT), the key gene in the metabolism of arsenic, have been associated with increased arsenic methylation efficiency.	Arsenic	26-33	arsenite methyltransferase	Homo sapiens	74-79
20014157-3	2010	Specifically, variants in arsenic (3+ oxidation state) methyltransferase (AS3MT), the key gene in the metabolism of arsenic, have been associated with increased arsenic methylation efficiency.	Arsenic	116-123	arsenite methyltransferase	Homo sapiens	26-72
20014157-3	2010	Specifically, variants in arsenic (3+ oxidation state) methyltransferase (AS3MT), the key gene in the metabolism of arsenic, have been associated with increased arsenic methylation efficiency.	Arsenic	116-123	arsenite methyltransferase	Homo sapiens	74-79
20014157-5	2010	In an effort to characterize the extent of the region in LD, we genotyped 46 SNPs in a 347,000 base region of chromosome 10 that included AS3MT in arsenic-exposed subjects from Mexico.	Arsenic	147-154	arsenite methyltransferase	Homo sapiens	138-143
20014157-7	2010	Genetic association analysis with arsenic metabolism confirmed the previously observed association between AS3MT variants, including this large cluster of linked polymorphisms, and arsenic methylation efficiency.	Arsenic	34-41	arsenite methyltransferase	Homo sapiens	107-112
20014157-7	2010	Genetic association analysis with arsenic metabolism confirmed the previously observed association between AS3MT variants, including this large cluster of linked polymorphisms, and arsenic methylation efficiency.	Arsenic	181-188	arsenite methyltransferase	Homo sapiens	107-112
20141178-0	2010	Five-membered arsenic-sulfur-nitrogen heterocycles, RAs(S2N2) (R = Me, Et, (i)Pr, (t)Bu, Ph, Mes).	Arsenic	14-21	MKS transition zone complex subunit 1	Homo sapiens	93-96
20374644-3	2010	METHODS: Development of AIA was investigated in wildtype and PI3Kgamma-deficient mice as well as in mice treated with a specific inhibitor of PI3Kgamma (AS-605240) in comparison to untreated animals.	Arsenic	153-155	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Mus musculus	142-151
20005095-7	2010	The developed procedure was successfully applied for the removal of both As(III) and As(V) from arsenic contaminated drinking water samples.	Arsenic	96-103	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	85-90
20123963-3	2010	To elucidate the direct phosphorylation of p53 at Ser46 by ATM, an ATM mutant (ATM-AS) sensitive to ATP analogues was engineered.	Arsenic	83-85	tumor protein p53	Homo sapiens	43-46
20123963-3	2010	To elucidate the direct phosphorylation of p53 at Ser46 by ATM, an ATM mutant (ATM-AS) sensitive to ATP analogues was engineered.	Arsenic	83-85	ATM serine/threonine kinase	Homo sapiens	67-70
20123963-3	2010	To elucidate the direct phosphorylation of p53 at Ser46 by ATM, an ATM mutant (ATM-AS) sensitive to ATP analogues was engineered.	Arsenic	83-85	ATM serine/threonine kinase	Homo sapiens	67-70
19948193-4	2010	Ruthenium red (1 nmol), TRPV4 AS (40 microg, daily for 7 days) or L-NAME (300 nmol) decreased nitrite (an index of nitric oxide formation) in the DRG of CCD rats.	Arsenic	30-32	transient receptor potential cation channel, subfamily V, member 4	Rattus norvegicus	24-29
20036271-0	2010	Arsenite induced poly(ADP-ribosyl)ation of tumor suppressor P53 in human skin keratinocytes as a possible mechanism for carcinogenesis associated with arsenic exposure.	Arsenic	151-158	tumor protein p53	Homo sapiens	60-63
21787596-0	2010	Alpha-lipoic acid regulates heme oxygenase gene expression and nuclear Nrf2 activation as a mechanism of protection against arsenic exposure in HepG2 cells.	Arsenic	124-131	NFE2 like bZIP transcription factor 2	Homo sapiens	71-75
20221439-6	2010	METHODOLOGY/PRINCIPAL FINDINGS: Using molecular genetics approaches and functional in vivo assays we showed that HMT-1 from a multicellular organism, Caenorhabditis elegans, functions distinctly from its S. pombe counterpart in that in addition to Cd it confers tolerance to arsenic (As) and copper (Cu) while acting independently of pcs-1.	Arsenic	275-282	Heavy metal tolerance factor 1	Caenorhabditis elegans	113-118
20221439-6	2010	METHODOLOGY/PRINCIPAL FINDINGS: Using molecular genetics approaches and functional in vivo assays we showed that HMT-1 from a multicellular organism, Caenorhabditis elegans, functions distinctly from its S. pombe counterpart in that in addition to Cd it confers tolerance to arsenic (As) and copper (Cu) while acting independently of pcs-1.	Arsenic	284-286	Heavy metal tolerance factor 1	Caenorhabditis elegans	113-118
20039017-0	2010	Dietary intake of total and inorganic arsenic by adults in arsenic-contaminated area of Ron Phibun district, Thailand.	Arsenic	59-66	macrophage stimulating 1 receptor	Homo sapiens	88-91
20179202-6	2010	Arsenic activates Hedgehog signaling by decreasing the stability of the repressor form of GLI3, one of the transcription factors that ultimately regulate Hedgehog activity.	Arsenic	0-7	GLI family zinc finger 3	Homo sapiens	90-94
19765857-0	2010	Arsenic response of AtPCS1- and CePCS-expressing plants - effects of external As(V) concentration on As-accumulation pattern and NPT metabolism.	Arsenic	0-7	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	20-26
21069159-2	2010	GLUT1 may be the major pathway for arsenic uptake into heart and brain, where the metalloid causes cardiotoxicity and neurotoxicity.	Arsenic	35-42	solute carrier family 2 member 1	Homo sapiens	0-5
20026328-1	2010	The stress-activated kinase Hog1p mediates arsenic tolerance by decreasing arsenite influx through the aquaglyceroporin Fps1p in Saccharomyces cerevisiae.	Arsenic	43-50	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	28-33
20026328-1	2010	The stress-activated kinase Hog1p mediates arsenic tolerance by decreasing arsenite influx through the aquaglyceroporin Fps1p in Saccharomyces cerevisiae.	Arsenic	43-50	Fps1p	Saccharomyces cerevisiae S288C	120-125
20026328-2	2010	Unexpectedly, we found that overexpression of FPS1 increased arsenite tolerance suggesting a physiological role of Fps1p in arsenic detoxification.	Arsenic	124-131	Fps1p	Saccharomyces cerevisiae S288C	46-50
20026328-2	2010	Unexpectedly, we found that overexpression of FPS1 increased arsenite tolerance suggesting a physiological role of Fps1p in arsenic detoxification.	Arsenic	124-131	Fps1p	Saccharomyces cerevisiae S288C	115-120
19765857-2	2010	The aim of this study was to determine whether overexpression of either of two PC synthase (PCS) genes, AtPCS1 and CePCS in Nicotiana tabacum (previously shown to cause decrease and increase, respectively, of cadmium tolerance of tobacco - Wojas et al., 2008) also contributes to such contrasting phenotypes with respect to arsenic (As) tolerance and accumulation, and how observed responses relate to non-protein thiol (NPT) metabolism.	Arsenic	324-331	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	104-110
19765857-2	2010	The aim of this study was to determine whether overexpression of either of two PC synthase (PCS) genes, AtPCS1 and CePCS in Nicotiana tabacum (previously shown to cause decrease and increase, respectively, of cadmium tolerance of tobacco - Wojas et al., 2008) also contributes to such contrasting phenotypes with respect to arsenic (As) tolerance and accumulation, and how observed responses relate to non-protein thiol (NPT) metabolism.	Arsenic	333-335	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	104-110
19802720-7	2010	Hg(II), an aquaporin inhibitor, inhibited transport of As(III), MAs(III), MAs(V) and DMAs(V) via AQP9.	Arsenic	55-57	aquaporin 9	Homo sapiens	97-101
19802720-10	2010	The results suggest that in addition to the initial uptake of trivalent inorganic As(III) inside cells, AQP9 plays a dual role in the detoxification of arsenic metabolites by facilitating efflux from cells.	Arsenic	152-159	aquaporin 9	Homo sapiens	104-108
20028703-3	2010	Treatment with L-ascorbate was found effective in normalizing the arsenic-induced alteration of SOD and CAT activity and LPO level in rat hepatocytes.	Arsenic	66-73	catalase	Rattus norvegicus	104-107
20949432-2	2010	Identification of arsenic (+3 oxidation state) methyltransferase (As3mt) as the enzyme that could catalyze all the steps in the pathway for arsenic methylation suggests that expression of this enzyme could be a useful target for manipulation.	Arsenic	18-25	arsenite methyltransferase	Homo sapiens	66-71
20396854-1	2010	Environmental contamination by arsenic compounds in the Ribeira River Valley, Sao Paulo, Brazil has already been observed.	Arsenic	31-38	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	78-81
19932728-5	2010	Arsenic or acetaminophen increased serum ALT and AST activities and depleted CYP.	Arsenic	0-7	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-80
19932728-8	2010	Arsenic did not alter the effects of acetaminophen on serum biomarkers, caused further CYP depletion and decreased acetaminophen-mediated induction of drug-metabolizing enzymes.	Arsenic	0-7	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	87-90
19932728-10	2010	However, arsenic attenuated the higher dose-mediated lipid peroxidation and glutathione depletion with improvement in glutathione peroxidase and glutathione reductase activities, further decrease in catalase and no alterations in superoxide dismutase and glutathione-S-transferase activities.	Arsenic	9-16	glutathione-disulfide reductase	Rattus norvegicus	145-166
19932728-10	2010	However, arsenic attenuated the higher dose-mediated lipid peroxidation and glutathione depletion with improvement in glutathione peroxidase and glutathione reductase activities, further decrease in catalase and no alterations in superoxide dismutase and glutathione-S-transferase activities.	Arsenic	9-16	hematopoietic prostaglandin D synthase	Rattus norvegicus	255-280
20137371-7	2010	Agreement was evaluated between RSC and AS-OCT.	Arsenic	40-42	plexin A2	Homo sapiens	43-46
23459695-5	2010	The overall arsenic mobility of the tested samples increased in the following order: ASL &gt; RASL &gt; PFA &gt; M1 &gt; HPFA &gt; M2.	Arsenic	12-19	ras homolog family member T2	Homo sapiens	94-98
19874834-7	2010	The serum levels of total antioxidant, glutathione peroxidase and glutathione reductase were substantially reduced in arsenic-exposed groups, while supplementation of jaggery enhanced their levels in combined treatment groups.	Arsenic	118-125	glutathione reductase	Mus musculus	66-87
19874834-8	2010	The serum levels of interleukin-1beta, interleukin-6 and TNF-alpha were significantly increased in arsenic-exposed groups, while in the arsenic-exposed and jaggery supplemented groups their levels were normal.	Arsenic	99-106	interleukin 1 beta	Mus musculus	20-37
19874834-8	2010	The serum levels of interleukin-1beta, interleukin-6 and TNF-alpha were significantly increased in arsenic-exposed groups, while in the arsenic-exposed and jaggery supplemented groups their levels were normal.	Arsenic	99-106	interleukin 6	Mus musculus	39-52
19874834-8	2010	The serum levels of interleukin-1beta, interleukin-6 and TNF-alpha were significantly increased in arsenic-exposed groups, while in the arsenic-exposed and jaggery supplemented groups their levels were normal.	Arsenic	99-106	tumor necrosis factor	Mus musculus	57-66
20109206-0	2010	Water quality monitoring records for estimating tap water arsenic and nitrate: a validation study.	Arsenic	58-65	nuclear RNA export factor 1	Homo sapiens	48-51
20109206-1	2010	BACKGROUND: Tap water may be an important source of exposure to arsenic and nitrate.	Arsenic	64-71	nuclear RNA export factor 1	Homo sapiens	12-15
19874836-7	2010	In contrast, one of the prominent proteins that did not bind to trivalent arsenic was identified as calreticulin precursor.	Arsenic	74-81	calreticulin	Homo sapiens	100-112
19914269-1	2010	To elucidate the role of genetic factors in arsenic metabolism, we investigated associations of genetic polymorphisms in the members of glutathione S-transferase (GST) superfamily with the arsenic concentrations in hair and urine, and urinary arsenic profile in residents in the Red River Delta, Vietnam.	Arsenic	189-196	glutathione S-transferase kappa 1	Homo sapiens	136-161
19914269-1	2010	To elucidate the role of genetic factors in arsenic metabolism, we investigated associations of genetic polymorphisms in the members of glutathione S-transferase (GST) superfamily with the arsenic concentrations in hair and urine, and urinary arsenic profile in residents in the Red River Delta, Vietnam.	Arsenic	189-196	glutathione S-transferase kappa 1	Homo sapiens	163-166
19914269-1	2010	To elucidate the role of genetic factors in arsenic metabolism, we investigated associations of genetic polymorphisms in the members of glutathione S-transferase (GST) superfamily with the arsenic concentrations in hair and urine, and urinary arsenic profile in residents in the Red River Delta, Vietnam.	Arsenic	189-196	glutathione S-transferase kappa 1	Homo sapiens	136-161
19914269-1	2010	To elucidate the role of genetic factors in arsenic metabolism, we investigated associations of genetic polymorphisms in the members of glutathione S-transferase (GST) superfamily with the arsenic concentrations in hair and urine, and urinary arsenic profile in residents in the Red River Delta, Vietnam.	Arsenic	189-196	glutathione S-transferase kappa 1	Homo sapiens	163-166
19914269-6	2010	Strong correlations between GSTP1 Ile105Val and arsenic exposure level and profile were observed in this study.	Arsenic	48-55	glutathione S-transferase pi 1	Homo sapiens	28-33
19914269-7	2010	Especially, heterozygote of GSTP1 Ile105Val had a higher metabolic capacity from inorganic arsenic to monomethyl arsenic, while the opposite trend was observed for ability of metabolism from As(V) to As(III).	Arsenic	91-98	glutathione S-transferase pi 1	Homo sapiens	28-33
19914269-7	2010	Especially, heterozygote of GSTP1 Ile105Val had a higher metabolic capacity from inorganic arsenic to monomethyl arsenic, while the opposite trend was observed for ability of metabolism from As(V) to As(III).	Arsenic	113-120	glutathione S-transferase pi 1	Homo sapiens	28-33
19914269-8	2010	Furthermore, other factors including sex, age, body mass index, arsenic level in drinking water, and genotypes of As (+3 oxidation state) methyltransferase (AS3MT) were also significantly co-associated with arsenic level and profile in the Vietnamese.	Arsenic	207-214	arsenite methyltransferase	Homo sapiens	157-162
19914269-9	2010	To our knowledge, this is the first study indicating the associations of genetic factors of GST superfamily with arsenic metabolism in a Vietnamese population.	Arsenic	113-120	glutathione S-transferase kappa 1	Homo sapiens	92-95
19818359-0	2010	Nucleophosmin in the pathogenesis of arsenic-related bladder carcinogenesis revealed by quantitative proteomics.	Arsenic	37-44	nucleophosmin 1	Homo sapiens	0-13
19818359-9	2010	The results suggest that NPM may play a role in the As-related bladder carcinogenesis, and soybean-based foods may have potential in the suppression of As/NPM-related tumorigenesis.	Arsenic	52-54	nucleophosmin 1	Homo sapiens	25-28
19540908-10	2010	Combined exposure, with increased levels of As and Cd in urine, caused considerably higher biomarker values of renal tubular damage, measured as increased urinary levels of B2M or NAG, than each of the exposures alone.	Arsenic	44-46	beta-2-microglobulin	Homo sapiens	173-176
20390892-3	2010	The arsenic and gallium content of waste slurries was analyzed using inductively coupled plasma mass-spectrometry (ICP-MS) and it is reported that the arsenic content of the waste streams was related to the wafer thinning process, with slurries from wafer polishing having the highest dissolved arsenic content at over 1,900 mgL(-1).	Arsenic	151-158	LLGL scribble cell polarity complex component 1	Homo sapiens	325-331
19834688-3	2010	This study was focused on a possible involvement of XPD/ERCC2 G23591A and A35931C polymorphisms in risk modulation of skin lesions and in the body burden of As in this unique case of As exposure.	Arsenic	157-159	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	52-55
19834688-3	2010	This study was focused on a possible involvement of XPD/ERCC2 G23591A and A35931C polymorphisms in risk modulation of skin lesions and in the body burden of As in this unique case of As exposure.	Arsenic	157-159	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	56-61
19834688-3	2010	This study was focused on a possible involvement of XPD/ERCC2 G23591A and A35931C polymorphisms in risk modulation of skin lesions and in the body burden of As in this unique case of As exposure.	Arsenic	183-185	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	52-55
19834688-3	2010	This study was focused on a possible involvement of XPD/ERCC2 G23591A and A35931C polymorphisms in risk modulation of skin lesions and in the body burden of As in this unique case of As exposure.	Arsenic	183-185	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	56-61
20134088-4	2010	In this paper we have examined the in vitro effect of arsenic (As(V)) on the rheologic properties of human erythrocytes in relation with membrane fluidity and internal microviscosity.	Arsenic	54-61	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	63-68
19782400-9	2010	Arsenic or acetaminophen given alone depleted GSH and decreased the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase and these effects remained mostly unaffected after co-exposure.	Arsenic	0-7	catalase	Rattus norvegicus	104-112
19782400-9	2010	Arsenic or acetaminophen given alone depleted GSH and decreased the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase and these effects remained mostly unaffected after co-exposure.	Arsenic	0-7	glutathione-disulfide reductase	Rattus norvegicus	138-159
19782400-9	2010	Arsenic or acetaminophen given alone depleted GSH and decreased the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase and these effects remained mostly unaffected after co-exposure.	Arsenic	0-7	hematopoietic prostaglandin D synthase	Rattus norvegicus	164-189
20039738-5	2010	Even in the presence of the more toxic arsenic species, arsenite, cell metabolism was significantly impaired only at the highest arsenite concentration (500 muM) for one of the Fe(II)-oxidizers.	Arsenic	39-46	latexin	Homo sapiens	157-160
20932244-3	2010	Arsenic treatment resulted in a significant increase in lipid peroxidase (LPO); however, glutathione (GSH) levels and the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT) were found to be significantly decreased following arsenic treatment.	Arsenic	0-7	lactoperoxidase	Rattus norvegicus	56-72
20932244-3	2010	Arsenic treatment resulted in a significant increase in lipid peroxidase (LPO); however, glutathione (GSH) levels and the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT) were found to be significantly decreased following arsenic treatment.	Arsenic	0-7	lactoperoxidase	Rattus norvegicus	74-77
20146381-5	2010	Effective protection of gonadal weight loss, suppressed ovarian steroidogenesis, and altered ovarian and uterine peroxidase activities were noticed when 1.0 IU hCG/(100 g body weight day) is given in arsenic-intoxicated rats.	Arsenic	200-207	chorionic gonadotropin subunit beta 5	Homo sapiens	160-163
20932244-3	2010	Arsenic treatment resulted in a significant increase in lipid peroxidase (LPO); however, glutathione (GSH) levels and the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT) were found to be significantly decreased following arsenic treatment.	Arsenic	0-7	glutathione-disulfide reductase	Rattus norvegicus	194-215
20390892-3	2010	The arsenic and gallium content of waste slurries was analyzed using inductively coupled plasma mass-spectrometry (ICP-MS) and it is reported that the arsenic content of the waste streams was related to the wafer thinning process, with slurries from wafer polishing having the highest dissolved arsenic content at over 1,900 mgL(-1).	Arsenic	151-158	LLGL scribble cell polarity complex component 1	Homo sapiens	325-331
20932244-3	2010	Arsenic treatment resulted in a significant increase in lipid peroxidase (LPO); however, glutathione (GSH) levels and the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT) were found to be significantly decreased following arsenic treatment.	Arsenic	0-7	glutathione-disulfide reductase	Rattus norvegicus	217-219
20932244-3	2010	Arsenic treatment resulted in a significant increase in lipid peroxidase (LPO); however, glutathione (GSH) levels and the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT) were found to be significantly decreased following arsenic treatment.	Arsenic	0-7	catalase	Rattus norvegicus	226-234
20932244-6	2010	Administration of zinc to arsenic-treated rats significantly decreased the level of LPO but increased the level of GSH compared with arsenic-treated rats.	Arsenic	26-33	lactoperoxidase	Rattus norvegicus	84-87
20390892-6	2010	Grinding slurries had the lowest dissolved arsenic content at 15 mgL(-1).	Arsenic	43-50	LLGL scribble cell polarity complex component 1	Homo sapiens	65-71
20134249-14	2010	While many isolates were genetically diverse, others were clonal in nature Additionally, the arsenic-resistant isolates were examined for the presence of arsenic resistance (ars) genes by using PCR, and 30% of the isolates were found to carry an arsenate reductase encoded by the arsC gene.	Arsenic	93-100	steroid sulfatase	Homo sapiens	280-284
22314828-5	2010	In this experimental study, we have evaluated the impact of arsenic, on blood and blood forming cells by the changes in their cellular morphology, immune functional capacity, alteration of bone marrow CD34 positive stem/progenitors and changes in the phenotype of Sca-1, c-Kit dual positive primitive stem cell population.	Arsenic	60-67	CD34 molecule	Homo sapiens	201-205
19808700-0	2010	Critical cysteine residues of Kelch-like ECH-associated protein 1 in arsenic sensing and suppression of nuclear factor erythroid 2-related factor 2.	Arsenic	69-76	kelch-like ECH-associated protein 1	Mus musculus	30-65
19808700-1	2010	Arsenic activates nuclear factor erythroid 2-related factor 2 (Nrf2) to induce phase II and antioxidative genes.	Arsenic	0-7	nuclear factor, erythroid derived 2, like 2	Mus musculus	18-61
19808700-1	2010	Arsenic activates nuclear factor erythroid 2-related factor 2 (Nrf2) to induce phase II and antioxidative genes.	Arsenic	0-7	nuclear factor, erythroid derived 2, like 2	Mus musculus	63-67
19808700-3	2010	Arsenic-based Nrf2 activators, fluorescent biarsenical labeling reagent (FlAsH) and phenylarsine oxide (PAO), were used to probe binding of arsenic to Keap1.	Arsenic	0-7	nuclear factor, erythroid derived 2, like 2	Mus musculus	14-18
19808700-3	2010	Arsenic-based Nrf2 activators, fluorescent biarsenical labeling reagent (FlAsH) and phenylarsine oxide (PAO), were used to probe binding of arsenic to Keap1.	Arsenic	0-7	kelch-like ECH-associated protein 1	Mus musculus	151-156
19808700-3	2010	Arsenic-based Nrf2 activators, fluorescent biarsenical labeling reagent (FlAsH) and phenylarsine oxide (PAO), were used to probe binding of arsenic to Keap1.	Arsenic	45-52	nuclear factor, erythroid derived 2, like 2	Mus musculus	14-18
19808700-7	2010	Arsenic, tBHQ, free PAO, or cadmium blocked Keap1 pulldown.	Arsenic	0-7	kelch-like ECH-associated protein 1	Mus musculus	44-49
19808700-8	2010	Furthermore, arsenic and free PAO significantly reduced the free thiol contents of purified or endogenous Keap1.	Arsenic	13-20	kelch-like ECH-associated protein 1	Mus musculus	106-111
19808700-9	2010	Thus, arsenic, FlAsH, and PAO, as well as tBHQ and cadmium, bind to Keap1 cysteine thiols in a similar fashion.	Arsenic	6-13	kelch-like ECH-associated protein 1	Mus musculus	68-73
19808700-13	2010	Mutation of Cys151 abolished Nrf2 activation by arsenic.	Arsenic	48-55	nuclear factor, erythroid derived 2, like 2	Mus musculus	29-33
19808700-14	2010	Overexpression of C273A, C288A, or C151A altered the basal and arsenic-induced expression of Nrf2 target genes.	Arsenic	63-70	nuclear factor, erythroid derived 2, like 2	Mus musculus	93-97
19808700-16	2010	Our findings support a model in which arsenic binds to different sets of Keap1 cysteine residues to regulate divergent functions in Nrf2 signal transduction.	Arsenic	38-45	kelch-like ECH-associated protein 1	Mus musculus	73-78
19808700-16	2010	Our findings support a model in which arsenic binds to different sets of Keap1 cysteine residues to regulate divergent functions in Nrf2 signal transduction.	Arsenic	38-45	nuclear factor, erythroid derived 2, like 2	Mus musculus	132-136
22314828-5	2010	In this experimental study, we have evaluated the impact of arsenic, on blood and blood forming cells by the changes in their cellular morphology, immune functional capacity, alteration of bone marrow CD34 positive stem/progenitors and changes in the phenotype of Sca-1, c-Kit dual positive primitive stem cell population.	Arsenic	60-67	ataxin 1	Homo sapiens	264-269
22314828-5	2010	In this experimental study, we have evaluated the impact of arsenic, on blood and blood forming cells by the changes in their cellular morphology, immune functional capacity, alteration of bone marrow CD34 positive stem/progenitors and changes in the phenotype of Sca-1, c-Kit dual positive primitive stem cell population.	Arsenic	60-67	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	271-276
19921855-1	2009	This study describes the sorption of As(V) and As(III) to schwertmannite as a function of pH and arsenic loading.	Arsenic	97-104	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	37-42
19936779-1	2010	A glutaredoxin of the fern Pteris vittata PvGRX5 was previously implicated in arsenic tolerance.	Arsenic	78-85	CAX interacting protein 1	Arabidopsis thaliana	2-14
22294918-2	2010	Enzymatic amperometric procedures for measuring arsenic, based on the inhibitive action of this metal on acetylcholinesterase enzyme activity, have been developed.	Arsenic	48-55	acetylcholinesterase (Cartwright blood group)	Homo sapiens	105-125
22294918-4	2010	The amperometric response of acetylcholinesterase was affected by the presence of arsenic ions, which caused a decrease in the current intensity.	Arsenic	82-89	acetylcholinesterase (Cartwright blood group)	Homo sapiens	29-49
19933942-7	2009	Inhibition of arsenic biomethylation with sodium selenite abolished arsenic-induced ODD and invasiveness, colony formation, and MMP-2 and -9 hypersecretion in TRL1215 cells.	Arsenic	14-21	matrix metallopeptidase 2	Homo sapiens	128-140
19933942-7	2009	Inhibition of arsenic biomethylation with sodium selenite abolished arsenic-induced ODD and invasiveness, colony formation, and MMP-2 and -9 hypersecretion in TRL1215 cells.	Arsenic	68-75	matrix metallopeptidase 2	Homo sapiens	128-140
19933942-8	2009	Arsenic induced ODD in methylation-competent UROtsa/F35 cells (eg, at 16 weeks, with 1.0 microM arsenite 225% of control, 95% CI = 188% to 262%) but not in arsenic methylation-deficient UROtsa cells, and ODD levels corresponded to the levels of increased invasiveness, colony formation, and hypersecretion of active MMP-2 and -9 seen after transformation to an in vitro cancer phenotype.	Arsenic	0-7	matrix metallopeptidase 2	Homo sapiens	316-328
20001046-10	2009	The value of the arsenic quadrupole coupling constant (eqQ=-202 MHz) suggests that the As-C bond has a mixture of covalent and ionic characters, consistent with theoretical predictions that both pi backbonding and electron transfer play a role in creating a linear, as opposed to a cyclic, structure for certain heteroatom dicarbides.	Arsenic	17-24	steroid sulfatase	Homo sapiens	87-91
19732783-11	2009	Based on these findings, we propose a novel role for the MYST1 gene in human sensitivity to arsenic.	Arsenic	92-99	lysine acetyltransferase 8	Homo sapiens	57-62
19732783-0	2009	Acetylated H4K16 by MYST1 protects UROtsa cells from arsenic toxicity and is decreased following chronic arsenic exposure.	Arsenic	53-60	lysine acetyltransferase 8	Homo sapiens	20-25
19732783-0	2009	Acetylated H4K16 by MYST1 protects UROtsa cells from arsenic toxicity and is decreased following chronic arsenic exposure.	Arsenic	105-112	lysine acetyltransferase 8	Homo sapiens	20-25
19732783-7	2009	The expression of MYST1 was knocked down in UROtsa cells, a model of bladder epithelium that has been used to study arsenic-induced carcinogenesis.	Arsenic	116-123	lysine acetyltransferase 8	Homo sapiens	18-23
19452132-8	2009	Nevertheless, activity of glucose-6-phosphatase in the liver was stimulated by insulin treatment to diabetic and arsenic-fed rats.	Arsenic	113-120	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	26-47
19799857-7	2009	Accordingly, atrial lipin-1 and lipin-3 mRNA expression in diabetic patients was 50% and 59% lower as in non-diabetic patients, respectively.	Arsenic	78-80	lipin 1	Homo sapiens	20-27
19799857-7	2009	Accordingly, atrial lipin-1 and lipin-3 mRNA expression in diabetic patients was 50% and 59% lower as in non-diabetic patients, respectively.	Arsenic	78-80	lipin 3	Homo sapiens	32-39
19787300-7	2009	The chronic exposure to arsenic upregulates the expression of tumor necrosis factor-alpha, interleukin-1, vascular cell adhesion molecule and vascular endothelial growth factor to induce cardiovascular pathogenesis.	Arsenic	24-31	tumor necrosis factor	Homo sapiens	62-89
19787300-7	2009	The chronic exposure to arsenic upregulates the expression of tumor necrosis factor-alpha, interleukin-1, vascular cell adhesion molecule and vascular endothelial growth factor to induce cardiovascular pathogenesis.	Arsenic	24-31	interleukin 1 alpha	Homo sapiens	91-104
19787300-7	2009	The chronic exposure to arsenic upregulates the expression of tumor necrosis factor-alpha, interleukin-1, vascular cell adhesion molecule and vascular endothelial growth factor to induce cardiovascular pathogenesis.	Arsenic	24-31	vascular endothelial growth factor A	Homo sapiens	142-176
19682479-0	2009	Arsenic exacerbates atherosclerotic lesion formation and inflammation in ApoE-/- mice.	Arsenic	0-7	apolipoprotein E	Mus musculus	73-77
19786557-5	2009	FlAsH (an arsenic-based fluorophore) and phenylarsine oxide (PAO) potently induce Nrf2 target genes and bind to Nrf2 in vitro and in vivo.	Arsenic	10-17	NFE2 like bZIP transcription factor 2	Homo sapiens	82-86
19786557-5	2009	FlAsH (an arsenic-based fluorophore) and phenylarsine oxide (PAO) potently induce Nrf2 target genes and bind to Nrf2 in vitro and in vivo.	Arsenic	10-17	NFE2 like bZIP transcription factor 2	Homo sapiens	112-116
19786557-10	2009	It is remarkable that the mutants fail to respond to arsenic for Nrf2 activation and gene induction.	Arsenic	53-60	NFE2 like bZIP transcription factor 2	Homo sapiens	65-69
19767444-8	2009	Finally, two well-characterized immunotoxicants, arsenic and benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide, using the CD40L-induced IgM AFC response were compared in both mouse and human B cells.	Arsenic	49-56	CD40 ligand	Mus musculus	116-121
19682479-9	2009	Expression of pro-inflammatory chemokine MCP-1 and cytokine IL-6 and markers of oxidative stress, protein-HNE and protein-MDA adducts were markedly increased in lesions of arsenic-exposed mice.	Arsenic	172-179	mast cell protease 1	Mus musculus	41-46
19682479-9	2009	Expression of pro-inflammatory chemokine MCP-1 and cytokine IL-6 and markers of oxidative stress, protein-HNE and protein-MDA adducts were markedly increased in lesions of arsenic-exposed mice.	Arsenic	172-179	interleukin 6	Mus musculus	60-64
19682479-10	2009	Plasma concentrations of MCP-1, IL-6 and MDA were also significantly elevated in arsenic-exposed mice.	Arsenic	81-88	mast cell protease 1	Mus musculus	25-30
19682479-10	2009	Plasma concentrations of MCP-1, IL-6 and MDA were also significantly elevated in arsenic-exposed mice.	Arsenic	81-88	interleukin 6	Mus musculus	32-36
19686770-2	2009	Therefore, the aim of this study is to investigate whether the effect of cigarette smoking, alcohol consumption, arsenic and occupational exposures on risk of UC could be modified by genetic polymorphisms of cytochrome P450 2E1 and glutathione S-transferase omega.	Arsenic	113-120	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	208-227
19966145-0	2009	Chronic exposure to arsenic in tap water reduces acetylcholine-induced relaxation in the aorta and increases oxidative stress in female rats.	Arsenic	20-27	nuclear RNA export factor 1	Rattus norvegicus	31-34
19680750-11	2009	Through GLM, significant gene effects of arsenic (+3 oxidation state)-methyltransferase (AS3MT) on MMA%, dimethylarsinic acid percentage (DMA%) and DMA/MMA, purine nucleoside phosphorylase (PNP) on DMA% and glutathione S-transferase omega 2 (GSTO2) on inorganic arsenics (InAs%) were found.	Arsenic	41-48	purine nucleoside phosphorylase	Homo sapiens	157-188
19680750-11	2009	Through GLM, significant gene effects of arsenic (+3 oxidation state)-methyltransferase (AS3MT) on MMA%, dimethylarsinic acid percentage (DMA%) and DMA/MMA, purine nucleoside phosphorylase (PNP) on DMA% and glutathione S-transferase omega 2 (GSTO2) on inorganic arsenics (InAs%) were found.	Arsenic	41-48	glutathione S-transferase omega 2	Homo sapiens	207-240
19680750-11	2009	Through GLM, significant gene effects of arsenic (+3 oxidation state)-methyltransferase (AS3MT) on MMA%, dimethylarsinic acid percentage (DMA%) and DMA/MMA, purine nucleoside phosphorylase (PNP) on DMA% and glutathione S-transferase omega 2 (GSTO2) on inorganic arsenics (InAs%) were found.	Arsenic	41-48	glutathione S-transferase omega 2	Homo sapiens	242-247
19680750-11	2009	Through GLM, significant gene effects of arsenic (+3 oxidation state)-methyltransferase (AS3MT) on MMA%, dimethylarsinic acid percentage (DMA%) and DMA/MMA, purine nucleoside phosphorylase (PNP) on DMA% and glutathione S-transferase omega 2 (GSTO2) on inorganic arsenics (InAs%) were found.	Arsenic	262-270	arsenite methyltransferase	Homo sapiens	89-94
19680750-11	2009	Through GLM, significant gene effects of arsenic (+3 oxidation state)-methyltransferase (AS3MT) on MMA%, dimethylarsinic acid percentage (DMA%) and DMA/MMA, purine nucleoside phosphorylase (PNP) on DMA% and glutathione S-transferase omega 2 (GSTO2) on inorganic arsenics (InAs%) were found.	Arsenic	41-48	arsenite methyltransferase	Homo sapiens	89-94
19680750-11	2009	Through GLM, significant gene effects of arsenic (+3 oxidation state)-methyltransferase (AS3MT) on MMA%, dimethylarsinic acid percentage (DMA%) and DMA/MMA, purine nucleoside phosphorylase (PNP) on DMA% and glutathione S-transferase omega 2 (GSTO2) on inorganic arsenics (InAs%) were found.	Arsenic	41-48	monocyte to macrophage differentiation associated	Homo sapiens	99-102
19966145-1	2009	The aim of this work is to determine whether consuming tap water containing arsenic (20 microg/L) alters oxidative stress levels in female rats and changes vascular response.	Arsenic	76-83	nuclear RNA export factor 1	Rattus norvegicus	55-58
19720680-3	2009	The aim of this study was to explore whether TNF-alpha promoter polymorphisms confer susceptibility to AS.	Arsenic	103-105	tumor necrosis factor	Homo sapiens	45-54
19672740-0	2009	Prophylactic role of taurine on arsenic mediated oxidative renal dysfunction via MAPKs/ NF-kappaB and mitochondria dependent pathways.	Arsenic	32-39	nuclear factor kappa B subunit 1	Homo sapiens	88-97
19631675-3	2009	The arsenic treated rats also exhibited a decrease in the binding of striatal dopamine receptors (32%) and tyrosine hydroxylase (TH) immunoreactivity (19%) in striatum.	Arsenic	4-11	tyrosine hydroxylase	Rattus norvegicus	107-127
19631675-3	2009	The arsenic treated rats also exhibited a decrease in the binding of striatal dopamine receptors (32%) and tyrosine hydroxylase (TH) immunoreactivity (19%) in striatum.	Arsenic	4-11	tyrosine hydroxylase	Rattus norvegicus	129-131
19631675-4	2009	Increased arsenic levels in corpus striatum (6.5 fold), frontal cortex (6.3 fold) and hippocampus (7.0 fold) associated with enhanced oxidative stress in these brain regions, as evident by an increase in lipid perioxidation, protein carbonyl and a decrease in the levels of glutathione and activity of superoxide dismutase, catalase and glutathione peroxidase with differential effects were observed in arsenic treated rats compared to controls.	Arsenic	10-17	catalase	Rattus norvegicus	324-332
19808868-4	2009	RA targets the RARA moiety of the fusion, whereas arsenic targets its PML part.	Arsenic	50-57	PML nuclear body scaffold	Homo sapiens	70-73
19691357-1	2009	The arsenic (+3 oxidation state) methyltransferase (As3mt) gene encodes a 43 kDa protein that catalyzes methylation of inorganic arsenic.	Arsenic	4-11	arsenite methyltransferase	Mus musculus	52-57
19691357-2	2009	Altered expression of AS3MT in cultured human cells controls arsenic methylation phenotypes, suggesting a critical role in arsenic metabolism.	Arsenic	61-68	arsenite methyltransferase	Homo sapiens	22-27
19691357-2	2009	Altered expression of AS3MT in cultured human cells controls arsenic methylation phenotypes, suggesting a critical role in arsenic metabolism.	Arsenic	123-130	arsenite methyltransferase	Homo sapiens	22-27
19691357-7	2009	At 2 and 24 h after dosing, livers of As3mt knockouts contained a greater proportion of inorganic and monomethylated arsenic than did livers of C57BL/6 mice.	Arsenic	117-124	arsenite methyltransferase	Mus musculus	38-43
19691357-8	2009	A similar predominance of inorganic and monomethylated arsenic was found in the urine of As3mt knockouts.	Arsenic	55-62	arsenite methyltransferase	Mus musculus	89-94
19691357-9	2009	At 24 h after dosing, As3mt knockouts retained significantly higher percentages of arsenic dose in liver, kidneys, urinary bladder, lungs, heart, and carcass than did C57BL/6 mice.	Arsenic	83-90	arsenite methyltransferase	Mus musculus	22-27
19691357-13	2009	These data confirm a central role for As3mt in the metabolism of inorganic arsenic and indicate that phenotypes for arsenic retention and distribution are markedly affected by the null genotype for arsenic methylation, indicating a close linkage between the metabolism and retention of arsenicals.	Arsenic	75-82	arsenite methyltransferase	Mus musculus	38-43
19595304-4	2009	In multiple linear regression models adjusted for age, BMI and smoking, PRL was inversely associated with arsenic, cadmium, copper, lead, manganese, molybdenum, and zinc, but positively associated with chromium.	Arsenic	106-113	prolactin	Homo sapiens	72-75
19672740-6	2009	Combining, results suggest that taurine possesses the ability to ameliorate arsenic-induced oxidative insult and renal damage, probably due to its antioxidant activity and functioning via MAPKs/NF-kappaB and mitochondria dependent pathways.	Arsenic	76-83	nuclear factor kappa B subunit 1	Homo sapiens	194-203
19616567-0	2009	Taurine prevents arsenic-induced cardiac oxidative stress and apoptotic damage: role of NF-kappa B, p38 and JNK MAPK pathway.	Arsenic	17-24	nuclear factor kappa B subunit 1	Homo sapiens	88-98
19429932-6	2009	RESULTS: In continuous and multi-category regression models, higher FGF23 was associated with a significant increase in the odds of having a high AS (OR 1.43, CI 1.06-1.92 to OR 3.01, CI 1.52-5.99).	Arsenic	146-148	fibroblast growth factor 23	Homo sapiens	68-73
19574057-0	2009	Characterization of glutathione reductase and catalase in the fronds of two Pteris ferns upon arsenic exposure.	Arsenic	94-101	catalase	Bos taurus	46-54
19574057-1	2009	To better understand the mechanisms of plant tolerance to high concentration of arsenic, we characterized two antioxidant enzymes, glutathione reductase (GR) and catalase (CAT), in the fronds of Pteris vittata, an arsenic-hyperaccumulating fern, and Pteris ensiformis, an arsenic-sensitive fern.	Arsenic	80-87	catalase	Bos taurus	162-170
19538980-5	2009	Previously, we demonstrated a protective role of Nrf2 against arsenic-induced toxicity using a cell culture model.	Arsenic	62-69	nuclear factor, erythroid derived 2, like 2	Mus musculus	49-53
19538980-6	2009	In this report, we present evidence that Nrf2 protects against liver and bladder injury in response to six weeks of arsenic exposure in a mouse model.	Arsenic	116-123	nuclear factor, erythroid derived 2, like 2	Mus musculus	41-45
19616567-0	2009	Taurine prevents arsenic-induced cardiac oxidative stress and apoptotic damage: role of NF-kappa B, p38 and JNK MAPK pathway.	Arsenic	17-24	mitogen-activated protein kinase 14	Homo sapiens	100-103
19538980-8	2009	Furthermore, Nrf2(-/-) mice were more sensitive to arsenic-induced DNA hypomethylation, oxidative DNA damage, and apoptotic cell death.	Arsenic	51-58	nuclear factor, erythroid derived 2, like 2	Mus musculus	13-17
19538980-10	2009	Hence, this work demonstrates the feasibility of using dietary compounds that target activation of the Nrf2 signaling pathway to alleviate arsenic-induced damage.	Arsenic	139-146	nuclear factor, erythroid derived 2, like 2	Mus musculus	103-107
19616567-0	2009	Taurine prevents arsenic-induced cardiac oxidative stress and apoptotic damage: role of NF-kappa B, p38 and JNK MAPK pathway.	Arsenic	17-24	mitogen-activated protein kinase 8	Homo sapiens	108-111
19616567-5	2009	Arsenic reduced cardiomyocyte viability, increased reactive oxygen species (ROS) production and intracellular calcium overload, and induced apoptotic cell death by mitochondrial dependent caspase-3 activation and poly-ADP ribose polymerase (PARP) cleavage.	Arsenic	0-7	caspase 3	Homo sapiens	188-197
19616567-5	2009	Arsenic reduced cardiomyocyte viability, increased reactive oxygen species (ROS) production and intracellular calcium overload, and induced apoptotic cell death by mitochondrial dependent caspase-3 activation and poly-ADP ribose polymerase (PARP) cleavage.	Arsenic	0-7	poly(ADP-ribose) polymerase 1	Homo sapiens	213-239
19616567-5	2009	Arsenic reduced cardiomyocyte viability, increased reactive oxygen species (ROS) production and intracellular calcium overload, and induced apoptotic cell death by mitochondrial dependent caspase-3 activation and poly-ADP ribose polymerase (PARP) cleavage.	Arsenic	0-7	poly(ADP-ribose) polymerase 1	Homo sapiens	241-245
19616567-6	2009	These changes due to arsenic exposure were found to be associated with increased IKK and NF-kappaB (p65) phosphorylation.	Arsenic	21-28	RELA proto-oncogene, NF-kB subunit	Homo sapiens	100-103
19616567-8	2009	Arsenic also markedly increased the activity of p38 and JNK MAPKs, but not ERK to that extent.	Arsenic	0-7	mitogen-activated protein kinase 14	Homo sapiens	48-51
19616567-8	2009	Arsenic also markedly increased the activity of p38 and JNK MAPKs, but not ERK to that extent.	Arsenic	0-7	mitogen-activated protein kinase 8	Homo sapiens	56-59
19616567-9	2009	Pre-treatment with SP600125 (JNK inhibitor) and SB203580 (p38 MAPK inhibitor) attenuated NF-kappaB and IKK phosphorylation indicating that p38 and JNK MAPKs are mainly involved in arsenic-induced NF-kappaB activation.	Arsenic	180-187	mitogen-activated protein kinase 14	Homo sapiens	58-61
19616567-9	2009	Pre-treatment with SP600125 (JNK inhibitor) and SB203580 (p38 MAPK inhibitor) attenuated NF-kappaB and IKK phosphorylation indicating that p38 and JNK MAPKs are mainly involved in arsenic-induced NF-kappaB activation.	Arsenic	180-187	mitogen-activated protein kinase 14	Homo sapiens	139-142
19797872-8	2009	In our cellular experiments, we found that arsenic exposure causes adaptive responses against oxidative stress and arsenic cytotoxicity through Nrf2 activation.	Arsenic	43-50	NFE2 like bZIP transcription factor 2	Homo sapiens	144-148
19616567-9	2009	Pre-treatment with SP600125 (JNK inhibitor) and SB203580 (p38 MAPK inhibitor) attenuated NF-kappaB and IKK phosphorylation indicating that p38 and JNK MAPKs are mainly involved in arsenic-induced NF-kappaB activation.	Arsenic	180-187	mitogen-activated protein kinase 8	Homo sapiens	147-150
19797872-8	2009	In our cellular experiments, we found that arsenic exposure causes adaptive responses against oxidative stress and arsenic cytotoxicity through Nrf2 activation.	Arsenic	115-122	NFE2 like bZIP transcription factor 2	Homo sapiens	144-148
19616567-10	2009	Taurine treatment suppressed these apoptotic actions, suggesting that its protective role in arsenic-induced cardiomyocyte apoptosis is mediated by attenuation of p38 and JNK MAPK signaling pathways.	Arsenic	93-100	mitogen-activated protein kinase 14	Homo sapiens	163-166
19616567-10	2009	Taurine treatment suppressed these apoptotic actions, suggesting that its protective role in arsenic-induced cardiomyocyte apoptosis is mediated by attenuation of p38 and JNK MAPK signaling pathways.	Arsenic	93-100	mitogen-activated protein kinase 8	Homo sapiens	171-174
19805235-0	2009	Reduced arsenic clearance and increased toxicity in aquaglyceroporin-9-null mice.	Arsenic	8-15	aquaporin 9	Mus musculus	52-70
19806747-1	2009	The emission of arsenic (As) with leachate from mechanically biologically pretreated municipal solid waste (MBP-MSW) was quantified over one year using landfill simulation reactors.	Arsenic	16-23	myelin basic protein	Homo sapiens	108-111
19806747-1	2009	The emission of arsenic (As) with leachate from mechanically biologically pretreated municipal solid waste (MBP-MSW) was quantified over one year using landfill simulation reactors.	Arsenic	25-27	myelin basic protein	Homo sapiens	108-111
19805235-4	2009	The highest tissue level of arsenic is in heart, with AQP9-null mice accumulating 10-20 times more arsenic than WT mice.	Arsenic	28-35	aquaporin 9	Mus musculus	54-58
19805235-4	2009	The highest tissue level of arsenic is in heart, with AQP9-null mice accumulating 10-20 times more arsenic than WT mice.	Arsenic	99-106	aquaporin 9	Mus musculus	54-58
19805235-6	2009	Increased arsenic levels are also present in liver, lung, spleen, and testis of AQP9-null mice.	Arsenic	10-17	aquaporin 9	Mus musculus	80-84
19805235-7	2009	Arsenic levels in the feces and urine of AQP9-null mice are only approximately 10% of the WT levels, and reduced clearance of multiple arsenic species by the AQP9-null mice suggests that AQP9 is involved in the export of multiple forms of arsenic.	Arsenic	0-7	aquaporin 9	Mus musculus	41-45
19805235-10	2009	We propose that AQP9 provides a route for excretion of arsenic by the liver, thereby providing partial protection of the whole animal from arsenic toxicity.	Arsenic	55-62	aquaporin 9	Mus musculus	16-20
19484295-0	2009	Diversity of arsenate reductase genes (arsC Genes) from arsenic-resistant environmental isolates of E. coli.	Arsenic	56-63	Arsenate reductase	Escherichia coli	13-31
21784005-9	2009	Treatment with arsenic decreased the CYP and cytochrome b(5) contents by 39 and 36%, than with malathion by 54 and 22% and the coexposure by 45 and 28%, respectively.	Arsenic	15-22	cytochrome b5 type A	Gallus gallus	45-60
19487254-3	2009	The hypothesis that sex-dependent Bcrp expression influences the hepatobiliary disposition of phase II metabolites was tested in the present study using acetaminophen (APAP) and the generated APAP glucuronide (AG) and sulfate (AS) metabolites in single-pass in situ perfused livers from male and female wild-type and Abcg(-/-) (Bcrp-deficient) mice.	Arsenic	227-229	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	34-38
19764221-1	2009	The objective of this study was to explore a bioremediation strategy based on injecting NO3- to support the anoxic oxidation of ferrous iron (Fe(II)) and arsenite (As(II)) in the subsurface as a means to immobilize As in the form of arsenate (As(V)) adsorbed onto biogenic ferric (Fe(III)) (hydr)oxides.	Arsenic	164-166	NBL1, DAN family BMP antagonist	Homo sapiens	88-91
19764221-3	2009	During operation for 250 days, the average influent arsenic concentration of 567 microg L(-1) was reduced to 10.6 (+/-9.6) microg L(-1) in the effluent of column SF1.	Arsenic	52-59	splicing factor 1	Homo sapiens	162-165
21784005-12	2009	The activities of hepatic microsomal and cytosolic GST were increased with all the three treatments [Arsenic (microsomal: 88% cytosolic: 113%), malathion (microsomal: 137%, cytosolic: 94%) and coexposure (microsomal: 140%, cytosolic: 148%)].	Arsenic	101-108	glutathione S-transferase alpha 3	Gallus gallus	51-54
19764221-5	2009	The dominant speciation of the immobilized iron and arsenic was Fe(III) and As(V) in SF1, compared with Fe(II) and As(III) in SF2.	Arsenic	52-59	splicing factor 1	Homo sapiens	85-88
19410645-0	2009	Arsenic down-regulates the expression of Camk4, an important gene related to cerebellar LTD in mice.	Arsenic	0-7	calcium/calmodulin-dependent protein kinase IV	Mus musculus	41-46
19513820-3	2009	Parameters studied included cell adhesion capacity, expression of CD54 and F-actin, nitric oxide production, phagocytic capacity, and effect of arsenic on Rho A-ROCK pathway.	Arsenic	144-151	ras homolog family member A	Homo sapiens	155-160
19513820-5	2009	Additionally, chronic arsenic exposure affected Rho A-ROCK pathway which in turn impaired macrophage functions.	Arsenic	22-29	ras homolog family member A	Homo sapiens	48-53
19635583-2	2009	Glutathione-S-transferase omega (GSTO) 1 and 2 are known to have the activity of monomethyl arsenate [MMA(V)] reductase, which is the rate-limiting enzyme for the biotransformation of inorganic arsenic.	Arsenic	194-201	glutathione S-transferase omega 1	Homo sapiens	0-46
19635583-2	2009	Glutathione-S-transferase omega (GSTO) 1 and 2 are known to have the activity of monomethyl arsenate [MMA(V)] reductase, which is the rate-limiting enzyme for the biotransformation of inorganic arsenic.	Arsenic	194-201	glutathione S-transferase omega 1	Homo sapiens	102-119
19635583-3	2009	This study was conducted to investigate the relationship between polymorphisms in the GSTO1 and GSTO2 genes and arsenic metabolism and oxidative stress status in Chinese populations chronically exposed to different levels of arsenic in drinking water.	Arsenic	112-119	glutathione S-transferase omega 1	Homo sapiens	86-91
19635583-3	2009	This study was conducted to investigate the relationship between polymorphisms in the GSTO1 and GSTO2 genes and arsenic metabolism and oxidative stress status in Chinese populations chronically exposed to different levels of arsenic in drinking water.	Arsenic	112-119	glutathione S-transferase omega 2	Homo sapiens	96-101
19635583-3	2009	This study was conducted to investigate the relationship between polymorphisms in the GSTO1 and GSTO2 genes and arsenic metabolism and oxidative stress status in Chinese populations chronically exposed to different levels of arsenic in drinking water.	Arsenic	225-232	glutathione S-transferase omega 1	Homo sapiens	86-91
19635583-3	2009	This study was conducted to investigate the relationship between polymorphisms in the GSTO1 and GSTO2 genes and arsenic metabolism and oxidative stress status in Chinese populations chronically exposed to different levels of arsenic in drinking water.	Arsenic	225-232	glutathione S-transferase omega 2	Homo sapiens	96-101
19410645-2	2009	Our results showed the increased level of As concentration in cerebellar tissue of the exposed mice in a dose-response manner, longer escape latency in the experimental group than controls and the down-regulated expression of Ca(2+)/calmodulin dependent protein kinase IV (Camk4), a very important regulator in the LTD pathway.	Arsenic	42-44	calcium/calmodulin-dependent protein kinase IV	Mus musculus	273-278
19410645-3	2009	We further analyzed the influence of As on cerebellar Camk4 expression by Western blot.	Arsenic	37-39	calcium/calmodulin-dependent protein kinase IV	Mus musculus	54-59
19410645-6	2009	Therefore, the Camk4 may be target of As-induced neurotoxicity.	Arsenic	38-40	calcium/calmodulin-dependent protein kinase IV	Mus musculus	15-20
19556897-3	2009	Here we report for the first time that REGgamma interacts with the promyelocytic leukemia protein (PML), accumulates in PML nuclear bodies (PML-NBs), but it does not play any role in normal or arsenic-induced PML degradation.	Arsenic	193-200	PML nuclear body scaffold	Homo sapiens	99-102
19538983-5	2009	In this study, we evaluated the association of the polymorphism in AS3MT gene with iAs metabolism and with the presence of arsenic (As) premalignant skin lesions.	Arsenic	123-130	arsenite methyltransferase	Homo sapiens	67-72
19538983-5	2009	In this study, we evaluated the association of the polymorphism in AS3MT gene with iAs metabolism and with the presence of arsenic (As) premalignant skin lesions.	Arsenic	84-86	arsenite methyltransferase	Homo sapiens	67-72
19661343-0	2009	Elevated ERCC1 gene expression in blood cells associated with exposure to arsenic from drinking water in Inner Mongolia.	Arsenic	74-81	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	9-14
19661343-2	2009	The objective of this study was to investigate the effects of arsenic exposure on a DNA nucleotide excision repair gene, ERCC1, expression in human blood cells.	Arsenic	62-69	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	121-126
19661343-5	2009	RESULTS: The mRNA levels of ERCC1 expression were positively associated with water arsenic concentration (slope=0.313, p=0.0043) and nail arsenic concentration (slope=0.474, p=0.0073).	Arsenic	83-90	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	28-33
19661343-5	2009	RESULTS: The mRNA levels of ERCC1 expression were positively associated with water arsenic concentration (slope=0.313, p=0.0043) and nail arsenic concentration (slope=0.474, p=0.0073).	Arsenic	138-145	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	28-33
19661343-7	2009	CONCLUSION: The results showed that mRNA levels of ERCC1 expression were significantly associated with arsenic concentrations in drinking water, implicating the DNA repair response was induced by arsenic exposure.	Arsenic	103-110	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	51-56
19661343-7	2009	CONCLUSION: The results showed that mRNA levels of ERCC1 expression were significantly associated with arsenic concentrations in drinking water, implicating the DNA repair response was induced by arsenic exposure.	Arsenic	196-203	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	51-56
18618274-5	2009	Arsenic and lead were found to trigger apoptosis as revealed by DNA ladder formation, Western blots of apoptotic factors, and reverse transcriptase polymerase chain reaction analyses of bax and bcl-2.	Arsenic	0-7	BCL2 associated X, apoptosis regulator	Rattus norvegicus	186-189
18618274-5	2009	Arsenic and lead were found to trigger apoptosis as revealed by DNA ladder formation, Western blots of apoptotic factors, and reverse transcriptase polymerase chain reaction analyses of bax and bcl-2.	Arsenic	0-7	BCL2, apoptosis regulator	Rattus norvegicus	194-199
18618274-6	2009	Results clearly indicate that both arsenic and lead induced apoptosis is caspase-mediated and accompanied by extracellular signal-regulated kinase (ERK) dephosphorylation.	Arsenic	35-42	Eph receptor B1	Rattus norvegicus	109-146
18618274-6	2009	Results clearly indicate that both arsenic and lead induced apoptosis is caspase-mediated and accompanied by extracellular signal-regulated kinase (ERK) dephosphorylation.	Arsenic	35-42	Eph receptor B1	Rattus norvegicus	148-151
18618274-7	2009	Full-length BH3-interacting-domain death agonist expression in presence of caspase 3 inhibitor unravels a direct involvement of caspase in As and Pb induced apoptosis.	Arsenic	139-141	caspase 3	Rattus norvegicus	75-84
19453443-0	2009	ARS5 is a component of the 26S proteasome complex, and negatively regulates thiol biosynthesis and arsenic tolerance in Arabidopsis.	Arsenic	99-106	proteasome alpha subunit F1	Arabidopsis thaliana	0-4
19453443-4	2009	ars5 is shown to exhibit an increased accumulation of arsenic and thiol compounds during arsenic stress.	Arsenic	54-61	proteasome alpha subunit F1	Arabidopsis thaliana	0-4
19453443-4	2009	ars5 is shown to exhibit an increased accumulation of arsenic and thiol compounds during arsenic stress.	Arsenic	89-96	proteasome alpha subunit F1	Arabidopsis thaliana	0-4
19453443-6	2009	Characterization of an independent paf1 T-DNA insertion allele and complementation by PAF1 confirmed that paf1 mutation is responsible for the enhanced thiol accumulation and arsenic tolerance phenotypes.	Arsenic	175-182	proteasome alpha subunit F1	Arabidopsis thaliana	86-90
19453443-6	2009	Characterization of an independent paf1 T-DNA insertion allele and complementation by PAF1 confirmed that paf1 mutation is responsible for the enhanced thiol accumulation and arsenic tolerance phenotypes.	Arsenic	175-182	proteasome alpha subunit F1	Arabidopsis thaliana	106-110
19453443-7	2009	Arsenic tolerance was not observed in a knock-out mutant of the highly homologous PAF2 gene.	Arsenic	0-7	20S proteasome alpha subunit F2	Arabidopsis thaliana	82-86
19453443-9	2009	No detectible difference was observed in total ubiquitinylated protein profiles between ars5 and wild-type (WT) Arabidopsis, suggesting that the arsenic tolerance observed in ars5 is not derived from a general impairment in proteasome-mediated protein degradation.	Arsenic	145-152	proteasome alpha subunit F1	Arabidopsis thaliana	175-179
19453443-10	2009	Quantitative RT-PCR showed that arsenic induces the enhanced transcriptional activation of several key genes that function in glutathione and phytochelatin biosynthesis in the WT, and this arsenic induction of gene expression is more dramatic in ars5.	Arsenic	32-39	proteasome alpha subunit F1	Arabidopsis thaliana	246-250
19453443-10	2009	Quantitative RT-PCR showed that arsenic induces the enhanced transcriptional activation of several key genes that function in glutathione and phytochelatin biosynthesis in the WT, and this arsenic induction of gene expression is more dramatic in ars5.	Arsenic	189-196	proteasome alpha subunit F1	Arabidopsis thaliana	246-250
19453443-11	2009	The enhanced transcriptional response to arsenic and the increased accumulation of thiol compounds in ars5, compared with WT, suggest the presence of a positive regulation pathway for thiol biosynthesis that is enhanced in the ars5 background.	Arsenic	41-48	proteasome alpha subunit F1	Arabidopsis thaliana	227-231
19121333-0	2009	Chronic low-level arsenic exposure causes gender-specific alterations in locomotor activity, dopaminergic systems, and thioredoxin expression in mice.	Arsenic	18-25	thioredoxin 1	Mus musculus	119-130
19152805-3	2009	Only recently have genes encoding enzymes responsible for arsenic metabolism, such as AS3MT and GSTO, been cloned and characterized.	Arsenic	58-65	arsenite methyltransferase	Homo sapiens	86-91
19707557-0	2009	Disruption of histone modification and CARM1 recruitment by arsenic represses transcription at glucocorticoid receptor-regulated promoters.	Arsenic	60-67	coactivator associated arginine methyltransferase 1	Homo sapiens	39-44
19707557-0	2009	Disruption of histone modification and CARM1 recruitment by arsenic represses transcription at glucocorticoid receptor-regulated promoters.	Arsenic	60-67	nuclear receptor subfamily 3 group C member 1	Homo sapiens	95-118
19792665-4	2009	It is surprising that STM images the different Fe-As orbitals associated with the orthorhombic structure, but not the As atoms in the surface plane.	Arsenic	50-52	sulfotransferase family 1A member 3	Homo sapiens	22-25
19494047-3	2009	Eel testicular fragments were cultured in vitro with 0.1-100 microM arsenic with or without human chorionic gonadotropin (hCG) for 6 or 15 days at 20 degrees C. Arsenic treatment provoked a dose-dependent inhibition of hCG-induced germ cell proliferation as revealed by 5-bromo-2-deoxyuridine immunohistochemistry.	Arsenic	161-168	chorionic gonadotropin subunit beta 5	Homo sapiens	122-125
19494047-4	2009	Time-resolved fluorescent immunoassay showed that arsenic suppressed hCG-induced synthesis of 11-ketotestosterone (11-KT) in testicular fragments incubated with 0.0001-100 microM arsenic and hCG for 18 h. A 0.1 microM (7 microg/l) dose of arsenic which is lower than the World Health Organization drinking water quality guideline of 10 microg/l most effectively reduced 11-KT production.	Arsenic	50-57	chorionic gonadotropin subunit beta 5	Homo sapiens	191-194
19494047-3	2009	Eel testicular fragments were cultured in vitro with 0.1-100 microM arsenic with or without human chorionic gonadotropin (hCG) for 6 or 15 days at 20 degrees C. Arsenic treatment provoked a dose-dependent inhibition of hCG-induced germ cell proliferation as revealed by 5-bromo-2-deoxyuridine immunohistochemistry.	Arsenic	161-168	chorionic gonadotropin subunit beta 5	Homo sapiens	219-222
19494047-4	2009	Time-resolved fluorescent immunoassay showed that arsenic suppressed hCG-induced synthesis of 11-ketotestosterone (11-KT) in testicular fragments incubated with 0.0001-100 microM arsenic and hCG for 18 h. A 0.1 microM (7 microg/l) dose of arsenic which is lower than the World Health Organization drinking water quality guideline of 10 microg/l most effectively reduced 11-KT production.	Arsenic	50-57	chorionic gonadotropin subunit beta 5	Homo sapiens	69-72
19494047-4	2009	Time-resolved fluorescent immunoassay showed that arsenic suppressed hCG-induced synthesis of 11-ketotestosterone (11-KT) in testicular fragments incubated with 0.0001-100 microM arsenic and hCG for 18 h. A 0.1 microM (7 microg/l) dose of arsenic which is lower than the World Health Organization drinking water quality guideline of 10 microg/l most effectively reduced 11-KT production.	Arsenic	179-186	chorionic gonadotropin subunit beta 5	Homo sapiens	69-72
19494047-4	2009	Time-resolved fluorescent immunoassay showed that arsenic suppressed hCG-induced synthesis of 11-ketotestosterone (11-KT) in testicular fragments incubated with 0.0001-100 microM arsenic and hCG for 18 h. A 0.1 microM (7 microg/l) dose of arsenic which is lower than the World Health Organization drinking water quality guideline of 10 microg/l most effectively reduced 11-KT production.	Arsenic	179-186	chorionic gonadotropin subunit beta 5	Homo sapiens	69-72
19494047-5	2009	The hCG-induced synthesis of progesterone from pregnenolone was significantly inhibited by low doses of arsenic (0.1-1 microM), implying an inhibition of 3beta-hydroxysteroid dehydrogenase activity.	Arsenic	104-111	chorionic gonadotropin subunit beta 5	Homo sapiens	4-7
18682255-5	2009	RESULTS: Genetic factors affecting arsenic metabolite pattern included two polymorphisms in arsenic (+III) methyltransferase (AS3MT) (rs3740400, rs7085104), where carriers had lower %MMA and higher %DMA.	Arsenic	35-42	arsenite methyltransferase	Homo sapiens	126-131
19577786-0	2009	Preparation and evaluation of iron-chitosan composites for removal of As(III) and As(V) from arsenic contaminated real life groundwater.	Arsenic	93-100	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	82-87
19442679-10	2009	Because the cellular uptake of iAs(III) is mediated by aquaporin proteins, and because the resistance of cells to arsenite can be influenced by lower arsenic uptake due to lower expression of aquaporin proteins (AQP 3, 7 and 9), the expression of several members of the aquaporin family was also examined.	Arsenic	150-157	aquaporin 3 (Gill blood group)	Homo sapiens	212-226
18682255-10	2009	CONCLUSIONS: Polymorphisms in AS3MT and in genes involved in one-carbon metabolism and reduction reactions affects arsenic metabolism.	Arsenic	115-122	arsenite methyltransferase	Homo sapiens	30-35
18682255-6	2009	These single nucleotide polymorphisms (SNPs) were in strong linkage disequilibrium (LD) with three intronic AS3MT SNPs, previously reported to be associated with arsenic metabolism, indicating the existence of a strongly methylating, population-specific haplotype.	Arsenic	162-169	arsenite methyltransferase	Homo sapiens	108-113
19393262-11	2009	PON1 192R alloform predicted significantly higher levels of arsenic and lead.	Arsenic	60-67	paraoxonase 1	Homo sapiens	0-4
19422848-0	2009	Subchronic exposure to arsenic decreased Sdha expression in the brain of mice.	Arsenic	23-30	succinate dehydrogenase complex, subunit A, flavoprotein (Fp)	Mus musculus	41-45
19070955-1	2009	Acid mine drainage (AMD) is often accompanied with elevated concentrations of arsenic, in the forms of arsenite, As(III), and/or arsenate, As(V), due to the high affinity of arsenic for sulfide mineral ores.	Arsenic	78-85	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	139-144
19422848-7	2009	We further analyzed the influence of As on brain Sdha expression using Western blot method.	Arsenic	37-39	succinate dehydrogenase complex, subunit A, flavoprotein (Fp)	Mus musculus	49-53
19422848-12	2009	It implies that the increased level of ROS by As may also be a factor in the disrupting Sdha expression in brain tissue of mice exposed to As.	Arsenic	46-48	succinate dehydrogenase complex, subunit A, flavoprotein (Fp)	Mus musculus	88-92
19328227-9	2009	These findings demonstrate that distinct transcriptional and posttranscriptional mechanisms mediate the coordinate induction of the Gclc and Gclm subunits of GCL in response to As(3+) and highlight the potential importance of the GSH antioxidant defense system in regulating As(3+)-induced responses in hepatocytes.	Arsenic	177-179	glutamate-cysteine ligase, catalytic subunit	Mus musculus	132-136
19328227-9	2009	These findings demonstrate that distinct transcriptional and posttranscriptional mechanisms mediate the coordinate induction of the Gclc and Gclm subunits of GCL in response to As(3+) and highlight the potential importance of the GSH antioxidant defense system in regulating As(3+)-induced responses in hepatocytes.	Arsenic	177-179	glutamate-cysteine ligase, modifier subunit	Mus musculus	141-145
19513507-4	2009	Three ABC transporter proteins, ABCB1, ABCC1 and ABCC2, were expressed increasingly and differently in two arsenic-resistant cell lines.	Arsenic	107-114	ATP binding cassette subfamily B member 1	Homo sapiens	32-37
19513507-4	2009	Three ABC transporter proteins, ABCB1, ABCC1 and ABCC2, were expressed increasingly and differently in two arsenic-resistant cell lines.	Arsenic	107-114	ATP binding cassette subfamily C member 1	Homo sapiens	39-44
19513507-4	2009	Three ABC transporter proteins, ABCB1, ABCC1 and ABCC2, were expressed increasingly and differently in two arsenic-resistant cell lines.	Arsenic	107-114	ATP binding cassette subfamily C member 2	Homo sapiens	49-54
19513507-5	2009	Further, tumor suppressor p53 was overexpressed in two arsenic-resistant cell lines, but the levels of p53 mediators MDM2 and gankyrin, which regulate the ubiquitination of p53, increased simultaneously.	Arsenic	55-62	tumor protein p53	Homo sapiens	26-29
19513507-5	2009	Further, tumor suppressor p53 was overexpressed in two arsenic-resistant cell lines, but the levels of p53 mediators MDM2 and gankyrin, which regulate the ubiquitination of p53, increased simultaneously.	Arsenic	55-62	tumor protein p53	Homo sapiens	103-106
19513507-5	2009	Further, tumor suppressor p53 was overexpressed in two arsenic-resistant cell lines, but the levels of p53 mediators MDM2 and gankyrin, which regulate the ubiquitination of p53, increased simultaneously.	Arsenic	55-62	MDM2 proto-oncogene	Homo sapiens	117-121
19513507-5	2009	Further, tumor suppressor p53 was overexpressed in two arsenic-resistant cell lines, but the levels of p53 mediators MDM2 and gankyrin, which regulate the ubiquitination of p53, increased simultaneously.	Arsenic	55-62	proteasome 26S subunit, non-ATPase 10	Homo sapiens	126-134
19513507-5	2009	Further, tumor suppressor p53 was overexpressed in two arsenic-resistant cell lines, but the levels of p53 mediators MDM2 and gankyrin, which regulate the ubiquitination of p53, increased simultaneously.	Arsenic	55-62	tumor protein p53	Homo sapiens	103-106
19070955-1	2009	Acid mine drainage (AMD) is often accompanied with elevated concentrations of arsenic, in the forms of arsenite, As(III), and/or arsenate, As(V), due to the high affinity of arsenic for sulfide mineral ores.	Arsenic	174-181	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	139-144
19397590-6	2009	Western blot analysis showed that As(2)O(3) significantly blocked phosphorylation of BubR1, Cdc20, and Cdc27 in cells treated with paclitaxel, suggesting that arsenic compromised the activation of the spindle checkpoint.	Arsenic	159-166	BUB1 mitotic checkpoint serine/threonine kinase B	Homo sapiens	85-90
19376847-0	2009	Differential effects of arsenic on cutaneous and systemic immunity: focusing on CD4+ cell apoptosis in patients with arsenic-induced Bowen"s disease.	Arsenic	117-124	CD4 molecule	Homo sapiens	80-83
19376847-6	2009	However, the CD4+ cells from As-BD patients were less susceptible to arsenic-induced apoptosis, due to reduced tumor necrosis factor receptor 1 expression.	Arsenic	69-76	CD4 molecule	Homo sapiens	13-16
19376847-7	2009	Interestingly, arsenic was found to induce Fas expression on CD4+ cells and increase the soluble Fas ligand (sFasL) production from keratinocytes.	Arsenic	15-22	CD4 molecule	Homo sapiens	61-64
19486684-4	2009	We address this controversy by showing that ErbB1 TM domain dimerizes in lipid bilayers and by calculating its contribution to stability as -2.5 kcal/mol.	Arsenic	137-139	epidermal growth factor receptor	Homo sapiens	44-49
19397590-6	2009	Western blot analysis showed that As(2)O(3) significantly blocked phosphorylation of BubR1, Cdc20, and Cdc27 in cells treated with paclitaxel, suggesting that arsenic compromised the activation of the spindle checkpoint.	Arsenic	159-166	cell division cycle 27	Homo sapiens	103-108
19376847-7	2009	Interestingly, arsenic was found to induce Fas expression on CD4+ cells and increase the soluble Fas ligand (sFasL) production from keratinocytes.	Arsenic	15-22	Fas ligand	Homo sapiens	97-107
19376847-11	2009	These residual CD4+ cells were less susceptible to arsenic-induced apoptosis.	Arsenic	51-58	CD4 molecule	Homo sapiens	15-18
19240355-5	2009	Among 253 respondents who consumed water: (a) 177/253 (70%) of tap water samples contained more than 10 microg l(-1) total inorganic arsenic (ave. 66 microg l(-1), median 20 microg l(-1)); (b) As((III)) occurred as a small proportion of total arsenic in most samples (ave. 22%, median 3%); and (c) tungsten occurred in concentrations ranging from below the detection limit (3 microg l(-1)) to a maximum of 610 microg l(-1) (ave. 30 microg l(-1), median 3 microg l(-1)).	Arsenic	133-140	nuclear RNA export factor 1	Homo sapiens	63-66
19429254-0	2009	Effects of an epidermal growth factor receptor inhibitor on arsenic associated toxicity in the rat bladder epithelium.	Arsenic	60-67	epidermal growth factor receptor	Rattus norvegicus	14-46
19369641-0	2009	Potential clinical significance of EGFR-mediated signaling following inorganic arsenic exposure in human lung.	Arsenic	79-86	epidermal growth factor receptor	Homo sapiens	35-39
19341753-0	2009	Role of aquaporin 9 in cellular accumulation of arsenic and its cytotoxicity in primary mouse hepatocytes.	Arsenic	48-55	aquaporin 9	Mus musculus	8-19
19341753-3	2009	In the present study, we examined the contribution of AQP9 to the uptake of inorganic arsenite, thereby increasing arsenic-induced cytotoxicity in primary mouse hepatocytes.	Arsenic	115-122	aquaporin 9	Mus musculus	54-58
19341753-5	2009	Furthermore, overexpression of AQP9 in HEK293 cells led to the enhancement of intracellular arsenic concentration, resulting in enhanced cytotoxicity after arsenite exposure.	Arsenic	92-99	aquaporin 9	Homo sapiens	31-35
19429254-13	2009	These data suggest that an EGFR inhibitor has the ability to block As(III)-induced cell proliferation in vitro but not in vivo in a short-term study.	Arsenic	67-69	epidermal growth factor receptor	Rattus norvegicus	27-31
18930593-5	2009	The assay of As(III) was based on subtracting As(V) from total As.	Arsenic	13-15	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	46-51
19168569-0	2009	Arsenic activates EGFR pathway signaling in the lung.	Arsenic	0-7	epidermal growth factor receptor	Homo sapiens	18-22
19168569-2	2009	Phosphorylation of the epidermal growth factor receptor (EGFR) has been reported with arsenic exposure in bladder cells.	Arsenic	86-93	epidermal growth factor receptor	Homo sapiens	23-55
19168569-2	2009	Phosphorylation of the epidermal growth factor receptor (EGFR) has been reported with arsenic exposure in bladder cells.	Arsenic	86-93	epidermal growth factor receptor	Homo sapiens	57-61
19168569-4	2009	We investigated the mechanisms of EGFR pathway activation by levels of arsenic relevant to human exposure scenarios both in vitro using cultured lung epithelial cells, and in lung tumors samples from New England Lung Cancer Study participants.	Arsenic	71-78	epidermal growth factor receptor	Homo sapiens	34-38
19168569-6	2009	Our in vitro data suggest that arsenic increases levels of the EGFR ligand, heparin binding-EGF, and activate EGFR phosphorylation in the lung.	Arsenic	31-38	epidermal growth factor receptor	Homo sapiens	63-67
19168569-6	2009	Our in vitro data suggest that arsenic increases levels of the EGFR ligand, heparin binding-EGF, and activate EGFR phosphorylation in the lung.	Arsenic	31-38	epidermal growth factor receptor	Homo sapiens	110-114
19168569-7	2009	Downstream of EGFR, arsenic exposure increased pERK and cyclin D1 levels.	Arsenic	20-27	epidermal growth factor receptor	Homo sapiens	14-18
19168569-7	2009	Downstream of EGFR, arsenic exposure increased pERK and cyclin D1 levels.	Arsenic	20-27	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	47-51
19168569-7	2009	Downstream of EGFR, arsenic exposure increased pERK and cyclin D1 levels.	Arsenic	20-27	cyclin D1	Homo sapiens	56-65
19168569-10	2009	These data suggest that arsenic exposure may stimulate EGFR pathway activation in the lung.	Arsenic	24-31	epidermal growth factor receptor	Homo sapiens	55-59
19168569-11	2009	Moreover, the tumors that arise in arsenic-exposed individuals also exhibit signs of EGFR pathway dysregulation.	Arsenic	35-42	epidermal growth factor receptor	Homo sapiens	85-89
19168569-12	2009	Further work is needed to assess the clinical utility of targeting the EGFR pathway in subgroups of lung cancer patients who have been exposed to elevated levels of arsenic.	Arsenic	165-172	epidermal growth factor receptor	Homo sapiens	71-75
19429237-6	2009	Gene-environment interaction with arsenic exposure was observed in relation to bladder cancer risk for a variant allele of the double-strand break repair gene XRCC3 T241M (adjusted OR 2.8 (1.1-7.3)) comparing to homozygous wild type among those in the top arsenic exposure decile (interaction p-value 0.01).	Arsenic	34-41	X-ray repair cross complementing 3	Homo sapiens	159-164
19429237-6	2009	Gene-environment interaction with arsenic exposure was observed in relation to bladder cancer risk for a variant allele of the double-strand break repair gene XRCC3 T241M (adjusted OR 2.8 (1.1-7.3)) comparing to homozygous wild type among those in the top arsenic exposure decile (interaction p-value 0.01).	Arsenic	256-263	X-ray repair cross complementing 3	Homo sapiens	159-164
19544866-1	2009	Arsenic is a redox-active metalloid whose toxicity and mobility strongly depends on its oxidation state, with arsenite (As(III)) being more toxic and mobile than arsenate (As(V)).	Arsenic	0-7	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	172-177
19167370-5	2009	The metabolism of inorganic arsenic in human is different from rat and mouse in some aspects though the AS3MT has a high degree of similarity in these species.	Arsenic	28-35	arsenite methyltransferase	Mus musculus	104-109
19544866-8	2009	The results from this study can be used to better predict the fate of arsenic in the environment and potentially explain the occurrence of oxidized As(V) in anoxic environments.	Arsenic	70-77	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	148-153
19544888-1	2009	The preoxidation of As(III) to As(V) is a desirable process to increase the removal efficiency of arsenic in water treatment In this work, the photooxidation of As(III) under 254 nm irradiation was investigated in the concentration range of 1-1000 microM in the presence of potassium iodide (typically 100 microM).	Arsenic	98-105	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	31-36
19349368-3	2009	While Rac1-GTPase and NADPH oxidase activities are essential for arsenic-stimulated endothelial cell signaling for angiogenesis or liver sinusoid capillarization, the mechanism for initiating these effects is unknown.	Arsenic	65-72	Rac family small GTPase 1	Homo sapiens	6-10
19269474-10	2009	The results showed that the soluble arsenic was found oxidized as As(V).	Arsenic	36-43	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	66-71
19276070-0	2009	Induction of metallothionein I by arsenic via metal-activated transcription factor 1: critical role of C-terminal cysteine residues in arsenic sensing.	Arsenic	34-41	metallothionein 1	Mus musculus	13-30
19276070-0	2009	Induction of metallothionein I by arsenic via metal-activated transcription factor 1: critical role of C-terminal cysteine residues in arsenic sensing.	Arsenic	135-142	metallothionein 1	Mus musculus	13-30
19276070-3	2009	We analyzed the interaction between arsenic (As(3+)) and MTF1 for Mt1 induction.	Arsenic	36-43	metallothionein 1	Mus musculus	66-69
19276070-9	2009	Preincubation with As(3+), Cd(2+), Co(2+), Ni(2+), Ag(+), Hg(2+), and Bi(3+) blocks pulldown of MTF1(321-675) by PAO beads in vitro and in vivo, indicating that binding of the metal inducers to the same C-terminal cysteine cluster as PAO occurs.	Arsenic	19-21	metal response element binding transcription factor 1	Mus musculus	96-100
19276070-11	2009	The findings demonstrate a critical role of the C-terminal cysteine cluster of MTF1 in arsenic sensing and gene transcription via arsenic-cysteine thiol interaction.	Arsenic	87-94	metal response element binding transcription factor 1	Mus musculus	79-83
19349368-5	2009	Incubating human microvascular endothelial cells with the sphingosine-1-phosphate type 1 receptor (S1P(1)) inhibitor VPC23019 or performing small interfering RNA knockdown of S1P(1) blocked arsenic-stimulated HMVEC angiogenic gene expression and tube formation, but did not affect induction of either HMOX1 or IL8.	Arsenic	190-197	sphingosine-1-phosphate receptor 1	Homo sapiens	58-97
19349368-5	2009	Incubating human microvascular endothelial cells with the sphingosine-1-phosphate type 1 receptor (S1P(1)) inhibitor VPC23019 or performing small interfering RNA knockdown of S1P(1) blocked arsenic-stimulated HMVEC angiogenic gene expression and tube formation, but did not affect induction of either HMOX1 or IL8.	Arsenic	190-197	sphingosine-1-phosphate receptor 1	Homo sapiens	99-105
19349368-5	2009	Incubating human microvascular endothelial cells with the sphingosine-1-phosphate type 1 receptor (S1P(1)) inhibitor VPC23019 or performing small interfering RNA knockdown of S1P(1) blocked arsenic-stimulated HMVEC angiogenic gene expression and tube formation, but did not affect induction of either HMOX1 or IL8.	Arsenic	190-197	sphingosine-1-phosphate receptor 1	Homo sapiens	175-181
19349368-5	2009	Incubating human microvascular endothelial cells with the sphingosine-1-phosphate type 1 receptor (S1P(1)) inhibitor VPC23019 or performing small interfering RNA knockdown of S1P(1) blocked arsenic-stimulated HMVEC angiogenic gene expression and tube formation, but did not affect induction of either HMOX1 or IL8.	Arsenic	190-197	heme oxygenase 1	Homo sapiens	301-306
19349368-5	2009	Incubating human microvascular endothelial cells with the sphingosine-1-phosphate type 1 receptor (S1P(1)) inhibitor VPC23019 or performing small interfering RNA knockdown of S1P(1) blocked arsenic-stimulated HMVEC angiogenic gene expression and tube formation, but did not affect induction of either HMOX1 or IL8.	Arsenic	190-197	C-X-C motif chemokine ligand 8	Homo sapiens	310-313
19349368-7	2009	We found that S1P(1) was enriched on LSECs in vivo and in primary cell culture and that VPC23019 inhibited both sphingosine-1-phosphate-stimulated and arsenic-stimulated LSEC oxidant generation and defenestration.	Arsenic	151-158	sphingosine-1-phosphate receptor 1	Homo sapiens	14-20
19349368-8	2009	These studies identified novel roles for S1P(1) in mediating arsenic stimulation of both angiogenesis and pathogenic LSEC capillarization, as well as demonstrating a role for S1P(1) in mediating environmental responses in the liver vasculature, providing possible mechanistic insight into arsenic-induced vascular pathogenesis and disease.	Arsenic	61-68	sphingosine-1-phosphate receptor 1	Homo sapiens	41-47
19416086-7	2009	In this review, we shed light on the effect of seven heavy metals, namely arsenic, mercury, lead, cadmium, chromium, copper and vanadium, on CYP1A1 and the consequences on drug metabolism.	Arsenic	74-81	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	141-147
19103198-9	2009	In fibroblastic cells, the normally rapid rate of degradation of Cx43 after its transport to the plasma membrane is reduced by treatments that either directly (ALLN; epoxomicin) or indirectly (generation of oxidatively un/mis-folded proteins by arsenic compounds) prevent the ubiquitin/proteasome system (UPS) from acting on its normal substrates.	Arsenic	245-252	gap junction protein alpha 1	Gallus gallus	65-69
18942077-0	2009	Characterization of an alternatively spliced GADD45alpha, GADD45alpha1 isoform, in arsenic-treated epithelial cells.	Arsenic	83-90	growth arrest and DNA damage inducible alpha	Homo sapiens	45-56
19395809-2	2009	Arsenic was examined to aid in discriminating its use as a preservative from that incorporated by ingestion and hence indicate poisoning (in the case of historical figures).	Arsenic	0-7	activation induced cytidine deaminase	Homo sapiens	24-27
18942077-1	2009	A new GADD45alpha isoform, GADD45alpha1, was identified in the cellular response to arsenic.	Arsenic	84-91	growth arrest and DNA damage inducible alpha	Homo sapiens	6-17
18942077-5	2009	In over-expression experiments, the full length GADD45alpha, but not the GADD45alpha1, sensitized cells to arsenic-induced prometaphase arrest of the cell cycle.	Arsenic	107-114	growth arrest and DNA damage inducible alpha	Homo sapiens	48-59
18942077-7	2009	Thus, these data suggest that the generation of the GADD45alpha1 isoform may not only offset but also antagonize the effects of arsenic and GADD45alpha on cell growth and cell cycle regulation.	Arsenic	128-135	growth arrest and DNA damage inducible alpha	Homo sapiens	52-63
19382146-0	2009	Impact of arsenic on nucleotide excision repair: XPC function, protein level, and gene expression.	Arsenic	10-17	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	49-52
19371612-1	2009	To elucidate the role of genetic factors in arsenic (As) metabolism, we studied associations of single nucleotide polymorphisms (SNPs) in As (+3 oxidation state) methyltransferase (AS3MT) with the As concentrations in hair and urine, and urinary As profile in residents in the Red River Delta, Vietnam.	Arsenic	138-140	arsenite methyltransferase	Homo sapiens	181-186
18723277-1	2009	The sorption characteristics of arsenic(As(V)) on iron-coated zeolite (ICZ) were investigated through batch and column studies.	Arsenic	32-39	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	40-45
19475968-4	2009	A BET isotherm equation provided the best fit to arsenic removal data, suggesting that surface precipitation occurred at a high arsenic/pyrite ratio.	Arsenic	49-56	delta/notch like EGF repeat containing	Homo sapiens	2-5
19475968-4	2009	A BET isotherm equation provided the best fit to arsenic removal data, suggesting that surface precipitation occurred at a high arsenic/pyrite ratio.	Arsenic	128-135	delta/notch like EGF repeat containing	Homo sapiens	2-5
19167132-9	2009	X-ray absorption near edge structure (XANES) spectra indicate that arsenic is sequestered in the solid phase as both As(III) and As(V) in coordination environments with O and S. Arsenic removal in the PRB probably results from several pathways, including adsorption to iron oxide and iron sulfide surfaces, and possible precipitation of ferrous arsenate.	Arsenic	67-74	RB transcriptional corepressor 1	Homo sapiens	201-204
19167132-9	2009	X-ray absorption near edge structure (XANES) spectra indicate that arsenic is sequestered in the solid phase as both As(III) and As(V) in coordination environments with O and S. Arsenic removal in the PRB probably results from several pathways, including adsorption to iron oxide and iron sulfide surfaces, and possible precipitation of ferrous arsenate.	Arsenic	178-185	RB transcriptional corepressor 1	Homo sapiens	201-204
19428935-9	2009	These results suggest that pentavalent arsenic compounds with both phenyl groups and hydroxyl groups are effective in the suppression of glutaminase.	Arsenic	39-46	glutaminase	Homo sapiens	137-148
19371607-0	2009	Risk of carotid atherosclerosis is associated with low serum paraoxonase (PON1) activity among arsenic exposed residents in Southwestern Taiwan.	Arsenic	95-102	paraoxonase 1	Homo sapiens	61-72
19371607-0	2009	Risk of carotid atherosclerosis is associated with low serum paraoxonase (PON1) activity among arsenic exposed residents in Southwestern Taiwan.	Arsenic	95-102	paraoxonase 1	Homo sapiens	74-78
19371607-1	2009	To understand whether human paraoxonase 1 (PON1) would modulate the risk for arsenic-related atherosclerosis, we studied 196 residents from an arseniasis-endemic area in Southwestern Taiwan and 291 age- and sex-matched residents from a nearby control area where arsenic exposure was found low.	Arsenic	77-84	paraoxonase 1	Homo sapiens	28-41
19371607-8	2009	However, genetic frequencies of certain alleles including PON1 Q192, PON2 G148 and PON2 C311 were found increased in the endemic group as compared to the controls and a general Chinese population, indicating a possible survival selection in the endemic group after a long arsenic exposure history.	Arsenic	272-279	paraoxonase 1	Homo sapiens	58-62
19371607-9	2009	Our results showed a significant joint effect between arsenic exposure and serum PON1 activity on carotid atherosclerosis, suggesting that subjects of low PON1 activity may be more susceptible to arsenic-related cardiovascular disease.	Arsenic	54-61	paraoxonase 1	Homo sapiens	155-159
19371607-9	2009	Our results showed a significant joint effect between arsenic exposure and serum PON1 activity on carotid atherosclerosis, suggesting that subjects of low PON1 activity may be more susceptible to arsenic-related cardiovascular disease.	Arsenic	196-203	paraoxonase 1	Homo sapiens	155-159
18789824-3	2009	The residents in Xing Ren have been using coal containing high arsenic levels all their life.	Arsenic	63-70	renin	Homo sapiens	22-25
18789824-4	2009	Urinary arsenic levels of villagers were 192.2+/-22 microg/g creatinine (n=113) in the coal-borne endemic area (Xing Ren county) and were significantly higher than 63.6+/-5.9 microg/g creatinine (n=30) in a neighbouring control site (a village in Xing Yi county).	Arsenic	8-15	renin	Homo sapiens	117-120
18809211-2	2009	Arsenic contamination in groundwater was found in four villages (Vinh Tru, Bo De, Hoa Hau, Nhan Dao) in Ha Nam province in northern Vietnam.	Arsenic	0-7	D-amino acid oxidase	Homo sapiens	96-99
18789824-6	2009	There was a strong correlation between age and urinary arsenic and MDA concentrations in the endemic area of Xing Ren; urinary arsenic and MDA levels decreased with age.	Arsenic	55-62	renin	Homo sapiens	114-117
18809211-2	2009	Arsenic contamination in groundwater was found in four villages (Vinh Tru, Bo De, Hoa Hau, Nhan Dao) in Ha Nam province in northern Vietnam.	Arsenic	0-7	SH3 and cysteine rich domain 3	Homo sapiens	107-110
18793801-5	2009	The NAG results also suggest that chronic arsenic exposure presents a significant adverse impact on the kidney function of villagers in the endemic areas.	Arsenic	42-49	O-GlcNAcase	Rattus norvegicus	4-7
19379560-2	2009	The apoptosis and cell cycle changes of APL cells treated with As(2)O(3) were detected by morphology and flow cytometry respectively, the protein and mRNA expressions of P27(Kip1), TGF-beta1, cyclin E and BCL-2 were measured by immunohistochemistry and RT-PCR.	Arsenic	63-65	dynactin subunit 6	Homo sapiens	170-173
19379560-2	2009	The apoptosis and cell cycle changes of APL cells treated with As(2)O(3) were detected by morphology and flow cytometry respectively, the protein and mRNA expressions of P27(Kip1), TGF-beta1, cyclin E and BCL-2 were measured by immunohistochemistry and RT-PCR.	Arsenic	63-65	cyclin dependent kinase inhibitor 1B	Homo sapiens	174-178
19379560-2	2009	The apoptosis and cell cycle changes of APL cells treated with As(2)O(3) were detected by morphology and flow cytometry respectively, the protein and mRNA expressions of P27(Kip1), TGF-beta1, cyclin E and BCL-2 were measured by immunohistochemistry and RT-PCR.	Arsenic	63-65	BCL2 apoptosis regulator	Homo sapiens	205-210
19337508-0	2009	Elevated human telomerase reverse transcriptase gene expression in blood cells associated with chronic arsenic exposure in Inner Mongolia, China.	Arsenic	103-110	telomerase reverse transcriptase	Homo sapiens	15-47
18687336-7	2009	From an evolutionary viewpoint, LmACR2 and the related arsenate reductases form, together with the known Cdc25 phosphatases, a well-defined subfamily of the rhodanese/Cdc25 phosphatase superfamily, characterized by a 7-amino-acid-long active-site loop that is able to selectively bind substrates containing phosphorous, arsenic, or antinomy.	Arsenic	320-327	Ras family guanine nucleotide exchange factor CDC25	Saccharomyces cerevisiae S288C	105-110
18687336-7	2009	From an evolutionary viewpoint, LmACR2 and the related arsenate reductases form, together with the known Cdc25 phosphatases, a well-defined subfamily of the rhodanese/Cdc25 phosphatase superfamily, characterized by a 7-amino-acid-long active-site loop that is able to selectively bind substrates containing phosphorous, arsenic, or antinomy.	Arsenic	320-327	Ras family guanine nucleotide exchange factor CDC25	Saccharomyces cerevisiae S288C	167-172
19154403-9	2009	Pretreatment with V-PROLI/NO suppressed phosphorylation of JNK1/2 after arsenic exposure.	Arsenic	72-79	mitogen-activated protein kinase 8	Homo sapiens	59-65
19167470-7	2009	Maternal urinary arsenic during pregnancy showed significant negative correlation with interleukin-7 (IL-7) and lactoferrin (Ltf) in breast milk and child thymic index (TI).	Arsenic	17-24	interleukin 7	Homo sapiens	87-100
19167470-7	2009	Maternal urinary arsenic during pregnancy showed significant negative correlation with interleukin-7 (IL-7) and lactoferrin (Ltf) in breast milk and child thymic index (TI).	Arsenic	17-24	interleukin 7	Homo sapiens	102-106
19167470-7	2009	Maternal urinary arsenic during pregnancy showed significant negative correlation with interleukin-7 (IL-7) and lactoferrin (Ltf) in breast milk and child thymic index (TI).	Arsenic	17-24	lactotransferrin	Homo sapiens	112-123
19167470-7	2009	Maternal urinary arsenic during pregnancy showed significant negative correlation with interleukin-7 (IL-7) and lactoferrin (Ltf) in breast milk and child thymic index (TI).	Arsenic	17-24	lactotransferrin	Homo sapiens	125-128
19100828-0	2009	Increased aquaglyceroporin 9 expression disrupts arsenic resistance in human lung cancer cells.	Arsenic	49-56	aquaporin 9	Homo sapiens	10-28
19131511-7	2009	However, chromatin immunoprecipitation studies revealed that arsenic inhibited AR recruitment to an AR target gene enhancer in vivo.	Arsenic	61-68	androgen receptor	Homo sapiens	79-81
19131511-7	2009	However, chromatin immunoprecipitation studies revealed that arsenic inhibited AR recruitment to an AR target gene enhancer in vivo.	Arsenic	61-68	androgen receptor	Homo sapiens	100-102
19131511-8	2009	Consistent with a deficiency in AR-chromatin binding, arsenic disrupted AR amino and carboxyl termini interaction.	Arsenic	54-61	androgen receptor	Homo sapiens	32-34
19131511-8	2009	Consistent with a deficiency in AR-chromatin binding, arsenic disrupted AR amino and carboxyl termini interaction.	Arsenic	54-61	androgen receptor	Homo sapiens	72-74
19131511-11	2009	Thus, arsenic-induced male infertility may be due to inhibition of AR activity.	Arsenic	6-13	androgen receptor	Homo sapiens	67-69
19100828-8	2009	By transfection of an aquaglyceroporin 9 (AQP9) gene, we showed that increased AQP9 expression significantly enhanced arsenic uptake and disrupted arsenic resistance of A549.	Arsenic	147-154	aquaporin 9	Homo sapiens	22-40
19100828-8	2009	By transfection of an aquaglyceroporin 9 (AQP9) gene, we showed that increased AQP9 expression significantly enhanced arsenic uptake and disrupted arsenic resistance of A549.	Arsenic	147-154	aquaporin 9	Homo sapiens	42-46
19100828-8	2009	By transfection of an aquaglyceroporin 9 (AQP9) gene, we showed that increased AQP9 expression significantly enhanced arsenic uptake and disrupted arsenic resistance of A549.	Arsenic	147-154	aquaporin 9	Homo sapiens	79-83
19100828-9	2009	The present study strongly suggests that membrane transporters responsible for arsenic uptake, such as AQP9, may play a critical role in development of arsenic resistance in human lung cancer cells.	Arsenic	79-86	aquaporin 9	Homo sapiens	103-107
19100828-9	2009	The present study strongly suggests that membrane transporters responsible for arsenic uptake, such as AQP9, may play a critical role in development of arsenic resistance in human lung cancer cells.	Arsenic	152-159	aquaporin 9	Homo sapiens	103-107
19440430-4	2009	Skin lesions were strongly associated with well water arsenic and there was an elevated prevalence among residents with water arsenic exposures as low as 5 microg/L-10 microg/L.	Arsenic	126-133	immunoglobulin kappa variable 3-7 (non-functional)	Homo sapiens	163-167
19131511-0	2009	Inhibition of androgen receptor transcriptional activity as a novel mechanism of action of arsenic.	Arsenic	91-98	androgen receptor	Homo sapiens	14-31
19131511-4	2009	Because the androgen receptor (AR) plays an important role in spermatogenesis and prostate cancer, we explored the possibility that trivalent arsenic regulates AR function.	Arsenic	142-149	androgen receptor	Homo sapiens	160-162
19131511-5	2009	We found that arsenic inhibited AR transcriptional activity in prostate cancer and Sertoli cells using reporter gene assays testing several androgen response element-containing regions and by assessing native target gene expression.	Arsenic	14-21	androgen receptor	Homo sapiens	32-34
19131511-6	2009	Arsenic inhibition of AR activity was not due to down-regulation of AR protein levels, decreased hormone binding to AR, disruption of AR nuclear translocation, or interference with AR-DNA binding in vitro.	Arsenic	0-7	androgen receptor	Homo sapiens	22-24
19100828-6	2009	After treatment with the respective As(2)O(3) at IC50, arsenic influx/efflux activity in CL3 was comparable to those in the other three arsenic-resistant cells.	Arsenic	55-62	adhesion G protein-coupled receptor L3	Homo sapiens	89-92
19100828-8	2009	By transfection of an aquaglyceroporin 9 (AQP9) gene, we showed that increased AQP9 expression significantly enhanced arsenic uptake and disrupted arsenic resistance of A549.	Arsenic	118-125	aquaporin 9	Homo sapiens	22-40
19100828-8	2009	By transfection of an aquaglyceroporin 9 (AQP9) gene, we showed that increased AQP9 expression significantly enhanced arsenic uptake and disrupted arsenic resistance of A549.	Arsenic	118-125	aquaporin 9	Homo sapiens	42-46
19100828-8	2009	By transfection of an aquaglyceroporin 9 (AQP9) gene, we showed that increased AQP9 expression significantly enhanced arsenic uptake and disrupted arsenic resistance of A549.	Arsenic	118-125	aquaporin 9	Homo sapiens	79-83
19217550-1	2009	A slurry bioreactor using a dissimilatory arsenate (As(V))-reducing bacterium is proposed for remediation of arsenic-contaminated soils.	Arsenic	109-116	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	52-57
19224052-16	2009	Compared with H-postC group, cell survival rate decreased by 8.98%, and apoptotic rate and LDH leakage increased by 1.74% and 13.6% in AS + H-postC group, respectively (P&lt;0.05), but intracellular Ca(2+) concentration, CaN activity, and expression of CaN and NFkappaB did not change significantly (P&gt;0.05), suggesting that CRT participates in endogenous protection, not through Ca(2+)-CaN pathway.	Arsenic	135-137	calreticulin	Rattus norvegicus	328-331
18636241-9	2009	Removal of extracellular Ca2+ or inhibition of the Ca2+-permeable cation channels with amiloride blunted the effects of arsenic on annexin V-binding and cell shrinkage.	Arsenic	120-127	annexin A5	Homo sapiens	131-140
19185119-4	2009	Under the optimized conditions, the detection limits of this method for As(III) were 0.0045 ng mL(-1) with an enrichment factor of 33 and 0.24 ng mL(-1) for As(V), and the relative standard deviations for As(III) and As(V) were 2.6% and 1.9% (n=9, c=1.0 ng mL(-1)), respectively.	Arsenic	72-74	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	157-162
19185119-4	2009	Under the optimized conditions, the detection limits of this method for As(III) were 0.0045 ng mL(-1) with an enrichment factor of 33 and 0.24 ng mL(-1) for As(V), and the relative standard deviations for As(III) and As(V) were 2.6% and 1.9% (n=9, c=1.0 ng mL(-1)), respectively.	Arsenic	72-74	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	217-222
18565654-2	2009	Influence of time on arsenic sorption efficiency of different sorbents reveals that NM, NC, SMNM and SMNC require about 20, 10, 110 and 20h, respectively to reach at state of equilibrium.	Arsenic	21-28	survival of motor neuron 2, centromeric	Homo sapiens	101-105
18565654-9	2009	Both SMNM and SMNC removed arsenic effectively over the initial pH range 6-10.	Arsenic	27-34	survival of motor neuron 2, centromeric	Homo sapiens	14-18
19111837-0	2009	Activity of the AtMRP3 promoter in transgenic Arabidopsis thaliana and Nicotiana tabacum plants is increased by cadmium, nickel, arsenic, cobalt and lead but not by zinc and iron.	Arsenic	129-136	multidrug resistance-associated protein 3	Arabidopsis thaliana	16-22
19217550-2	2009	Bacterial As(V) reduction can cause arsenic extraction from the solid to the liquid phase because arsenite, As(III), is much less adsorptive than As(V).	Arsenic	36-43	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	10-15
19073887-4	2009	Arsenic, mercury, and nickel cause reduction of transcription of ribosome biogenesis genes, which are under the control of Sfp1, a TORC1-regulated transcriptional activator.	Arsenic	0-7	zinc-coordinating transcription factor SFP1	Saccharomyces cerevisiae S288C	123-127
19073887-5	2009	We report that arsenic stress deactivates Sfp1 as it becomes dephosphorylated, dissociates from chromatin, and exits the nucleus.	Arsenic	15-22	zinc-coordinating transcription factor SFP1	Saccharomyces cerevisiae S288C	42-46
19073887-6	2009	Curiously, whereas loss of SFP1 function leads to increased arsenic resistance, absence of TOR1 or SCH9 has the opposite effect suggesting that TORC1 has a role beyond down-regulation of Sfp1.	Arsenic	60-67	zinc-coordinating transcription factor SFP1	Saccharomyces cerevisiae S288C	27-31
19073887-7	2009	Indeed, we show that arsenic activates the transcription factors Msn2 and Msn4 both of which are targets of TORC1 and protein kinase A (PKA).	Arsenic	21-28	stress-responsive transcriptional activator MSN2	Saccharomyces cerevisiae S288C	65-69
19073887-7	2009	Indeed, we show that arsenic activates the transcription factors Msn2 and Msn4 both of which are targets of TORC1 and protein kinase A (PKA).	Arsenic	21-28	stress-responsive transcriptional activator MSN4	Saccharomyces cerevisiae S288C	74-78
19073887-9	2009	A normal level of PKA activity might serve to dampen the stress response since hyperactive Msn2 will decrease arsenic tolerance.	Arsenic	110-117	stress-responsive transcriptional activator MSN2	Saccharomyces cerevisiae S288C	91-95
19015167-6	2009	Initial studies in these models show that arsenic exposure accelerates and exacerbates atherosclerosis in apolipoprotein E-knockout mice.	Arsenic	42-49	apolipoprotein E	Mus musculus	106-122
19033395-10	2009	Our findings provided clear evidence that arsenic can enhance CYP1A1 expression and activity via AhR activation, and the arsenic-induced AhR activation is probably triggered by oxidative stress.	Arsenic	42-49	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	62-68
19033395-0	2009	Involvement of oxidative stress and activation of aryl hydrocarbon receptor in elevation of CYP1A1 expression and activity in lung cells and tissues by arsenic: an in vitro and in vivo study.	Arsenic	152-159	aryl hydrocarbon receptor	Homo sapiens	50-75
19033395-0	2009	Involvement of oxidative stress and activation of aryl hydrocarbon receptor in elevation of CYP1A1 expression and activity in lung cells and tissues by arsenic: an in vitro and in vivo study.	Arsenic	152-159	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	92-98
19033395-5	2009	However, the effects of arsenic on cytochrome P450 1A1 (CYP1A1) status (expression and activity), which is essential for B[a]P metabolism, either in lung cells or in lung tissues, are never demonstrated.	Arsenic	24-31	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	35-54
19033395-5	2009	However, the effects of arsenic on cytochrome P450 1A1 (CYP1A1) status (expression and activity), which is essential for B[a]P metabolism, either in lung cells or in lung tissues, are never demonstrated.	Arsenic	24-31	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	56-62
19033395-6	2009	We hypothesized that arsenic would enhance aryl hydrocarbon receptor (AhR) activation leading to CYP1A1 expression and activity in lung cells.	Arsenic	21-28	aryl hydrocarbon receptor	Homo sapiens	43-68
18779381-0	2009	Investigating arsenic susceptibility from a genetic perspective in Drosophila reveals a key role for glutathione synthetase.	Arsenic	14-21	Glutathione synthetase 1	Drosophila melanogaster	101-123
19033395-10	2009	Our findings provided clear evidence that arsenic can enhance CYP1A1 expression and activity via AhR activation, and the arsenic-induced AhR activation is probably triggered by oxidative stress.	Arsenic	42-49	aryl hydrocarbon receptor	Homo sapiens	97-100
19033395-6	2009	We hypothesized that arsenic would enhance aryl hydrocarbon receptor (AhR) activation leading to CYP1A1 expression and activity in lung cells.	Arsenic	21-28	aryl hydrocarbon receptor	Homo sapiens	70-73
19033395-6	2009	We hypothesized that arsenic would enhance aryl hydrocarbon receptor (AhR) activation leading to CYP1A1 expression and activity in lung cells.	Arsenic	21-28	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	97-103
19033395-10	2009	Our findings provided clear evidence that arsenic can enhance CYP1A1 expression and activity via AhR activation, and the arsenic-induced AhR activation is probably triggered by oxidative stress.	Arsenic	121-128	aryl hydrocarbon receptor	Homo sapiens	137-140
19033395-7	2009	Indeed, our present study successfully demonstrated the elevation of CYP1A1 messenger RNA expression in H1355 cells, a human lung adenocarcinoma cell line, as well as CYP1A1 expression and activity in lung tissues of arsenic-exposed mice.	Arsenic	217-224	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	167-173
19128515-10	2009	Horizontal transfer of ACR3(2) and arsB appeared to have occurred in strains that were primarily isolated from the highly arsenic-contaminated soil.	Arsenic	122-129	arylsulfatase B	Homo sapiens	35-39
19033395-8	2009	We further demonstrated that this elevation of CYP1A1 expression could be effectively blocked with AhR antagonist, 3",4"-dimethoxyflavone, indicating that the arsenic-induced CYP1A1 expression and activity were via AhR activation.	Arsenic	159-166	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	47-53
19033395-8	2009	We further demonstrated that this elevation of CYP1A1 expression could be effectively blocked with AhR antagonist, 3",4"-dimethoxyflavone, indicating that the arsenic-induced CYP1A1 expression and activity were via AhR activation.	Arsenic	159-166	aryl hydrocarbon receptor	Homo sapiens	99-102
19033395-8	2009	We further demonstrated that this elevation of CYP1A1 expression could be effectively blocked with AhR antagonist, 3",4"-dimethoxyflavone, indicating that the arsenic-induced CYP1A1 expression and activity were via AhR activation.	Arsenic	159-166	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	175-181
19033395-8	2009	We further demonstrated that this elevation of CYP1A1 expression could be effectively blocked with AhR antagonist, 3",4"-dimethoxyflavone, indicating that the arsenic-induced CYP1A1 expression and activity were via AhR activation.	Arsenic	159-166	aryl hydrocarbon receptor	Homo sapiens	215-218
19033395-9	2009	Furthermore, we found that arsenic-induced AhR activation and -enhanced CYP1A1 expression can be further increased by a prooxidant, buthionine-(S,R)-sulfoximine, and suppressed by antioxidants, such as N-acetylcysteine and catalase.	Arsenic	27-34	aryl hydrocarbon receptor	Homo sapiens	43-46
19033395-9	2009	Furthermore, we found that arsenic-induced AhR activation and -enhanced CYP1A1 expression can be further increased by a prooxidant, buthionine-(S,R)-sulfoximine, and suppressed by antioxidants, such as N-acetylcysteine and catalase.	Arsenic	27-34	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	72-78
19041379-8	2009	Neurons and endothelial cells presented pathological changes and the expression of NR2A was down-regulated in hippocampus in arsenic exposed rats.	Arsenic	125-132	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	83-87
19041379-9	2009	Our data indicated that arsenic exposure of 68 mg/L caused spatial memory damage, of which the morphological and biochemical bases could be the ultra-structure changes and reduced NR2A expression in hippocampus.	Arsenic	24-31	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	180-184
18977016-3	2009	The aim of this study was to determine the long term arsenic effect on human small airway epithelial cells (SAEC) by analyzing two distinct apoptosis-inducing agents, Fas ligand (Fas L), which evokes death receptor-mediated apoptosis, and hydrogen peroxide H2O2, which induces apoptosis mediated by reactive oxygen species (ROS).	Arsenic	53-60	Fas ligand	Homo sapiens	167-177
18977016-3	2009	The aim of this study was to determine the long term arsenic effect on human small airway epithelial cells (SAEC) by analyzing two distinct apoptosis-inducing agents, Fas ligand (Fas L), which evokes death receptor-mediated apoptosis, and hydrogen peroxide H2O2, which induces apoptosis mediated by reactive oxygen species (ROS).	Arsenic	53-60	Fas ligand	Homo sapiens	179-184
18977016-5	2009	SAEC displayed decreased cell viability and increased apoptosis after treatment with Fas L and H2O2, compared to non-arsenic treated control cells.	Arsenic	117-124	Fas ligand	Homo sapiens	85-90
18977016-6	2009	Furthermore, treatment of these arsenic-exposed SAEC with Fas L or H2O2 induced cleavage of the DNA damage recognition protein, poly (ADP-ribose) polymerase (PARP), and the "effector" caspase, Caspase-3, both canonical indicators of apoptosis.	Arsenic	32-39	Fas ligand	Homo sapiens	58-63
18977016-6	2009	Furthermore, treatment of these arsenic-exposed SAEC with Fas L or H2O2 induced cleavage of the DNA damage recognition protein, poly (ADP-ribose) polymerase (PARP), and the "effector" caspase, Caspase-3, both canonical indicators of apoptosis.	Arsenic	32-39	poly(ADP-ribose) polymerase 1	Homo sapiens	128-156
18977016-6	2009	Furthermore, treatment of these arsenic-exposed SAEC with Fas L or H2O2 induced cleavage of the DNA damage recognition protein, poly (ADP-ribose) polymerase (PARP), and the "effector" caspase, Caspase-3, both canonical indicators of apoptosis.	Arsenic	32-39	poly(ADP-ribose) polymerase 1	Homo sapiens	158-162
18977016-6	2009	Furthermore, treatment of these arsenic-exposed SAEC with Fas L or H2O2 induced cleavage of the DNA damage recognition protein, poly (ADP-ribose) polymerase (PARP), and the "effector" caspase, Caspase-3, both canonical indicators of apoptosis.	Arsenic	32-39	caspase 3	Homo sapiens	193-202
19082730-0	2009	Arsenic induced apoptosis in malignant melanoma cells is enhanced by menadione through ROS generation, p38 signaling and p53 activation.	Arsenic	0-7	mitogen-activated protein kinase 14	Mus musculus	103-106
19082730-0	2009	Arsenic induced apoptosis in malignant melanoma cells is enhanced by menadione through ROS generation, p38 signaling and p53 activation.	Arsenic	0-7	transformation related protein 53, pseudogene	Mus musculus	121-124
19130933-8	2009	By using multivariable logistic regression, after adjustment for risk factors, in female subjects incident CVD/stroke events were associated with asthma (OR, 3.24; 95% CI, 1.55-6.78), with no effect modification by atopy (P for interaction = .61), and with as-required short-acting beta(2)-agonist use (OR, 2.66; 95% CI, 1.06-6.61).	Arsenic	130-132	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	282-288
19411561-2	2009	The enzymatic methylation of iAs that is catalyzed by arsenic (+3 oxidation state)-methyltransferase (AS3MT) generates reactive methylated intermediates that contribute to the toxic and carcinogenic effects of iAs.	Arsenic	54-61	arsenite methyltransferase	Homo sapiens	102-107
19452124-4	2009	After treatment with AS extract for 6 months, the AS extract group showed a significant increase in serum osteocalcin levels compared with the control group (P = 0.041).	Arsenic	21-23	bone gamma-carboxyglutamate protein	Homo sapiens	106-117
19452124-4	2009	After treatment with AS extract for 6 months, the AS extract group showed a significant increase in serum osteocalcin levels compared with the control group (P = 0.041).	Arsenic	50-52	bone gamma-carboxyglutamate protein	Homo sapiens	106-117
19049867-7	2009	The results from Fourier transform infrared spectroscopy analysis demonstrated that in AS-DCN cultures the mineral content was greater but the crystallinity of mineral was poorer than that of the controls at early stage of mineralization.	Arsenic	87-89	decorin	Mus musculus	90-93
18462831-0	2009	Exogenous spermidine, arsenic and beta-aminobutyric acid modulate tobacco resistance to tobacco mosaic virus, and affect local and systemic glucosylsalicylic acid levels and arginine decarboxylase gene expression in tobacco leaves.	Arsenic	22-29	arginine decarboxylase	Nicotiana tabacum	174-196
19634416-5	2009	The ability of this new adsorbent for arsenic (As(V)) removal was evaluated.	Arsenic	38-45	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	47-52
19033365-3	2009	The predicted AUF1 motif (29-39 nucleotides) contained 79% As and Us, consistent with the AU-rich sequences of reported AUF1 targets.	Arsenic	59-61	heterogeneous nuclear ribonucleoprotein D	Homo sapiens	14-18
19033365-3	2009	The predicted AUF1 motif (29-39 nucleotides) contained 79% As and Us, consistent with the AU-rich sequences of reported AUF1 targets.	Arsenic	59-61	heterogeneous nuclear ribonucleoprotein D	Homo sapiens	120-124
19192803-3	2008	Dissolved As exists in different oxidation states, mainly as As(III) and As(V), and the charge of individual species varies with pH.	Arsenic	10-12	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	73-78
18976679-0	2009	Ethnic differences in five intronic polymorphisms associated with arsenic metabolism within human arsenic (+3 oxidation state) methyltransferase (AS3MT) gene.	Arsenic	66-73	arsenite methyltransferase	Homo sapiens	98-144
18976679-0	2009	Ethnic differences in five intronic polymorphisms associated with arsenic metabolism within human arsenic (+3 oxidation state) methyltransferase (AS3MT) gene.	Arsenic	66-73	arsenite methyltransferase	Homo sapiens	146-151
18976679-1	2009	Human arsenic (+3 oxidation state) methyltransferase (AS3MT) is known to catalyze the methylation of arsenite, and intronic single-nucleotide polymorphisms (SNPs: G7395A, G12390C, T14215C, T35587C, and G35991A) in the AS3MT gene were shown to be related to inter-individual variation in the arsenic metabolism.	Arsenic	6-13	arsenite methyltransferase	Homo sapiens	54-59
18976679-1	2009	Human arsenic (+3 oxidation state) methyltransferase (AS3MT) is known to catalyze the methylation of arsenite, and intronic single-nucleotide polymorphisms (SNPs: G7395A, G12390C, T14215C, T35587C, and G35991A) in the AS3MT gene were shown to be related to inter-individual variation in the arsenic metabolism.	Arsenic	6-13	arsenite methyltransferase	Homo sapiens	218-223
18977105-2	2008	A recent study indicated that 2,3-dimercaptopropanol (BAL) could be used to derivatize arsenic compounds to make them detectable by LC coupled to UV detector.	Arsenic	87-94	solute carrier family 27 member 5	Rattus norvegicus	54-57
18977105-4	2008	The arsenic compounds were derivatized with BAL before solvent extraction was carried out.	Arsenic	4-11	solute carrier family 27 member 5	Rattus norvegicus	44-47
18977105-6	2008	However, our finding showed that BAL, being a thiol, reduced the pentavalent arsenic compounds, As(V) to a trivalent state, As(III).	Arsenic	77-84	solute carrier family 27 member 5	Rattus norvegicus	33-36
18977105-7	2008	The arsenic metabolites, monomethyl arsonate (MMA) and dimethyl arsenic acid (DMA) could also be reduced by BAL to As(V)- and As(III)-BAL adducts.	Arsenic	4-11	solute carrier family 27 member 5	Rattus norvegicus	108-111
18977105-7	2008	The arsenic metabolites, monomethyl arsonate (MMA) and dimethyl arsenic acid (DMA) could also be reduced by BAL to As(V)- and As(III)-BAL adducts.	Arsenic	4-11	solute carrier family 27 member 5	Rattus norvegicus	134-137
19322015-6	2009	The MPO and SULT genetic polymorphisms might modify the arsenic methylation profile and UC progression, and thus are worthy of further investigation.	Arsenic	56-63	myeloperoxidase	Homo sapiens	4-7
19445126-11	2009	The increase ranges of HO-1 activities at different time post administration changed with the arsenic concentration in rat serum.	Arsenic	94-101	heme oxygenase 1	Rattus norvegicus	23-27
18929588-0	2008	Gene expression profiling analysis reveals arsenic-induced cell cycle arrest and apoptosis in p53-proficient and p53-deficient cells through differential gene pathways.	Arsenic	43-50	transformation related protein 53, pseudogene	Mus musculus	94-97
18929588-0	2008	Gene expression profiling analysis reveals arsenic-induced cell cycle arrest and apoptosis in p53-proficient and p53-deficient cells through differential gene pathways.	Arsenic	43-50	transformation related protein 53, pseudogene	Mus musculus	113-116
18929588-3	2008	Tumor suppressor gene p53, a pivotal cell cycle checkpoint signaling protein, has been hypothesized to play a possible role in mediating As-induced toxicity and therapeutic efficiency.	Arsenic	137-139	transformation related protein 53, pseudogene	Mus musculus	22-25
18929588-4	2008	In this study, we found that arsenite (As(3+)) induced apoptosis and cell cycle arrest in a dose-dependent manner in both p53(+/+) and p53(-/-) mouse embryonic fibroblasts (MEFs).	Arsenic	39-41	transformation related protein 53, pseudogene	Mus musculus	122-125
18929588-4	2008	In this study, we found that arsenite (As(3+)) induced apoptosis and cell cycle arrest in a dose-dependent manner in both p53(+/+) and p53(-/-) mouse embryonic fibroblasts (MEFs).	Arsenic	39-41	transformation related protein 53, pseudogene	Mus musculus	135-138
18929386-7	2008	Biosorption studies indicated that SRB cell pellets removed about 6.6% of the As(III) and 10.5% of the As(V) from water containing an initial concentration of 1mg/L of either arsenic species after 24h contact.	Arsenic	103-105	chaperonin containing TCP1 subunit 4	Homo sapiens	35-38
18848598-6	2008	These data indicate that arsenic is widely distributed and significantly accumulated in various organs and influences on other trace elements, and also modulates MT-1 expression in the liver and kidney.	Arsenic	25-32	metallothionein 1	Rattus norvegicus	162-166
19029980-5	2008	Although retinoic acid and arsenic synergize to clear LICs through cooperative PML-RARA degradation, this combination does not enhance differentiation.	Arsenic	27-34	promyelocytic leukemia	Mus musculus	79-82
19029980-5	2008	Although retinoic acid and arsenic synergize to clear LICs through cooperative PML-RARA degradation, this combination does not enhance differentiation.	Arsenic	27-34	retinoic acid receptor, alpha	Mus musculus	83-87
19033667-5	2008	Furthermore, ex vivo arsenic exposure increased SEC superoxide generation, and this effect was inhibited by addition of a Nox2 inhibitor and quenched by the cell-permeant superoxide scavenger.	Arsenic	21-28	cytochrome b-245, beta polypeptide	Mus musculus	122-126
19033667-6	2008	In addition, inhibiting either oxidant generation or Rac1-GTPase blocked ex vivo arsenic-stimulated SEC differentiation and dysfunction.	Arsenic	81-88	Rac family small GTPase 1	Mus musculus	53-57
19033667-7	2008	Our data indicate that a Nox2-based oxidase is required for SEC capillarization and that it may play a central role in vessel remodeling following environmentally relevant arsenic exposures.	Arsenic	172-179	cytochrome b-245, beta polypeptide	Mus musculus	25-29
18929386-2	2008	During growth of a mixed SRB culture adapted to 0.1mg/L arsenic species through repeated sub-culturing, 1mg/L of either As(III) or As(V) was reduced to 0.3 and 0.13mg/L respectively.	Arsenic	56-63	chaperonin containing TCP1 subunit 4	Homo sapiens	25-28
18929386-3	2008	Sorption experiments on the precipitate produced by batch cultured sulphate-reducing bacteria (SRB-PP) indicated a removal of about 77 and 55% of As(V) and As(III) respectively under the following conditions: pH 6.9; biomass (2g/L); 24h contact time; initial arsenic concentration, 1mg/L of either species.	Arsenic	146-148	chaperonin containing TCP1 subunit 4	Homo sapiens	95-98
18929386-3	2008	Sorption experiments on the precipitate produced by batch cultured sulphate-reducing bacteria (SRB-PP) indicated a removal of about 77 and 55% of As(V) and As(III) respectively under the following conditions: pH 6.9; biomass (2g/L); 24h contact time; initial arsenic concentration, 1mg/L of either species.	Arsenic	156-158	chaperonin containing TCP1 subunit 4	Homo sapiens	95-98
18929386-3	2008	Sorption experiments on the precipitate produced by batch cultured sulphate-reducing bacteria (SRB-PP) indicated a removal of about 77 and 55% of As(V) and As(III) respectively under the following conditions: pH 6.9; biomass (2g/L); 24h contact time; initial arsenic concentration, 1mg/L of either species.	Arsenic	259-266	chaperonin containing TCP1 subunit 4	Homo sapiens	95-98
18929386-7	2008	Biosorption studies indicated that SRB cell pellets removed about 6.6% of the As(III) and 10.5% of the As(V) from water containing an initial concentration of 1mg/L of either arsenic species after 24h contact.	Arsenic	78-80	chaperonin containing TCP1 subunit 4	Homo sapiens	35-38
19099632-5	2008	The results showed that the expression of VEGF-C and VEGFR-3 in cancer cells significantly reduced in the arsenic -treated groups.	Arsenic	106-113	vascular endothelial growth factor C	Mus musculus	42-48
19099632-5	2008	The results showed that the expression of VEGF-C and VEGFR-3 in cancer cells significantly reduced in the arsenic -treated groups.	Arsenic	106-113	FMS-like tyrosine kinase 4	Mus musculus	53-60
18929386-7	2008	Biosorption studies indicated that SRB cell pellets removed about 6.6% of the As(III) and 10.5% of the As(V) from water containing an initial concentration of 1mg/L of either arsenic species after 24h contact.	Arsenic	175-182	chaperonin containing TCP1 subunit 4	Homo sapiens	35-38
18636556-0	2008	PML/RARalpha fusion protein mediates the unique sensitivity to arsenic cytotoxicity in acute promyelocytic leukemia cells: Mechanisms involve the impairment of cAMP signaling and the aberrant regulation of NADPH oxidase.	Arsenic	63-70	PML nuclear body scaffold	Homo sapiens	0-3
19260322-1	2008	OBJECTIVE: To investigate the occurrence of germ cell apoptosis and the expression of Bcl-2/Bax after aniso-doses arsenic (As2O3) administration in the testes of the adult male rats.	Arsenic	114-121	BCL2, apoptosis regulator	Rattus norvegicus	86-91
19260322-1	2008	OBJECTIVE: To investigate the occurrence of germ cell apoptosis and the expression of Bcl-2/Bax after aniso-doses arsenic (As2O3) administration in the testes of the adult male rats.	Arsenic	114-121	BCL2 associated X, apoptosis regulator	Rattus norvegicus	92-95
18674524-10	2008	In conclusion, we show that expression of mu- and m-calpain protein is increased by exposure to As, possibly leading to increased NF-L degradation.	Arsenic	96-98	calpain 2	Rattus norvegicus	50-59
18674524-10	2008	In conclusion, we show that expression of mu- and m-calpain protein is increased by exposure to As, possibly leading to increased NF-L degradation.	Arsenic	96-98	neurofilament light chain	Rattus norvegicus	130-134
19010883-0	2008	Induction of cytoplasmic accumulation of p53: a mechanism for low levels of arsenic exposure to predispose cells for malignant transformation.	Arsenic	76-83	tumor protein p53	Homo sapiens	41-44
18593383-1	2008	Saccharomyces cerevisiae uses several mechanisms for arsenic detoxification including the arsenate reductase Acr2p and the arsenite efflux protein Acr3p.	Arsenic	53-60	Arr3p	Saccharomyces cerevisiae S288C	147-152
18593383-3	2008	Yap8p has been shown to permanently associate with this promoter and to stimulate ACR2/ACR3 expression in response to arsenic.	Arsenic	118-125	Arr1p	Saccharomyces cerevisiae S288C	0-5
18593383-3	2008	Yap8p has been shown to permanently associate with this promoter and to stimulate ACR2/ACR3 expression in response to arsenic.	Arsenic	118-125	Arr2p	Saccharomyces cerevisiae S288C	82-86
18593383-3	2008	Yap8p has been shown to permanently associate with this promoter and to stimulate ACR2/ACR3 expression in response to arsenic.	Arsenic	118-125	Arr3p	Saccharomyces cerevisiae S288C	87-91
19010883-6	2008	Together, our data suggests that arsenic compounds predispose cells to malignant transformation by up-regulation of Hdm2 and subsequent p53 inactivation.	Arsenic	33-40	MDM2 proto-oncogene	Homo sapiens	116-120
19010883-6	2008	Together, our data suggests that arsenic compounds predispose cells to malignant transformation by up-regulation of Hdm2 and subsequent p53 inactivation.	Arsenic	33-40	tumor protein p53	Homo sapiens	136-139
18636556-0	2008	PML/RARalpha fusion protein mediates the unique sensitivity to arsenic cytotoxicity in acute promyelocytic leukemia cells: Mechanisms involve the impairment of cAMP signaling and the aberrant regulation of NADPH oxidase.	Arsenic	63-70	retinoic acid receptor alpha	Homo sapiens	4-12
18511430-0	2008	Decreased urinary beta-defensin-1 expression as a biomarker of response to arsenic.	Arsenic	75-82	defensin beta 1	Homo sapiens	18-33
18787995-3	2008	The goal of this study is to describe the clinical course and urinary arsenic concentrations of children who ingested ant bait containing arsenic trioxide (0.46%).	Arsenic	70-77	solute carrier family 25 member 6	Homo sapiens	118-121
18787995-10	2008	CONCLUSIONS: Children who ingest all or part of a household ant bait gel bar that contains relatively low concentration of arsenic trioxide can develop markedly elevated urine arsenic concentrations with minor initial symptoms.	Arsenic	123-130	solute carrier family 25 member 6	Homo sapiens	60-63
18511430-7	2008	In a separate in vitro experiment, gene expression analysis of As-treated cell lines demonstrated reduced HBD1 mRNA confirming that the observed decrease in HBD-1 resulted from As exposure.	Arsenic	177-179	defensin beta 1	Homo sapiens	157-162
18511430-9	2008	Recent studies support its role as a tumor suppressor gene for urological cancers suggesting that decreased HBD-1 levels may play a role in the development of cancers associated with As exposure.	Arsenic	183-185	defensin beta 1	Homo sapiens	108-113
18511430-7	2008	In a separate in vitro experiment, gene expression analysis of As-treated cell lines demonstrated reduced HBD1 mRNA confirming that the observed decrease in HBD-1 resulted from As exposure.	Arsenic	63-65	defensin beta 1	Homo sapiens	106-110
18511430-7	2008	In a separate in vitro experiment, gene expression analysis of As-treated cell lines demonstrated reduced HBD1 mRNA confirming that the observed decrease in HBD-1 resulted from As exposure.	Arsenic	63-65	defensin beta 1	Homo sapiens	157-162
18762312-1	2008	In this study, denitrification linked to the oxidation of arsenite (As(III)) to arsenate (As(V)) was shown to be a widespread microbial activity in anaerobic sludge and sediment samples that were not previously exposed to arsenic contamination.	Arsenic	222-229	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	90-95
19141569-9	2008	It is therefore concluded that caspase activation has a direct role in arsenic-induced apoptosis mediated by mitochondrial factors at 10 microM As(2)O(3), and JUN N-terminal kinase (JNK) and P38 activation are the major mediators of apoptosis at the higher test concentrations (20 and 40 microM) of As(2)O(3).	Arsenic	71-78	mitogen-activated protein kinase 8	Rattus norvegicus	159-180
19141569-9	2008	It is therefore concluded that caspase activation has a direct role in arsenic-induced apoptosis mediated by mitochondrial factors at 10 microM As(2)O(3), and JUN N-terminal kinase (JNK) and P38 activation are the major mediators of apoptosis at the higher test concentrations (20 and 40 microM) of As(2)O(3).	Arsenic	71-78	mitogen-activated protein kinase 8	Rattus norvegicus	182-185
19141569-9	2008	It is therefore concluded that caspase activation has a direct role in arsenic-induced apoptosis mediated by mitochondrial factors at 10 microM As(2)O(3), and JUN N-terminal kinase (JNK) and P38 activation are the major mediators of apoptosis at the higher test concentrations (20 and 40 microM) of As(2)O(3).	Arsenic	71-78	mitogen activated protein kinase 14	Rattus norvegicus	191-194
19141569-5	2008	The expression of the common stress proteins HSP 70 and 90 throughout the experimental duration confirmed the magnitude of toxic effect imposed by arsenic.	Arsenic	147-154	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	45-51
19141569-8	2008	Co-treatment of cells with arsenic and caspase inhibitor (Ac-DEVD-Cho) led to over expression of bcl-2, suppression of bax, and cytosolic sequestration of Bid and Bad.	Arsenic	27-34	BCL2, apoptosis regulator	Rattus norvegicus	97-102
19141569-8	2008	Co-treatment of cells with arsenic and caspase inhibitor (Ac-DEVD-Cho) led to over expression of bcl-2, suppression of bax, and cytosolic sequestration of Bid and Bad.	Arsenic	27-34	BCL2 associated X, apoptosis regulator	Rattus norvegicus	119-122
18762312-2	2008	When incubated with 0.5mM As(III) and 10mM NO(3)(-), the anoxic oxidation of As(III) commenced within a few days, achieving specific activities of up to 1.24mmol As(V) formed g(-1) volatile suspended solids d(-1) due to growth (doubling times of 0.74-1.4d).	Arsenic	26-28	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	162-167
19141569-8	2008	Co-treatment of cells with arsenic and caspase inhibitor (Ac-DEVD-Cho) led to over expression of bcl-2, suppression of bax, and cytosolic sequestration of Bid and Bad.	Arsenic	27-34	BH3 interacting domain death agonist	Rattus norvegicus	155-158
18762312-2	2008	When incubated with 0.5mM As(III) and 10mM NO(3)(-), the anoxic oxidation of As(III) commenced within a few days, achieving specific activities of up to 1.24mmol As(V) formed g(-1) volatile suspended solids d(-1) due to growth (doubling times of 0.74-1.4d).	Arsenic	77-79	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	162-167
18640142-1	2008	INTRODUCTION: Polymorphisms in p53, p21 and CCND1 could regulate the progression of the cell cycle and might increase the susceptibility to inorganic arsenic-related cancer risk.	Arsenic	150-157	tumor protein p53	Homo sapiens	31-34
18922899-8	2008	CD34, considered a marker for both KSCs and skin cancer stem cells, and Rac1, a key gene stimulating KSC self-renewal, were greatly increased in tumors produced by arsenic plus TPA exposure versus TPA alone, and both were elevated in arsenic-treated fetal skin.	Arsenic	164-171	CD34 molecule	Homo sapiens	0-4
18922899-8	2008	CD34, considered a marker for both KSCs and skin cancer stem cells, and Rac1, a key gene stimulating KSC self-renewal, were greatly increased in tumors produced by arsenic plus TPA exposure versus TPA alone, and both were elevated in arsenic-treated fetal skin.	Arsenic	164-171	Rac family small GTPase 1	Homo sapiens	72-76
18922899-8	2008	CD34, considered a marker for both KSCs and skin cancer stem cells, and Rac1, a key gene stimulating KSC self-renewal, were greatly increased in tumors produced by arsenic plus TPA exposure versus TPA alone, and both were elevated in arsenic-treated fetal skin.	Arsenic	234-241	Rac family small GTPase 1	Homo sapiens	72-76
18922899-9	2008	Greatly increased numbers of CD34-positive probable cancer stem cells and marked overexpression of RAC1 protein occurred in tumors induced by arsenic plus TPA compared with TPA alone.	Arsenic	142-149	CD34 molecule	Homo sapiens	29-33
18922899-9	2008	Greatly increased numbers of CD34-positive probable cancer stem cells and marked overexpression of RAC1 protein occurred in tumors induced by arsenic plus TPA compared with TPA alone.	Arsenic	142-149	Rac family small GTPase 1	Homo sapiens	99-103
18640142-1	2008	INTRODUCTION: Polymorphisms in p53, p21 and CCND1 could regulate the progression of the cell cycle and might increase the susceptibility to inorganic arsenic-related cancer risk.	Arsenic	150-157	H3 histone pseudogene 16	Homo sapiens	36-39
18640142-1	2008	INTRODUCTION: Polymorphisms in p53, p21 and CCND1 could regulate the progression of the cell cycle and might increase the susceptibility to inorganic arsenic-related cancer risk.	Arsenic	150-157	cyclin D1	Homo sapiens	44-49
18640142-12	2008	CONCLUSIONS: The results showed that the variant genotype of p21 might be a predictor of inorganic arsenic-related UC risk.	Arsenic	99-106	H3 histone pseudogene 16	Homo sapiens	61-64
18991936-7	2008	Arsenic in vitro induced a three-fold increase in the expression of alpha-fetoprotein (AFP), a biomarker associated with transplacental arsenic-induced mouse liver tumors.	Arsenic	0-7	alpha fetoprotein	Mus musculus	68-85
18767879-2	2008	The experimental results indicate that addition of NaF, NaCl, NaHCO 3, or NaNO 3 can result in phase inversion of ATPS-C formed by 12-3-12/AS systems; however, addition of NaBr cannot lead to phase inversion.	Arsenic	139-141	C-X-C motif chemokine ligand 8	Homo sapiens	51-54
18991936-7	2008	Arsenic in vitro induced a three-fold increase in the expression of alpha-fetoprotein (AFP), a biomarker associated with transplacental arsenic-induced mouse liver tumors.	Arsenic	0-7	alpha fetoprotein	Mus musculus	87-90
18991936-7	2008	Arsenic in vitro induced a three-fold increase in the expression of alpha-fetoprotein (AFP), a biomarker associated with transplacental arsenic-induced mouse liver tumors.	Arsenic	136-143	alpha fetoprotein	Mus musculus	68-85
18991936-7	2008	Arsenic in vitro induced a three-fold increase in the expression of alpha-fetoprotein (AFP), a biomarker associated with transplacental arsenic-induced mouse liver tumors.	Arsenic	136-143	alpha fetoprotein	Mus musculus	87-90
18707137-3	2008	The present study tests the hypothesis that arsenite not only induces oxidative stress but also inhibits the activity of the DNA base excision repair protein, poly(ADP-ribose) polymerase-1 (PARP-1), leading to exacerbation of the oxidative DNA damage induced by arsenic.	Arsenic	262-269	poly(ADP-ribose) polymerase 1	Homo sapiens	159-188
18439143-0	2008	Contribution of Yap1 towards Saccharomyces cerevisiae adaptation to arsenic-mediated oxidative stress.	Arsenic	68-75	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	16-20
18439143-1	2008	In the budding yeast Saccharomyces cerevisiae, arsenic detoxification involves the activation of Yap8, a member of the Yap (yeast AP-1-like) family of transcription factors, which in turn regulates ACR2 and ACR3, genes encoding an arsenate reductase and a plasma-membrane arsenite-efflux protein respectively.	Arsenic	47-54	Arr1p	Saccharomyces cerevisiae S288C	97-101
18439143-1	2008	In the budding yeast Saccharomyces cerevisiae, arsenic detoxification involves the activation of Yap8, a member of the Yap (yeast AP-1-like) family of transcription factors, which in turn regulates ACR2 and ACR3, genes encoding an arsenate reductase and a plasma-membrane arsenite-efflux protein respectively.	Arsenic	47-54	Arr2p	Saccharomyces cerevisiae S288C	198-202
18439143-1	2008	In the budding yeast Saccharomyces cerevisiae, arsenic detoxification involves the activation of Yap8, a member of the Yap (yeast AP-1-like) family of transcription factors, which in turn regulates ACR2 and ACR3, genes encoding an arsenate reductase and a plasma-membrane arsenite-efflux protein respectively.	Arsenic	47-54	Arr3p	Saccharomyces cerevisiae S288C	207-211
18439143-2	2008	In addition, Yap1 is involved in the arsenic adaptation process through regulation of the expression of the vacuolar pump encoded by YCF1 (yeast cadmium factor 1 gene) and also contributing to the regulation of ACR genes.	Arsenic	37-44	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	13-17
18439143-2	2008	In addition, Yap1 is involved in the arsenic adaptation process through regulation of the expression of the vacuolar pump encoded by YCF1 (yeast cadmium factor 1 gene) and also contributing to the regulation of ACR genes.	Arsenic	37-44	ATP-binding cassette glutathione S-conjugate transporter YCF1	Saccharomyces cerevisiae S288C	133-137
18439143-3	2008	Here we show that Yap1 is also involved in the removal of ROS (reactive oxygen species) generated by arsenic compounds.	Arsenic	101-108	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	18-22
19794907-8	2008	Arsenic exposure significantly reduced blood delta-aminolevulinic acid dehydratase (ALAD) activity, a key enzyme involved in the heme biosynthesis and enhanced zinc protoporphyrin (ZPP) level.	Arsenic	0-7	aminolevulinate dehydratase	Rattus norvegicus	45-82
19794907-8	2008	Arsenic exposure significantly reduced blood delta-aminolevulinic acid dehydratase (ALAD) activity, a key enzyme involved in the heme biosynthesis and enhanced zinc protoporphyrin (ZPP) level.	Arsenic	0-7	aminolevulinate dehydratase	Rattus norvegicus	84-88
18439143-4	2008	Data on lipid peroxidation and intracellular oxidation indicate that deletion of YAP1 and YAP8 triggers cellular oxidation mediated by inorganic arsenic.	Arsenic	145-152	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	81-85
18439143-4	2008	Data on lipid peroxidation and intracellular oxidation indicate that deletion of YAP1 and YAP8 triggers cellular oxidation mediated by inorganic arsenic.	Arsenic	145-152	Arr1p	Saccharomyces cerevisiae S288C	90-94
18439143-6	2008	In contrast, the yap1 mutant exhibits high contents of protein carbonyl groups and the GSSG/GSH ratio is severely disturbed on exposure to arsenic compounds in these cells.	Arsenic	139-146	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	17-21
18439143-7	2008	These results point to an additional level of Yap1 contribution to arsenic stress responses by preventing oxidative damage in cells exposed to these compounds.	Arsenic	67-74	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	46-50
18707137-3	2008	The present study tests the hypothesis that arsenite not only induces oxidative stress but also inhibits the activity of the DNA base excision repair protein, poly(ADP-ribose) polymerase-1 (PARP-1), leading to exacerbation of the oxidative DNA damage induced by arsenic.	Arsenic	262-269	poly(ADP-ribose) polymerase 1	Homo sapiens	190-196
18486177-0	2008	Arsenic alters vascular smooth muscle cell focal adhesion complexes leading to activation of FAK-src mediated pathways.	Arsenic	0-7	protein tyrosine kinase 2	Homo sapiens	93-96
18795156-0	2008	Oridonin confers protection against arsenic-induced toxicity through activation of the Nrf2-mediated defensive response.	Arsenic	36-43	NFE2 like bZIP transcription factor 2	Homo sapiens	87-91
18795156-4	2008	Recently, activation of the Nrf2 signaling pathway has been reported to confer protection against arsenic-induced toxicity in a cell culture model.	Arsenic	98-105	NFE2 like bZIP transcription factor 2	Homo sapiens	28-32
18795156-5	2008	OBJECTIVES: The goal of the present work was to identify a potent Nrf2 activator from plants as a chemopreventive compound and to demonstrate the efficacy of the compound in battling arsenic-induced toxicity.	Arsenic	183-190	NFE2 like bZIP transcription factor 2	Homo sapiens	66-70
18795156-7	2008	Pretreatment of UROtsa cells with 1.4 muM oridonin significantly enhanced the cellular redox capacity, reduced formation of reactive oxygen species (ROS), and improved cell survival after arsenic challenge.	Arsenic	188-195	latexin	Homo sapiens	38-41
18572023-0	2008	Arsenic-induced malignant transformation of human keratinocytes: involvement of Nrf2.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	80-84
18486177-0	2008	Arsenic alters vascular smooth muscle cell focal adhesion complexes leading to activation of FAK-src mediated pathways.	Arsenic	0-7	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	97-100
18602460-2	2008	Excision repair cross-complementing 1 and 2 (ERCC1 and ERCC2) have shown to be associated with arsenic-induced toxicity and carcinogenicity.	Arsenic	95-102	DNA excision repair protein ERCC-1	Cricetulus griseus	45-50
18486177-6	2008	In our model, arsenic treatment caused a sustained increase in FAK-src association and activation, and induced the formation of unique signaling complexes (beginning after 3-hour As(3+) exposure and continuing throughout the 12-hour time course studied).	Arsenic	14-21	protein tyrosine kinase 2	Homo sapiens	63-66
18602460-2	2008	Excision repair cross-complementing 1 and 2 (ERCC1 and ERCC2) have shown to be associated with arsenic-induced toxicity and carcinogenicity.	Arsenic	95-102	general transcription and DNA repair factor IIH helicase subunit XPD	Cricetulus griseus	55-60
18486177-6	2008	In our model, arsenic treatment caused a sustained increase in FAK-src association and activation, and induced the formation of unique signaling complexes (beginning after 3-hour As(3+) exposure and continuing throughout the 12-hour time course studied).	Arsenic	14-21	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	67-70
18572272-10	2008	The hydrogeochemistry and widespread As enrichment in groundwater of Chia-Nan plain result from multiple processes, e.g., de-watering of deep crustal fluids, seawater intrusion, and biogeochemical cycling of Fe, As, and S in alluvial sediments.	Arsenic	37-39	chitinase acidic	Homo sapiens	69-73
18656657-1	2008	A new, simple, and selective method has been presented for the separation and preconcentration of inorganic arsenic (As(III)/As(V)) and selenium (Se(IV)/Se(VI)) species by a microcolumn on-line coupled with inductively coupled plasma-optical emission spectrometry (ICP-OES).	Arsenic	108-115	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	125-130
18656657-5	2008	The assay of As(III) and Se(IV) were based on subtracting As(V) and Se(VI) from total As and total Se, respectively.	Arsenic	13-15	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	58-63
18754502-0	2008	Landfill disposal of CCA-treated wood with construction and demolition (C&amp;D) debris: arsenic, chromium, and copper concentrations in leachate.	Arsenic	89-96	fibrillin 2	Homo sapiens	21-24
18588996-2	2008	Inter-individual variation in arsenic metabolism has been reported and recent studies demonstrate that 287T allele in human arsenic (+3 oxidation state) methyltransferase (AS3MT) increase the percentage of monomethylated arsenic in urine.	Arsenic	30-37	arsenite methyltransferase	Homo sapiens	124-170
18588996-2	2008	Inter-individual variation in arsenic metabolism has been reported and recent studies demonstrate that 287T allele in human arsenic (+3 oxidation state) methyltransferase (AS3MT) increase the percentage of monomethylated arsenic in urine.	Arsenic	30-37	arsenite methyltransferase	Homo sapiens	172-177
18588996-2	2008	Inter-individual variation in arsenic metabolism has been reported and recent studies demonstrate that 287T allele in human arsenic (+3 oxidation state) methyltransferase (AS3MT) increase the percentage of monomethylated arsenic in urine.	Arsenic	124-131	arsenite methyltransferase	Homo sapiens	172-177
18795150-9	2008	TrxR1 expression was higher (P &lt; .01) in CR-CaP compared with AS-BP or AS-CaP.	Arsenic	65-67	thioredoxin reductase 1	Mus musculus	0-5
19105269-4	2008	CONCLUSION: VEGF are important factors in patients with active AS.	Arsenic	63-65	vascular endothelial growth factor A	Homo sapiens	12-16
19105269-6	2008	If we can reduce the expressions of VEGF in the patients with active AS, the process of osteoclasia and pathological new bone formation will be interrupted and this provides a new strategy for the treatment of ankylosing spondylitis.	Arsenic	69-71	vascular endothelial growth factor A	Homo sapiens	36-40
18621066-0	2008	Increased damage of exon 5 of p53 gene in workers from an arsenic plant.	Arsenic	58-65	tumor protein p53	Homo sapiens	30-33
18621066-11	2008	These results imply that base modification in exon 5 of p53 gene can be induced by arsenic.	Arsenic	83-90	tumor protein p53	Homo sapiens	56-59
18539681-0	2008	Arsenic upregulates MMP-9 and inhibits wound repair in human airway epithelial cells.	Arsenic	0-7	matrix metallopeptidase 9	Homo sapiens	20-25
18539681-6	2008	In an effort to understand functional contributions to epithelial wound repair altered by arsenic, we showed that acute arsenic exposure increases activity and expression of matrix metalloproteinase (MMP)-9, an important protease in lung function.	Arsenic	90-97	matrix metallopeptidase 9	Homo sapiens	174-206
18539681-6	2008	In an effort to understand functional contributions to epithelial wound repair altered by arsenic, we showed that acute arsenic exposure increases activity and expression of matrix metalloproteinase (MMP)-9, an important protease in lung function.	Arsenic	120-127	matrix metallopeptidase 9	Homo sapiens	174-206
18539681-7	2008	Furthermore, inhibition of MMP-9 in arsenic-treated cells improved wound repair.	Arsenic	36-43	matrix metallopeptidase 9	Homo sapiens	27-32
18539681-8	2008	We propose that arsenic in the airway can alter the airway epithelial barrier by restricting proper wound repair in part through the upregulation of MMP-9 by lung epithelial cells.	Arsenic	16-23	matrix metallopeptidase 9	Homo sapiens	149-154
18602135-2	2008	Determination of inorganic arsenic in each oxidation state is important because As(III) is much more toxic than As(V).	Arsenic	27-34	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	112-117
18839561-11	2008	The concentrations of available arsenic in the sediments, which were estimated by the method of acetate cellulose composite membrane embedded with iron oxides (FeO/CAM), accounted for 0.6% to 3.9% (averaged as 2.1%) of the total arsenic concentrations.	Arsenic	32-39	calmodulin 3	Homo sapiens	164-167
18451318-10	2008	Moreover, the arsenic compounds were able to activate caspase-3 expression when examined by Western blot analysis.	Arsenic	14-21	caspase 3	Homo sapiens	54-63
19083458-0	2008	Glutamine reduces the expression of leukocyte integrins leukocyte function-associated antigen-1 and macrophage antigen-1 in mice exposed to arsenic.	Arsenic	140-147	macrophage antigen 1	Mus musculus	36-120
19083458-10	2008	beta(2) intergins, including leukocyte function-associated antigen-1 and macrophage antigen-1 expressed by leukocytes, were significantly higher in the arsenic group than the control groups.	Arsenic	152-159	macrophage antigen 1	Mus musculus	0-93
18417180-4	2008	Paradoxically, arsenic has been reported to induce the Nrf2-dependent signaling pathway.	Arsenic	15-22	NFE2 like bZIP transcription factor 2	Homo sapiens	55-59
18417180-5	2008	Here, we report the unique mechanism of Nrf2 induction by arsenic.	Arsenic	58-65	NFE2 like bZIP transcription factor 2	Homo sapiens	40-44
18417180-6	2008	Similar to tert-butylhydroquinone (tBHQ) or sulforaphane (SF), arsenic induced the Nrf2-dependent response through enhancing Nrf2 protein levels by inhibiting Nrf2 ubiquitination and degradation.	Arsenic	63-70	NFE2 like bZIP transcription factor 2	Homo sapiens	83-87
18417180-6	2008	Similar to tert-butylhydroquinone (tBHQ) or sulforaphane (SF), arsenic induced the Nrf2-dependent response through enhancing Nrf2 protein levels by inhibiting Nrf2 ubiquitination and degradation.	Arsenic	63-70	NFE2 like bZIP transcription factor 2	Homo sapiens	125-129
18417180-6	2008	Similar to tert-butylhydroquinone (tBHQ) or sulforaphane (SF), arsenic induced the Nrf2-dependent response through enhancing Nrf2 protein levels by inhibiting Nrf2 ubiquitination and degradation.	Arsenic	63-70	NFE2 like bZIP transcription factor 2	Homo sapiens	125-129
18417180-7	2008	However, the detailed action of arsenic in Nrf2 induction is different from that of tBHQ or SF.	Arsenic	32-39	NFE2 like bZIP transcription factor 2	Homo sapiens	43-47
18417180-8	2008	Arsenic markedly enhanced the interaction between Keap1 and Cul3, subunits of the E3 ubiquitin ligase for Nrf2, which led to impaired dynamic assembly/disassembly of the E3 ubiquitin ligase and thus decreased its ligase activity.	Arsenic	0-7	kelch like ECH associated protein 1	Homo sapiens	50-55
18417180-8	2008	Arsenic markedly enhanced the interaction between Keap1 and Cul3, subunits of the E3 ubiquitin ligase for Nrf2, which led to impaired dynamic assembly/disassembly of the E3 ubiquitin ligase and thus decreased its ligase activity.	Arsenic	0-7	cullin 3	Homo sapiens	60-64
18417180-8	2008	Arsenic markedly enhanced the interaction between Keap1 and Cul3, subunits of the E3 ubiquitin ligase for Nrf2, which led to impaired dynamic assembly/disassembly of the E3 ubiquitin ligase and thus decreased its ligase activity.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	106-110
18417180-9	2008	Furthermore, induction of Nrf2 by arsenic is independent of the previously identified C151 residue in Keap1 that is required for Nrf2 activation by tBHQ or SF.	Arsenic	34-41	NFE2 like bZIP transcription factor 2	Homo sapiens	26-30
18524450-3	2008	The expression of two enzymes responsible for arsenic biotransformation arsenic methyltranferase (AS3MT) and glutathione S-transferase omega 1 (GSTO1) was evaluated in human cord blood cells.	Arsenic	46-53	arsenite methyltransferase	Homo sapiens	98-103
18407307-0	2008	Arsenic interferes with the signaling transduction pathway of T cell receptor activation by increasing basal and induced phosphorylation of Lck and Fyn in spleen cells.	Arsenic	0-7	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	140-143
18407307-0	2008	Arsenic interferes with the signaling transduction pathway of T cell receptor activation by increasing basal and induced phosphorylation of Lck and Fyn in spleen cells.	Arsenic	0-7	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	148-151
18407307-3	2008	Intra-gastric exposure to arsenic (as sodium arsenite) for 30 days (1, 0.1, or 0.01 mg/kg/day), reduced the proportion of CD4+ cells and the CD4+/CD8+ ratio in the spleen, increasing the proportion of CD11b+ cells.	Arsenic	26-33	integrin subunit alpha M	Homo sapiens	201-206
18407307-7	2008	Arsenic exposure reduced the proliferative response of SMC to Con-A, and also reduced secretion of IL-2, IL-6, IL-12 and IFNgamma.	Arsenic	0-7	interleukin 2	Homo sapiens	99-103
18407307-7	2008	Arsenic exposure reduced the proliferative response of SMC to Con-A, and also reduced secretion of IL-2, IL-6, IL-12 and IFNgamma.	Arsenic	0-7	interleukin 6	Homo sapiens	105-109
18407307-7	2008	Arsenic exposure reduced the proliferative response of SMC to Con-A, and also reduced secretion of IL-2, IL-6, IL-12 and IFNgamma.	Arsenic	0-7	interferon gamma	Homo sapiens	121-129
18407307-10	2008	This study demonstrates that repeated and prolonged exposure to arsenic alters cell populations and produces functional changes depending on the specific activation pathway, and could be related with the phosphorylation status of lck and fyn kinases.	Arsenic	64-71	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	230-233
18407307-10	2008	This study demonstrates that repeated and prolonged exposure to arsenic alters cell populations and produces functional changes depending on the specific activation pathway, and could be related with the phosphorylation status of lck and fyn kinases.	Arsenic	64-71	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	238-241
18573533-4	2008	Compared to controls, offspring exposed to 50 parts per billion arsenic during the perinatal period had significantly elevated serum corticosterone levels, reduced whole hippocampal CRFR 1 protein level and elevated dorsal hippocampal serotonin 5HT 1A receptor binding and receptor-effector coupling.	Arsenic	64-71	corticotropin releasing hormone receptor 1	Mus musculus	182-188
18504054-0	2008	Overexpressing GSH1 and AsPCS1 simultaneously increases the tolerance and accumulation of cadmium and arsenic in Arabidopsis thaliana.	Arsenic	102-109	glutamate-cysteine ligase	Arabidopsis thaliana	15-19
18085531-0	2008	Attenuation of DNA damage-induced p53 expression by arsenic: a possible mechanism for arsenic co-carcinogenesis.	Arsenic	52-59	tumor protein p53	Homo sapiens	34-37
18085531-0	2008	Attenuation of DNA damage-induced p53 expression by arsenic: a possible mechanism for arsenic co-carcinogenesis.	Arsenic	86-93	tumor protein p53	Homo sapiens	34-37
18085531-10	2008	Because p53 is required for proficient global NER, our data suggest that arsenic inhibits NER through suppressing p53 induction in response to DNA damage in cells with normal p53 gene expression.	Arsenic	73-80	tumor protein p53	Homo sapiens	8-11
18085531-10	2008	Because p53 is required for proficient global NER, our data suggest that arsenic inhibits NER through suppressing p53 induction in response to DNA damage in cells with normal p53 gene expression.	Arsenic	73-80	tumor protein p53	Homo sapiens	114-117
18085531-10	2008	Because p53 is required for proficient global NER, our data suggest that arsenic inhibits NER through suppressing p53 induction in response to DNA damage in cells with normal p53 gene expression.	Arsenic	73-80	tumor protein p53	Homo sapiens	114-117
18451774-5	2008	There was a trend for a differential effect between groups for CRP as it decreased 32% in the AS group but increased 50% for P (P=0.076).	Arsenic	94-96	C-reactive protein	Homo sapiens	63-66
18249029-6	2008	Previously we have reported that the p53 codon 72 arginine (Arg) homozygous genotype is associated with the development of arsenic-induced keratosis.	Arsenic	123-130	tumor protein p53	Homo sapiens	37-40
18249029-13	2008	This study suggests that individuals with keratosis are more susceptible to arsenic-induced health effects and genetic damage and that the arginine variant of p53 can further influence the repair capacity of arsenic-exposed individuals, leading to increased accumulation of chromosomal aberrations.	Arsenic	208-215	tumor protein p53	Homo sapiens	159-162
18354491-6	2008	Arsenic treatment of NB4 cells resulted in a partial but significant reduction of ATRA-dependent induction of COX-1 expression and activity.	Arsenic	0-7	prostaglandin-endoperoxide synthase 1	Homo sapiens	110-115
18093733-7	2008	Column adsorption tests suggested that complete removal of arsenic was achievable at up to 120 Bed Volumes (BV) for As(V) and 8 0BV for As(III).	Arsenic	59-66	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	116-121
18640604-8	2008	When the recombinant strain B3 established symbiosis with A. sinicus, the introduction of AtIRT1 in the recombinant strain B3 advantaged the accumulation of Cu and As in the nodules of A. sinicus, compared with that of Cd and Zn.	Arsenic	164-166	iron-regulated transporter 1	Arabidopsis thaliana	90-96
18839526-0	2008	[Study on the relationship between GSTM1, GSTT1 gene polymorphisms and arsenic methylation level].	Arsenic	71-78	glutathione S-transferase mu 1	Homo sapiens	35-40
18839526-0	2008	[Study on the relationship between GSTM1, GSTT1 gene polymorphisms and arsenic methylation level].	Arsenic	71-78	glutathione S-transferase theta 1	Homo sapiens	42-47
18839526-1	2008	OBJECTIVE: To investigate the relationship between genetic polymorphisms of GSTT1, GSTM1 and arsenic methylation level.	Arsenic	93-100	glutathione S-transferase theta 1	Homo sapiens	76-81
18839526-1	2008	OBJECTIVE: To investigate the relationship between genetic polymorphisms of GSTT1, GSTM1 and arsenic methylation level.	Arsenic	93-100	glutathione S-transferase mu 1	Homo sapiens	83-88
18435919-2	2008	Loss of function in AtNIP7;1 led to increased plant tolerance to AsIII and reduced total As in planta.	Arsenic	65-67	NOD26-like intrinsic protein 7;1	Arabidopsis thaliana	20-28
18336854-0	2008	Reactive oxygen species-dependent HSP90 protein cleavage participates in arsenical As(+3)- and MMA(+3)-induced apoptosis through inhibition of telomerase activity via JNK activation.	Arsenic	83-85	heat shock protein 86, pseudogene 2	Mus musculus	34-39
18299328-5	2008	Importantly, arsenic-induced apoptosis is enhanced in cells with targeted disruption of the Mnk1 and/or Mnk2 genes, suggesting that these kinases are activated in a negative-feedback regulatory manner, to control generation of arsenic trioxide responses.	Arsenic	13-20	MAPK interacting serine/threonine kinase 1	Homo sapiens	92-96
18299328-5	2008	Importantly, arsenic-induced apoptosis is enhanced in cells with targeted disruption of the Mnk1 and/or Mnk2 genes, suggesting that these kinases are activated in a negative-feedback regulatory manner, to control generation of arsenic trioxide responses.	Arsenic	13-20	MAPK interacting serine/threonine kinase 2	Homo sapiens	104-108
18328529-8	2008	Particularly, Cd, Se, As and Li preserve their ratios in all study area, and are interpreted as principal components of the MGF emissions.	Arsenic	22-24	signal transducer and activator of transcription 5A	Homo sapiens	124-127
18183357-3	2008	Arsenic exposure led to a significant depletion of blood delta-aminolevulinic acid dehydratase (ALAD) activity, glutathione, white (WBC) and red blood cell (RBC) counts, and an increase in platelet levels while significantly increasing the level of reactive oxygen species (in RBCs).	Arsenic	0-7	aminolevulinate, delta-, dehydratase	Mus musculus	57-94
18183357-3	2008	Arsenic exposure led to a significant depletion of blood delta-aminolevulinic acid dehydratase (ALAD) activity, glutathione, white (WBC) and red blood cell (RBC) counts, and an increase in platelet levels while significantly increasing the level of reactive oxygen species (in RBCs).	Arsenic	0-7	aminolevulinate, delta-, dehydratase	Mus musculus	96-100
18252256-5	2008	To address this question we have investigated the regulation of DNA polymerase beta (Pol beta) and AP endonuclease (APE1), in response to low, physiologically relevant doses of arsenic.	Arsenic	177-184	DNA polymerase beta	Homo sapiens	64-83
17574535-6	2008	Crustal enrichments (EFc) for As (97), Cr (6), Cu (10), Pb (121), V (7), and Hg (17) were highest for North Lilbourn soils.	Arsenic	30-32	regulatory factor X1	Homo sapiens	21-24
17879257-7	2008	Real-time RT-PCR confirmed that arsenic increased mRNA levels of the following genes: retinoblastoma 1 (RB1) (5.4-fold), retinoblastoma-binding protein 1 (ARID4A) (6.8-fold), transforming growth factor beta-stimulated protein (TSC22D1) (6.84-fold), MAX binding protein (MNT) (2.44-fold), and RAD50 (4.24-fold).	Arsenic	32-39	RB transcriptional corepressor 1	Homo sapiens	86-102
17879257-7	2008	Real-time RT-PCR confirmed that arsenic increased mRNA levels of the following genes: retinoblastoma 1 (RB1) (5.4-fold), retinoblastoma-binding protein 1 (ARID4A) (6.8-fold), transforming growth factor beta-stimulated protein (TSC22D1) (6.84-fold), MAX binding protein (MNT) (2.44-fold), and RAD50 (4.24-fold).	Arsenic	32-39	RB transcriptional corepressor 1	Homo sapiens	104-107
17879257-7	2008	Real-time RT-PCR confirmed that arsenic increased mRNA levels of the following genes: retinoblastoma 1 (RB1) (5.4-fold), retinoblastoma-binding protein 1 (ARID4A) (6.8-fold), transforming growth factor beta-stimulated protein (TSC22D1) (6.84-fold), MAX binding protein (MNT) (2.44-fold), and RAD50 (4.24-fold).	Arsenic	32-39	AT-rich interaction domain 4A	Homo sapiens	121-153
17879257-7	2008	Real-time RT-PCR confirmed that arsenic increased mRNA levels of the following genes: retinoblastoma 1 (RB1) (5.4-fold), retinoblastoma-binding protein 1 (ARID4A) (6.8-fold), transforming growth factor beta-stimulated protein (TSC22D1) (6.84-fold), MAX binding protein (MNT) (2.44-fold), and RAD50 (4.24-fold).	Arsenic	32-39	AT-rich interaction domain 4A	Homo sapiens	155-161
17879257-7	2008	Real-time RT-PCR confirmed that arsenic increased mRNA levels of the following genes: retinoblastoma 1 (RB1) (5.4-fold), retinoblastoma-binding protein 1 (ARID4A) (6.8-fold), transforming growth factor beta-stimulated protein (TSC22D1) (6.84-fold), MAX binding protein (MNT) (2.44-fold), and RAD50 (4.24-fold).	Arsenic	32-39	TSC22 domain family member 1	Homo sapiens	227-234
17879257-7	2008	Real-time RT-PCR confirmed that arsenic increased mRNA levels of the following genes: retinoblastoma 1 (RB1) (5.4-fold), retinoblastoma-binding protein 1 (ARID4A) (6.8-fold), transforming growth factor beta-stimulated protein (TSC22D1) (6.84-fold), MAX binding protein (MNT) (2.44-fold), and RAD50 (4.24-fold).	Arsenic	32-39	MAX network transcriptional repressor	Homo sapiens	249-268
17879257-7	2008	Real-time RT-PCR confirmed that arsenic increased mRNA levels of the following genes: retinoblastoma 1 (RB1) (5.4-fold), retinoblastoma-binding protein 1 (ARID4A) (6.8-fold), transforming growth factor beta-stimulated protein (TSC22D1) (6.84-fold), MAX binding protein (MNT) (2.44-fold), and RAD50 (4.24-fold).	Arsenic	32-39	MAX network transcriptional repressor	Homo sapiens	270-273
17879257-7	2008	Real-time RT-PCR confirmed that arsenic increased mRNA levels of the following genes: retinoblastoma 1 (RB1) (5.4-fold), retinoblastoma-binding protein 1 (ARID4A) (6.8-fold), transforming growth factor beta-stimulated protein (TSC22D1) (6.84-fold), MAX binding protein (MNT) (2.44-fold), and RAD50 (4.24-fold).	Arsenic	32-39	RAD50 double strand break repair protein	Homo sapiens	292-297
17988793-4	2008	As the adsorbent dosage and initial arsenic concentration were fixed, both the As(V) and As(III) removals decrease with increasing initial solution pH.	Arsenic	36-43	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	79-84
17988793-6	2008	Moreover, adsorption isotherms of As(V) and As(III) fit the Langmuir model satisfactorily for the four different initial pH conditions as well as for the studied range of initial arsenic concentrations.	Arsenic	179-186	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	34-39
18252256-5	2008	To address this question we have investigated the regulation of DNA polymerase beta (Pol beta) and AP endonuclease (APE1), in response to low, physiologically relevant doses of arsenic.	Arsenic	177-184	DNA polymerase beta	Homo sapiens	85-93
18252256-5	2008	To address this question we have investigated the regulation of DNA polymerase beta (Pol beta) and AP endonuclease (APE1), in response to low, physiologically relevant doses of arsenic.	Arsenic	177-184	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	116-120
18308733-3	2008	Met4 regulates expression of genes involved in the sulfur assimilation pathway and coordinates the transcriptional program and cell cycle progression in response to cadmium and arsenic stress.	Arsenic	177-184	Met4p	Saccharomyces cerevisiae S288C	0-4
19022878-8	2008	We observed a significant increase in blood and brain ROS levels accompanied by the depletion of GSH/GSSG ratio and glucose-6-phosphate dehydrogenase (G6PD) activity in different brain regions of arsenic-exposed rats.	Arsenic	196-203	glucose-6-phosphate dehydrogenase	Rattus norvegicus	116-149
19022878-8	2008	We observed a significant increase in blood and brain ROS levels accompanied by the depletion of GSH/GSSG ratio and glucose-6-phosphate dehydrogenase (G6PD) activity in different brain regions of arsenic-exposed rats.	Arsenic	196-203	glucose-6-phosphate dehydrogenase	Rattus norvegicus	151-155
18497140-7	2008	Our results demonstrate that mobility of arsenic in groundwater and removal in engineered treatment systems are more complicated when both As(III) and As(V) are present than anticipated based on single-adsorbate experimental results.	Arsenic	41-48	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	151-156
18304716-9	2008	We also observed that chronic arsenic exposure reduced Bcl-2/Bax ratio and also resulted in cell cycle arrest of PBMC in G0/G1 phase.	Arsenic	30-37	BCL2 apoptosis regulator	Homo sapiens	55-60
18304716-9	2008	We also observed that chronic arsenic exposure reduced Bcl-2/Bax ratio and also resulted in cell cycle arrest of PBMC in G0/G1 phase.	Arsenic	30-37	BCL2 associated X, apoptosis regulator	Homo sapiens	61-64
18408733-0	2008	Arsenic degrades PML or PML-RARalpha through a SUMO-triggered RNF4/ubiquitin-mediated pathway.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	17-20
18408733-0	2008	Arsenic degrades PML or PML-RARalpha through a SUMO-triggered RNF4/ubiquitin-mediated pathway.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	24-27
18408733-0	2008	Arsenic degrades PML or PML-RARalpha through a SUMO-triggered RNF4/ubiquitin-mediated pathway.	Arsenic	0-7	retinoic acid receptor alpha	Homo sapiens	28-36
18408733-0	2008	Arsenic degrades PML or PML-RARalpha through a SUMO-triggered RNF4/ubiquitin-mediated pathway.	Arsenic	0-7	ring finger protein 4	Homo sapiens	62-66
18408733-0	2008	Arsenic degrades PML or PML-RARalpha through a SUMO-triggered RNF4/ubiquitin-mediated pathway.	Arsenic	0-7	ubiquitin	Saccharomyces cerevisiae S288C	67-76
18408733-3	2008	Here, we demonstrate that arsenic-induced PML SUMOylation triggers its Lys 48-linked polyubiquitination and proteasome-dependent degradation.	Arsenic	26-33	PML nuclear body scaffold	Homo sapiens	42-45
18408733-4	2008	When exposed to arsenic, SUMOylated PML recruits RNF4, the human orthologue of the yeast SUMO-dependent E3 ubiquitin-ligase, as well as ubiquitin and proteasomes onto PML nuclear bodies.	Arsenic	16-23	PML nuclear body scaffold	Homo sapiens	36-39
18408733-4	2008	When exposed to arsenic, SUMOylated PML recruits RNF4, the human orthologue of the yeast SUMO-dependent E3 ubiquitin-ligase, as well as ubiquitin and proteasomes onto PML nuclear bodies.	Arsenic	16-23	ring finger protein 4	Homo sapiens	49-53
18408733-4	2008	When exposed to arsenic, SUMOylated PML recruits RNF4, the human orthologue of the yeast SUMO-dependent E3 ubiquitin-ligase, as well as ubiquitin and proteasomes onto PML nuclear bodies.	Arsenic	16-23	ubiquitin	Saccharomyces cerevisiae S288C	107-116
18408733-4	2008	When exposed to arsenic, SUMOylated PML recruits RNF4, the human orthologue of the yeast SUMO-dependent E3 ubiquitin-ligase, as well as ubiquitin and proteasomes onto PML nuclear bodies.	Arsenic	16-23	ubiquitin	Saccharomyces cerevisiae S288C	136-145
18408733-4	2008	When exposed to arsenic, SUMOylated PML recruits RNF4, the human orthologue of the yeast SUMO-dependent E3 ubiquitin-ligase, as well as ubiquitin and proteasomes onto PML nuclear bodies.	Arsenic	16-23	PML nuclear body scaffold	Homo sapiens	167-170
18408733-5	2008	Arsenic-induced differentiation is impaired in cells transformed by a non-degradable PML-RARalpha SUMOylation mutant or in APL cells transduced with a dominant-negative RNF4, directly implicating PML-RARalpha catabolism in the therapeutic response.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	85-88
18408733-5	2008	Arsenic-induced differentiation is impaired in cells transformed by a non-degradable PML-RARalpha SUMOylation mutant or in APL cells transduced with a dominant-negative RNF4, directly implicating PML-RARalpha catabolism in the therapeutic response.	Arsenic	0-7	retinoic acid receptor alpha	Homo sapiens	89-97
18408733-5	2008	Arsenic-induced differentiation is impaired in cells transformed by a non-degradable PML-RARalpha SUMOylation mutant or in APL cells transduced with a dominant-negative RNF4, directly implicating PML-RARalpha catabolism in the therapeutic response.	Arsenic	0-7	ring finger protein 4	Homo sapiens	169-173
18408733-5	2008	Arsenic-induced differentiation is impaired in cells transformed by a non-degradable PML-RARalpha SUMOylation mutant or in APL cells transduced with a dominant-negative RNF4, directly implicating PML-RARalpha catabolism in the therapeutic response.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	196-199
18408733-5	2008	Arsenic-induced differentiation is impaired in cells transformed by a non-degradable PML-RARalpha SUMOylation mutant or in APL cells transduced with a dominant-negative RNF4, directly implicating PML-RARalpha catabolism in the therapeutic response.	Arsenic	0-7	retinoic acid receptor alpha	Homo sapiens	200-208
18408734-0	2008	RNF4 is a poly-SUMO-specific E3 ubiquitin ligase required for arsenic-induced PML degradation.	Arsenic	62-69	ring finger protein 4	Homo sapiens	0-4
18408734-0	2008	RNF4 is a poly-SUMO-specific E3 ubiquitin ligase required for arsenic-induced PML degradation.	Arsenic	62-69	PML nuclear body scaffold	Homo sapiens	78-81
18408734-2	2008	This disease can be treated effectively with arsenic, which induces PML modification by small ubiquitin-like modifiers (SUMO) and proteasomal degradation.	Arsenic	45-52	PML nuclear body scaffold	Homo sapiens	68-71
18414623-0	2008	Transformation of human urothelial cells (UROtsa) by as and cd induces the expression of keratin 6a.	Arsenic	53-55	keratin 6A	Homo sapiens	89-99
18199464-9	2008	Our preliminary results showed the XRCC1 Arg194Trp were associated with arsenic-related urinary TCC and the interaction between the genotype and the exposure was statistically significant.	Arsenic	72-79	X-ray repair cross complementing 1	Homo sapiens	35-40
18213641-9	2008	Exposure to arsenic compounds, chlorophenols, diesel fuel, herbicides, nitrites/nitrates/nitrosamines, and organic dusts were associated with NHL(high) and NHL(low), while exhibiting little association with CLL.	Arsenic	12-19	regulator of telomere elongation helicase 1	Homo sapiens	142-145
18213641-9	2008	Exposure to arsenic compounds, chlorophenols, diesel fuel, herbicides, nitrites/nitrates/nitrosamines, and organic dusts were associated with NHL(high) and NHL(low), while exhibiting little association with CLL.	Arsenic	12-19	regulator of telomere elongation helicase 1	Homo sapiens	156-164
18157160-8	2008	Alteration of TRX1 from its reduced form to oxidized form in vivo by 2,4-dinitrochlorobenzene (DNCB), a specific inhibitor of TRX reductase, also sensitized HepG(2) cells to As(2)O(3)-induced apoptosis.	Arsenic	174-176	thioredoxin	Homo sapiens	14-18
18414634-2	2008	Metabolism of arsenic proceeds through sequential reduction and oxidative methylation being mediated by the following genes: purine nucleoside phosphorylase (PNP), arsenic (+3) methyltransferase (As3MT), glutathione S-transferase omega 1 (GSTO1), and omega 2 (GSTO2).	Arsenic	14-21	purine nucleoside phosphorylase	Homo sapiens	158-161
18414634-2	2008	Metabolism of arsenic proceeds through sequential reduction and oxidative methylation being mediated by the following genes: purine nucleoside phosphorylase (PNP), arsenic (+3) methyltransferase (As3MT), glutathione S-transferase omega 1 (GSTO1), and omega 2 (GSTO2).	Arsenic	14-21	arsenite methyltransferase	Homo sapiens	196-201
18414634-2	2008	Metabolism of arsenic proceeds through sequential reduction and oxidative methylation being mediated by the following genes: purine nucleoside phosphorylase (PNP), arsenic (+3) methyltransferase (As3MT), glutathione S-transferase omega 1 (GSTO1), and omega 2 (GSTO2).	Arsenic	14-21	glutathione S-transferase omega 1	Homo sapiens	204-237
18414634-2	2008	Metabolism of arsenic proceeds through sequential reduction and oxidative methylation being mediated by the following genes: purine nucleoside phosphorylase (PNP), arsenic (+3) methyltransferase (As3MT), glutathione S-transferase omega 1 (GSTO1), and omega 2 (GSTO2).	Arsenic	14-21	glutathione S-transferase omega 1	Homo sapiens	239-244
18414634-2	2008	Metabolism of arsenic proceeds through sequential reduction and oxidative methylation being mediated by the following genes: purine nucleoside phosphorylase (PNP), arsenic (+3) methyltransferase (As3MT), glutathione S-transferase omega 1 (GSTO1), and omega 2 (GSTO2).	Arsenic	14-21	glutathione S-transferase omega 2	Homo sapiens	260-265
18414634-3	2008	PNP functions as arsenate reductase; As3MT methylates inorganic arsenic and its metabolites; and both GSTO1 and GSTO2 reduce the metabolites.	Arsenic	64-71	purine nucleoside phosphorylase	Homo sapiens	0-3
18414634-3	2008	PNP functions as arsenate reductase; As3MT methylates inorganic arsenic and its metabolites; and both GSTO1 and GSTO2 reduce the metabolites.	Arsenic	64-71	arsenite methyltransferase	Homo sapiens	37-42
18414634-10	2008	CONCLUSIONS: The results indicate that the three PNP variants render individuals susceptible toward developing arsenic-induced skin lesions.	Arsenic	111-118	purine nucleoside phosphorylase	Homo sapiens	49-52
18272248-8	2008	Inhibition of caspase-3 inhibited the early phase of ALR-AS-induced death but not the late phase that included ALR and LDH release.	Arsenic	57-59	caspase 3	Rattus norvegicus	14-23
18272248-8	2008	Inhibition of caspase-3 inhibited the early phase of ALR-AS-induced death but not the late phase that included ALR and LDH release.	Arsenic	57-59	growth factor, augmenter of liver regeneration	Rattus norvegicus	53-56
18334919-3	2008	Thus, genetic variations in the AS3MT gene could explain, at least partly, the interindividual variation in the response to arsenic exposure.	Arsenic	124-131	arsenite methyltransferase	Homo sapiens	32-37
18334919-4	2008	In an earlier study, we have demonstrated that the AS3MT Met(287)Thr (C/T) polymorphism affected the urinary arsenic profile in a Chilean group of men (n=50) occupationally exposed to arsenic.	Arsenic	109-116	arsenite methyltransferase	Homo sapiens	51-56
18334919-4	2008	In an earlier study, we have demonstrated that the AS3MT Met(287)Thr (C/T) polymorphism affected the urinary arsenic profile in a Chilean group of men (n=50) occupationally exposed to arsenic.	Arsenic	184-191	arsenite methyltransferase	Homo sapiens	51-56
18174314-6	2008	Upon exposure to heat and arsenic stress, PCBP2 became predominantly accumulated at the SG, but was still present in Dcp1a-positive P-bodies.	Arsenic	26-33	poly(rC) binding protein 2	Homo sapiens	42-47
18182400-10	2008	Differential effects of selective PKC inhibitors on induced gene expression combined with a lack of interaction for induction of hemeoxygenase-1 further demonstrated that arsenic-responsive signaling pathways differ in sensitivity to EtOH interactions.	Arsenic	171-178	protein kinase C delta	Homo sapiens	34-37
18296743-7	2008	Arsenic exposure increased the expression of inflammation genes, such as TNF-alpha, IL-6, iNOS, chemokines, and macrophage inflammatory protein-2.	Arsenic	0-7	tumor necrosis factor	Mus musculus	73-82
18296743-7	2008	Arsenic exposure increased the expression of inflammation genes, such as TNF-alpha, IL-6, iNOS, chemokines, and macrophage inflammatory protein-2.	Arsenic	0-7	interleukin 6	Mus musculus	84-88
18296743-7	2008	Arsenic exposure increased the expression of inflammation genes, such as TNF-alpha, IL-6, iNOS, chemokines, and macrophage inflammatory protein-2.	Arsenic	0-7	chemokine (C-X-C motif) ligand 2	Mus musculus	112-145
18296743-8	2008	The expression of the stress-related gene heme oxygenase-1 was increased, while metallothionein-1 and GSH S-transferase-pi were decreased when arsenic was combined with the high fat diet.	Arsenic	143-150	heme oxygenase 1	Mus musculus	42-58
18296743-8	2008	The expression of the stress-related gene heme oxygenase-1 was increased, while metallothionein-1 and GSH S-transferase-pi were decreased when arsenic was combined with the high fat diet.	Arsenic	143-150	metallothionein 1	Mus musculus	80-97
18242949-0	2008	Mechanism of arsenic-induced neurotoxicity may be explained through cleavage of p35 to p25 by calpain.	Arsenic	13-20	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	80-83
18242949-0	2008	Mechanism of arsenic-induced neurotoxicity may be explained through cleavage of p35 to p25 by calpain.	Arsenic	13-20	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	87-90
18242949-2	2008	To further examine the mechanism of arsenic-induced neurotoxicity with various arsenate metabolites (iAsV, MMAV and DMAV) and arsenite metabolites (iAsIII, MMAIII and DMAIII), we investigated the role of the proteolytic enzyme calpain and its involvement in the cleavage of p35 protein to p25, and also mRNA expression levels of calpain, cyclin-dependent kinase 5 (cdk5) and glycogen synthase kinase 3 beta (gsk3ss).	Arsenic	36-43	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	274-277
18242949-2	2008	To further examine the mechanism of arsenic-induced neurotoxicity with various arsenate metabolites (iAsV, MMAV and DMAV) and arsenite metabolites (iAsIII, MMAIII and DMAIII), we investigated the role of the proteolytic enzyme calpain and its involvement in the cleavage of p35 protein to p25, and also mRNA expression levels of calpain, cyclin-dependent kinase 5 (cdk5) and glycogen synthase kinase 3 beta (gsk3ss).	Arsenic	36-43	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	289-292
18242949-2	2008	To further examine the mechanism of arsenic-induced neurotoxicity with various arsenate metabolites (iAsV, MMAV and DMAV) and arsenite metabolites (iAsIII, MMAIII and DMAIII), we investigated the role of the proteolytic enzyme calpain and its involvement in the cleavage of p35 protein to p25, and also mRNA expression levels of calpain, cyclin-dependent kinase 5 (cdk5) and glycogen synthase kinase 3 beta (gsk3ss).	Arsenic	36-43	cyclin dependent kinase 5	Homo sapiens	338-363
18242949-2	2008	To further examine the mechanism of arsenic-induced neurotoxicity with various arsenate metabolites (iAsV, MMAV and DMAV) and arsenite metabolites (iAsIII, MMAIII and DMAIII), we investigated the role of the proteolytic enzyme calpain and its involvement in the cleavage of p35 protein to p25, and also mRNA expression levels of calpain, cyclin-dependent kinase 5 (cdk5) and glycogen synthase kinase 3 beta (gsk3ss).	Arsenic	36-43	cyclin dependent kinase 5	Homo sapiens	365-369
18242949-2	2008	To further examine the mechanism of arsenic-induced neurotoxicity with various arsenate metabolites (iAsV, MMAV and DMAV) and arsenite metabolites (iAsIII, MMAIII and DMAIII), we investigated the role of the proteolytic enzyme calpain and its involvement in the cleavage of p35 protein to p25, and also mRNA expression levels of calpain, cyclin-dependent kinase 5 (cdk5) and glycogen synthase kinase 3 beta (gsk3ss).	Arsenic	36-43	glycogen synthase kinase 3 beta	Homo sapiens	375-406
18242949-8	2008	These results suggest that cleavage of p35 to p25 by calpain, probably As-induced Ca2+-influx, may explain the mechanism by which arsenic induces its neurotoxic effects.	Arsenic	130-137	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	39-42
18242949-8	2008	These results suggest that cleavage of p35 to p25 by calpain, probably As-induced Ca2+-influx, may explain the mechanism by which arsenic induces its neurotoxic effects.	Arsenic	130-137	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	46-49
17697749-1	2008	An enhanced electrokinetic remediation process for removal of arsenic, presented as As(V) form, from spiked soil has been investigated with groundwater (GW) and chemical reagents of cetylpyridinium chloride (CPC, a cationic surfactant), ethylenediaminetetraacetic acid (EDTA) and citric acid (CA) under potential gradient of 2.0-3.3V/cm for 5 days treatment.	Arsenic	62-69	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	84-89
18191166-1	2008	Chronic drinking water exposure to inorganic arsenic and its metabolites increases tumor frequency in the skin of K6/ODC transgenic mice.	Arsenic	45-52	keratin 6	Mus musculus	114-120
18028863-1	2008	Glutathione transferase omega 1-1 (GSTO1-1) catalyzes the biotransformation of arsenic and is implicated as a factor influencing the age-at-onset of Alzheimer"s disease and the posttranslational activation of interleukin 1beta (IL-1beta).	Arsenic	79-86	glutathione S-transferase omega 1	Homo sapiens	35-42
18028863-1	2008	Glutathione transferase omega 1-1 (GSTO1-1) catalyzes the biotransformation of arsenic and is implicated as a factor influencing the age-at-onset of Alzheimer"s disease and the posttranslational activation of interleukin 1beta (IL-1beta).	Arsenic	79-86	interleukin 1 beta	Homo sapiens	209-226
18028863-1	2008	Glutathione transferase omega 1-1 (GSTO1-1) catalyzes the biotransformation of arsenic and is implicated as a factor influencing the age-at-onset of Alzheimer"s disease and the posttranslational activation of interleukin 1beta (IL-1beta).	Arsenic	79-86	interleukin 1 beta	Homo sapiens	228-236
18247522-10	2008	Furthermore, this new arsenic peak was consistent with the As-BP identified in the plasma in vivo, suggesting that arsenic bound to Hb further binds to haptoglobin (Hp), forming the ternary As-Hb-Hp complex.	Arsenic	22-29	par-3 family cell polarity regulator	Rattus norvegicus	59-64
18247522-10	2008	Furthermore, this new arsenic peak was consistent with the As-BP identified in the plasma in vivo, suggesting that arsenic bound to Hb further binds to haptoglobin (Hp), forming the ternary As-Hb-Hp complex.	Arsenic	22-29	haptoglobin	Rattus norvegicus	152-163
18247522-10	2008	Furthermore, this new arsenic peak was consistent with the As-BP identified in the plasma in vivo, suggesting that arsenic bound to Hb further binds to haptoglobin (Hp), forming the ternary As-Hb-Hp complex.	Arsenic	115-122	par-3 family cell polarity regulator	Rattus norvegicus	59-64
18247522-10	2008	Furthermore, this new arsenic peak was consistent with the As-BP identified in the plasma in vivo, suggesting that arsenic bound to Hb further binds to haptoglobin (Hp), forming the ternary As-Hb-Hp complex.	Arsenic	115-122	haptoglobin	Rattus norvegicus	152-163
18174314-6	2008	Upon exposure to heat and arsenic stress, PCBP2 became predominantly accumulated at the SG, but was still present in Dcp1a-positive P-bodies.	Arsenic	26-33	decapping mRNA 1A	Homo sapiens	117-122
18199454-4	2008	We found that the light-induced reduction in D occurs in transducers of lengths 120 and 157 residues (Tr120 and Tr157), which are both predicted to contain a HAMP domain consisting of two amphipathic alpha-helices (AS-1 and AS-2).	Arsenic	215-217	hepcidin antimicrobial peptide	Homo sapiens	158-162
18177893-5	2008	cdr-4 expression is induced by arsenic, cadmium, mercury, and zinc exposure as well as by hypotonic stress.	Arsenic	31-38	CaDmium Responsive	Caenorhabditis elegans	0-5
18022660-0	2008	Risk of carotid atherosclerosis associated with genetic polymorphisms of apolipoprotein E and inflammatory genes among arsenic exposed residents in Taiwan.	Arsenic	119-126	apolipoprotein E	Homo sapiens	73-89
18685814-0	2008	The minimal arsenic concentration required to inhibit the activity of thyroid peroxidase activity in vitro.	Arsenic	12-19	thyroid peroxidase	Homo sapiens	70-88
17570581-11	2008	When the complete breakthrough of total arsenic occurred, the total arsenic removed by 1 kg of MCS was 79.0 mg, suggesting MCS acts as an adsorbent for As(V), as well as an oxidant for As(III).	Arsenic	40-47	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	152-157
17626301-0	2008	Enhanced arsenic accumulation by engineered yeast cells expressing Arabidopsis thaliana phytochelatin synthase.	Arsenic	9-16	phytochelatin synthase 1 (PCS1)	Arabidopsis thaliana	88-110
17626301-3	2008	In this study, PCs were introduced by expressing Arabidopsis thaliana Phytochelatin Synthase (AtPCS) in the yeast Saccharomyces cerevisiae for enhanced As accumulation and removal.	Arsenic	152-154	phytochelatin synthase 1 (PCS1)	Arabidopsis thaliana	70-92
17976671-2	2008	We believe that arsenic will enhance the expression of hepatic CYP2A enzyme and NNK metabolism (a cigarette smoke component), thus its metabolites, and carcinogenic DNA adducts.	Arsenic	16-23	cytochrome P450, family 2, subfamily a	Mus musculus	63-68
17976671-5	2008	Both the cyp2a4/5 mRNA levels and the CYP2A enzyme activity were significantly elevated in arsenic-treated mice liver.	Arsenic	91-98	cytochrome P450, family 2, subfamily a, polypeptide 4	Mus musculus	9-15
17976671-5	2008	Both the cyp2a4/5 mRNA levels and the CYP2A enzyme activity were significantly elevated in arsenic-treated mice liver.	Arsenic	91-98	cytochrome P450, family 2, subfamily a	Mus musculus	38-43
17976671-8	2008	Our findings provide clear evidence that arsenic increased NNK metabolism by up-regulation of CYP2A expression and activity leading to an increased NNK metabolism and DNA adducts (N(7)-methylguanine and O(6)-methylguanine).	Arsenic	41-48	cytochrome P450, family 2, subfamily a	Mus musculus	94-99
18288313-0	2008	Arsenic as an endocrine disruptor: arsenic disrupts retinoic acid receptor-and thyroid hormone receptor-mediated gene regulation and thyroid hormone-mediated amphibian tail metamorphosis.	Arsenic	0-7	nuclear receptor subfamily 4 group A member 1	Homo sapiens	87-103
18288313-0	2008	Arsenic as an endocrine disruptor: arsenic disrupts retinoic acid receptor-and thyroid hormone receptor-mediated gene regulation and thyroid hormone-mediated amphibian tail metamorphosis.	Arsenic	35-42	nuclear receptor subfamily 4 group A member 1	Homo sapiens	87-103
18288317-3	2008	OBJECTIVES: We examined the relationship of the serum level of Clara cell protein CC16--a novel biomarker for respiratory illnesses--with well As, total urinary As, and urinary As methylation indices.	Arsenic	143-145	secretoglobin family 1A member 1	Homo sapiens	82-86
18288317-6	2008	RESULTS: We observed an inverse association between urinary As and serum CC16 among persons with skin lesions (beta = -0.13, p = 0.01).	Arsenic	60-62	secretoglobin family 1A member 1	Homo sapiens	73-77
18288317-7	2008	We also observed a positive association between secondary methylation index in urinary As and CC16 levels (beta = 0.12, p = 0.05) in the overall study population; the association was stronger among people without skin lesions (beta = 0.18, p = 0.04), indicating that increased methylation capability may be protective against As-induced respiratory damage.	Arsenic	87-89	secretoglobin family 1A member 1	Homo sapiens	94-98
18288317-7	2008	We also observed a positive association between secondary methylation index in urinary As and CC16 levels (beta = 0.12, p = 0.05) in the overall study population; the association was stronger among people without skin lesions (beta = 0.18, p = 0.04), indicating that increased methylation capability may be protective against As-induced respiratory damage.	Arsenic	326-328	secretoglobin family 1A member 1	Homo sapiens	94-98
18288323-8	2008	Cox"s regression models were used to analyze possible relationships between arsenic and cancer.	Arsenic	76-83	cytochrome c oxidase subunit 8A	Homo sapiens	0-3
18218843-5	2008	Real-time RT-PCR analysis showed that the levels of IGF-I and IGF binding protein (IGFBP)3 mRNAs in the AS-ODN group were significantly decreased.	Arsenic	104-106	insulin-like growth factor 1	Rattus norvegicus	52-57
18218843-5	2008	Real-time RT-PCR analysis showed that the levels of IGF-I and IGF binding protein (IGFBP)3 mRNAs in the AS-ODN group were significantly decreased.	Arsenic	104-106	insulin-like growth factor binding protein 3	Rattus norvegicus	83-90
17822735-2	2008	Removal of arsenic (III) (As(III)) and arsenic (V) (As(V)) was studied through adsorption on the biosorbent at pH 4.0 under equilibrium and dynamic conditions.	Arsenic	11-18	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	52-57
17822735-2	2008	Removal of arsenic (III) (As(III)) and arsenic (V) (As(V)) was studied through adsorption on the biosorbent at pH 4.0 under equilibrium and dynamic conditions.	Arsenic	39-46	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	52-57
17822735-6	2008	The difference in adsorption capacity for As(III) and As(V) was explained on the basis of speciation of arsenic at pH 4.0.	Arsenic	104-111	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	54-59
18685814-4	2008	The results of this study indicate a significant dose-response relationship with the highest concentration of arsenic producing the greatest amount of TPO inhibition.	Arsenic	110-117	thyroid peroxidase	Homo sapiens	151-154
18685814-6	2008	Incubation for 2 min in the presence of 1.0, 5.0, or 10 ppm arsenic inhibited TPO activity to 4%, 9%, and 9% of control, respectively.	Arsenic	60-67	thyroid peroxidase	Homo sapiens	78-81
18685814-7	2008	After 10 min incubation in the presence of 1.0 or 5.0 ppm arsenic, TPO activity returned to 92% and 54% of control, respectively, while the presence of 10 ppm arsenic further inhibited TPO activity to 1% of control.	Arsenic	58-65	thyroid peroxidase	Homo sapiens	67-70
18685814-7	2008	After 10 min incubation in the presence of 1.0 or 5.0 ppm arsenic, TPO activity returned to 92% and 54% of control, respectively, while the presence of 10 ppm arsenic further inhibited TPO activity to 1% of control.	Arsenic	58-65	thyroid peroxidase	Homo sapiens	185-188
18685814-7	2008	After 10 min incubation in the presence of 1.0 or 5.0 ppm arsenic, TPO activity returned to 92% and 54% of control, respectively, while the presence of 10 ppm arsenic further inhibited TPO activity to 1% of control.	Arsenic	159-166	thyroid peroxidase	Homo sapiens	185-188
18685814-3	2008	The activity of commercially prepared human TPO was assayed spectrophotometrically in the absence (control) or presence of arsenic (0.1, 1.0, 5.0, and 10 ppm) during a 10-min incubation period.	Arsenic	123-130	thyroid peroxidase	Homo sapiens	44-47
18172319-2	2008	Whereas TRAIL-mediated proteolytic processing of procaspase-3 was partially blocked in glioma cells, treatment with As(2)O(3) efficiently recovered TRAIL-induced activation of caspases.	Arsenic	116-118	TNF superfamily member 10	Homo sapiens	148-153
18571971-1	2008	The Omega class glutathione transferase GSTO1-1 can catalyze the reduction of pentavalent methylated arsenic species and is responsible for the biotransfomation of potentially toxic alpha-haloketones.	Arsenic	101-108	glutathione S-transferase omega 1	Homo sapiens	40-47
18571971-8	2008	In this study GSTO1-1 deficient T47-D cells were used to determine if GSTO1-1 contributes directly to arsenic and drug resistance.	Arsenic	102-109	glutathione S-transferase omega 1	Homo sapiens	70-77
19013355-6	2008	Generation of reactive oxygen species, accumulation of Ca(2+), upregulation of caspase-3, down regulation of bcl-2, and deficiency of p-53 lead to arsenic-induced apoptosis.	Arsenic	147-154	caspase 3	Homo sapiens	79-88
19209639-1	2008	Microbial reduction of As(V) (i.e., arsenate) plays an important role in arsenic (As) mobilization in aqueous environment.	Arsenic	73-80	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	23-28
19209639-2	2008	In this study, we investigated As(V) reduction characteristics of the bacteria enriched from the arsenic-contaminated soil at an abandoned smelter site.	Arsenic	97-104	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	31-36
19209639-9	2008	53% of the adsorbed As(V) was reduced to As(III) by the bacteria, which resulted in an appreciable release of arsenic into aqueous phase.	Arsenic	110-117	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	20-25
18569616-0	2008	Arsenic enhances matrix metalloproteinase-14 expression in fibroblasts.	Arsenic	0-7	matrix metallopeptidase 14	Homo sapiens	17-44
18569616-1	2008	This study focused on the effects of arsenic (As) on fibroblast-derived matrix metalloproteinase (MMP)-2 and -14 levels, as these proteins were reported to be associated with tumor progression.	Arsenic	37-44	matrix metallopeptidase 2	Homo sapiens	72-112
18569616-1	2008	This study focused on the effects of arsenic (As) on fibroblast-derived matrix metalloproteinase (MMP)-2 and -14 levels, as these proteins were reported to be associated with tumor progression.	Arsenic	46-48	matrix metallopeptidase 2	Homo sapiens	72-112
18569616-2	2008	Arsenic was found to promote production of the fibroblast-derived active form of MMP-2.	Arsenic	0-7	matrix metallopeptidase 2	Homo sapiens	81-86
19013355-6	2008	Generation of reactive oxygen species, accumulation of Ca(2+), upregulation of caspase-3, down regulation of bcl-2, and deficiency of p-53 lead to arsenic-induced apoptosis.	Arsenic	147-154	BCL2 apoptosis regulator	Homo sapiens	109-114
19013355-6	2008	Generation of reactive oxygen species, accumulation of Ca(2+), upregulation of caspase-3, down regulation of bcl-2, and deficiency of p-53 lead to arsenic-induced apoptosis.	Arsenic	147-154	tumor protein p53	Homo sapiens	134-138
18216717-1	2008	OBJECTIVES AND METHODS: The aim of this study was to investigate genetic variation in glutathione transferase omega 1 (GSTO1-1) in Atacamenos, an indigenous population from Chile that has been exposed to environmental arsenic for many generations.	Arsenic	218-225	glutathione S-transferase omega 1	Homo sapiens	119-126
18037969-5	2008	In addition, arsenic-treated cells showed an increase in c-H-ras, c-myc, and c-fos protein expression relative to controls.	Arsenic	13-20	HRas proto-oncogene, GTPase	Homo sapiens	57-64
18037969-5	2008	In addition, arsenic-treated cells showed an increase in c-H-ras, c-myc, and c-fos protein expression relative to controls.	Arsenic	13-20	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	66-71
18037969-5	2008	In addition, arsenic-treated cells showed an increase in c-H-ras, c-myc, and c-fos protein expression relative to controls.	Arsenic	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	77-82
18037969-7	2008	Taken together, these results strongly suggest that h-TERT immortalized human small airway epithelial cells underwent step-wise transformation after inorganic arsenic treatment.	Arsenic	159-166	telomerase reverse transcriptase	Homo sapiens	54-58
19189537-4	2008	The aim of this research was to assess the influence of occupational exposure of copper-foundry workers to heavy metals (arsenic, cadmium, lead) on total activity of N-acetyl-beta-D-glucosaminidase and its molecular forms in urine.	Arsenic	121-128	O-GlcNAcase	Homo sapiens	166-197
19189537-14	2008	It was confirmed, that the activity of N-acetyl-beta-D-glucosaminidase is a good factor in the assessment of occupational exposure to heavy metals like arsenic, cadmium and lead.	Arsenic	152-159	O-GlcNAcase	Homo sapiens	39-70
18421855-5	2008	-SH in sulfhydryl compound, could play an important role in the reduction of As(V), and at the concentration of 60 mmol/L -SH (both GSH and Cys) could reduce 60%, of As(V) to As(III) for 30 min.	Arsenic	77-79	helicase, lymphoid specific	Homo sapiens	120-125
20467584-0	2008	Environmental arsenic as a disruptor of insulin signaling.	Arsenic	14-21	insulin	Homo sapiens	40-47
17850829-0	2008	Role of the Met(287)Thr polymorphism in the AS3MT gene on the metabolic arsenic profile.	Arsenic	72-79	arsenite methyltransferase	Homo sapiens	44-49
17850829-3	2008	Coding and flanking regions of the human arsenic methyltransferase (AS3MT) gene have been analysed in 50 Chilean men exposed to arsenic.	Arsenic	41-48	arsenite methyltransferase	Homo sapiens	68-73
17850829-8	2008	Our results indicate that genetic polymorphisms in AS3MT contribute to inter-individual variation in arsenic biotransformation and, therefore, may contribute to inter-individual variations in risk of arsenic toxicity and arsenic carcinogenesis.	Arsenic	101-108	arsenite methyltransferase	Homo sapiens	51-56
18231637-6	2008	Overactivation of RhoA by transfection with the V14RhoA mutant prevented gastric cancer line SGC-7901 cells from arsenic-induced apoptosis and conferred anoikis resistance through, at least in part, promoting formations of F-actin fibers and focal adhesion.	Arsenic	113-120	ras homolog family member A	Homo sapiens	18-22
18231637-6	2008	Overactivation of RhoA by transfection with the V14RhoA mutant prevented gastric cancer line SGC-7901 cells from arsenic-induced apoptosis and conferred anoikis resistance through, at least in part, promoting formations of F-actin fibers and focal adhesion.	Arsenic	113-120	ras homolog family member A	Homo sapiens	51-55
18982996-20	2008	Historical arsenic contamination exists in Cornwall, UK; an example of a recent arsenic pollution event is that of Ron Phibun town in southern Thailand, where arsenic-related human health effects have been reported.	Arsenic	80-87	macrophage stimulating 1 receptor	Homo sapiens	115-118
18982996-20	2008	Historical arsenic contamination exists in Cornwall, UK; an example of a recent arsenic pollution event is that of Ron Phibun town in southern Thailand, where arsenic-related human health effects have been reported.	Arsenic	80-87	macrophage stimulating 1 receptor	Homo sapiens	115-118
18824809-3	2008	After As(III) oxidation to arsenate, As(V), arsenic is easily removable from contaminated groundwater because As(V) is more adsorptive to absorbents than As(III).	Arsenic	44-51	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	37-42
18824809-3	2008	After As(III) oxidation to arsenate, As(V), arsenic is easily removable from contaminated groundwater because As(V) is more adsorptive to absorbents than As(III).	Arsenic	44-51	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	110-115
18824809-7	2008	Arsenic removal by activated alumina was greatly enhanced by bacterial oxidation of As(III) to As(V).	Arsenic	0-7	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	95-100
18216717-2	2008	GSTO1-1 is thought to catalyse the rate-limiting step in the biotransformation of arsenic in humans and may modulate the response of cancer patients to arsenic trioxide therapy.	Arsenic	82-89	glutathione S-transferase omega 1	Homo sapiens	0-7
18161919-10	2007	The fluorescence intensity levels of Flt-1 and KDR were significantly less in the arsenic-treated mice than in the control group.	Arsenic	82-89	FMS-like tyrosine kinase 1	Mus musculus	37-42
18161919-10	2007	The fluorescence intensity levels of Flt-1 and KDR were significantly less in the arsenic-treated mice than in the control group.	Arsenic	82-89	kinase insert domain protein receptor	Mus musculus	47-50
17889916-3	2007	Recently, a single nucleotide polymorphism (SNPs; rs17885947, M287T (T860C)) in the AS3MT gene was shown to be related to enzyme activity and considered to be related to genetic susceptibility to arsenic.	Arsenic	196-203	arsenite methyltransferase	Homo sapiens	84-89
17688991-12	2007	Furthermore, CYP4A might be more important than ACE in contributing to arsenic-induced hypertension.	Arsenic	71-78	angiotensin I converting enzyme	Rattus norvegicus	48-51
18053222-0	2007	GSTM1 and APE1 genotypes affect arsenic-induced oxidative stress: a repeated measures study.	Arsenic	32-39	glutathione S-transferase mu 1	Homo sapiens	0-5
18053222-0	2007	GSTM1 and APE1 genotypes affect arsenic-induced oxidative stress: a repeated measures study.	Arsenic	32-39	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	10-14
18053222-8	2007	RESULTS: A consistent negative effect for APE1 was observed across water, toenail and urinary arsenic models.	Arsenic	94-101	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	42-46
18053222-10	2007	An association between total urinary arsenic and 8-OHdG was observed among women with the GSTM1 null genotype but not in women with GSTM1 positive.	Arsenic	37-44	glutathione S-transferase mu 1	Homo sapiens	90-95
18053222-11	2007	Among women with GSTM1 null, a comparison of the second, third, and fourth quartiles of total urinary arsenic to the first quartile resulted in a 0.84 increase (95% CI 0.27, 1.42), a 0.98 increase (95% CI 033, 1.66) and a 0.85 increase (95% CI 0.27, 1.44) in logged 8-OHdG, respectively.	Arsenic	102-109	glutathione S-transferase mu 1	Homo sapiens	17-22
18053222-13	2007	CONCLUSION: These results suggest the APE1 variant genotype decreases repair of 8-OHdG and that arsenic exposure is associated with oxidative stress in women who lack a functional GSTM1 detoxification enzyme.	Arsenic	96-103	glutathione S-transferase mu 1	Homo sapiens	180-185
17765279-8	2007	These results, obtained by both loss of function and gain of function analyses, clearly demonstrate the protective role of Nrf2 in arsenic-induced toxicity.	Arsenic	131-138	NFE2 like bZIP transcription factor 2	Homo sapiens	123-127
17953697-5	2007	In the subset of patients from living environments which were contaminated with arsenic, there was a statistically significant association between DAPK hypermethylation and patient"s age, tumour invasiveness, histological grade and recurrence.	Arsenic	80-87	death associated protein kinase 1	Homo sapiens	147-151
17953697-8	2007	CONCLUSION: Exposure to arsenic may induce DAPK promoter hypermethylation and inactivate the function of DAPK in urothelial carcinoma.	Arsenic	24-31	death associated protein kinase 1	Homo sapiens	43-47
17953697-8	2007	CONCLUSION: Exposure to arsenic may induce DAPK promoter hypermethylation and inactivate the function of DAPK in urothelial carcinoma.	Arsenic	24-31	death associated protein kinase 1	Homo sapiens	105-109
17624716-9	2007	Besides, taurine administration normalized the arsenic-induced enhanced levels of the marker enzymes ALT and ALP in hepatocytes.	Arsenic	47-54	glutamic pyruvic transaminase, soluble	Mus musculus	101-104
17953697-0	2007	Urothelial carcinomas arising in arsenic-contaminated areas are associated with hypermethylation of the gene promoter of the death-associated protein kinase.	Arsenic	33-40	death associated protein kinase 1	Homo sapiens	125-156
17953697-2	2007	The aim was to determine whether hypermethylation of death-associated protein kinase (DAPK) gene is associated with chronic arsenic exposure.	Arsenic	124-131	death associated protein kinase 1	Homo sapiens	53-84
17953697-2	2007	The aim was to determine whether hypermethylation of death-associated protein kinase (DAPK) gene is associated with chronic arsenic exposure.	Arsenic	124-131	death associated protein kinase 1	Homo sapiens	86-90
17953697-4	2007	DAPK hypermethylation status was significantly higher in urothelial cancers arising in arsenic-contaminated areas when compared with tumours from patients from non-contaminated areas (P = 0.018).	Arsenic	87-94	death associated protein kinase 1	Homo sapiens	0-4
17936320-5	2007	Arsenic affects insulin sensitivity in peripheral tissue by modifying the expression of genes involved in insulin resistance and shifting away cells from differentiation to the proliferation pathway.	Arsenic	0-7	insulin	Homo sapiens	16-23
17765279-9	2007	The current work lays the groundwork for using Nrf2 activators for therapeutic and dietary interventions against adverse effects of arsenic.	Arsenic	132-139	NFE2 like bZIP transcription factor 2	Homo sapiens	47-51
17936320-5	2007	Arsenic affects insulin sensitivity in peripheral tissue by modifying the expression of genes involved in insulin resistance and shifting away cells from differentiation to the proliferation pathway.	Arsenic	0-7	insulin	Homo sapiens	106-113
17660305-7	2007	Comparative analysis of the Saccharomyces cerevisiae SEO1 (ScSEO1) promoter revealed that the ScSEO1 promoter has a broader specificity for heavy metals and is responsive to arsenic and mercury in addition to Cd.	Arsenic	174-181	putative permease SEO1	Saccharomyces cerevisiae S288C	53-57
17945324-0	2007	Arsenic promotes centrosome abnormalities and cell colony formation in p53 compromised human lung cells.	Arsenic	0-7	tumor protein p53	Homo sapiens	71-74
17945324-11	2007	Our present investigation demonstrated that arsenic would act specifically on p53 compromised cells (either with p53 dysfunction or inhibited) to induce centrosomal abnormality and colony formation.	Arsenic	44-51	tumor protein p53	Homo sapiens	78-81
17945324-11	2007	Our present investigation demonstrated that arsenic would act specifically on p53 compromised cells (either with p53 dysfunction or inhibited) to induce centrosomal abnormality and colony formation.	Arsenic	44-51	tumor protein p53	Homo sapiens	113-116
17945324-12	2007	These findings provided strong evidence on the carcinogenic promotional role of arsenic, especially under the condition of p53 dysfunction.	Arsenic	80-87	tumor protein p53	Homo sapiens	123-126
17662298-7	2007	Arsenic adsorption in the filter from As-spiked tap water was relatively lower than that from artificial As solution because high HCO(-)(3) concentration restrained siderite dissolution and thus suppressed production of the fresh Fe oxides on the siderite grains.	Arsenic	0-7	nuclear RNA export factor 1	Homo sapiens	48-51
17928125-0	2007	Folate deficiency enhances arsenic effects on expression of genes involved in epidermal differentiation in transgenic K6/ODC mouse skin.	Arsenic	27-34	ornithine decarboxylase, structural 1	Mus musculus	121-124
17928125-9	2007	In particular, expression of markers of epidermal differentiation, e.g., loricrin, small proline rich proteins and involucrin, was significantly reduced by arsenic in the folate sufficient animals, and reduced further or at a lower arsenic dose in the folate deficient animals.	Arsenic	156-163	loricrin	Mus musculus	73-81
17961518-0	2007	Arsenic inhibits neurofilament transport and induces perikaryal accumulation of phosphorylated neurofilaments: roles of JNK and GSK-3beta.	Arsenic	0-7	mitogen-activated protein kinase 8	Mus musculus	120-123
17961518-0	2007	Arsenic inhibits neurofilament transport and induces perikaryal accumulation of phosphorylated neurofilaments: roles of JNK and GSK-3beta.	Arsenic	0-7	glycogen synthase kinase 3 beta	Mus musculus	128-137
17453351-3	2007	Arsenic exposure led to a significant depletion of blood delta-aminolevulinic acid dehydratase (ALAD) activity, hematocrit, and white blood cell (WBC) counts accompanied by small decline in blood hemoglobin level.	Arsenic	0-7	aminolevulinate, delta-, dehydratase	Mus musculus	57-94
17453351-3	2007	Arsenic exposure led to a significant depletion of blood delta-aminolevulinic acid dehydratase (ALAD) activity, hematocrit, and white blood cell (WBC) counts accompanied by small decline in blood hemoglobin level.	Arsenic	0-7	aminolevulinate, delta-, dehydratase	Mus musculus	96-100
17453351-5	2007	Liver aspartate and alanine transaminases (AST and ALT) activities also decreased significantly on arsenic exposure.	Arsenic	99-106	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	43-46
17453351-5	2007	Liver aspartate and alanine transaminases (AST and ALT) activities also decreased significantly on arsenic exposure.	Arsenic	99-106	glutamic pyruvic transaminase, soluble	Mus musculus	51-54
17950580-7	2007	Our data also demonstrate that Dpp regulates adhesion between epidermis and AS, and mediates expression of the transcription factor U-shaped in a gradient across both the AS and the epidermis.	Arsenic	76-78	decapentaplegic	Drosophila melanogaster	31-34
17950580-7	2007	Our data also demonstrate that Dpp regulates adhesion between epidermis and AS, and mediates expression of the transcription factor U-shaped in a gradient across both the AS and the epidermis.	Arsenic	171-173	decapentaplegic	Drosophila melanogaster	31-34
17950580-8	2007	In summary, we show that Dpp plays a crucial role in coordinating the activity of the AS and its interactions with the LE cells during dorsal closure.	Arsenic	86-88	decapentaplegic	Drosophila melanogaster	25-28
17658681-10	2007	Activation of the c-Jun N-terminal kinase (JNK) pathway can be critical to apoptosis and pretreatment with V-PYRRO/NO suppressed arsenic-induced JNK activation.	Arsenic	129-136	mitogen-activated protein kinase 8	Rattus norvegicus	18-41
17658681-10	2007	Activation of the c-Jun N-terminal kinase (JNK) pathway can be critical to apoptosis and pretreatment with V-PYRRO/NO suppressed arsenic-induced JNK activation.	Arsenic	129-136	mitogen-activated protein kinase 8	Rattus norvegicus	43-46
17658681-10	2007	Activation of the c-Jun N-terminal kinase (JNK) pathway can be critical to apoptosis and pretreatment with V-PYRRO/NO suppressed arsenic-induced JNK activation.	Arsenic	129-136	mitogen-activated protein kinase 8	Rattus norvegicus	145-148
17936104-3	2007	Based on this fact, a new speciation scheme for inorganic arsenic was established, which involved determining total As at pH 6.0 and As(III) at pH 10, with As(V) obtained by difference.	Arsenic	58-65	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	156-161
17588644-0	2007	Electrolytic arsenic removal for recycling of washing solutions in a remediation process of CCA-treated wood.	Arsenic	13-20	fibrillin 2	Homo sapiens	92-95
18284027-2	2007	The environmental neurotoxin arsenic has recently been linked with decreased neurofilament (NF) content in peripheral nerve.	Arsenic	29-36	neurofascin	Homo sapiens	92-94
18284027-3	2007	We examined herein, whether or not folate deprivation potentiated the impact of arsenic on NF dynamics.	Arsenic	80-87	neurofascin	Homo sapiens	91-93
18284027-4	2007	Arsenic inhibited translocation of NFs into axonal neurites in culture and increased perikaryal NF phosphoepitopes.	Arsenic	0-7	neurofascin	Homo sapiens	35-37
17952781-6	2007	Analysis of the clinical symptoms based on skin manifestations showed the levels of both IgG and IgE were significantly elevated during the initial stages while IgE were further elevated with the duration of arsenic exposure.	Arsenic	208-215	immunoglobulin heavy constant epsilon	Homo sapiens	97-100
17952781-6	2007	Analysis of the clinical symptoms based on skin manifestations showed the levels of both IgG and IgE were significantly elevated during the initial stages while IgE were further elevated with the duration of arsenic exposure.	Arsenic	208-215	immunoglobulin heavy constant epsilon	Homo sapiens	161-164
17952781-8	2007	The eosinophil counts in the patients did not differ significantly from the unexposed subjects indicating that elevated levels of serum IgE might not be due to allergic diseases, rather it could be due to direct effects of arsenic.	Arsenic	223-230	immunoglobulin heavy constant epsilon	Homo sapiens	136-139
17952781-9	2007	We found significant linear relationships between the levels of serum IgE and inorganic phosphorus (P&lt;0.05), and serum IgA levels with urinary excretion of arsenic (P&lt;0.001).	Arsenic	159-166	CD79a molecule	Homo sapiens	122-125
17934333-6	2007	Pretreatment of antisense oligodeoxynucleotide (AS) against NCX depressed this transient Ca2+ rise and raised the basal level of [Ca2+]i.	Arsenic	48-50	solute carrier family 8 member A1	Rattus norvegicus	60-63
17643460-7	2007	This correlation between our in vivo and in vitro data provides further evidence for a direct link between altered renal HKII expression and arsenic exposure.	Arsenic	141-148	hexokinase 2	Mus musculus	121-125
17643460-8	2007	Thus, our data suggest that alterations in renal HKII expression may be involved in arsenic-induced pathological conditions involving the kidney.	Arsenic	84-91	hexokinase 2	Mus musculus	49-53
17499915-7	2007	Arsenic-binding properties of two of these proteins, beta-tubulin and pyruvate kinase M2 (PKM2), were studied further in vitro and the biological consequences of this binding was evaluated.	Arsenic	0-7	pyruvate kinase M1/2	Homo sapiens	70-88
17499915-7	2007	Arsenic-binding properties of two of these proteins, beta-tubulin and pyruvate kinase M2 (PKM2), were studied further in vitro and the biological consequences of this binding was evaluated.	Arsenic	0-7	pyruvate kinase M1/2	Homo sapiens	90-94
17499915-8	2007	Binding assay with Western blotting confirmed binding of beta-tubulin and PKM2 by arsenic in a concentration-dependent manner.	Arsenic	82-89	pyruvate kinase M1/2	Homo sapiens	74-78
17499915-12	2007	In summary, this study confirmed beta-tubulin and PKM2 as arsenic-binding proteins in MCF-7 cells.	Arsenic	58-65	pyruvate kinase M1/2	Homo sapiens	50-54
17567589-0	2007	p53 response to arsenic exposure in epithelial cells: protein kinase B/Akt involvement.	Arsenic	16-23	tumor protein p53	Homo sapiens	0-3
17567589-0	2007	p53 response to arsenic exposure in epithelial cells: protein kinase B/Akt involvement.	Arsenic	16-23	AKT serine/threonine kinase 1	Homo sapiens	71-74
17567589-5	2007	To further understand the molecular mechanisms involved in the arsenic mode of action, we explored the effects of this metalloid on the activation of the phosphatidyl inositol 3-kinase (PI3K)/Ca2+/diacylglicerol dependent protein kinase/protein kinase B (PKB) signaling cascade and its repercussion in p53 activation in two epithelial cell types: primary normal human keratinocytes cultures (NHK) and the carcinoma-derived C33-A cell line.	Arsenic	63-70	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	154-184
17567589-6	2007	Although in both cell systems arsenic leads to an increase in p53 and its binding to DNA, the final outcome is different.	Arsenic	30-37	tumor protein p53	Homo sapiens	62-65
17567589-7	2007	In NHK, arsenic triggers a sustained activation of the PI3K/PKB/glycogen synthase kinase-3 beta pathway, driving the cell into a cell-differentiated stage in which the proliferation signals are turned down.	Arsenic	8-15	AKT serine/threonine kinase 1	Homo sapiens	60-63
17567589-7	2007	In NHK, arsenic triggers a sustained activation of the PI3K/PKB/glycogen synthase kinase-3 beta pathway, driving the cell into a cell-differentiated stage in which the proliferation signals are turned down.	Arsenic	8-15	glycogen synthase kinase 3 beta	Homo sapiens	64-95
17567589-8	2007	In sharp contrast, in C33-A cells, arsenic leads to a transient increase in p53 followed by a drastic reduction in its nuclear levels and an increase in cell proliferation.	Arsenic	35-42	tumor protein p53	Homo sapiens	76-79
17567589-9	2007	These findings favor the notion that p53-stage and transcriptional abilities are important to understand modifications in the proliferation-differentiation balance, an equilibrium that is severely impaired by arsenic.	Arsenic	209-216	tumor protein p53	Homo sapiens	37-40
17643460-0	2007	Increased hexokinase II expression in the renal glomerulus of mice in response to arsenic.	Arsenic	82-89	hexokinase 2	Mus musculus	10-23
17643460-4	2007	Here we report increased renal hexokinase II (HKII) expression in response to arsenic exposure both in vivo and in vitro.	Arsenic	78-85	hexokinase 2	Mus musculus	31-44
17643460-4	2007	Here we report increased renal hexokinase II (HKII) expression in response to arsenic exposure both in vivo and in vitro.	Arsenic	78-85	hexokinase 2	Mus musculus	46-50
17643460-5	2007	In our model, HKII was up-regulated in the renal glomeruli of mice exposed to low levels of arsenic (10 ppb or 50 ppb) via their drinking water for up to 21 days.	Arsenic	92-99	hexokinase 2	Mus musculus	14-18
17561435-1	2007	This study was undertaken to investigate the genotoxic interactions between the common environmental pollutants: arsenic (As), cadmium (Cd) and benzo(a)pyrene (BaP), which are known to be human carcinogens.	Arsenic	113-120	prohibitin 2	Homo sapiens	160-163
17689208-9	2007	Our data suggest that arsenic-mediated inactivation of the JAK-STAT signaling pathway might be caused by Bcl-6 interaction with JAK tyrosine kinase or STAT.	Arsenic	22-29	BCL6 transcription repressor	Homo sapiens	105-110
17687452-3	2007	OBJECTIVE: We tested whether polymorphisms in the NER genes XPA (A23G) and XPD (Asp312Asn and Lys751Gln) modify the association between arsenic and NMSC.	Arsenic	136-143	XPA, DNA damage recognition and repair factor	Homo sapiens	60-63
17922641-0	2007	Tim18, a component of the mitochondrial translocator, mediates yeast cell death induced by arsenic.	Arsenic	91-98	Tim18p	Saccharomyces cerevisiae S288C	0-5
17922641-6	2007	These results suggest that Tim18 is important for yeast cell death induced by arsenic, and it may act downstream of ROS production.	Arsenic	78-85	Tim18p	Saccharomyces cerevisiae S288C	27-32
17687452-3	2007	OBJECTIVE: We tested whether polymorphisms in the NER genes XPA (A23G) and XPD (Asp312Asn and Lys751Gln) modify the association between arsenic and NMSC.	Arsenic	136-143	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	75-78
17687452-8	2007	RESULTS: There was an increased BCC risk associated with high arsenic exposure among those homozygous variant for XPA [odds ratio (OR) = 1.8; 95% confidence interval (CI), 0.9-3.7].	Arsenic	62-69	XPA, DNA damage recognition and repair factor	Homo sapiens	114-117
17687452-10	2007	In the stratum of subjects who have variant for both XPD polymorphisms, there was a 2-fold increased risk of SCC associated with elevated arsenic (OR = 2.2; 95% CI, 1.0-5.0).	Arsenic	138-145	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	53-56
17687452-10	2007	In the stratum of subjects who have variant for both XPD polymorphisms, there was a 2-fold increased risk of SCC associated with elevated arsenic (OR = 2.2; 95% CI, 1.0-5.0).	Arsenic	138-145	serpin family B member 3	Homo sapiens	109-112
17687452-11	2007	The test for interaction between XPD and arsenic in SCC was of borderline significance (p &lt; 0.07, 3 degrees of freedom).	Arsenic	41-48	serpin family B member 3	Homo sapiens	52-55
17239412-6	2007	Two urinary arsenic excretion peaks were observed: an initial peak several (4-8) hours after ingestion corresponding to the excretion of predominantly As(III), and a larger peak at 14 h corresponding predominantly to DMAA and MMAA.	Arsenic	12-19	metabolism of cobalamin associated A	Homo sapiens	226-230
17470448-0	2007	Polymorphisms in XPD (Asp312Asn and Lys751Gln) genes, sunburn and arsenic-related skin lesions.	Arsenic	66-73	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	17-20
17470448-8	2007	CONCLUSION: XPD polymorphisms modified the relationship between tendency to sunburn and skin lesions in an arsenic exposed population.	Arsenic	107-114	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	12-15
17470448-9	2007	Further study is necessary to explore the effect of XPD polymorphisms and sun exposure on risk of arsenic-related skin lesions.	Arsenic	98-105	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	52-55
17509635-4	2007	As compared to the referent category (below limit of detection to 20 microg of As/L), the overall population mean systolic blood pressure rose 1.29 mm Hg (95% CI 0.82, 1.75), 1.28 mm Hg (95% CI 0.49, 2.07), and 2.22 mm Hg (95% CI 1.46, 2.97) as drinking water arsenic concentration increased from 21 to 50, 51 to 100, and &gt;100 microg of As/L, respectively.	Arsenic	260-267	argininosuccinate lyase	Homo sapiens	79-83
17467962-4	2007	The aim of this study was to investigate whether Mrp2 plays a role in exportation of arsenic in vivo and its protective effects on liver function.	Arsenic	85-92	ATP binding cassette subfamily B member 4	Rattus norvegicus	49-53
17467962-11	2007	A positive correlation between Mrp2 expression level and total arsenic concentration in bile indicated that Mrp2 accelerated the transport of arsenic.	Arsenic	63-70	ATP binding cassette subfamily B member 4	Rattus norvegicus	31-35
17467962-11	2007	A positive correlation between Mrp2 expression level and total arsenic concentration in bile indicated that Mrp2 accelerated the transport of arsenic.	Arsenic	63-70	ATP binding cassette subfamily B member 4	Rattus norvegicus	108-112
17467962-11	2007	A positive correlation between Mrp2 expression level and total arsenic concentration in bile indicated that Mrp2 accelerated the transport of arsenic.	Arsenic	142-149	ATP binding cassette subfamily B member 4	Rattus norvegicus	31-35
17467962-11	2007	A positive correlation between Mrp2 expression level and total arsenic concentration in bile indicated that Mrp2 accelerated the transport of arsenic.	Arsenic	142-149	ATP binding cassette subfamily B member 4	Rattus norvegicus	108-112
17467962-16	2007	In conclusion, overexpression of Mrp2 may explain increased biliary excretion of arsenic and it may protect liver function.	Arsenic	81-88	ATP binding cassette subfamily B member 4	Rattus norvegicus	33-37
17306315-9	2007	Male CD1 mice treated with arsenic in utero develop tumors of the liver and adrenal and renal hyperplasia while females develop tumors of urogenital system, ovary, uterus and adrenal and hyperplasia of the oviduct.	Arsenic	27-34	CD1 antigen complex	Mus musculus	5-8
17306315-10	2007	Additional postnatal treatment with diethylstilbestrol or tamoxifen after prenatal arsenic in CD1 mice induces urinary bladder transitional cell proliferative lesions, including carcinoma and papilloma, and enhances the carcinogenic response in the liver of both sexes.	Arsenic	83-90	CD1 antigen complex	Mus musculus	94-97
17306849-5	2007	Subsequent analyses revealed that the high D/M values associated with variant AS3MT alleles were primarily due to lower levels of monomethylarsonic acid as percent of total urinary arsenic (%MMA5).	Arsenic	181-188	arsenite methyltransferase	Homo sapiens	78-83
17306849-6	2007	In light of several reports of arsenic-induced disease being associated with relatively high %MMA5 levels, these findings raise the possibility that variant AS3MT individuals may suffer less risk from arsenic exposure than non-variant individuals.	Arsenic	31-38	arsenite methyltransferase	Homo sapiens	157-162
17306849-6	2007	In light of several reports of arsenic-induced disease being associated with relatively high %MMA5 levels, these findings raise the possibility that variant AS3MT individuals may suffer less risk from arsenic exposure than non-variant individuals.	Arsenic	201-208	arsenite methyltransferase	Homo sapiens	157-162
17316729-7	2007	Here, we report new data on the mutagenicity of the trivalent methylated arsenic metabolites MMA(III) and dimethylarsinous acid [DMA(III)] at the gpt locus in Chinese hamster G12 cells.	Arsenic	73-80	alanine aminotransferase 1	Cricetulus griseus	146-149
17267001-0	2007	Chronic arsenic exposure increases TGFalpha concentration in bladder urothelial cells of Mexican populations environmentally exposed to inorganic arsenic.	Arsenic	8-15	transforming growth factor alpha	Homo sapiens	35-43
17267001-0	2007	Chronic arsenic exposure increases TGFalpha concentration in bladder urothelial cells of Mexican populations environmentally exposed to inorganic arsenic.	Arsenic	146-153	transforming growth factor alpha	Homo sapiens	35-43
17267001-7	2007	Results show a statistically significant positive correlation between TGF-alpha concentration in BUC and each of the six arsenic species present in urine.	Arsenic	121-128	transforming growth factor alpha	Homo sapiens	70-79
17267001-8	2007	The multivariate linear regression analyses show that the increment of TGF-alpha levels in BUC was importantly associated with the presence of arsenic species after adjusting by age, and presence of urinary infection.	Arsenic	143-150	transforming growth factor alpha	Homo sapiens	71-80
17606337-11	2007	We clearly demonstrated that As(3+), Cd(2+), and Cr(6+) increase Cyp1a1 mRNA levels at the transcriptional and posttranscriptional levels while decreasing Cyp1a1 activity at the posttranslational level.	Arsenic	29-31	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	65-71
17267001-9	2007	People from areas with high arsenic exposure had a significantly higher TGF-alpha concentration in BUC than people from areas of low arsenic exposure (128.8 vs. 64.4 pg/mg protein; p&lt;0.05).	Arsenic	28-35	transforming growth factor alpha	Homo sapiens	72-81
17606337-11	2007	We clearly demonstrated that As(3+), Cd(2+), and Cr(6+) increase Cyp1a1 mRNA levels at the transcriptional and posttranscriptional levels while decreasing Cyp1a1 activity at the posttranslational level.	Arsenic	29-31	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	155-161
17526490-6	2007	Pretreatment with the antioxidant N-acetylcysteine (NAC) and expression of MT1 in the Ikkbeta(-)(/)(-) cells prevented JNK activation; moreover, NAC pretreatment, MT1 expression, MKK4 ablation, and JNK inhibition all protected cells from death induced by arsenic.	Arsenic	255-262	metallothionein 1	Mus musculus	75-78
17526490-5	2007	In contrast to wild type and IKKbeta-reconstituted Ikkbeta(-)(/)(-) cells, IKKbeta-null cells display a marked increase in arsenic-induced reactive oxygen species (ROS) accumulation, which leads to activation of the MKK4-c-Jun NH(2)-terminal kinase (JNK) pathway, c-Jun phosphorylation, and apoptosis.	Arsenic	123-130	inhibitor of kappaB kinase beta	Mus musculus	75-82
17526490-6	2007	Pretreatment with the antioxidant N-acetylcysteine (NAC) and expression of MT1 in the Ikkbeta(-)(/)(-) cells prevented JNK activation; moreover, NAC pretreatment, MT1 expression, MKK4 ablation, and JNK inhibition all protected cells from death induced by arsenic.	Arsenic	255-262	inhibitor of kappaB kinase beta	Mus musculus	86-93
17526490-5	2007	In contrast to wild type and IKKbeta-reconstituted Ikkbeta(-)(/)(-) cells, IKKbeta-null cells display a marked increase in arsenic-induced reactive oxygen species (ROS) accumulation, which leads to activation of the MKK4-c-Jun NH(2)-terminal kinase (JNK) pathway, c-Jun phosphorylation, and apoptosis.	Arsenic	123-130	mitogen-activated protein kinase 8	Mus musculus	216-248
17526490-5	2007	In contrast to wild type and IKKbeta-reconstituted Ikkbeta(-)(/)(-) cells, IKKbeta-null cells display a marked increase in arsenic-induced reactive oxygen species (ROS) accumulation, which leads to activation of the MKK4-c-Jun NH(2)-terminal kinase (JNK) pathway, c-Jun phosphorylation, and apoptosis.	Arsenic	123-130	mitogen-activated protein kinase 8	Mus musculus	250-253
17468136-5	2007	The mitogenic activity of TGF-beta1 on ASM cells was inhibited by selective inhibitors of TGF-beta receptor I kinase (SD-208), phosphatidylinositol 3-kinase (PI3K, LY-294002), ERK (PD-98059), JNK (SP-600125), and NF-kappaB (AS-602868).	Arsenic	39-41	transforming growth factor beta 1	Homo sapiens	26-35
17526490-5	2007	In contrast to wild type and IKKbeta-reconstituted Ikkbeta(-)(/)(-) cells, IKKbeta-null cells display a marked increase in arsenic-induced reactive oxygen species (ROS) accumulation, which leads to activation of the MKK4-c-Jun NH(2)-terminal kinase (JNK) pathway, c-Jun phosphorylation, and apoptosis.	Arsenic	123-130	jun proto-oncogene	Mus musculus	221-226
17718444-0	2007	[Real-time PCR used to detect p53 gene damage in workers exposed to arsenic].	Arsenic	68-75	tumor protein p53	Homo sapiens	30-33
17374727-3	2007	Adjusted for toenail arsenic, body mass index, education, smoking and betel nut use, individuals with the APE1 148Glu/Glu polymorphism had a 2-fold increased odds of skin lesions compared with individuals with the 148Asp/Asp genotype (1.93; 95% confidence interval 1.15, 3.19).	Arsenic	21-28	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	106-110
17374727-4	2007	Gene-environment interactions between toenail arsenic and XRCC1 Arg194Trp and APE1 Asp148Glu were observed.	Arsenic	46-53	X-ray repair cross complementing 1	Homo sapiens	58-63
17374727-4	2007	Gene-environment interactions between toenail arsenic and XRCC1 Arg194Trp and APE1 Asp148Glu were observed.	Arsenic	46-53	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	78-82
17374727-5	2007	Within the lowest arsenic tertile, APE1 148Glu/Glu had 2.5 times the odds ratio compared with wild-type, whereas within the highest tertile of arsenic the odds ratios for skin lesions did not differ.	Arsenic	18-25	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	35-39
17374727-7	2007	However, at the highest tertile of arsenic, the XRCC1 194Arg/Arg polymorphism conferred a 3-fold larger odds ratio for skin lesions compared with XRCC1 194Trp/Trp.	Arsenic	35-42	X-ray repair cross complementing 1	Homo sapiens	48-53
17608860-7	2007	RESULTS: Arsenic exposure gradually increased portal pressure and venous endothelin-1 levels in rats.	Arsenic	9-16	endothelin 1	Rattus norvegicus	73-85
17608860-8	2007	Endothelin-1 concentration in the supernatant did not change in every cell type stimulated with arsenic, but it increased in B lymphocytes and monocyte-derived macrophages treated with lipopolysaccharide and interferon-gamma.	Arsenic	96-103	endothelin 1	Homo sapiens	0-12
17608860-9	2007	CONCLUSIONS: The in vivo study indicated that arsenic might elevate portal pressure through mechanisms involving endothelin-1.	Arsenic	46-53	endothelin 1	Homo sapiens	113-125
17558810-7	2007	Increased expression of cell proliferation marker genes (PCNA, CyclinD1) and DNA methylation (DNA Methyl Transferase I) and decreased expression of genes for DNA repair (DNA Polymerase beta, ERCC6) with lower concentrations of arsenic was also observed.	Arsenic	227-234	proliferating cell nuclear antigen	Mus musculus	57-61
17558810-7	2007	Increased expression of cell proliferation marker genes (PCNA, CyclinD1) and DNA methylation (DNA Methyl Transferase I) and decreased expression of genes for DNA repair (DNA Polymerase beta, ERCC6) with lower concentrations of arsenic was also observed.	Arsenic	227-234	polymerase (DNA directed), beta	Mus musculus	170-189
17558810-7	2007	Increased expression of cell proliferation marker genes (PCNA, CyclinD1) and DNA methylation (DNA Methyl Transferase I) and decreased expression of genes for DNA repair (DNA Polymerase beta, ERCC6) with lower concentrations of arsenic was also observed.	Arsenic	227-234	excision repair cross-complementing rodent repair deficiency, complementation group 6	Mus musculus	191-196
17283378-0	2007	Arsenic as an endocrine disruptor: effects of arsenic on estrogen receptor-mediated gene expression in vivo and in cell culture.	Arsenic	0-7	estrogen receptor 1	Homo sapiens	57-74
17283378-0	2007	Arsenic as an endocrine disruptor: effects of arsenic on estrogen receptor-mediated gene expression in vivo and in cell culture.	Arsenic	46-53	estrogen receptor 1	Homo sapiens	57-74
17400579-9	2007	Bacterial infection, post arsenic exposure, demonstrated at least 2.5- and 4-fold declines in interleukin-1beta and tumor necrosis factor-alpha mRNA levels, respectively.	Arsenic	26-33	interleukin 1, beta	Danio rerio	94-143
17616671-0	2007	Incorporation of an internal ribosome entry site-dependent mechanism in arsenic-induced GADD45 alpha expression.	Arsenic	72-79	growth arrest and DNA damage inducible alpha	Homo sapiens	88-100
17616671-1	2007	We have previously shown that trivalent arsenic (arsenite, As(3+)) is able to induce GADD45 alpha expression in human bronchial epithelial cells through activation of c-Jun NH(2)-terminal kinase and nucleolin-dependent mRNA stabilization.	Arsenic	40-47	growth arrest and DNA damage inducible alpha	Homo sapiens	85-97
17616671-1	2007	We have previously shown that trivalent arsenic (arsenite, As(3+)) is able to induce GADD45 alpha expression in human bronchial epithelial cells through activation of c-Jun NH(2)-terminal kinase and nucleolin-dependent mRNA stabilization.	Arsenic	40-47	nucleolin	Homo sapiens	199-208
17309668-7	2007	With HER2 staining, 64.4% were scored as 0, 24.4% as 1+, 6.9% as 2+, and 4.4% as 3+.	Arsenic	38-40	erb-b2 receptor tyrosine kinase 2	Homo sapiens	5-9
17390107-0	2007	Transgenic Indian mustard (Brassica juncea) plants expressing an Arabidopsis phytochelatin synthase (AtPCS1) exhibit enhanced As and Cd tolerance.	Arsenic	126-128	phytochelatin synthase 1 (PCS1)	Arabidopsis thaliana	77-99
17390107-0	2007	Transgenic Indian mustard (Brassica juncea) plants expressing an Arabidopsis phytochelatin synthase (AtPCS1) exhibit enhanced As and Cd tolerance.	Arsenic	126-128	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	101-107
17451858-9	2007	Other expression alterations observed in the arsenic-treated male mouse newborn liver included the overexpression of cdk-inhibitors and stress response genes including increased expression of metallothionein-1 and decreased expression of betaine-homocysteine methyltransferase and thioether S-methyltransferase.	Arsenic	45-52	metallothionein 1	Mus musculus	192-209
17451858-9	2007	Other expression alterations observed in the arsenic-treated male mouse newborn liver included the overexpression of cdk-inhibitors and stress response genes including increased expression of metallothionein-1 and decreased expression of betaine-homocysteine methyltransferase and thioether S-methyltransferase.	Arsenic	45-52	betaine-homocysteine methyltransferase	Mus musculus	238-276
17451858-9	2007	Other expression alterations observed in the arsenic-treated male mouse newborn liver included the overexpression of cdk-inhibitors and stress response genes including increased expression of metallothionein-1 and decreased expression of betaine-homocysteine methyltransferase and thioether S-methyltransferase.	Arsenic	45-52	indolethylamine N-methyltransferase	Mus musculus	281-310
17718444-1	2007	OBJECTIVE: To evaluate the relationship between the metabolism of arsenic and the damage of exon 5 and 8 of p53 gene from workers in a arsenic mill, and with real-time PCR technique, to establish the method probing the gene-specific DNA damage in people.	Arsenic	66-73	tumor protein p53	Homo sapiens	108-111
17718444-1	2007	OBJECTIVE: To evaluate the relationship between the metabolism of arsenic and the damage of exon 5 and 8 of p53 gene from workers in a arsenic mill, and with real-time PCR technique, to establish the method probing the gene-specific DNA damage in people.	Arsenic	135-142	tumor protein p53	Homo sapiens	108-111
17650541-0	2007	Arsenic: extension of its endocrine disruption potential to interference with estrogen receptor-mediated signaling.	Arsenic	0-7	estrogen receptor 1	Homo sapiens	78-95
17718444-2	2007	METHODS: By real-time PCR, the damages of exon 5 and 8 of p53 gene were probed in 37 workers exposed highly to, 16 manager and logistic employees exposed less to an arsenic mill in Yunnan province, and also 25 local people who did not contact with any white arsenic in near past time.	Arsenic	165-172	tumor protein p53	Homo sapiens	58-61
17718444-2	2007	METHODS: By real-time PCR, the damages of exon 5 and 8 of p53 gene were probed in 37 workers exposed highly to, 16 manager and logistic employees exposed less to an arsenic mill in Yunnan province, and also 25 local people who did not contact with any white arsenic in near past time.	Arsenic	258-265	tumor protein p53	Homo sapiens	58-61
17718444-4	2007	The correlation between metabolism of arsenic and damage of p53 gene was evaluated.	Arsenic	38-45	tumor protein p53	Homo sapiens	60-63
17718444-9	2007	The Ct relative value of exon 5 of p53 gene in high exposed group was higher than that in control male (P &lt; 0.05), and the increased tendency of Ct relative value of exon 5 of p53 gene was found in workers with organic arsenic concentration going up (r(s) = 0.355, P = 0.011).	Arsenic	222-229	tumor protein p53	Homo sapiens	35-38
17718444-9	2007	The Ct relative value of exon 5 of p53 gene in high exposed group was higher than that in control male (P &lt; 0.05), and the increased tendency of Ct relative value of exon 5 of p53 gene was found in workers with organic arsenic concentration going up (r(s) = 0.355, P = 0.011).	Arsenic	222-229	tumor protein p53	Homo sapiens	179-182
17718444-11	2007	CONCLUSION: The damages in exon 5 and 8 of p53 gene in workers exposed to arsenic may be induced.	Arsenic	74-81	tumor protein p53	Homo sapiens	43-46
17439954-2	2007	ArsD is a metallochaperone that delivers As(III) to ArsA, increasing its affinity for As(III), thus conferring resistance to environmental concentrations of arsenic.	Arsenic	157-164	ArsD	Escherichia coli	0-4
17646145-2	2007	By case-control study in 79 AS patients and 132 healthy subjects, the distribution of TNF-alpha-850 genotype TT is higher in AS group than that in normal control group (P=0.027); Mutational allele T has a significant statistically difference between AS group and normal control group (P=0.002).	Arsenic	28-30	tumor necrosis factor	Homo sapiens	86-95
17646145-4	2007	The result hints that there may be susceptible sites of AS in this 15 kb region, which may be TNF-alpha-850 C--&gt;T mutation or other sites that around the TNF-alpha-850.	Arsenic	56-58	tumor necrosis factor	Homo sapiens	94-103
17646145-4	2007	The result hints that there may be susceptible sites of AS in this 15 kb region, which may be TNF-alpha-850 C--&gt;T mutation or other sites that around the TNF-alpha-850.	Arsenic	56-58	tumor necrosis factor	Homo sapiens	157-166
17512921-0	2007	Preferential binding of human XPA to the mitomycin C-DNA interstrand crosslink and modulation by arsenic and cadmium.	Arsenic	97-104	XPA, DNA damage recognition and repair factor	Homo sapiens	30-33
17521968-2	2007	Our results show that a single intraarterial bolus injection of AT1-AS in 30-day-old rats results in a prolonged lowering of systolic blood pressure (SBP) for a period of 18 days with an average difference in SBP of 30 mm Hg between AS-treated and untreated TGR.	Arsenic	68-70	angiotensin II receptor, type 1a	Rattus norvegicus	64-67
18072624-1	2007	OBJECTIVE: To investigate the apoptosis-induction, P-glycoprotein (P-gp) and mdr1 mRNA inhibition effects of arsenic trioxide (As2O3) and buthionine sulfoximine (BSO) on multidrug-resistant cell line K562/ADM cells, and to determine the relationship between intracellular GSH content and arsenic effect.	Arsenic	109-116	ATP binding cassette subfamily B member 1	Homo sapiens	67-71
18072624-1	2007	OBJECTIVE: To investigate the apoptosis-induction, P-glycoprotein (P-gp) and mdr1 mRNA inhibition effects of arsenic trioxide (As2O3) and buthionine sulfoximine (BSO) on multidrug-resistant cell line K562/ADM cells, and to determine the relationship between intracellular GSH content and arsenic effect.	Arsenic	109-116	ATP binding cassette subfamily B member 1	Homo sapiens	77-81
18072624-9	2007	At 48 hours, the mdr1 mRNA inhibition effect of the combination group was obviously stronger than that of high dose arsenic alone group.	Arsenic	116-123	ATP binding cassette subfamily B member 1	Homo sapiens	17-21
18072624-10	2007	At 72 hours, the P-gp inhibition effect of the combination group (clinic dose arsenic group, 0.5, 2.0 micromol/L) was obviously stronger than that of high dose arsenic alone group (5.0 micromol/L).	Arsenic	78-85	ATP binding cassette subfamily B member 1	Homo sapiens	17-21
18072624-10	2007	At 72 hours, the P-gp inhibition effect of the combination group (clinic dose arsenic group, 0.5, 2.0 micromol/L) was obviously stronger than that of high dose arsenic alone group (5.0 micromol/L).	Arsenic	160-167	ATP binding cassette subfamily B member 1	Homo sapiens	17-21
18072624-12	2007	The combination of conventional dose arsenic and BSO significantly induces K562/ADM cell apoptosis and inhibits P-gp and mdr1 mRNA expression in the cells.	Arsenic	37-44	ATP binding cassette subfamily B member 1	Homo sapiens	112-116
18072624-12	2007	The combination of conventional dose arsenic and BSO significantly induces K562/ADM cell apoptosis and inhibits P-gp and mdr1 mRNA expression in the cells.	Arsenic	37-44	ATP binding cassette subfamily B member 1	Homo sapiens	121-125
16973168-5	2007	In addition, the high-arsenic exposure group with one or two variant genotypes of GSTP1 and p53 had 2.8- and 6.1-fold higher risks of carotid atherosclerosis, respectively, and showed a dose-dependent relationship.	Arsenic	22-29	glutathione S-transferase pi 1	Homo sapiens	82-87
17420081-0	2007	Conditioned flavor aversion and brain Fos expression following exposure to arsenic.	Arsenic	75-82	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	38-41
17420081-5	2007	Our experiments indicate that arsenic ingestion is readily detected by the brain, as shown by increased Fos expression after oral administration of arsenic.	Arsenic	30-37	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	104-107
16973168-4	2007	The high-arsenic exposure group with GSTP1 variant genotypes of Ile/Val and Val/Val, and with the p53 variant genotypes of Arg/Pro and Pro/Pro had 6.0- and 3.1-fold higher risks of carotid atherosclerosis, respectively.	Arsenic	9-16	glutathione S-transferase pi 1	Homo sapiens	37-42
16973168-5	2007	In addition, the high-arsenic exposure group with one or two variant genotypes of GSTP1 and p53 had 2.8- and 6.1-fold higher risks of carotid atherosclerosis, respectively, and showed a dose-dependent relationship.	Arsenic	22-29	tumor protein p53	Homo sapiens	92-95
16973168-7	2007	Our study showed the joint effects on the risk of carotid atherosclerosis between the genetic polymorphisms of GSTP1 and p53, and arsenic exposure.	Arsenic	130-137	glutathione S-transferase pi 1	Homo sapiens	111-116
17317095-0	2007	In utero arsenic exposure induces early onset of atherosclerosis in ApoE-/- mice.	Arsenic	9-16	apolipoprotein E	Mus musculus	68-72
17619801-3	2007	Arsenic is also reported to phosphorylate eNOS in cultured keratinocyte and Human T cell leukemia Jurkat cells, respectively.	Arsenic	0-7	nitric oxide synthase 3	Homo sapiens	42-46
17619801-11	2007	And the initial up-regulation of eNOS phosphorylation by MMA(III )seems to be an adaptive response against disruption of eNOS bioactivity during arsenic exposure.	Arsenic	145-152	nitric oxide synthase 3	Homo sapiens	33-37
17619801-11	2007	And the initial up-regulation of eNOS phosphorylation by MMA(III )seems to be an adaptive response against disruption of eNOS bioactivity during arsenic exposure.	Arsenic	145-152	nitric oxide synthase 3	Homo sapiens	121-125
17420275-10	2007	Gfi-1B knockdown by RNA interference diminished imatinib-induced apoptosis, while the overexpression of Gfi-1B sensitized K562 cells to arsenic-induced death.	Arsenic	136-143	growth factor independent 1B transcriptional repressor	Homo sapiens	104-110
17363038-2	2007	Arsenic-spiked tap water and synthetic As solution with As concentrations from 200 to 500 mug/L were used for the experiments.	Arsenic	0-7	nuclear RNA export factor 1	Homo sapiens	15-18
17453740-0	2007	Serum levels of the extracellular domain of the epidermal growth factor receptor in individuals exposed to arsenic in drinking water in Bangladesh.	Arsenic	107-114	epidermal growth factor receptor	Homo sapiens	48-80
17453740-5	2007	The purpose of this study was to examine the EGFR ECD as a potential biomarker of arsenic exposure and/or effect in this population.	Arsenic	82-89	epidermal growth factor receptor	Homo sapiens	45-49
17453740-6	2007	Levels of the EGFR ECD were determined by enzyme-linked immunosorbent assay in the serum samples from 574 individuals with a range of arsenic exposures from drinking water in the Araihazar area of Bangladesh.	Arsenic	134-141	epidermal growth factor receptor	Homo sapiens	14-18
17453740-7	2007	In multiple regression analysis, serum EGFR ECD was found to be positively associated with three different measures of arsenic exposure (well water arsenic, urinary arsenic and a cumulative arsenic index) at statistically significant levels (p&lt;or=0.034), and this association was strongest among the individuals with arsenic-induced skin lesions (p &lt;or= 0.002).	Arsenic	119-126	epidermal growth factor receptor	Homo sapiens	39-43
17453740-7	2007	In multiple regression analysis, serum EGFR ECD was found to be positively associated with three different measures of arsenic exposure (well water arsenic, urinary arsenic and a cumulative arsenic index) at statistically significant levels (p&lt;or=0.034), and this association was strongest among the individuals with arsenic-induced skin lesions (p &lt;or= 0.002).	Arsenic	148-155	epidermal growth factor receptor	Homo sapiens	39-43
17453740-7	2007	In multiple regression analysis, serum EGFR ECD was found to be positively associated with three different measures of arsenic exposure (well water arsenic, urinary arsenic and a cumulative arsenic index) at statistically significant levels (p&lt;or=0.034), and this association was strongest among the individuals with arsenic-induced skin lesions (p &lt;or= 0.002).	Arsenic	148-155	epidermal growth factor receptor	Homo sapiens	39-43
17453740-7	2007	In multiple regression analysis, serum EGFR ECD was found to be positively associated with three different measures of arsenic exposure (well water arsenic, urinary arsenic and a cumulative arsenic index) at statistically significant levels (p&lt;or=0.034), and this association was strongest among the individuals with arsenic-induced skin lesions (p &lt;or= 0.002).	Arsenic	148-155	epidermal growth factor receptor	Homo sapiens	39-43
17453740-7	2007	In multiple regression analysis, serum EGFR ECD was found to be positively associated with three different measures of arsenic exposure (well water arsenic, urinary arsenic and a cumulative arsenic index) at statistically significant levels (p&lt;or=0.034), and this association was strongest among the individuals with arsenic-induced skin lesions (p &lt;or= 0.002).	Arsenic	148-155	epidermal growth factor receptor	Homo sapiens	39-43
17453740-8	2007	When the study subjects were stratified in tertiles of serum EGFR ECD levels, the risk of skin lesions increased progressively for each increase in all three arsenic measures (also stratified in tertiles) and this increasing risk became more pronounced among subjects within the highest tertile of EGFR ECD levels.	Arsenic	158-165	epidermal growth factor receptor	Homo sapiens	61-65
17453740-8	2007	When the study subjects were stratified in tertiles of serum EGFR ECD levels, the risk of skin lesions increased progressively for each increase in all three arsenic measures (also stratified in tertiles) and this increasing risk became more pronounced among subjects within the highest tertile of EGFR ECD levels.	Arsenic	158-165	epidermal growth factor receptor	Homo sapiens	298-302
17453740-9	2007	These results suggest that serum EGFR ECD levels may be a potential biomarker of effect of arsenic exposure and may indicate those exposed individuals at greatest risk for the development of arsenic-induced skin lesions.	Arsenic	91-98	epidermal growth factor receptor	Homo sapiens	33-37
17453740-9	2007	These results suggest that serum EGFR ECD levels may be a potential biomarker of effect of arsenic exposure and may indicate those exposed individuals at greatest risk for the development of arsenic-induced skin lesions.	Arsenic	191-198	epidermal growth factor receptor	Homo sapiens	33-37
17520061-0	2007	Molecular mechanisms of the diabetogenic effects of arsenic: inhibition of insulin signaling by arsenite and methylarsonous acid.	Arsenic	52-59	insulin	Homo sapiens	75-82
17539544-3	2007	The groundwater contained an extremely high arsenic concentration (341 mg L(-1)) and the results of ion chromatography and inductively coupled plasma mass spectrometry (IC-ICP-MS) analysis showed that the dominant arsenic species were arsenite (45.1%) and monomethyl arsenic acid (MMAA, 22.7%), while dimethyl arsenic acid (DMAA) and arsenate were only 2.4 and 1.3%, respectively.	Arsenic	214-221	metabolism of cobalamin associated A	Homo sapiens	281-285
17539544-8	2007	The results of pH-controlled DCBR tests using different synthetic species of arsenic solution showed that the humic acid inhibited the MMAA removal of Fe (25%)-diatomite more than arsenite.	Arsenic	77-84	metabolism of cobalamin associated A	Homo sapiens	135-139
17301066-18	2007	In addition, IL-6 secretion was measured in CS, AS, and nano-sized ZnO-exposed cocultures.	Arsenic	48-50	interleukin 6	Rattus norvegicus	13-17
17440589-1	2007	OBJECTIVE: To study the relationship between 5,10-methylenetetrahydrofolate reductase(MTHFR) genetic polymorphism and arsenic metabolism and the role of folate in it.	Arsenic	118-125	methylenetetrahydrofolate reductase	Homo sapiens	86-91
17440589-2	2007	METHODS: Forty-three individuals who were exposed to arsenic more than 0.05 mg/L in well water were chosen and the vein blood and morning urine was collected; The MTHFR C677 polymorphism was analyzed by PCR-RFLP method ; Urinary inorganic and methylated arsenic were speciated by high performance liquid chromatography combined with hydride-generation atomic fluorescence spectrometry; Microbiological assay was used to estimate serum folate.	Arsenic	53-60	methylenetetrahydrofolate reductase	Homo sapiens	163-168
17440589-5	2007	CONCLUSION: Genetic polymorphism of MTHFR C677 was significantly associated with arsenic methylation and this effect was not associated with the serum folate.	Arsenic	81-88	methylenetetrahydrofolate reductase	Homo sapiens	36-41
17307329-6	2007	Inevitably, arsenic treatment showed dose-dependent augmentation in the incidences of SCE and CCPI/RI together with AGT and PDT.	Arsenic	12-19	granzyme B	Homo sapiens	94-98
17321213-1	2007	Human exposure risk to environmental arsenic is evaluated by combining drinking water and atmospheric deposition, assessed tap water analysis and a moss biomonitoring survey.	Arsenic	37-44	nuclear RNA export factor 1	Homo sapiens	123-126
17317095-10	2007	These results indicate that in utero arsenic exposure induces an early onset of atherosclerosis in ApoE(-/-) mice without a hyperlipidemic diet and support the hypothesis that in utero arsenic exposure may be atherogenic in humans.	Arsenic	37-44	apolipoprotein E	Mus musculus	99-103
17386680-1	2007	The determination of arsenic in sea and freshwater by anodic stripping voltammetry (ASV) was revisited because of problems related to unstable peaks and inconveniently strong acidic conditions used by existing methods.	Arsenic	21-28	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	32-35
17409701-11	2007	Our present studies found that MT-I/II knockout mice have an increased sensitivity to harmful metals such as cadmium, mercury, and arsenic, oxidative stress, chemical carcinogenesis and neurodegenerative diseases.	Arsenic	131-138	metallothionein 3	Mus musculus	31-38
17386680-9	2007	The method was applied successfully to the determination of arsenic as well as copper in samples from the Irish Sea, mineral water and tap water.	Arsenic	60-67	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	112-115
17386680-9	2007	The method was applied successfully to the determination of arsenic as well as copper in samples from the Irish Sea, mineral water and tap water.	Arsenic	60-67	nuclear RNA export factor 1	Homo sapiens	135-138
17050553-0	2007	Polymorphism in the ERCC2 codon 751 is associated with arsenic-induced premalignant hyperkeratosis and significant chromosome aberrations.	Arsenic	55-62	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	20-25
17050553-10	2007	This study indicates that ERCC2 codon 751 Lys/Lys genotype is significantly associated with arsenic-induced premalignant hyperkeratosis and is possibly due to sub-optimal DNA repair capacity of the ERCC2 codon 751 Lys/Lys genotype.	Arsenic	92-99	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	26-31
17050553-10	2007	This study indicates that ERCC2 codon 751 Lys/Lys genotype is significantly associated with arsenic-induced premalignant hyperkeratosis and is possibly due to sub-optimal DNA repair capacity of the ERCC2 codon 751 Lys/Lys genotype.	Arsenic	92-99	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	198-203
17439919-8	2007	Results of the current study indicate neurosensory effects of arsenic exposure at concentrations well below the 1000 microg/L drinking water level specified by NRC, and suggest that non-carcinogenic end-points, such as vibration thresholds, are useful in the risk assessment of exposure to arsenic in drinking water.	Arsenic	62-69	nuclear receptor coactivator 6	Homo sapiens	160-163
17086449-7	2007	Arsenic exposure led to the inhibition of blood delta-aminolevulinic acid dehydratase (ALAD) activity and depletion of glutathione (GSH) level.	Arsenic	0-7	aminolevulinate dehydratase	Rattus norvegicus	48-85
17086449-7	2007	Arsenic exposure led to the inhibition of blood delta-aminolevulinic acid dehydratase (ALAD) activity and depletion of glutathione (GSH) level.	Arsenic	0-7	aminolevulinate dehydratase	Rattus norvegicus	87-91
17431481-10	2007	The interaction between GSTT1 wildtype and secondary methylation ratio modifies risk of skin lesions among arsenic-exposed individuals.	Arsenic	107-114	glutathione S-transferase theta 1	Homo sapiens	24-29
17339181-0	2007	Arsenic but not all-trans retinoic acid overcomes the aberrant stem cell capacity of PML/RARalpha-positive leukemic stem cells.	Arsenic	0-7	promyelocytic leukemia	Mus musculus	85-88
17339181-0	2007	Arsenic but not all-trans retinoic acid overcomes the aberrant stem cell capacity of PML/RARalpha-positive leukemic stem cells.	Arsenic	0-7	retinoic acid receptor, alpha	Mus musculus	89-97
17339181-7	2007	Here we compared the effects of ATRA and arsenic on PML/RARalpha-positive stem cell compartments.	Arsenic	41-48	promyelocytic leukemia	Mus musculus	52-55
17339181-7	2007	Here we compared the effects of ATRA and arsenic on PML/RARalpha-positive stem cell compartments.	Arsenic	41-48	retinoic acid receptor, alpha	Mus musculus	56-64
17339181-9	2007	RESULTS: In contrast to ATRA, arsenic abolishes the aberrant stem cell capacity of PML/RARalpha-positive stem cells.	Arsenic	30-37	promyelocytic leukemia	Mus musculus	83-86
17339181-9	2007	RESULTS: In contrast to ATRA, arsenic abolishes the aberrant stem cell capacity of PML/RARalpha-positive stem cells.	Arsenic	30-37	retinoic acid receptor, alpha	Mus musculus	87-95
17335514-0	2007	Identification of an arsenic tolerant double mutant with a thiol-mediated component and increased arsenic tolerance in phyA mutants.	Arsenic	21-28	phytochrome A	Arabidopsis thaliana	119-123
17335514-10	2007	Compared with wild type, the total thiol levels in ars4, ars5 and ars4ars5 mutants were increased up to 80% with combined buthionine sulfoximine and arsenic treatments, suggesting the enhancement of mechanisms that mediate thiol synthesis in the mutants.	Arsenic	149-156	proteasome alpha subunit F1	Arabidopsis thaliana	57-61
17335514-10	2007	Compared with wild type, the total thiol levels in ars4, ars5 and ars4ars5 mutants were increased up to 80% with combined buthionine sulfoximine and arsenic treatments, suggesting the enhancement of mechanisms that mediate thiol synthesis in the mutants.	Arsenic	149-156	proteasome alpha subunit F1	Arabidopsis thaliana	66-74
17400898-0	2007	A mutant of the Arabidopsis phosphate transporter PHT1;1 displays enhanced arsenic accumulation.	Arsenic	75-82	phosphate transporter 1;1	Arabidopsis thaliana	50-56
17400898-3	2007	pht1;1-3 displays a slow rate of As(V) uptake that ultimately enables the mutant to accumulate double the arsenic found in wild-type plants.	Arsenic	106-113	phosphate transporter 1;1	Arabidopsis thaliana	0-6
17335514-11	2007	The presented findings show that PHYA negatively regulates a pathway conferring arsenic tolerance, and that an enhanced thiol synthesis mechanism contributes to the arsenic tolerance of ars4ars5.	Arsenic	80-87	phytochrome A	Arabidopsis thaliana	33-37
17335514-0	2007	Identification of an arsenic tolerant double mutant with a thiol-mediated component and increased arsenic tolerance in phyA mutants.	Arsenic	98-105	phytochrome A	Arabidopsis thaliana	119-123
17335514-11	2007	The presented findings show that PHYA negatively regulates a pathway conferring arsenic tolerance, and that an enhanced thiol synthesis mechanism contributes to the arsenic tolerance of ars4ars5.	Arsenic	165-172	proteasome alpha subunit F1	Arabidopsis thaliana	186-194
17335514-3	2007	Genetic analyses of the mutant indicate that the mutant contains two loci that contribute to arsenic tolerance, designated ars4 and ars5.	Arsenic	93-100	proteasome alpha subunit F1	Arabidopsis thaliana	132-136
17335514-4	2007	The ars4ars5 double mutant contains a single T-DNA insertion, ars4, which co-segregates with arsenic tolerance and is inserted in the Phytochrome A (PHYA) gene, strongly reducing the expression of PHYA.	Arsenic	93-100	proteasome alpha subunit F1	Arabidopsis thaliana	4-12
17335514-7	2007	Analyses of the ars5 single mutant show that ars5 exhibits stronger arsenic tolerance than ars4, and that ars5 is not linked to ars4.	Arsenic	68-75	proteasome alpha subunit F1	Arabidopsis thaliana	16-20
17335514-7	2007	Analyses of the ars5 single mutant show that ars5 exhibits stronger arsenic tolerance than ars4, and that ars5 is not linked to ars4.	Arsenic	68-75	proteasome alpha subunit F1	Arabidopsis thaliana	45-49
17335514-7	2007	Analyses of the ars5 single mutant show that ars5 exhibits stronger arsenic tolerance than ars4, and that ars5 is not linked to ars4.	Arsenic	68-75	proteasome alpha subunit F1	Arabidopsis thaliana	45-49
17038445-8	2007	Arsenic prevented acclimation to seawater and decreased CFTR protein abundance.	Arsenic	0-7	cystic fibrosis transmembrane conductance regulator	Fundulus heteroclitus	56-60
17203165-12	2007	Because BFD has been closely related to arsenic ingestion, our results suggested that continual intake of arsenic in drinking water might provoke AKR1C2 expression that could in turn induce drug resistance in UBC, and AKR1C2 could be a tumor marker for UBC.	Arsenic	106-113	aldo-keto reductase family 1 member C2	Homo sapiens	146-152
17203165-12	2007	Because BFD has been closely related to arsenic ingestion, our results suggested that continual intake of arsenic in drinking water might provoke AKR1C2 expression that could in turn induce drug resistance in UBC, and AKR1C2 could be a tumor marker for UBC.	Arsenic	106-113	aldo-keto reductase family 1 member C2	Homo sapiens	218-224
16968895-0	2007	Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in leukemia cells.	Arsenic	54-61	aquaporin 9	Homo sapiens	30-48
17077188-7	2007	In utero arsenic exposure also induced overexpression of alpha-fetoprotein, epidermal growth factor receptor, L-myc, and metallothionein-1 in fetal lung, all of which are associated with lung cancer.	Arsenic	9-16	alpha fetoprotein	Mus musculus	57-74
17077188-7	2007	In utero arsenic exposure also induced overexpression of alpha-fetoprotein, epidermal growth factor receptor, L-myc, and metallothionein-1 in fetal lung, all of which are associated with lung cancer.	Arsenic	9-16	epidermal growth factor receptor	Mus musculus	76-108
17077188-7	2007	In utero arsenic exposure also induced overexpression of alpha-fetoprotein, epidermal growth factor receptor, L-myc, and metallothionein-1 in fetal lung, all of which are associated with lung cancer.	Arsenic	9-16	v-myc avian myelocytomatosis viral oncogene lung carcinoma derived	Mus musculus	110-115
17077188-7	2007	In utero arsenic exposure also induced overexpression of alpha-fetoprotein, epidermal growth factor receptor, L-myc, and metallothionein-1 in fetal lung, all of which are associated with lung cancer.	Arsenic	9-16	metallothionein 1	Mus musculus	121-138
17077188-8	2007	Lung adenoma and adenocarcinoma from adult female mice exposed to arsenic in utero showed widespread, intense nuclear ER-alpha expression.	Arsenic	66-73	estrogen receptor 1 (alpha)	Mus musculus	118-126
17077188-11	2007	ER-alpha activation was specifically associated with arsenic-induced lung adenocarcinoma and adenoma but not with nitrosamine-induced lung tumors.	Arsenic	53-60	estrogen receptor 1 (alpha)	Mus musculus	0-8
16968895-2	2007	Aquaglyceroporin 9 (AQP9) is a transmembrane protein that may be involved in arsenic uptake.	Arsenic	77-84	aquaporin 9	Homo sapiens	0-18
16968895-2	2007	Aquaglyceroporin 9 (AQP9) is a transmembrane protein that may be involved in arsenic uptake.	Arsenic	77-84	aquaporin 9	Homo sapiens	20-24
16968895-6	2007	The K562(EGFP-AQP9) transfectant accumulated significantly higher levels of intracellular arsenic than control K562(EGFP) when incubated with As2O3, resulting in significantly increased As2O3-induced cytotoxicity.	Arsenic	90-97	aquaporin 9	Homo sapiens	9-18
16968895-7	2007	Pretreatment of the myeloid leukemia line HL-60 with all-trans retinoic acid (ATRA) up-regulated AQP9, leading to a significantly increased arsenic uptake and As2O3-induced cytotoxicity on incubation with As2O3, which might explain the synergism between ATRA and As2O3.	Arsenic	140-147	aquaporin 9	Homo sapiens	97-101
16968895-8	2007	Therefore, AQP9 controlled arsenic transport and might determine As2O3 sensitivity.	Arsenic	27-34	aquaporin 9	Homo sapiens	11-15
17200139-2	2007	The Saccharomyces cerevisiae AP-1-like protein Yap8p (systematic name YPR199c; also known as Acr1p and Arr1p) confers arsenic tolerance by stimulating enhanced transcription of the arsenic-specific detoxification genes ACR2 and ACR3.	Arsenic	118-125	Arr1p	Saccharomyces cerevisiae S288C	47-52
17200139-2	2007	The Saccharomyces cerevisiae AP-1-like protein Yap8p (systematic name YPR199c; also known as Acr1p and Arr1p) confers arsenic tolerance by stimulating enhanced transcription of the arsenic-specific detoxification genes ACR2 and ACR3.	Arsenic	118-125	Arr1p	Saccharomyces cerevisiae S288C	93-98
17365576-6	2007	When arsenic intake from consumption of tap water and beverages made from tap water (microg/L arsenic x L/d = microg/d) was used as a predictor variable, the correlation was markedly increased for individuals with &gt;1 microg/L arsenic (R2 = .48).	Arsenic	5-12	nuclear RNA export factor 1	Homo sapiens	40-43
17365576-6	2007	When arsenic intake from consumption of tap water and beverages made from tap water (microg/L arsenic x L/d = microg/d) was used as a predictor variable, the correlation was markedly increased for individuals with &gt;1 microg/L arsenic (R2 = .48).	Arsenic	5-12	nuclear RNA export factor 1	Homo sapiens	74-77
17200139-2	2007	The Saccharomyces cerevisiae AP-1-like protein Yap8p (systematic name YPR199c; also known as Acr1p and Arr1p) confers arsenic tolerance by stimulating enhanced transcription of the arsenic-specific detoxification genes ACR2 and ACR3.	Arsenic	118-125	Arr3p	Saccharomyces cerevisiae S288C	228-232
17200139-2	2007	The Saccharomyces cerevisiae AP-1-like protein Yap8p (systematic name YPR199c; also known as Acr1p and Arr1p) confers arsenic tolerance by stimulating enhanced transcription of the arsenic-specific detoxification genes ACR2 and ACR3.	Arsenic	181-188	Arr1p	Saccharomyces cerevisiae S288C	47-52
17200139-2	2007	The Saccharomyces cerevisiae AP-1-like protein Yap8p (systematic name YPR199c; also known as Acr1p and Arr1p) confers arsenic tolerance by stimulating enhanced transcription of the arsenic-specific detoxification genes ACR2 and ACR3.	Arsenic	181-188	Arr1p	Saccharomyces cerevisiae S288C	93-98
17365576-6	2007	When arsenic intake from consumption of tap water and beverages made from tap water (microg/L arsenic x L/d = microg/d) was used as a predictor variable, the correlation was markedly increased for individuals with &gt;1 microg/L arsenic (R2 = .48).	Arsenic	94-101	nuclear RNA export factor 1	Homo sapiens	40-43
17365576-6	2007	When arsenic intake from consumption of tap water and beverages made from tap water (microg/L arsenic x L/d = microg/d) was used as a predictor variable, the correlation was markedly increased for individuals with &gt;1 microg/L arsenic (R2 = .48).	Arsenic	94-101	nuclear RNA export factor 1	Homo sapiens	40-43
17200139-2	2007	The Saccharomyces cerevisiae AP-1-like protein Yap8p (systematic name YPR199c; also known as Acr1p and Arr1p) confers arsenic tolerance by stimulating enhanced transcription of the arsenic-specific detoxification genes ACR2 and ACR3.	Arsenic	118-125	Arr1p	Saccharomyces cerevisiae S288C	103-108
17200139-2	2007	The Saccharomyces cerevisiae AP-1-like protein Yap8p (systematic name YPR199c; also known as Acr1p and Arr1p) confers arsenic tolerance by stimulating enhanced transcription of the arsenic-specific detoxification genes ACR2 and ACR3.	Arsenic	118-125	Arr2p	Saccharomyces cerevisiae S288C	219-223
17365577-0	2007	Genetic polymorphisms in MTHFR 677 and 1298, GSTM1 and T1, and metabolism of arsenic.	Arsenic	77-84	methylenetetrahydrofolate reductase	Homo sapiens	25-30
17200139-2	2007	The Saccharomyces cerevisiae AP-1-like protein Yap8p (systematic name YPR199c; also known as Acr1p and Arr1p) confers arsenic tolerance by stimulating enhanced transcription of the arsenic-specific detoxification genes ACR2 and ACR3.	Arsenic	181-188	Arr1p	Saccharomyces cerevisiae S288C	103-108
17365577-8	2007	This is the first study to report (1) associations between MTHFR and arsenic metabolism in humans, and (2) gender differences between genetic polymorphisms and urinary arsenic methylation patterns.	Arsenic	69-76	methylenetetrahydrofolate reductase	Homo sapiens	59-64
17200139-2	2007	The Saccharomyces cerevisiae AP-1-like protein Yap8p (systematic name YPR199c; also known as Acr1p and Arr1p) confers arsenic tolerance by stimulating enhanced transcription of the arsenic-specific detoxification genes ACR2 and ACR3.	Arsenic	181-188	Arr2p	Saccharomyces cerevisiae S288C	219-223
17200139-2	2007	The Saccharomyces cerevisiae AP-1-like protein Yap8p (systematic name YPR199c; also known as Acr1p and Arr1p) confers arsenic tolerance by stimulating enhanced transcription of the arsenic-specific detoxification genes ACR2 and ACR3.	Arsenic	181-188	Arr3p	Saccharomyces cerevisiae S288C	228-232
17365577-5	2007	In this study, it was found that subjects with the TT/AA variant of MTHFR 677/1298 excreted a significantly higher proportion of ingested arsenic as inorganic arsenic and a lower proportion as dimethylarsinic acid.	Arsenic	138-145	methylenetetrahydrofolate reductase	Homo sapiens	68-73
17365577-6	2007	Women with the null genotype of GSTM1 excreted a significantly higher proportion of arsenic as monomethylarsonate than women with the active genotype.	Arsenic	84-91	glutathione S-transferase mu 1	Homo sapiens	32-37
17365577-9	2007	Overall, this study provides evidence that MTHFR and GSTM1 are involved in arsenic metabolism in humans, and polymorphisms in the genes that encode these enzymes may play a role in susceptibility to arsenic-induced cancer.	Arsenic	75-82	methylenetetrahydrofolate reductase	Homo sapiens	43-48
17365577-9	2007	Overall, this study provides evidence that MTHFR and GSTM1 are involved in arsenic metabolism in humans, and polymorphisms in the genes that encode these enzymes may play a role in susceptibility to arsenic-induced cancer.	Arsenic	75-82	glutathione S-transferase mu 1	Homo sapiens	53-58
17107663-5	2007	We find that arsenic causes the depletion of S-adenosylmethionine, the main cellular methyl donor, and represses the expression of the DNA methyltransferase genes DNMT1 and DNMT3A.	Arsenic	13-20	DNA methyltransferase 1	Homo sapiens	163-168
17188728-6	2007	Similarly, arsenic treatment lowered the activities of testicular 3beta-hydroxysteroid dehydrogenase (HSD) and 17beta-HSD, which play important roles in steroidogenesis, and this was reversed by co-treatment with ascorbic acid.	Arsenic	11-18	hydroxysteroid (17-beta) dehydrogenase 1	Mus musculus	111-121
17107663-5	2007	We find that arsenic causes the depletion of S-adenosylmethionine, the main cellular methyl donor, and represses the expression of the DNA methyltransferase genes DNMT1 and DNMT3A.	Arsenic	13-20	DNA methyltransferase 3 alpha	Homo sapiens	173-179
16824580-1	2007	The performance of a new anion exchanger (AE) prepared from coconut coir pith (CP), for the removal of arsenic(V) [As(V)] from aqueous solutions was evaluated in this study.	Arsenic	103-110	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	115-120
17055307-7	2007	Exposure to arsenic (2.5 mg/kg, intraperitoneally for 6weeks) led to a significant increase in the levels of tissue reactive oxygen species (ROS), metallothionein (MT) and thiobarbituric acid reactive substance (TBARS) which were accompanied by a decrease in the activities in the antioxidant enzymes such as superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) in mice.	Arsenic	12-19	catalase	Mus musculus	337-345
17055307-8	2007	Arsenic exposed mice also exhibited liver injury as reflected by reduced acid phosphatase (ACP), alkaline phosphatase (ALP) and aspartate aminotransferase (AST) activities and altered heme synthesis pathway as shown by inhibited blood delta-aminolevulinic acid dehydratase (delta-ALAD) activity.	Arsenic	0-7	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	128-154
17055307-8	2007	Arsenic exposed mice also exhibited liver injury as reflected by reduced acid phosphatase (ACP), alkaline phosphatase (ALP) and aspartate aminotransferase (AST) activities and altered heme synthesis pathway as shown by inhibited blood delta-aminolevulinic acid dehydratase (delta-ALAD) activity.	Arsenic	0-7	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	156-159
17055307-8	2007	Arsenic exposed mice also exhibited liver injury as reflected by reduced acid phosphatase (ACP), alkaline phosphatase (ALP) and aspartate aminotransferase (AST) activities and altered heme synthesis pathway as shown by inhibited blood delta-aminolevulinic acid dehydratase (delta-ALAD) activity.	Arsenic	0-7	aminolevulinate, delta-, dehydratase	Mus musculus	235-272
17055307-8	2007	Arsenic exposed mice also exhibited liver injury as reflected by reduced acid phosphatase (ACP), alkaline phosphatase (ALP) and aspartate aminotransferase (AST) activities and altered heme synthesis pathway as shown by inhibited blood delta-aminolevulinic acid dehydratase (delta-ALAD) activity.	Arsenic	0-7	aminolevulinate, delta-, dehydratase	Mus musculus	274-284
17055307-9	2007	Co-administration of M. oleifera seed powder (250 and 500 mg/kg, orally) with arsenic significantly increased the activities of SOD, catalase, GPx with elevation in reduced GSH level in tissues (liver, kidney and brain).	Arsenic	78-85	catalase	Mus musculus	133-141
16963107-4	2007	The results indicated the presence of inorganic arsenic species with daily means of 262mugl(-1) for As(V) and 107 microg l(-1) for As(III).	Arsenic	48-55	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	100-105
16963107-10	2007	An explanation for the arsenic diel cycles observed is the light induced photooxidation of As(III) and the elimination of As(V) due to its adsorption onto Fe precipitates during the daytime.	Arsenic	23-30	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	122-127
17613011-6	2007	Exposure to arsenic or fluoride caused a significant depletion in blood delta-aminolevulinic acid dehydratase (ALAD) activity, platelet counts (PLT), and glutathione (GSH) level.	Arsenic	12-19	aminolevulinate, delta-, dehydratase	Mus musculus	72-109
17613011-6	2007	Exposure to arsenic or fluoride caused a significant depletion in blood delta-aminolevulinic acid dehydratase (ALAD) activity, platelet counts (PLT), and glutathione (GSH) level.	Arsenic	12-19	aminolevulinate, delta-, dehydratase	Mus musculus	111-115
17613011-11	2007	Hepatic catalase activity, on the other hand, increased significantly on exposure to arsenic and fluoride.	Arsenic	85-92	catalase	Mus musculus	8-16
17056641-5	2007	Furthermore, the arsenic-induced vascular leakage could be significantly reduced when the neurogenic inflammation process was interrupted (via either disruption on the release of substance P, interference on the action of substance P, or blockage of endothelial NK-1 receptor) showing that the neurogenic inflammation process was indeed involved.	Arsenic	17-24	tachykinin precursor 1	Homo sapiens	179-190
17969647-3	2007	The contents of O2*-, MDA, soluble protein and peroxidase (POD) activity all increased with increasing As concentrations.	Arsenic	103-105	peroxidase-like	Triticum aestivum	47-57
17969647-3	2007	The contents of O2*-, MDA, soluble protein and peroxidase (POD) activity all increased with increasing As concentrations.	Arsenic	103-105	peroxidase-like	Triticum aestivum	59-62
17969647-4	2007	Soluble sugar content, ascorbate peroxidase (APX), and superoxide dismutase (SOD) activities decreased at low concentrations of As, and increased at high concentrations of As.	Arsenic	128-130	SOD	Triticum aestivum	77-80
17388894-2	2007	The rice genome contains two ACR2-like genes, OsACR2.1 and OsACR2.2, which may be involved in regulating arsenic metabolism in rice.	Arsenic	105-112	Arr2p	Saccharomyces cerevisiae S288C	29-33
21783745-2	2007	Although it has been demonstrated that the methylation of arsenic is catalyzed by arsenic methyltransferase, Cyt19, very little is known about the characteristics of this enzyme.	Arsenic	58-65	arsenite methyltransferase	Rattus norvegicus	109-114
17969647-5	2007	While acetylsalicylic acid (ASA) and chlorophyll contents, catalase (CAT) activity displayed increasing trend when the concentrations of As was lower than 1 mg/kg, and then decreasing trend.	Arsenic	137-139	catalase-1	Triticum aestivum	59-67
17969647-5	2007	While acetylsalicylic acid (ASA) and chlorophyll contents, catalase (CAT) activity displayed increasing trend when the concentrations of As was lower than 1 mg/kg, and then decreasing trend.	Arsenic	137-139	catalase-1	Triticum aestivum	69-72
17070597-15	2007	When performed under dark conditions, AS-OCT identified 98% of those subjects found to have angle closure on gonioscopy (95% confidence interval [CI], 92.2-99.6) and led to the characterization of 44.6% of those found to have open angles on gonioscopy to have angle closure as well.	Arsenic	38-40	plexin A2	Homo sapiens	41-44
17939155-2	2007	However, little is known about how arsenic affects Trx chemically.	Arsenic	35-42	thioredoxin	Homo sapiens	51-54
17939155-4	2007	The objective of this study is to characterize the binding of seven arsenic species with Trx from E. coli and humans, using two mass spectrometry techniques.	Arsenic	68-75	thioredoxin	Homo sapiens	89-92
17939155-5	2007	The arsenic-Trx complexes and the free arsenicals were well separated by size-exclusion liquid chromatography (LC) and detected with inductively coupled plasma mass spectrometry (ICPMS).	Arsenic	4-11	thioredoxin	Homo sapiens	12-15
17939155-6	2007	The LC/ICPMS analyses showed that the trivalent arsenic species were able to form complexes with both human and E. coli Trx.	Arsenic	48-55	thioredoxin	Homo sapiens	120-123
17939155-9	2007	Binding stoichiometries for different arsenic species were consistent with the available cysteine residues in the Trx.	Arsenic	38-45	thioredoxin	Homo sapiens	114-117
17939155-11	2007	This study provides the first detailed chemical characterization of the interactions between Trx and arsenic species.	Arsenic	101-108	thioredoxin	Homo sapiens	93-96
17056641-0	2007	Involvement of substance P and neurogenic inflammation in arsenic-induced early vascular dysfunction.	Arsenic	58-65	tachykinin precursor 1	Homo sapiens	15-26
17056641-3	2007	Based on our previous studies, we hypothesized that arsenic exerted its action on blood vessels via the neurogenic inflammation process involving release of a neuropeptide (substance P) and activation of endothelial Neurokinin 1 (NK-1) receptor in vivo.	Arsenic	52-59	tachykinin precursor 1	Homo sapiens	173-184
17056641-3	2007	Based on our previous studies, we hypothesized that arsenic exerted its action on blood vessels via the neurogenic inflammation process involving release of a neuropeptide (substance P) and activation of endothelial Neurokinin 1 (NK-1) receptor in vivo.	Arsenic	52-59	tachykinin precursor 1	Homo sapiens	216-228
17056641-3	2007	Based on our previous studies, we hypothesized that arsenic exerted its action on blood vessels via the neurogenic inflammation process involving release of a neuropeptide (substance P) and activation of endothelial Neurokinin 1 (NK-1) receptor in vivo.	Arsenic	52-59	tachykinin receptor 1	Homo sapiens	230-244
17056641-4	2007	Indeed, our present study demonstrated a significantly higher substance P levels in arsenic-treated tissues when compared to saline-treated controls indicating a rapid release of substance P under the influence of arsenic.	Arsenic	84-91	tachykinin precursor 1	Homo sapiens	62-73
17056641-4	2007	Indeed, our present study demonstrated a significantly higher substance P levels in arsenic-treated tissues when compared to saline-treated controls indicating a rapid release of substance P under the influence of arsenic.	Arsenic	84-91	tachykinin precursor 1	Homo sapiens	179-190
17056641-4	2007	Indeed, our present study demonstrated a significantly higher substance P levels in arsenic-treated tissues when compared to saline-treated controls indicating a rapid release of substance P under the influence of arsenic.	Arsenic	214-221	tachykinin precursor 1	Homo sapiens	62-73
17056641-5	2007	Furthermore, the arsenic-induced vascular leakage could be significantly reduced when the neurogenic inflammation process was interrupted (via either disruption on the release of substance P, interference on the action of substance P, or blockage of endothelial NK-1 receptor) showing that the neurogenic inflammation process was indeed involved.	Arsenic	17-24	tachykinin precursor 1	Homo sapiens	222-233
17056641-4	2007	Indeed, our present study demonstrated a significantly higher substance P levels in arsenic-treated tissues when compared to saline-treated controls indicating a rapid release of substance P under the influence of arsenic.	Arsenic	214-221	tachykinin precursor 1	Homo sapiens	179-190
17056641-5	2007	Furthermore, the arsenic-induced vascular leakage could be significantly reduced when the neurogenic inflammation process was interrupted (via either disruption on the release of substance P, interference on the action of substance P, or blockage of endothelial NK-1 receptor) showing that the neurogenic inflammation process was indeed involved.	Arsenic	17-24	tachykinin receptor 1	Homo sapiens	262-275
17056641-7	2007	Our present study affirmed a de novo concept that a pathophysiological mechanism involving the neurogenic release of substance P and activation of endothelial NK-1 receptor underlies the arsenic-induced vascular injury and dysfunction in vivo.	Arsenic	187-194	tachykinin precursor 1	Homo sapiens	117-128
17056641-7	2007	Our present study affirmed a de novo concept that a pathophysiological mechanism involving the neurogenic release of substance P and activation of endothelial NK-1 receptor underlies the arsenic-induced vascular injury and dysfunction in vivo.	Arsenic	187-194	tachykinin receptor 1	Homo sapiens	159-172
16678950-0	2006	Arsenic in sediments from the southeastern Baltic Sea.	Arsenic	0-7	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	50-53
17128987-7	2006	Similarly, certain arsenic complexes (i.e., arsenate and arsenic trioxide) may inactivate RhoA by bridging the cysteine residues in the GXXXCGK(S/T)C motif.	Arsenic	19-26	ras homolog family member A	Homo sapiens	90-94
17128987-8	2006	Thus, in addition to redox agents, platinated-chemotherapeutic agents and arsenic complexes may modulate the activity of GTPases containing the GXXXCGK(S/T)C motif (i.e., RhoA and RhoB).	Arsenic	74-81	ras homolog family member A	Homo sapiens	171-175
17128987-8	2006	Thus, in addition to redox agents, platinated-chemotherapeutic agents and arsenic complexes may modulate the activity of GTPases containing the GXXXCGK(S/T)C motif (i.e., RhoA and RhoB).	Arsenic	74-81	ras homolog family member B	Homo sapiens	180-184
17173375-6	2006	Mutations in the DBD that alter the conformation of the dimerization domain (D-loop) to a DNA-bound GR conformation abolished the stimulatory effect and enhanced the inhibitory response to As.	Arsenic	189-191	nuclear receptor subfamily 3 group C member 1	Homo sapiens	100-102
17173375-9	2006	Moreover, a well-characterized GR dimerization mutant displayed a wild-type biphasic response to As for several divergent reporter genes, suggesting that dimerization is not critical for the response to As.	Arsenic	97-99	nuclear receptor subfamily 3 group C member 1	Homo sapiens	31-33
17305125-6	2007	After breakthrough of arsenic, concentration of As(III) in the effluents was below 40 ppb for the entire reaction period in all configurations, and most arsenic was identified as As(V) owing to near complete conversion of As(III) to As(V) by MCS.	Arsenic	153-160	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	179-184
17064664-10	2006	Thus GLUT1 may be a major pathway uptake of both inorganic and methylated arsenicals in erythrocytes or the epithelial cells of the blood-brain barrier, contributing to arsenic-related cardiovascular problems and neurotoxicity.	Arsenic	74-81	solute carrier family 2 member 1	Rattus norvegicus	5-10
17145805-3	2006	We investigated the role of TOPK in arsenic-induced apoptosis in RPMI7951 human melanoma cells.	Arsenic	36-43	PDZ binding kinase	Homo sapiens	28-32
17145805-5	2006	Immunofluorescence, Western blot, and flow cytometry were used to assess the effect of arsenic on TOPK, histone H2AX, and apoptosis in RPMI7951 cells.	Arsenic	87-94	PDZ binding kinase	Homo sapiens	98-102
17145805-5	2006	Immunofluorescence, Western blot, and flow cytometry were used to assess the effect of arsenic on TOPK, histone H2AX, and apoptosis in RPMI7951 cells.	Arsenic	87-94	H2A.X variant histone	Homo sapiens	104-116
16678950-1	2006	Arsenic occurs as a persistent constituent in many of the chemical weapons dumped into the Baltic Sea; it can be used as an indicator of leakage and dispersal of released munitions to the marine environment.	Arsenic	0-7	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	98-101
17056473-4	2006	Immunoassays were used to determine the plasma levels of TGF-alpha and epidermal growth factor receptor (EGFR), which is the receptor for TGF-alpha, in residents of an arseniasis area of Taiwan in relation to their estimated cumulative arsenic exposure from drinking water.	Arsenic	236-243	epidermal growth factor receptor	Homo sapiens	71-103
17108810-15	2006	The GSTP1 A1578G (Ile105Val) status might be a susceptibility factor for arsenic-related skin lesions.	Arsenic	73-80	glutathione S-transferase pi 1	Homo sapiens	4-9
17105159-6	2006	The calibration curve is linear up to 20 microg L-1 arsenic, and the detection limit is 0.5 microg L-1 (6.6 x 10(-9) mol L-1).	Arsenic	52-59	immunoglobulin kappa variable 1-16	Homo sapiens	48-51
17105159-6	2006	The calibration curve is linear up to 20 microg L-1 arsenic, and the detection limit is 0.5 microg L-1 (6.6 x 10(-9) mol L-1).	Arsenic	52-59	immunoglobulin kappa variable 1-16	Homo sapiens	99-102
17105159-6	2006	The calibration curve is linear up to 20 microg L-1 arsenic, and the detection limit is 0.5 microg L-1 (6.6 x 10(-9) mol L-1).	Arsenic	52-59	immunoglobulin kappa variable 1-16	Homo sapiens	99-102
17105159-8	2006	Furthermore, it is possible to detect concentrations as low as 1 microg L-1 arsenic visually using this method.	Arsenic	76-83	immunoglobulin kappa variable 1-16	Homo sapiens	72-75
17105159-12	2006	Since this method is specific for As(V), it is applicable to the speciation of arsenic oxidation states.	Arsenic	79-86	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	34-39
16766112-9	2006	Interestingly, targeting AtPCS1 to chloroplasts induced a marked sensitivity to arsenic while plants over-expressing AtPCS1 in the cytoplasm were more tolerant to this metalloid.	Arsenic	80-87	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	25-31
17056473-7	2006	There was a significant linear trend between cumulative arsenic exposure and the prevalence of plasma TGF-alpha over-expression after adjusting for age and sex (p=0.019).	Arsenic	56-63	transforming growth factor alpha	Homo sapiens	102-111
16487958-6	2006	Household tap water arsenic levels in Ajo (20.3+/-3.7 microg/L) were higher than in those Tucson (4.0+/-2.3 microg/L), as were mean urinary total inorganic arsenic levels (29.1+/-20.4 and 11.0+/-12.0 microg/L, respectively).	Arsenic	20-27	nuclear RNA export factor 1	Homo sapiens	10-13
17194918-6	2006	Arsenic intake significantly increased (p&lt;0.05) serum gamma-gultamyltransferase (GGT), glutamic-pyruvic transaminase (GPT), and alkaline phosphatase (ALP) activities, and decreased (p&lt;0.05) total protein, urea nitrogen, creatinine, and triglycerides.	Arsenic	0-7	alanine aminotransferase 1	Sus scrofa	90-119
17194918-6	2006	Arsenic intake significantly increased (p&lt;0.05) serum gamma-gultamyltransferase (GGT), glutamic-pyruvic transaminase (GPT), and alkaline phosphatase (ALP) activities, and decreased (p&lt;0.05) total protein, urea nitrogen, creatinine, and triglycerides.	Arsenic	0-7	alanine aminotransferase 1	Sus scrofa	121-124
17194918-6	2006	Arsenic intake significantly increased (p&lt;0.05) serum gamma-gultamyltransferase (GGT), glutamic-pyruvic transaminase (GPT), and alkaline phosphatase (ALP) activities, and decreased (p&lt;0.05) total protein, urea nitrogen, creatinine, and triglycerides.	Arsenic	0-7	ALPA	Sus scrofa	131-151
17194918-6	2006	Arsenic intake significantly increased (p&lt;0.05) serum gamma-gultamyltransferase (GGT), glutamic-pyruvic transaminase (GPT), and alkaline phosphatase (ALP) activities, and decreased (p&lt;0.05) total protein, urea nitrogen, creatinine, and triglycerides.	Arsenic	0-7	ALPA	Sus scrofa	153-156
16487958-8	2006	However, after adjusting for town, asthma, diabetes, urinary monomethylarsonic acid/inorganic arsenic, and smoking history, total urinary arsenic was negatively associated with MMP-2 and TIMP-1 levels in sputum and positively associated with the ratio of MMP-2/TIMP-1 and MMP-9/TIMP-1 in sputum.	Arsenic	138-145	matrix metallopeptidase 2	Homo sapiens	177-182
16487958-8	2006	However, after adjusting for town, asthma, diabetes, urinary monomethylarsonic acid/inorganic arsenic, and smoking history, total urinary arsenic was negatively associated with MMP-2 and TIMP-1 levels in sputum and positively associated with the ratio of MMP-2/TIMP-1 and MMP-9/TIMP-1 in sputum.	Arsenic	138-145	TIMP metallopeptidase inhibitor 1	Homo sapiens	187-193
16487958-8	2006	However, after adjusting for town, asthma, diabetes, urinary monomethylarsonic acid/inorganic arsenic, and smoking history, total urinary arsenic was negatively associated with MMP-2 and TIMP-1 levels in sputum and positively associated with the ratio of MMP-2/TIMP-1 and MMP-9/TIMP-1 in sputum.	Arsenic	138-145	matrix metallopeptidase 2	Homo sapiens	255-260
16487958-8	2006	However, after adjusting for town, asthma, diabetes, urinary monomethylarsonic acid/inorganic arsenic, and smoking history, total urinary arsenic was negatively associated with MMP-2 and TIMP-1 levels in sputum and positively associated with the ratio of MMP-2/TIMP-1 and MMP-9/TIMP-1 in sputum.	Arsenic	138-145	TIMP metallopeptidase inhibitor 1	Homo sapiens	261-267
16487958-8	2006	However, after adjusting for town, asthma, diabetes, urinary monomethylarsonic acid/inorganic arsenic, and smoking history, total urinary arsenic was negatively associated with MMP-2 and TIMP-1 levels in sputum and positively associated with the ratio of MMP-2/TIMP-1 and MMP-9/TIMP-1 in sputum.	Arsenic	138-145	matrix metallopeptidase 9	Homo sapiens	272-277
16487958-8	2006	However, after adjusting for town, asthma, diabetes, urinary monomethylarsonic acid/inorganic arsenic, and smoking history, total urinary arsenic was negatively associated with MMP-2 and TIMP-1 levels in sputum and positively associated with the ratio of MMP-2/TIMP-1 and MMP-9/TIMP-1 in sputum.	Arsenic	138-145	TIMP metallopeptidase inhibitor 1	Homo sapiens	261-267
17029826-0	2006	Increased glycophorin A somatic cell variant frequency in arsenic-exposed patients of Guizhou, China.	Arsenic	58-65	glycophorin A (MNS blood group)	Homo sapiens	10-23
16930657-3	2006	In the biotransformation of inorganic arsenic, GSTO1 catalyzes the reduction of arsenate, MMA(V), and DMA(V) to the more toxic +3 arsenic species.	Arsenic	38-45	glutathione S-transferase omega 1	Mus musculus	47-52
17029826-2	2006	The glycophorin A (GPA) assay is a human mutation assay detecting somatic variation in erythrocytes expressing the MN blood type, and was used to assess genotoxicity of arsenic-exposed patients.	Arsenic	169-176	glycophorin A (MNS blood group)	Homo sapiens	4-17
16930657-3	2006	In the biotransformation of inorganic arsenic, GSTO1 catalyzes the reduction of arsenate, MMA(V), and DMA(V) to the more toxic +3 arsenic species.	Arsenic	130-137	glutathione S-transferase omega 1	Mus musculus	47-52
17029826-2	2006	The glycophorin A (GPA) assay is a human mutation assay detecting somatic variation in erythrocytes expressing the MN blood type, and was used to assess genotoxicity of arsenic-exposed patients.	Arsenic	169-176	glycophorin A (MNS blood group)	Homo sapiens	19-22
17029826-8	2006	Total GPA variant frequency in arsenic-exposed patients bearing skin tumors was significantly increased compared to patients without skin tumors (167 versus 290).	Arsenic	31-38	glycophorin A (MNS blood group)	Homo sapiens	6-9
17029826-9	2006	The relationship between arsenic exposure history and GPA variant frequency was less evident.	Arsenic	25-32	glycophorin A (MNS blood group)	Homo sapiens	54-57
17029826-10	2006	These data demonstrate that arsenic exposure is associated with mutations at the GPA locus, an effect exaggerated in patients bearing arsenic-induced skin tumors.	Arsenic	28-35	glycophorin A (MNS blood group)	Homo sapiens	81-84
17029826-10	2006	These data demonstrate that arsenic exposure is associated with mutations at the GPA locus, an effect exaggerated in patients bearing arsenic-induced skin tumors.	Arsenic	134-141	glycophorin A (MNS blood group)	Homo sapiens	81-84
17029826-11	2006	The variant frequency of GPA could be a useful biomarker for arsenic exposure and arsenic carcinogenesis.	Arsenic	61-68	glycophorin A (MNS blood group)	Homo sapiens	25-28
16904653-7	2006	In vivo, Tet/AS but not control mice showed stress-associated hippocampal deposits of heat-shock protein 70 and GRP78 (BiP), predicting posttranscriptional changes in neuronal reactions.	Arsenic	13-15	heat shock protein 5	Mus musculus	112-117
16930632-0	2006	Association of specific p53 polymorphisms with keratosis in individuals exposed to arsenic through drinking water in West Bengal, India.	Arsenic	83-90	tumor protein p53	Homo sapiens	24-27
16930632-5	2006	This prompted us to study the association of three p53 polymorphisms with arsenic induced keratosis in a population exposed to arsenic through drinking water.	Arsenic	74-81	tumor protein p53	Homo sapiens	51-54
16930632-5	2006	This prompted us to study the association of three p53 polymorphisms with arsenic induced keratosis in a population exposed to arsenic through drinking water.	Arsenic	127-134	tumor protein p53	Homo sapiens	51-54
17003472-5	2006	The intrarenal arsenic concentration was significantly higher in IFN-gamma-/- mice later than 10 hours after NaAs treatment, with attenuated intrarenal expression of multidrug resistance-associated protein (MRP) 1, a main transporter for NaAs efflux, compared with WT mice.	Arsenic	15-22	interferon gamma	Mus musculus	65-74
17030823-6	2006	ArsD transfers trivalent metalloids to ArsA, the catalytic subunit of an As(III)/Sb(III) efflux pump.	Arsenic	73-75	ArsD	Escherichia coli	0-4
16904653-7	2006	In vivo, Tet/AS but not control mice showed stress-associated hippocampal deposits of heat-shock protein 70 and GRP78 (BiP), predicting posttranscriptional changes in neuronal reactions.	Arsenic	13-15	heat shock protein 5	Mus musculus	119-122
16713074-0	2006	Arsenic inhibits induction of cytochrome P450 1A1 by 2,3,7,8-tetrachlorodibenzo-p-dioxin in human hepatoma cells.	Arsenic	0-7	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	30-49
17051793-6	2006	Dom values were fitted as a function of the As/DOC ratio for As(III) and As(V).	Arsenic	44-46	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	73-78
16600567-5	2006	It is highly suggestive that CAT gene expression and protein levels are affected by arsenic.	Arsenic	84-91	catalase	Homo sapiens	29-32
17007042-10	2006	The fluorescence intensity levels of VEGF in tumor cells were significantly lowered in the arsenic-treated groups (P&lt;0.01, P&lt;0.01).	Arsenic	91-98	vascular endothelial growth factor A	Mus musculus	37-41
16713074-6	2006	In the present study, we demonstrated that arsenic not only inhibited the TCDD-induced CYP1A1 activation but also interfered with DRE-CALUX bioassay in human hepatoma cells.	Arsenic	43-50	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	87-93
16775837-3	2006	To investigate the mechanisms for this inhibition, Cr(VI) effects on basal and arsenic (As(III))-induced HO-1 expression were examined in cultured human bronchial epithelial (BEAS-2B) cells.	Arsenic	79-86	heme oxygenase 1	Homo sapiens	105-109
16713074-1	2006	The aim of this study was to examine the arsenic effect on activation of aryl hydrocarbon receptor (AhR)-mediated gene expression by 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) in human hepatoma cells.	Arsenic	41-48	aryl hydrocarbon receptor	Homo sapiens	73-98
16713074-1	2006	The aim of this study was to examine the arsenic effect on activation of aryl hydrocarbon receptor (AhR)-mediated gene expression by 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) in human hepatoma cells.	Arsenic	41-48	aryl hydrocarbon receptor	Homo sapiens	100-103
16807664-7	2006	The most common arsenic-induced skin cancers are Bowen"s disease (carcinoma in situ), basal cell carcinoma (BCC) and squamous cell carcinoma (SCC).	Arsenic	16-23	serpin family B member 3	Homo sapiens	142-145
16338065-2	2006	We further demonstrated that arsenic treatment of the immortalized bladder cell line, E7, increased Aurora-A expression.	Arsenic	29-36	aurora kinase A	Homo sapiens	100-108
16338065-4	2006	In addition, Aurora-A overexpression and up-regulated by arsenic exposure opens a new direction for exploring the occurrence of bladder cancer occurrence in Taiwan.	Arsenic	57-64	aurora kinase A	Homo sapiens	13-21
17119258-7	2006	Arsenic exposure, measured as toenail arsenic, was associated with RASSF1A (P &lt; 0.02) and PRSS3 (P &lt; 0.1) but not p16(INK4A) or SFRP promotor methylation, in models adjusted for stage and other risk factors.	Arsenic	0-7	Ras association domain family member 1	Homo sapiens	67-74
17119258-7	2006	Arsenic exposure, measured as toenail arsenic, was associated with RASSF1A (P &lt; 0.02) and PRSS3 (P &lt; 0.1) but not p16(INK4A) or SFRP promotor methylation, in models adjusted for stage and other risk factors.	Arsenic	0-7	serine protease 3	Homo sapiens	93-98
17119258-7	2006	Arsenic exposure, measured as toenail arsenic, was associated with RASSF1A (P &lt; 0.02) and PRSS3 (P &lt; 0.1) but not p16(INK4A) or SFRP promotor methylation, in models adjusted for stage and other risk factors.	Arsenic	38-45	Ras association domain family member 1	Homo sapiens	67-74
17119258-7	2006	Arsenic exposure, measured as toenail arsenic, was associated with RASSF1A (P &lt; 0.02) and PRSS3 (P &lt; 0.1) but not p16(INK4A) or SFRP promotor methylation, in models adjusted for stage and other risk factors.	Arsenic	38-45	serine protease 3	Homo sapiens	93-98
16970300-9	2006	The electrode was applicable for analysis of spiked arsenic in tap water containing a significant amount of various ion elements.	Arsenic	52-59	nuclear RNA export factor 1	Homo sapiens	63-66
16712894-0	2006	Enhanced urinary bladder and liver carcinogenesis in male CD1 mice exposed to transplacental inorganic arsenic and postnatal diethylstilbestrol or tamoxifen.	Arsenic	103-110	CD1 antigen complex	Mus musculus	58-61
16712894-9	2006	Thus, in male CD1 mice, gestational arsenic exposure alone induced liver adenoma and carcinoma, lung adenocarcinoma, adrenal adenoma and renal cystic hyperplasia.	Arsenic	36-43	CD1 antigen complex	Mus musculus	14-17
16930595-6	2006	The generation of H(2)O(2) and activation of caspase 3 were identified as critical components of As(2)O(3)-induced apoptosis in all of the above cell lines.	Arsenic	97-99	caspase 3	Homo sapiens	45-54
16807664-8	2006	Arsenic-induced Bowen"s disease (As-BD) is able to transform into invasive BCC and SCC.	Arsenic	0-7	serpin family B member 3	Homo sapiens	83-86
16807664-12	2006	These cellular abnormalities relate to the p53 dysfunction induced by arsenic.	Arsenic	70-77	tumor protein p53	Homo sapiens	43-46
16807664-21	2006	A decrease in peripheral CD4+ cells was noticed in the inhabitants of arsenic exposure areas.	Arsenic	70-77	CD4 molecule	Homo sapiens	25-28
16807664-23	2006	Since CD4+ cells are the target cell affected by As, the interaction between CD4+ cells and epidermal keratinocytes under As affection might be closely linked to the pathogenesis of multiple occurrence of arsenic-induced skin cancer.	Arsenic	49-51	CD4 molecule	Homo sapiens	6-9
16807664-23	2006	Since CD4+ cells are the target cell affected by As, the interaction between CD4+ cells and epidermal keratinocytes under As affection might be closely linked to the pathogenesis of multiple occurrence of arsenic-induced skin cancer.	Arsenic	49-51	CD4 molecule	Homo sapiens	77-80
16807664-23	2006	Since CD4+ cells are the target cell affected by As, the interaction between CD4+ cells and epidermal keratinocytes under As affection might be closely linked to the pathogenesis of multiple occurrence of arsenic-induced skin cancer.	Arsenic	205-212	CD4 molecule	Homo sapiens	6-9
16807664-23	2006	Since CD4+ cells are the target cell affected by As, the interaction between CD4+ cells and epidermal keratinocytes under As affection might be closely linked to the pathogenesis of multiple occurrence of arsenic-induced skin cancer.	Arsenic	205-212	CD4 molecule	Homo sapiens	77-80
17366771-4	2006	The mean total arsenic (microg/L) in tap-water was 20.3+/-3.7 in Ajo and 4.0+/-2.3 in Tucson.	Arsenic	15-22	nuclear RNA export factor 1	Homo sapiens	37-40
16828073-4	2006	Exposure to arsenic or fluoride led to a significant depletion of blood delta-aminolevulinic acid dehydratase (ALAD) activity and glutathione (GSH) level.	Arsenic	12-19	aminolevulinate, delta-, dehydratase	Mus musculus	72-109
16917909-2	2006	The detection rate for TBX5 mutations in HOS patients has been given as 30-35% in most reports.	Arsenic	55-57	T-box transcription factor 5	Homo sapiens	23-27
16828073-4	2006	Exposure to arsenic or fluoride led to a significant depletion of blood delta-aminolevulinic acid dehydratase (ALAD) activity and glutathione (GSH) level.	Arsenic	12-19	aminolevulinate, delta-, dehydratase	Mus musculus	111-115
16785233-0	2006	Arsenic induces NAD(P)H-quinone oxidoreductase I by disrupting the Nrf2 x Keap1 x Cul3 complex and recruiting Nrf2 x Maf to the antioxidant response element enhancer.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	67-71
16785233-0	2006	Arsenic induces NAD(P)H-quinone oxidoreductase I by disrupting the Nrf2 x Keap1 x Cul3 complex and recruiting Nrf2 x Maf to the antioxidant response element enhancer.	Arsenic	0-7	kelch like ECH associated protein 1	Homo sapiens	74-79
16785233-10	2006	In addition, Keap1 was shown to be ubiquitinated in the cytoplasm and deubiquitinated in the nucleus in the presence of arsenic without changing the protein level, implicating nuclear-cytoplasmic recycling of Keap1.	Arsenic	120-127	kelch like ECH associated protein 1	Homo sapiens	13-18
16785233-0	2006	Arsenic induces NAD(P)H-quinone oxidoreductase I by disrupting the Nrf2 x Keap1 x Cul3 complex and recruiting Nrf2 x Maf to the antioxidant response element enhancer.	Arsenic	0-7	cullin 3	Homo sapiens	82-86
16785233-11	2006	Our data reveal that arsenic activates the Nrf2/Keap1 signaling pathway through a distinct mechanism from that by antioxidants and suggest an "on-switch" model of Nqo1 transcription in which the binding of Nrf2 x Maf to ARE controls both the basal and inducible expression of Nqo1.	Arsenic	21-28	NFE2 like bZIP transcription factor 2	Homo sapiens	43-47
16785233-11	2006	Our data reveal that arsenic activates the Nrf2/Keap1 signaling pathway through a distinct mechanism from that by antioxidants and suggest an "on-switch" model of Nqo1 transcription in which the binding of Nrf2 x Maf to ARE controls both the basal and inducible expression of Nqo1.	Arsenic	21-28	kelch like ECH associated protein 1	Homo sapiens	48-53
16785233-0	2006	Arsenic induces NAD(P)H-quinone oxidoreductase I by disrupting the Nrf2 x Keap1 x Cul3 complex and recruiting Nrf2 x Maf to the antioxidant response element enhancer.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	110-114
16785233-11	2006	Our data reveal that arsenic activates the Nrf2/Keap1 signaling pathway through a distinct mechanism from that by antioxidants and suggest an "on-switch" model of Nqo1 transcription in which the binding of Nrf2 x Maf to ARE controls both the basal and inducible expression of Nqo1.	Arsenic	21-28	NAD(P)H quinone dehydrogenase 1	Homo sapiens	163-167
16785233-11	2006	Our data reveal that arsenic activates the Nrf2/Keap1 signaling pathway through a distinct mechanism from that by antioxidants and suggest an "on-switch" model of Nqo1 transcription in which the binding of Nrf2 x Maf to ARE controls both the basal and inducible expression of Nqo1.	Arsenic	21-28	NFE2 like bZIP transcription factor 2	Homo sapiens	206-210
16785233-11	2006	Our data reveal that arsenic activates the Nrf2/Keap1 signaling pathway through a distinct mechanism from that by antioxidants and suggest an "on-switch" model of Nqo1 transcription in which the binding of Nrf2 x Maf to ARE controls both the basal and inducible expression of Nqo1.	Arsenic	21-28	MAF bZIP transcription factor	Homo sapiens	213-216
16785233-11	2006	Our data reveal that arsenic activates the Nrf2/Keap1 signaling pathway through a distinct mechanism from that by antioxidants and suggest an "on-switch" model of Nqo1 transcription in which the binding of Nrf2 x Maf to ARE controls both the basal and inducible expression of Nqo1.	Arsenic	21-28	NAD(P)H quinone dehydrogenase 1	Homo sapiens	276-280
16785233-0	2006	Arsenic induces NAD(P)H-quinone oxidoreductase I by disrupting the Nrf2 x Keap1 x Cul3 complex and recruiting Nrf2 x Maf to the antioxidant response element enhancer.	Arsenic	0-7	MAF bZIP transcription factor	Homo sapiens	117-120
16785233-3	2006	We analyzed the signaling pathway for induction of detoxification gene NAD(P)H-quinone oxidoreductase (Nqo1) by arsenic.	Arsenic	112-119	NAD(P)H quinone dehydrogenase 1	Homo sapiens	103-107
16785233-5	2006	Arsenic stabilized Nrf2 protein, extending the t(1/2) of Nrf2 from 21 to 200 min by inhibiting the Keap1 x Cul3-dependent ubiquitination and proteasomal turnover of Nrf2.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	19-23
16785233-5	2006	Arsenic stabilized Nrf2 protein, extending the t(1/2) of Nrf2 from 21 to 200 min by inhibiting the Keap1 x Cul3-dependent ubiquitination and proteasomal turnover of Nrf2.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	57-61
16785233-5	2006	Arsenic stabilized Nrf2 protein, extending the t(1/2) of Nrf2 from 21 to 200 min by inhibiting the Keap1 x Cul3-dependent ubiquitination and proteasomal turnover of Nrf2.	Arsenic	0-7	kelch like ECH associated protein 1	Homo sapiens	99-104
16785233-5	2006	Arsenic stabilized Nrf2 protein, extending the t(1/2) of Nrf2 from 21 to 200 min by inhibiting the Keap1 x Cul3-dependent ubiquitination and proteasomal turnover of Nrf2.	Arsenic	0-7	cullin 3	Homo sapiens	107-111
16785233-5	2006	Arsenic stabilized Nrf2 protein, extending the t(1/2) of Nrf2 from 21 to 200 min by inhibiting the Keap1 x Cul3-dependent ubiquitination and proteasomal turnover of Nrf2.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	57-61
16785233-6	2006	Arsenic markedly inhibited the ubiquitination of Nrf2 but did not disrupt the Nrf2 x Keap1 x Cul3 association in the cytoplasm.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	49-53
16785233-7	2006	In the nucleus, arsenic, but not phenolic antioxidant tert-butylhydroquinone, dissociated Nrf2 from Keap1 and Cul3 followed by dimerization of Nrf2 with a Maf protein (Maf G/Maf K).	Arsenic	16-23	NFE2 like bZIP transcription factor 2	Homo sapiens	90-94
16785233-7	2006	In the nucleus, arsenic, but not phenolic antioxidant tert-butylhydroquinone, dissociated Nrf2 from Keap1 and Cul3 followed by dimerization of Nrf2 with a Maf protein (Maf G/Maf K).	Arsenic	16-23	kelch like ECH associated protein 1	Homo sapiens	100-105
16785233-7	2006	In the nucleus, arsenic, but not phenolic antioxidant tert-butylhydroquinone, dissociated Nrf2 from Keap1 and Cul3 followed by dimerization of Nrf2 with a Maf protein (Maf G/Maf K).	Arsenic	16-23	cullin 3	Homo sapiens	110-114
16785233-7	2006	In the nucleus, arsenic, but not phenolic antioxidant tert-butylhydroquinone, dissociated Nrf2 from Keap1 and Cul3 followed by dimerization of Nrf2 with a Maf protein (Maf G/Maf K).	Arsenic	16-23	NFE2 like bZIP transcription factor 2	Homo sapiens	143-147
16785233-7	2006	In the nucleus, arsenic, but not phenolic antioxidant tert-butylhydroquinone, dissociated Nrf2 from Keap1 and Cul3 followed by dimerization of Nrf2 with a Maf protein (Maf G/Maf K).	Arsenic	16-23	MAF bZIP transcription factor	Homo sapiens	155-158
16785233-7	2006	In the nucleus, arsenic, but not phenolic antioxidant tert-butylhydroquinone, dissociated Nrf2 from Keap1 and Cul3 followed by dimerization of Nrf2 with a Maf protein (Maf G/Maf K).	Arsenic	16-23	MAF bZIP transcription factor	Homo sapiens	168-171
16785233-7	2006	In the nucleus, arsenic, but not phenolic antioxidant tert-butylhydroquinone, dissociated Nrf2 from Keap1 and Cul3 followed by dimerization of Nrf2 with a Maf protein (Maf G/Maf K).	Arsenic	16-23	MAF bZIP transcription factor	Homo sapiens	168-171
16785233-9	2006	Arsenic substantially increased the ARE occupancy by Nrf2 and Maf.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	53-57
16785233-9	2006	Arsenic substantially increased the ARE occupancy by Nrf2 and Maf.	Arsenic	0-7	MAF bZIP transcription factor	Homo sapiens	62-65
16966277-0	2006	Down-regulation of wt1 expression in leukemia cell lines as part of apoptotic effect in arsenic treatment using two compounds.	Arsenic	88-95	WT1 transcription factor	Homo sapiens	19-22
16762916-4	2006	Arsenic-induced apoptosis was enhanced in cells in which MSK1 expression was decreased using small interfering RNA and in Msk1 knock-out mouse embryonic fibroblasts, suggesting that this kinase is activated in a negative feedback regulatory manner to regulate As2O3 responses.	Arsenic	0-7	ribosomal protein S6 kinase, polypeptide 5	Mus musculus	57-61
16762916-4	2006	Arsenic-induced apoptosis was enhanced in cells in which MSK1 expression was decreased using small interfering RNA and in Msk1 knock-out mouse embryonic fibroblasts, suggesting that this kinase is activated in a negative feedback regulatory manner to regulate As2O3 responses.	Arsenic	0-7	ribosomal protein S6 kinase, polypeptide 5	Mus musculus	122-126
16882524-6	2006	Arsenic exposure was associated with decreased expression of ERCC1 in isolated lymphocytes at the mRNA and protein levels.	Arsenic	0-7	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	61-66
16966277-6	2006	Low concentrations of 0.1 microM arsenic induced expression of the anti-apoptotic bcl-2 gene in both cell lines HL-60 and K562.	Arsenic	33-40	BCL2 apoptosis regulator	Homo sapiens	82-87
16966277-8	2006	After arsenic treatment of the leukemia cell lines HL-60 and K562 the up-regulation of par-4 may contribute to the induction of apoptosis rather than down-regulation of bcl-2.	Arsenic	6-13	Prader Willi/Angelman region RNA 4	Homo sapiens	87-92
16966277-9	2006	The therapeutic effect of arsenic is the induction of apoptosis by modulating the gene expression profile of pro- and anti-apoptotic genes including the wt1 gene.	Arsenic	26-33	WT1 transcription factor	Homo sapiens	153-156
16672223-0	2006	Enhanced expression of multidrug resistance-associated protein 2 and reduced expression of aquaglyceroporin 3 in an arsenic-resistant human cell line.	Arsenic	116-123	ATP binding cassette subfamily C member 2	Homo sapiens	23-64
16814109-4	2006	Here, we investigate the effects of arsenic exposure on the induction of the growth arrest and DNA damage protein 45 alpha (GADD45 alpha), which is thought to play roles in apoptosis, DNA damage response, and cell cycle arrest.	Arsenic	36-43	growth arrest and DNA damage inducible alpha	Homo sapiens	123-136
16814109-5	2006	We found that arsenic transcriptionally activates the gadd45 alpha promoter located in a 153-bp region between -234 and -81, relative to the transcriptional start site.	Arsenic	14-21	growth arrest and DNA damage inducible alpha	Homo sapiens	54-66
16672223-0	2006	Enhanced expression of multidrug resistance-associated protein 2 and reduced expression of aquaglyceroporin 3 in an arsenic-resistant human cell line.	Arsenic	116-123	aquaporin 3 (Gill blood group)	Homo sapiens	91-109
16672223-6	2006	Thus, increased arsenic extrusion by MRP2 may contribute to arsenic resistance in R15 cells.	Arsenic	16-23	ATP binding cassette subfamily C member 2	Rattus norvegicus	37-41
16672223-6	2006	Thus, increased arsenic extrusion by MRP2 may contribute to arsenic resistance in R15 cells.	Arsenic	60-67	ATP binding cassette subfamily C member 2	Rattus norvegicus	37-41
16672223-10	2006	Conversely, overexpression of AQP3 in human embryonic kidney 293T cells increased arsenic accumulation, and the cells were more susceptible to As(III) than 293T cells transfected with vector alone.	Arsenic	82-89	aquaporin 3 (Gill blood group)	Homo sapiens	30-34
16672223-12	2006	Taken together, our results suggest that enhanced expression of MRP2 and lower expression of AQP3 are responsible for lower arsenic accumulation in arsenic-resistant R15 cells.	Arsenic	124-131	ATP binding cassette subfamily C member 2	Rattus norvegicus	64-68
16672223-12	2006	Taken together, our results suggest that enhanced expression of MRP2 and lower expression of AQP3 are responsible for lower arsenic accumulation in arsenic-resistant R15 cells.	Arsenic	124-131	aquaporin 3 (Gill blood group)	Rattus norvegicus	93-97
16672223-12	2006	Taken together, our results suggest that enhanced expression of MRP2 and lower expression of AQP3 are responsible for lower arsenic accumulation in arsenic-resistant R15 cells.	Arsenic	148-155	ATP binding cassette subfamily C member 2	Rattus norvegicus	64-68
16672223-12	2006	Taken together, our results suggest that enhanced expression of MRP2 and lower expression of AQP3 are responsible for lower arsenic accumulation in arsenic-resistant R15 cells.	Arsenic	148-155	aquaporin 3 (Gill blood group)	Rattus norvegicus	93-97
16405955-10	2006	Arsenic sorption kinetics were biphasic, similar to what has been observed with P sorption by the WTRs.	Arsenic	0-7	WTRS	Homo sapiens	98-102
16781109-5	2006	Human GST omega 1-1 (hGSTO1-1) is identical to human monomethylarsenic acid (MMAV), the rate-limiting enzyme for biotransformation of inorganic arsenic.	Arsenic	63-70	glutathione S-transferase omega 1	Homo sapiens	21-29
16841956-3	2006	Arsenic (+3 oxidation state) methyltransferase (AS3MT) that is expressed in rat and human hepatocytes catalyzes the conversion of iAs, yielding methylated metabolites that contain arsenic in +3 or +5 oxidation states.	Arsenic	180-187	arsenite methyltransferase	Rattus norvegicus	0-46
16841956-3	2006	Arsenic (+3 oxidation state) methyltransferase (AS3MT) that is expressed in rat and human hepatocytes catalyzes the conversion of iAs, yielding methylated metabolites that contain arsenic in +3 or +5 oxidation states.	Arsenic	180-187	arsenite methyltransferase	Rattus norvegicus	48-53
16479312-0	2006	Organic anion transporting polypeptide-C mediates arsenic uptake in HEK-293 cells.	Arsenic	50-57	solute carrier organic anion transporter family member 1B1	Homo sapiens	0-40
16479312-3	2006	In order to examine whether organic anion transporting polypeptide-C (OATP-C) also plays a role in arsenic transport, OATP-C cDNA was transfected into cells of a human embryonic kidney cell line (HEK-293).	Arsenic	99-106	solute carrier organic anion transporter family member 1B1	Homo sapiens	28-68
16479312-3	2006	In order to examine whether organic anion transporting polypeptide-C (OATP-C) also plays a role in arsenic transport, OATP-C cDNA was transfected into cells of a human embryonic kidney cell line (HEK-293).	Arsenic	99-106	solute carrier organic anion transporter family member 1B1	Homo sapiens	70-76
16055167-4	2006	Irrespective of organic matter content, As(V) was the predominant soil bound and aqueous phase arsenic species.	Arsenic	95-102	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	40-45
16598798-7	2006	The trend of the BDE of H(2)B(+)-CO and H(2)B(+)-EC(5)H(5) is N&gt;P&gt;As&gt;Sb&gt;Bi&gt;CO. A surprising result is found for H(2)B(+)-CO, which has a significantly stronger and yet substantially longer bond than H(3)B-CO.	Arsenic	72-74	homeobox D13	Homo sapiens	17-20
16841956-0	2006	shRNA silencing of AS3MT expression minimizes arsenic methylation capacity of HepG2 cells.	Arsenic	46-53	arsenite methyltransferase	Homo sapiens	19-24
16479312-9	2006	Our results suggest that OATP-C can transport inorganic arsenic in a (GSH)-dependent manner.	Arsenic	56-63	solute carrier organic anion transporter family member 1B1	Homo sapiens	25-31
16413591-7	2006	We also showed a significant decrease in insulin mRNA expression of cells exposed to 5 microM sodium arsenite during 72 h. Our data suggest that arsenic may contribute to the development of diabetes mellitus by impairing pancreatic beta-cell functions, particularly insulin synthesis and secretion.	Arsenic	145-152	insulin	Homo sapiens	41-48
16368122-5	2006	Arsenic/TPA treatment resulted in increased expression of alpha-fetoprotein, k-ras, c-myc, estrogen receptor-alpha, cyclin D1, cdk2na, plasminogen activator inhibitor-1, cytokeratin-8, cytokeratin-18, glutathione S-transferases and insulin-like growth factor binding proteins in liver and liver tumors from both male and female mice.	Arsenic	0-7	alpha fetoprotein	Mus musculus	58-75
16368122-5	2006	Arsenic/TPA treatment resulted in increased expression of alpha-fetoprotein, k-ras, c-myc, estrogen receptor-alpha, cyclin D1, cdk2na, plasminogen activator inhibitor-1, cytokeratin-8, cytokeratin-18, glutathione S-transferases and insulin-like growth factor binding proteins in liver and liver tumors from both male and female mice.	Arsenic	0-7	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	77-82
16368122-5	2006	Arsenic/TPA treatment resulted in increased expression of alpha-fetoprotein, k-ras, c-myc, estrogen receptor-alpha, cyclin D1, cdk2na, plasminogen activator inhibitor-1, cytokeratin-8, cytokeratin-18, glutathione S-transferases and insulin-like growth factor binding proteins in liver and liver tumors from both male and female mice.	Arsenic	0-7	estrogen receptor 1 (alpha)	Mus musculus	91-114
16368122-5	2006	Arsenic/TPA treatment resulted in increased expression of alpha-fetoprotein, k-ras, c-myc, estrogen receptor-alpha, cyclin D1, cdk2na, plasminogen activator inhibitor-1, cytokeratin-8, cytokeratin-18, glutathione S-transferases and insulin-like growth factor binding proteins in liver and liver tumors from both male and female mice.	Arsenic	0-7	cyclin D1	Mus musculus	116-125
16368122-5	2006	Arsenic/TPA treatment resulted in increased expression of alpha-fetoprotein, k-ras, c-myc, estrogen receptor-alpha, cyclin D1, cdk2na, plasminogen activator inhibitor-1, cytokeratin-8, cytokeratin-18, glutathione S-transferases and insulin-like growth factor binding proteins in liver and liver tumors from both male and female mice.	Arsenic	0-7	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	127-168
16368122-5	2006	Arsenic/TPA treatment resulted in increased expression of alpha-fetoprotein, k-ras, c-myc, estrogen receptor-alpha, cyclin D1, cdk2na, plasminogen activator inhibitor-1, cytokeratin-8, cytokeratin-18, glutathione S-transferases and insulin-like growth factor binding proteins in liver and liver tumors from both male and female mice.	Arsenic	0-7	keratin 8	Mus musculus	170-183
16368122-5	2006	Arsenic/TPA treatment resulted in increased expression of alpha-fetoprotein, k-ras, c-myc, estrogen receptor-alpha, cyclin D1, cdk2na, plasminogen activator inhibitor-1, cytokeratin-8, cytokeratin-18, glutathione S-transferases and insulin-like growth factor binding proteins in liver and liver tumors from both male and female mice.	Arsenic	0-7	keratin 18	Mus musculus	185-199
16368122-6	2006	Arsenic/TPA also decreased the expression of BRCA1, betaine-homocysteine methyltransferase, CYP7B1, CYP2F2 and insulin-like growth factor-1 in normal and cancerous livers.	Arsenic	0-7	breast cancer 1, early onset	Mus musculus	45-50
16368122-6	2006	Arsenic/TPA also decreased the expression of BRCA1, betaine-homocysteine methyltransferase, CYP7B1, CYP2F2 and insulin-like growth factor-1 in normal and cancerous livers.	Arsenic	0-7	betaine-homocysteine methyltransferase	Mus musculus	52-90
16368122-6	2006	Arsenic/TPA also decreased the expression of BRCA1, betaine-homocysteine methyltransferase, CYP7B1, CYP2F2 and insulin-like growth factor-1 in normal and cancerous livers.	Arsenic	0-7	cytochrome P450, family 7, subfamily b, polypeptide 1	Mus musculus	92-98
16368122-6	2006	Arsenic/TPA also decreased the expression of BRCA1, betaine-homocysteine methyltransferase, CYP7B1, CYP2F2 and insulin-like growth factor-1 in normal and cancerous livers.	Arsenic	0-7	cytochrome P450, family 2, subfamily f, polypeptide 2	Mus musculus	100-106
16368122-6	2006	Arsenic/TPA also decreased the expression of BRCA1, betaine-homocysteine methyltransferase, CYP7B1, CYP2F2 and insulin-like growth factor-1 in normal and cancerous livers.	Arsenic	0-7	insulin-like growth factor 1	Mus musculus	111-139
16914093-0	2006	Arsenic enhances the apoptosis induced by interferon gamma: key role of IRF-1.	Arsenic	0-7	interferon gamma	Homo sapiens	42-58
16759981-0	2006	Chronic arsenic exposure and oxidative stress: OGG1 expression and arsenic exposure, nail selenium, and skin hyperkeratosis in Inner Mongolia.	Arsenic	8-15	8-oxoguanine DNA glycosylase	Homo sapiens	47-51
16709846-4	2006	PreBCR complexes retained in the TGN or shunted from the TGN to lysosomes were as or 50% as active as the corresponding wild-type preBCRs in directing preBCR-dependent events, including CD2 and CD22 expression and proliferation in primary pro-B cells.	Arsenic	79-81	CD2 molecule	Homo sapiens	186-189
16709846-4	2006	PreBCR complexes retained in the TGN or shunted from the TGN to lysosomes were as or 50% as active as the corresponding wild-type preBCRs in directing preBCR-dependent events, including CD2 and CD22 expression and proliferation in primary pro-B cells.	Arsenic	79-81	CD22 molecule	Homo sapiens	194-198
16565513-0	2006	Metallothionein-1 and -2 expression in cadmium- or arsenic-derived human malignant urothelial cells and tumor heterotransplants and as a prognostic indicator in human bladder cancer.	Arsenic	51-58	metallothionein 2A	Homo sapiens	0-24
16353154-10	2006	Individuals with GSTM1-positive (at least one allele) had significantly higher risk of arsenic-induced skin lesions (odds ratio, 1.73; 95% confidence interval, 1.24-2.22).	Arsenic	87-94	glutathione S-transferase mu 1	Homo sapiens	17-22
16403505-1	2006	The present study reports removal of As(V) by adsorption onto laboratory-prepared pure and Cu(II)-, Ni(II)-, and Co(II)-doped goethite samples.	Arsenic	37-39	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	113-119
16914093-0	2006	Arsenic enhances the apoptosis induced by interferon gamma: key role of IRF-1.	Arsenic	0-7	interferon regulatory factor 1	Homo sapiens	72-77
16214333-4	2006	Results showed that, compared to control group, there was a significant increase in the levels of nitric oxide (NO), malondialdehyde (MDA) and hydroxyl radical (OH-) formation in the pancreatic tissue of arsenic-treated rats, while the activity of antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT), and cellular content of antioxidant glutathione (GSH) were low in these animals.	Arsenic	204-211	catalase	Rattus norvegicus	300-308
16214333-4	2006	Results showed that, compared to control group, there was a significant increase in the levels of nitric oxide (NO), malondialdehyde (MDA) and hydroxyl radical (OH-) formation in the pancreatic tissue of arsenic-treated rats, while the activity of antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT), and cellular content of antioxidant glutathione (GSH) were low in these animals.	Arsenic	204-211	catalase	Rattus norvegicus	310-313
16531489-4	2006	Analyses demonstrated that TaPCS1 is expressed only in shoots and that CAB2TaPCS1/cad1-3 lines complement the cadmium (Cd) and arsenic metal sensitivity of cad1-3 shoots.	Arsenic	127-134	glutathione gamma-glutamylcysteinyltransferase 1	Triticum aestivum	27-33
16629649-7	2006	The expressions of TNF-alpha on KC and of intercellular adhesion molecule-1 on sinusoidal endothelial cells were completely suppressed in TNF-AS-treated livers.	Arsenic	142-144	tumor necrosis factor	Homo sapiens	19-28
16629649-7	2006	The expressions of TNF-alpha on KC and of intercellular adhesion molecule-1 on sinusoidal endothelial cells were completely suppressed in TNF-AS-treated livers.	Arsenic	142-144	intercellular adhesion molecule 1	Homo sapiens	42-75
16629649-7	2006	The expressions of TNF-alpha on KC and of intercellular adhesion molecule-1 on sinusoidal endothelial cells were completely suppressed in TNF-AS-treated livers.	Arsenic	142-144	tumor necrosis factor	Homo sapiens	19-22
16581878-0	2006	The shoot-specific expression of gamma-glutamylcysteine synthetase directs the long-distance transport of thiol-peptides to roots conferring tolerance to mercury and arsenic.	Arsenic	166-173	glutamate-cysteine ligase	Arabidopsis thaliana	33-66
16531489-4	2006	Analyses demonstrated that TaPCS1 is expressed only in shoots and that CAB2TaPCS1/cad1-3 lines complement the cadmium (Cd) and arsenic metal sensitivity of cad1-3 shoots.	Arsenic	127-134	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	71-81
16531489-4	2006	Analyses demonstrated that TaPCS1 is expressed only in shoots and that CAB2TaPCS1/cad1-3 lines complement the cadmium (Cd) and arsenic metal sensitivity of cad1-3 shoots.	Arsenic	127-134	cinnamyl-alcohol dehydrogenase	Arabidopsis thaliana	82-88
16531489-4	2006	Analyses demonstrated that TaPCS1 is expressed only in shoots and that CAB2TaPCS1/cad1-3 lines complement the cadmium (Cd) and arsenic metal sensitivity of cad1-3 shoots.	Arsenic	127-134	cinnamyl-alcohol dehydrogenase	Arabidopsis thaliana	82-86
16609772-15	2006	The calculations are in accordance with the experimentally preferred reactions when the As atom and the AsH fragment are generated in the quartet and triplet state, respectively.	Arsenic	88-90	arylsulfatase family member H	Homo sapiens	104-107
16436460-7	2006	The long-term arsenic exposure increased glutathione S-transferase (GST) activity and cellular glutathione (GSH) levels.	Arsenic	14-21	glutathione S-transferase kappa 1	Homo sapiens	41-66
16436460-7	2006	The long-term arsenic exposure increased glutathione S-transferase (GST) activity and cellular glutathione (GSH) levels.	Arsenic	14-21	glutathione S-transferase kappa 1	Homo sapiens	68-71
16436460-9	2006	The depletion of cellular GSH and the inhibition of Mrps and P-gp functions increased cellular arsenic uptake and reduced arsenic tolerance in these cells.	Arsenic	95-102	phosphoglycolate phosphatase	Homo sapiens	61-65
16436460-9	2006	The depletion of cellular GSH and the inhibition of Mrps and P-gp functions increased cellular arsenic uptake and reduced arsenic tolerance in these cells.	Arsenic	122-129	phosphoglycolate phosphatase	Homo sapiens	61-65
16737587-12	2006	Expression of hepatic MRP2 was increased with intragastric arsenic concentration.	Arsenic	59-66	ATP binding cassette subfamily C member 2	Rattus norvegicus	22-26
16737587-13	2006	A positive correlation between biliary arsenic concentration and MRP2 levels was found in liver (r = 0.986, P &lt; 0.05).	Arsenic	39-46	ATP binding cassette subfamily C member 2	Rattus norvegicus	65-69
16737587-17	2006	The function of MRP2 for transportation of arsenic and its metabolites is associated with the intracellular GSH level.	Arsenic	43-50	ATP binding cassette subfamily C member 2	Rattus norvegicus	16-20
16567632-0	2006	Hyperaccumulation of arsenic in the shoots of Arabidopsis silenced for arsenate reductase (ACR2).	Arsenic	21-28	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	71-89
16567632-0	2006	Hyperaccumulation of arsenic in the shoots of Arabidopsis silenced for arsenate reductase (ACR2).	Arsenic	21-28	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	91-95
16567632-1	2006	Endogenous plant arsenate reductase (ACR) activity converts arsenate to arsenite in roots, immobilizing arsenic below ground.	Arsenic	104-111	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	17-35
16567632-8	2006	Reducing expression of ACR2 homologs in tree, shrub, and grass species should play a vital role in the phytoremediation of environmental arsenic contamination.	Arsenic	137-144	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	23-27
16598022-0	2006	Arsenic resistance in Campylobacter spp.	Arsenic	0-7	histocompatibility minor 13	Homo sapiens	36-39
16516206-0	2006	Sulforaphane, an activator of Nrf2, suppresses cellular accumulation of arsenic and its cytotoxicity in primary mouse hepatocytes.	Arsenic	72-79	nuclear factor, erythroid derived 2, like 2	Mus musculus	30-34
16571148-9	2006	The decrease in the antioxidant status of konbu rats was related to the high As content of this alga, which led to a compensatory increase in glutathione reductase activity in these animals.	Arsenic	77-79	glutathione-disulfide reductase	Rattus norvegicus	142-163
16581540-3	2006	We have previously shown that aquaglyceroporin channels, including Escherichia coli GlpF, Saccharomyces cerevisiae Fps1p, AQP7, and AQP9 from rat and human, conduct trivalent inorganic arsenic [As(III)] as arsenic trioxide, the protonated form of arsenite.	Arsenic	185-192	Fps1p	Saccharomyces cerevisiae S288C	115-120
16581540-3	2006	We have previously shown that aquaglyceroporin channels, including Escherichia coli GlpF, Saccharomyces cerevisiae Fps1p, AQP7, and AQP9 from rat and human, conduct trivalent inorganic arsenic [As(III)] as arsenic trioxide, the protonated form of arsenite.	Arsenic	185-192	aquaporin 9	Homo sapiens	132-136
16597375-5	2006	Treatment with either arsenic or imatinib, or both, resulted in significant increases in serum creatine kinase isoenzyme (CK-MB), glutathione peroxidase (GPx), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) activity levels.	Arsenic	22-29	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	192-218
16597375-5	2006	Treatment with either arsenic or imatinib, or both, resulted in significant increases in serum creatine kinase isoenzyme (CK-MB), glutathione peroxidase (GPx), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) activity levels.	Arsenic	22-29	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	220-223
16581540-10	2006	This is similar to that found for As(III), suggesting that As(III) and MAs(III) use the same translocation pathway in AQP9.	Arsenic	34-36	aquaporin 9	Rattus norvegicus	118-122
16581540-11	2006	Identification of MAs(III) as an AQP9 substrate is an important step in understanding physiologic responses to arsenic in mammals, including humans.	Arsenic	111-118	aquaporin 9	Homo sapiens	33-37
16461332-6	2006	Increased urine arsenic levels were associated with a reduced proliferative response to phytohemaglutinin (PHA) stimulation (P=0.005), CD4 subpopulation proportion (P=0.092), CD4/CD8 ratio (P=0.056), and IL-2 secretion levels (P=0.003).	Arsenic	16-23	CD4 molecule	Homo sapiens	135-138
16461332-6	2006	Increased urine arsenic levels were associated with a reduced proliferative response to phytohemaglutinin (PHA) stimulation (P=0.005), CD4 subpopulation proportion (P=0.092), CD4/CD8 ratio (P=0.056), and IL-2 secretion levels (P=0.003).	Arsenic	16-23	CD4 molecule	Homo sapiens	175-178
16461332-6	2006	Increased urine arsenic levels were associated with a reduced proliferative response to phytohemaglutinin (PHA) stimulation (P=0.005), CD4 subpopulation proportion (P=0.092), CD4/CD8 ratio (P=0.056), and IL-2 secretion levels (P=0.003).	Arsenic	16-23	CD8a molecule	Homo sapiens	179-182
16461332-6	2006	Increased urine arsenic levels were associated with a reduced proliferative response to phytohemaglutinin (PHA) stimulation (P=0.005), CD4 subpopulation proportion (P=0.092), CD4/CD8 ratio (P=0.056), and IL-2 secretion levels (P=0.003).	Arsenic	16-23	interleukin 2	Homo sapiens	204-208
16461332-7	2006	Increased arsenic exposure was also associated with an increase in GM-CSF secretion by mononucleated cells (P=0.000).	Arsenic	10-17	colony stimulating factor 2	Homo sapiens	67-73
16461332-9	2006	These data indicate that arsenic exposure could alter the activation processes of T cells, such that an immunosuppression status that favors opportunistic infections and carcinogenesis is produced together with increased GM-CSF secretion that may be associated with chronic inflammation.	Arsenic	25-32	colony stimulating factor 2	Homo sapiens	221-227
23105572-7	2006	Mean arsenic level detected in samples collected from tap water supply was 0.013 ppm (Range 0-0.0430 ppm, Standard Deviation 0.00911 and Standard error of Mean 0.000515).	Arsenic	5-12	nuclear RNA export factor 1	Homo sapiens	54-57
16507454-0	2006	The impact of diet and betel nut use on skin lesions associated with drinking-water arsenic in Pabna, Bangladesh.	Arsenic	84-91	NUT midline carcinoma family member 1	Homo sapiens	29-32
16407288-12	2006	These results raise the possibility that inherited variation in AS3MT may contribute to variation in arsenic metabolism and, perhaps, arsenic-dependent carcinogenesis in humans.	Arsenic	101-108	arsenite methyltransferase	Homo sapiens	64-69
16407288-12	2006	These results raise the possibility that inherited variation in AS3MT may contribute to variation in arsenic metabolism and, perhaps, arsenic-dependent carcinogenesis in humans.	Arsenic	134-141	arsenite methyltransferase	Homo sapiens	64-69
16406071-4	2006	We present atomic-resolution crystal structures and biophysical data for human SOD1 in three metallation states: Zn-Zn, Cu-Zn and as-isolated.	Arsenic	130-132	superoxide dismutase 1	Homo sapiens	79-83
23105572-9	2006	The mean arsenic level detected in water samples of booster pumping station was within WHO/EPA permissible limit while mean arsenic level detected in tap water samples was marginally higher.	Arsenic	124-131	nuclear RNA export factor 1	Homo sapiens	150-153
23105572-10	2006	Mixing of ground water and contamination through broken or leaking channel could be the possible reason of higher arsenic level in tap water.	Arsenic	114-121	nuclear RNA export factor 1	Homo sapiens	131-134
16428081-12	2006	Lysosomal enzyme release from splenic macrophages decreased upon simultaneous exposure to arsenic and lead, as is evident from the decrease in myeloperoxidase release in multimetal group from that in control.	Arsenic	90-97	myeloperoxidase	Mus musculus	143-158
16452187-0	2006	Urogenital carcinogenesis in female CD1 mice induced by in utero arsenic exposure is exacerbated by postnatal diethylstilbestrol treatment.	Arsenic	65-72	CD1 antigen complex	Mus musculus	36-39
16428081-16	2006	Simultaneous exposure to lead and arsenic appears to be additive as is further established from the isobologram constructed by plotting the concentration of arsenic against the concentration of lead at which effect (in this case myeloperoxidase release) remained constant, a convex line showing synergism was demonstrated.	Arsenic	34-41	myeloperoxidase	Mus musculus	229-244
16452187-11	2006	In neonatal uteri, prenatal arsenic increased ER-alpha expression and enhanced estrogen-related gene expression induced by postnatal diethylstilbestrol.	Arsenic	28-35	estrogen receptor 1 (alpha)	Mus musculus	46-54
16531839-0	2006	Metabolic profile in workers occupationally exposed to arsenic: role of GST polymorphisms.	Arsenic	55-62	glutathione S-transferase kappa 1	Homo sapiens	72-75
16338954-3	2006	However, roles of securin on the arsenic-induced cell cycle arrest and apoptosis remain unknown.	Arsenic	33-40	PTTG1 regulator of sister chromatid separation, securin	Homo sapiens	18-25
16572798-1	2006	The risk posed from incidental ingestion to humans of arsenic-contaminated soil may depend on sorption of arsenate (As(V)) to oxide surfaces in soil.	Arsenic	54-61	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	116-121
16452187-2	2006	Pregnant CD1 mice received 85 ppm arsenic in the drinking water from gestation days 8 to 18 and were allowed to give birth.	Arsenic	34-41	CD1 antigen complex	Mus musculus	9-12
19771260-5	2006	Western blot analysis was performed to identify the activated caspases after As(2)O(3) exposure, and we compared the possible target molecules of apoptosis.	Arsenic	77-79	caspase 9	Homo sapiens	62-70
16452187-10	2006	Uterine and bladder carcinoma induced by arsenic plus diethylstilbestrol greatly overexpressed estrogen receptor-alpha (ER-alpha) and pS2, an estrogen-regulated gene.	Arsenic	41-48	estrogen receptor 1 (alpha)	Mus musculus	95-118
16452187-10	2006	Uterine and bladder carcinoma induced by arsenic plus diethylstilbestrol greatly overexpressed estrogen receptor-alpha (ER-alpha) and pS2, an estrogen-regulated gene.	Arsenic	41-48	estrogen receptor 1 (alpha)	Mus musculus	120-128
16452187-10	2006	Uterine and bladder carcinoma induced by arsenic plus diethylstilbestrol greatly overexpressed estrogen receptor-alpha (ER-alpha) and pS2, an estrogen-regulated gene.	Arsenic	41-48	trefoil factor 1	Mus musculus	134-137
16251483-0	2006	DNA hypermethylation of promoter of gene p53 and p16 in arsenic-exposed people with and without malignancy.	Arsenic	56-63	tumor protein p53	Homo sapiens	41-44
16420308-0	2006	Defective beta1-integrins expression in arsenical keratosis and arsenic-treated cultured human keratinocytes.	Arsenic	40-47	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	10-15
16420308-7	2006	Western blotting was used to assess the expression of integrin beta1 and focal adhesion kinase (FAK) in arsenic-treated cultured keratinocytes.	Arsenic	104-111	integrin subunit beta 1	Homo sapiens	54-68
16420308-7	2006	Western blotting was used to assess the expression of integrin beta1 and focal adhesion kinase (FAK) in arsenic-treated cultured keratinocytes.	Arsenic	104-111	protein tyrosine kinase 2	Homo sapiens	73-94
16420308-7	2006	Western blotting was used to assess the expression of integrin beta1 and focal adhesion kinase (FAK) in arsenic-treated cultured keratinocytes.	Arsenic	104-111	protein tyrosine kinase 2	Homo sapiens	96-99
16420308-9	2006	The expressions of integrin beta1 and FAK were both decreased in arsenic-treated keratinocytes.	Arsenic	65-72	integrin subunit beta 1	Homo sapiens	19-33
16420308-9	2006	The expressions of integrin beta1 and FAK were both decreased in arsenic-treated keratinocytes.	Arsenic	65-72	protein tyrosine kinase 2	Homo sapiens	38-41
16251483-4	2006	Significant DNA hypermethylation of promoter region of p53 gene was observed in DNA of arsenic-exposed people compared to control subjects.	Arsenic	87-94	tumor protein p53	Homo sapiens	55-58
16251483-0	2006	DNA hypermethylation of promoter of gene p53 and p16 in arsenic-exposed people with and without malignancy.	Arsenic	56-63	cyclin dependent kinase inhibitor 2A	Homo sapiens	49-52
16251483-6	2006	Further, hypermethylation of p53 gene was also observed in arsenic-induced skin cancer patients compared to subjects having skin cancer unrelated to arsenic, though not at significant level.	Arsenic	59-66	tumor protein p53	Homo sapiens	29-32
16251483-6	2006	Further, hypermethylation of p53 gene was also observed in arsenic-induced skin cancer patients compared to subjects having skin cancer unrelated to arsenic, though not at significant level.	Arsenic	149-156	tumor protein p53	Homo sapiens	29-32
16421274-0	2006	Nucleolin links to arsenic-induced stabilization of GADD45alpha mRNA.	Arsenic	19-26	nucleolin	Homo sapiens	0-9
16251483-8	2006	Significant hypermethylation of gene p16 was also observed in cases of arsenicosis exposed to high level of arsenic.	Arsenic	71-78	cyclin dependent kinase inhibitor 2A	Homo sapiens	37-40
16251483-9	2006	In man, arsenic has the ability to alter DNA methylation patterns in gene p53 and p16, which are important in carcinogenesis.	Arsenic	8-15	tumor protein p53	Homo sapiens	74-77
16251483-9	2006	In man, arsenic has the ability to alter DNA methylation patterns in gene p53 and p16, which are important in carcinogenesis.	Arsenic	8-15	cyclin dependent kinase inhibitor 2A	Homo sapiens	82-85
16421274-0	2006	Nucleolin links to arsenic-induced stabilization of GADD45alpha mRNA.	Arsenic	19-26	growth arrest and DNA damage inducible alpha	Homo sapiens	52-63
16421274-1	2006	The present study shows that arsenic induces GADD45alpha (growth arrest and DNA damage inducible gene 45alpha) mainly through post-transcriptional mechanism.	Arsenic	29-36	growth arrest and DNA damage inducible alpha	Homo sapiens	45-56
16288947-9	2006	RESULTS: A significant increase in cytochrome-P450 and lipid peroxidation accompanied with a significant alteration in the activity of many of the antioxidants was observed, all suggestive of arsenic induced oxidative stress.	Arsenic	192-199	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	35-50
16260785-7	2006	Our homology model of Arr4p shows that the antimony (arsenic) metal binding site of ArsA is not conserved in Arr4p.	Arsenic	53-60	guanine nucleotide exchange factor GET3	Saccharomyces cerevisiae S288C	22-27
16791002-0	2006	Arsenic inhibits CFTR-mediated chloride secretion by killifish (Fundulus heteroclitus) opercular membrane.	Arsenic	0-7	cystic fibrosis transmembrane conductance regulator	Fundulus heteroclitus	17-21
16475721-9	2006	Bcl-2 and c-Fos may play important roles in arsenic-mediated carcinogenesis of the urothelium.	Arsenic	44-51	BCL2 apoptosis regulator	Homo sapiens	0-5
16475721-9	2006	Bcl-2 and c-Fos may play important roles in arsenic-mediated carcinogenesis of the urothelium.	Arsenic	44-51	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	10-15
16487037-0	2006	Induction of endogenous Nrf2/small maf heterodimers by arsenic-mediated stress in placental choriocarcinoma cells.	Arsenic	55-62	NFE2 like bZIP transcription factor 2	Homo sapiens	24-28
16487037-0	2006	Induction of endogenous Nrf2/small maf heterodimers by arsenic-mediated stress in placental choriocarcinoma cells.	Arsenic	55-62	MAF bZIP transcription factor	Homo sapiens	35-38
15987713-7	2006	Arsenic exposure, measured as toenail arsenic, was associated with RASSF1A (P&lt;0.02) and PRSS3 (P&lt;0.1) but not p16INK4A promoter methylation, in models adjusted for stage and other factors.	Arsenic	0-7	Ras association domain family member 1	Homo sapiens	67-74
15987713-7	2006	Arsenic exposure, measured as toenail arsenic, was associated with RASSF1A (P&lt;0.02) and PRSS3 (P&lt;0.1) but not p16INK4A promoter methylation, in models adjusted for stage and other factors.	Arsenic	0-7	serine protease 3	Homo sapiens	91-96
15987713-7	2006	Arsenic exposure, measured as toenail arsenic, was associated with RASSF1A (P&lt;0.02) and PRSS3 (P&lt;0.1) but not p16INK4A promoter methylation, in models adjusted for stage and other factors.	Arsenic	38-45	Ras association domain family member 1	Homo sapiens	67-74
16487037-3	2006	The nuclear protein levels of the CNC transcription factor Nrf2 were strongly induced in the presence of arsenic.	Arsenic	105-112	NFE2 like bZIP transcription factor 2	Homo sapiens	59-63
16487037-4	2006	Dosage response experiments showed that 0.5 microM of arsenic is sufficient to augment Nrf2 levels.	Arsenic	54-61	NFE2 like bZIP transcription factor 2	Homo sapiens	87-91
16487037-6	2006	Arsenic also induced the binding of endogenous Nrf2/small Maf DNA-binding complexes to a stress response element (StRE) recognition site.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	47-51
16487037-6	2006	Arsenic also induced the binding of endogenous Nrf2/small Maf DNA-binding complexes to a stress response element (StRE) recognition site.	Arsenic	0-7	MAF bZIP transcription factor	Homo sapiens	58-61
16487037-8	2006	Expression of the enzyme heme oxygenase-1 (HO-1), a known Nrf2 target gene, was upregulated by exposure of JAR cells to arsenic.	Arsenic	120-127	heme oxygenase 1	Homo sapiens	25-41
16487037-8	2006	Expression of the enzyme heme oxygenase-1 (HO-1), a known Nrf2 target gene, was upregulated by exposure of JAR cells to arsenic.	Arsenic	120-127	NFE2 like bZIP transcription factor 2	Homo sapiens	58-62
16487037-9	2006	These results suggest that Nrf2/small Maf heterodimers may play an important role in the response to arsenic-mediated stress in placental cells.	Arsenic	101-108	NFE2 like bZIP transcription factor 2	Homo sapiens	27-31
16487037-9	2006	These results suggest that Nrf2/small Maf heterodimers may play an important role in the response to arsenic-mediated stress in placental cells.	Arsenic	101-108	MAF bZIP transcription factor	Homo sapiens	38-41
16845179-5	2006	Arsenic has been shown to increase the formation of peroxynitrite in bovine aortic endothelial cells (BAECs) and promote the formation of 3-nitrotyrosine (3-NY) in the atherosclerotic plaque of ApoE-/-/LDLr-/- mice.	Arsenic	0-7	apolipoprotein E	Bos taurus	194-198
16845179-5	2006	Arsenic has been shown to increase the formation of peroxynitrite in bovine aortic endothelial cells (BAECs) and promote the formation of 3-nitrotyrosine (3-NY) in the atherosclerotic plaque of ApoE-/-/LDLr-/- mice.	Arsenic	0-7	low density lipoprotein receptor	Bos taurus	202-206
16845179-6	2006	Arsenic exposure also increases leukotriene E4 (LTE4) formation in both the mice and BAECs, an effect that is partially reversed by the addition of Nomega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor.	Arsenic	0-7	nitric oxide synthase 1, neuronal	Mus musculus	197-218
16791002-6	2006	To determine if arsenic blocked acclimation by inhibiting CFTR mediated Cl- secretion (Isc), opercular membranes were isolated and mounted in Ussing chambers and the effects of arsenic on Isc were measured.	Arsenic	16-23	cystic fibrosis transmembrane conductance regulator	Fundulus heteroclitus	58-62
16283526-0	2005	Deficiency in Ikkbeta gene enhances arsenic-induced gadd45alpha expression.	Arsenic	36-43	growth arrest and DNA damage inducible alpha	Homo sapiens	52-63
16931443-6	2006	Arsenic-induced decreased glutathione reductase activity in liver and increased activity in kidney was appreciably counteracted by melatonin.	Arsenic	0-7	glutathione-disulfide reductase	Rattus norvegicus	26-47
17278761-1	2006	It was observed that the atomic fluorescence emission due to As(V) could has a 10% to 40% of fluorescence emission signal during the determination of As(III) in the mixture of As(III) and As(V).	Arsenic	61-63	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	188-193
15986429-9	2005	The incidence of lung metastasis was increased from 6% in AS to 98% in AS-SMAGP tumor-bearing rats.	Arsenic	71-73	small cell adhesion glycoprotein	Rattus norvegicus	74-79
16475353-9	2005	The reaction products produced by the media in domestic tap water had average As-to-Fe ratios that were approximately 25% higher than those for a commercially available adsorbent.	Arsenic	78-80	SEC14 like lipid binding 2	Homo sapiens	56-59
16323906-4	2005	Both the syn and anti macrocycles show close contacts between the arsenic(III) ions and the aromatic carbons, consistent with intramolecular arsenic-pi interactions.	Arsenic	66-73	synemin	Homo sapiens	9-12
16205725-5	2005	There was a significant decrease in cardiac angiotensin II type 1 receptor (AT(1)R) expression in AS-treated rats compared to vehicle-treated rats; cardiac AT(1)R was decreased to 80+/-6% in comparison to 100%.	Arsenic	98-100	angiotensin II receptor, type 1b	Rattus norvegicus	44-74
16205725-5	2005	There was a significant decrease in cardiac angiotensin II type 1 receptor (AT(1)R) expression in AS-treated rats compared to vehicle-treated rats; cardiac AT(1)R was decreased to 80+/-6% in comparison to 100%.	Arsenic	98-100	angiotensin II receptor, type 1b	Rattus norvegicus	76-82
16205725-5	2005	There was a significant decrease in cardiac angiotensin II type 1 receptor (AT(1)R) expression in AS-treated rats compared to vehicle-treated rats; cardiac AT(1)R was decreased to 80+/-6% in comparison to 100%.	Arsenic	98-100	angiotensin II receptor, type 1b	Rattus norvegicus	156-162
16205725-6	2005	AT(1)R immunoreactivity was also reduced in IGF-IR AS-treated tail arteries.IGF-IR AS treatment resulted in structural changes in both the heart and aortae, with small but significant differences observed between left ventricle/bodyweight ratios of AS and both vehicle- and MM-18-treated rats (n=8, P&lt;0.05).	Arsenic	51-53	angiotensin II receptor, type 1b	Rattus norvegicus	0-6
16322246-4	2005	As poly(ADP-ribose) polymerase (PARP) is critical for genomic DNA stability, role of PARP-1 was evaluated in arsenic-induced cytotoxic and genotoxic effects.	Arsenic	109-116	poly(ADP-ribose) polymerase 1	Homo sapiens	3-30
16027966-9	2005	The arsenic content in polluted paddy soils and river/brook water is 46.26-496.19 microg g(-1), 0.3-16.5 mgL(-1), respectively.	Arsenic	4-11	LLGL scribble cell polarity complex component 1	Homo sapiens	105-111
16290184-6	2005	The Mn-minerals promoted the oxidation of As(III) to As(V), for both sorbed and dissolved As-species.	Arsenic	42-44	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	53-58
16084078-5	2005	Among the arsenic groups, the expression of CAMs on ECs and CD11b, and IL-8 receptor on PMNs was lowest with 0 microM compared with the other GLN concentrations.	Arsenic	10-17	integrin subunit alpha M	Homo sapiens	60-65
16283521-3	2005	Currently, we have investigated whether the eukaryotic translation initiation factor 4E (eIF4E), the mRNA cap binding and rate limiting factor required for translation, is a target for As-induced cytotoxicity and cell death.	Arsenic	185-187	eukaryotic translation initiation factor 4E	Homo sapiens	44-87
16283521-3	2005	Currently, we have investigated whether the eukaryotic translation initiation factor 4E (eIF4E), the mRNA cap binding and rate limiting factor required for translation, is a target for As-induced cytotoxicity and cell death.	Arsenic	185-187	eukaryotic translation initiation factor 4E	Homo sapiens	89-94
16283521-4	2005	We have also investigated the potential cellular mechanisms underlying the As-induced de-regulation of expression of eIF4E that are most likely responsible for the cytotoxicity and cell death induced by As.	Arsenic	75-77	eukaryotic translation initiation factor 4E	Homo sapiens	117-122
16283521-4	2005	We have also investigated the potential cellular mechanisms underlying the As-induced de-regulation of expression of eIF4E that are most likely responsible for the cytotoxicity and cell death induced by As.	Arsenic	203-205	eukaryotic translation initiation factor 4E	Homo sapiens	117-122
17145702-12	2006	A large percentage of the altered genes and proteins are known to be regulated by redox-sensitive transcription factors, (SP1, NF kappaB, AP-1), suggesting that, at environmentally relevant levels of chronic exposure, arsenic may be acting through alteration of cellular redox status.	Arsenic	218-225	nuclear factor kappa B subunit 1	Homo sapiens	127-136
17145702-12	2006	A large percentage of the altered genes and proteins are known to be regulated by redox-sensitive transcription factors, (SP1, NF kappaB, AP-1), suggesting that, at environmentally relevant levels of chronic exposure, arsenic may be acting through alteration of cellular redox status.	Arsenic	218-225	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	138-142
16337887-5	2006	Arsenic, cadmium, and mercury showed little oxidation of GSH but significantly oxidized both Trx1 and Trx2.	Arsenic	0-7	thioredoxin	Homo sapiens	93-97
16337887-5	2006	Arsenic, cadmium, and mercury showed little oxidation of GSH but significantly oxidized both Trx1 and Trx2.	Arsenic	0-7	thioredoxin 2	Homo sapiens	102-106
16337887-6	2006	The magnitude of effects of arsenic, cadmium, and mercury was greater for the mitochondrial Trx2 (&gt;60 mV) compared to the cytoplasmic Trx1 (20 to 40 mV).	Arsenic	28-35	thioredoxin 2	Homo sapiens	92-96
16959597-6	2006	Concomitant administration of zinc with arsenic showed remarkable protection against blood delta-aminolevulinic acid dehydratase (ALAD) activity as well as providing protection to hepatic biochemical variables indicative of oxidative stress (like thiobarbituric acid reactive substances (TBARS) level, catalase) and tissue injury.	Arsenic	40-47	aminolevulinate dehydratase	Rattus norvegicus	91-128
16959597-6	2006	Concomitant administration of zinc with arsenic showed remarkable protection against blood delta-aminolevulinic acid dehydratase (ALAD) activity as well as providing protection to hepatic biochemical variables indicative of oxidative stress (like thiobarbituric acid reactive substances (TBARS) level, catalase) and tissue injury.	Arsenic	40-47	aminolevulinate dehydratase	Rattus norvegicus	130-134
16959597-6	2006	Concomitant administration of zinc with arsenic showed remarkable protection against blood delta-aminolevulinic acid dehydratase (ALAD) activity as well as providing protection to hepatic biochemical variables indicative of oxidative stress (like thiobarbituric acid reactive substances (TBARS) level, catalase) and tissue injury.	Arsenic	40-47	catalase	Rattus norvegicus	302-310
15998567-6	2005	Supplementation of DL-alpha-lipoic acid and meso 2,3 dimercapto succinic acid to arsenic fed rats significantly increased the activities of superoxide dismutase, catalase, glutathione peroxidase with elevation in the levels of reduced glutathione, total sulfhydryl, ascorbic acid and alpha-tocopherol.	Arsenic	81-88	catalase	Rattus norvegicus	162-170
16322246-4	2005	As poly(ADP-ribose) polymerase (PARP) is critical for genomic DNA stability, role of PARP-1 was evaluated in arsenic-induced cytotoxic and genotoxic effects.	Arsenic	109-116	poly(ADP-ribose) polymerase 1	Homo sapiens	85-91
16274885-10	2005	Our data clearly show that As(3+)-, Cd(2+)-, and Cr(6+)-induced oxidative stress modulates Cyp1a1 at transcriptional and posttranscriptional levels but induces Nqo1 and Gst ya at the transcriptional level.	Arsenic	27-29	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	91-97
16274885-10	2005	Our data clearly show that As(3+)-, Cd(2+)-, and Cr(6+)-induced oxidative stress modulates Cyp1a1 at transcriptional and posttranscriptional levels but induces Nqo1 and Gst ya at the transcriptional level.	Arsenic	27-29	NAD(P)H quinone dehydrogenase 1	Homo sapiens	160-164
16135519-4	2005	Nox4 protein expression was increased in diabetic kidney cortex compared with non-diabetic controls and was down-regulated in AS-treated animals.	Arsenic	126-128	NADPH oxidase 4	Rattus norvegicus	0-4
16135519-8	2005	Moreover, the increased expression of fibronectin protein was markedly reduced in renal cortex including glomeruli of AS-treated diabetic rats.	Arsenic	118-120	fibronectin 1	Rattus norvegicus	38-49
16283526-6	2005	Thus, these results uncover the molecular mechanism by which NF-kappaB signalling contributes to the regulation of gadd family gene expression induced by arsenic.	Arsenic	154-161	nuclear factor kappa B subunit 1	Homo sapiens	61-70
16283526-4	2005	Ikkbeta deficiency prevented the induction of gadd45beta and gadd45gamma by arsenic, whereas the induction of gadd45alpha and gadd153 was appreciably enhanced in Ikkbeta-/- cells.	Arsenic	76-83	growth arrest and DNA damage inducible beta	Homo sapiens	46-56
16283526-4	2005	Ikkbeta deficiency prevented the induction of gadd45beta and gadd45gamma by arsenic, whereas the induction of gadd45alpha and gadd153 was appreciably enhanced in Ikkbeta-/- cells.	Arsenic	76-83	growth arrest and DNA damage inducible gamma	Homo sapiens	61-72
16283526-4	2005	Ikkbeta deficiency prevented the induction of gadd45beta and gadd45gamma by arsenic, whereas the induction of gadd45alpha and gadd153 was appreciably enhanced in Ikkbeta-/- cells.	Arsenic	76-83	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	0-7
16099114-9	2005	In this work we demonstrate that genetic biomarkers such as CYP1A1 2A and GSTM1 polymorphisms in addition to DR70 as screening biomarkers might provide relevant information to identify individuals with higher risk for lung cancer, due to arsenic exposure.	Arsenic	238-245	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	60-66
16239170-2	2005	Recent research has also linked this vascular damage to impairment of endothelial nitric oxide synthase (eNOS) function by arsenic exposure.	Arsenic	123-130	nitric oxide synthase 3	Homo sapiens	70-103
16239170-2	2005	Recent research has also linked this vascular damage to impairment of endothelial nitric oxide synthase (eNOS) function by arsenic exposure.	Arsenic	123-130	nitric oxide synthase 3	Homo sapiens	105-109
16099114-9	2005	In this work we demonstrate that genetic biomarkers such as CYP1A1 2A and GSTM1 polymorphisms in addition to DR70 as screening biomarkers might provide relevant information to identify individuals with higher risk for lung cancer, due to arsenic exposure.	Arsenic	238-245	glutathione S-transferase mu 1	Homo sapiens	74-79
16333752-7	2005	These results indicate that GCS-1 is essential for the synthesis of intracellular GSH in C. elegans and consequently that the intracellular GSH status plays a critical role in protection of C. elegans from arsenic-induced oxidative stress.	Arsenic	206-213	Glutamate--cysteine ligase	Caenorhabditis elegans	28-33
19956532-11	2005	CONCLUSION: Taken together, these findings suggest that a novel arsenic compound, As(4)O(6), possesses more potent anti-proliferative effects on human cervical cancer cells, with the induction of apoptosis also, at least via the activation of Bax protein in vitro.	Arsenic	64-71	BCL2 associated X, apoptosis regulator	Homo sapiens	243-246
16333752-0	2005	Caenorhabditis elegans gcs-1 confers resistance to arsenic-induced oxidative stress.	Arsenic	51-58	Glutamate--cysteine ligase	Caenorhabditis elegans	23-28
16014739-10	2005	These results suggest that regulation of glutathione levels by GCLM determines the sensitivity to arsenic-induced apoptosis by setting the overall ability of the cells to mount an effective antioxidant response.	Arsenic	98-105	glutamate-cysteine ligase, modifier subunit	Mus musculus	63-67
16076760-6	2005	These results suggested that the NADPH oxidase, MnSOD, and e-NOS polymorphisms, but not catalase, might play a role in the development of arsenic-related hypertension, especially in subjects with high triglyceride levels.	Arsenic	138-145	superoxide dismutase 2	Homo sapiens	48-53
16171347-4	2005	In this work, we show that the as-deposited films are structurally unstable above 125 K on Au(111)/mica surfaces and above 100 K on the organic self-assembled monolayers.	Arsenic	31-33	MHC class I polypeptide-related sequence A	Homo sapiens	99-103
16102566-0	2005	Metabolism and toxicity of arsenic in human urothelial cells expressing rat arsenic (+3 oxidation state)-methyltransferase.	Arsenic	27-34	arsenite methyltransferase	Rattus norvegicus	76-122
15961223-1	2005	The effect of the organic species oxalate, citrate and acetate and the inorganic species silicate and phosphate on release of As(V) from synthetic arsenic-loaded ferrihydrite and Al-ferrihydrite in the pH range 4-8 was investigated.	Arsenic	147-154	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	126-131
16162327-8	2005	The correlation between DHA and soluble arsenic containing both As(V) and As(III) was not significant (r=0.24).	Arsenic	40-47	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	64-69
16007375-4	2005	Respiratory burst activity and TNF-alpha expression were decreased upon arsenic exposure, indicating inhibition of TNF-alpha priming of the respiratory burst response.	Arsenic	72-79	tumor necrosis factor a (TNF superfamily, member 2)	Danio rerio	31-40
16007375-4	2005	Respiratory burst activity and TNF-alpha expression were decreased upon arsenic exposure, indicating inhibition of TNF-alpha priming of the respiratory burst response.	Arsenic	72-79	tumor necrosis factor a (TNF superfamily, member 2)	Danio rerio	115-124
16007375-5	2005	Arsenic enhanced IFN expression slightly over time, but reduced MX : expression.	Arsenic	0-7	interferon phi 1	Danio rerio	17-20
16007375-6	2005	In zebrafish infected with snakehead rhabdovirus, arsenic decreased induction and altered the kinetics of IFN and MX : upon infection.	Arsenic	50-57	interferon phi 1	Danio rerio	106-109
16007375-7	2005	Differences in IFN and MX : expression in arsenic-exposed larvae point toward an interruption of the Janus kinase-signal transducer and activator of transcription (JAK/STAT) pathway.	Arsenic	42-49	interferon phi 1	Danio rerio	15-25
16007375-7	2005	Differences in IFN and MX : expression in arsenic-exposed larvae point toward an interruption of the Janus kinase-signal transducer and activator of transcription (JAK/STAT) pathway.	Arsenic	42-49	signal transducer and activator of transcription 4	Danio rerio	168-172
16132727-13	2005	These results suggest that cellular injury by arsenic is mediated through ROS generation resulting in the expression of Hsp70.	Arsenic	46-53	heat shock protein family A (Hsp70) member 4	Homo sapiens	120-125
16132727-14	2005	It is possible that Hsp70 may prove to be a sensitive biomarker for arsenic exposure with other markers of oxidative stress in human serum.	Arsenic	68-75	heat shock protein family A (Hsp70) member 4	Homo sapiens	20-25
16076760-6	2005	These results suggested that the NADPH oxidase, MnSOD, and e-NOS polymorphisms, but not catalase, might play a role in the development of arsenic-related hypertension, especially in subjects with high triglyceride levels.	Arsenic	138-145	nitric oxide synthase 3	Homo sapiens	59-64
16329590-1	2005	OBJECTIVE: Effects of arsenic on the levels of estradiol (E2), follicle stimulating hormone (FSH), luteinizing hormone (LH) and prolactin (PRL) in serum of female rats, as well as histopathological changes of ovary and adrenal gland were researched.	Arsenic	22-29	prolactin	Rattus norvegicus	128-137
16087744-9	2005	We conclude that the toxic effects of arsenic are not strongly connected to oxidative stress and that although Spc1 is activated by arsenic exposure, the basal activity of Spc1 is largely sufficient for the survival of arsenic.	Arsenic	132-139	signal peptidase complex subunit 1	Homo sapiens	111-115
15967209-5	2005	Both mutation type and hot spots of p53 gene were significantly different in arsenic-induced and non-arsenic-induced TCCs.	Arsenic	77-84	tumor protein p53	Homo sapiens	36-39
15967209-5	2005	Both mutation type and hot spots of p53 gene were significantly different in arsenic-induced and non-arsenic-induced TCCs.	Arsenic	101-108	tumor protein p53	Homo sapiens	36-39
16173569-10	2005	However, for Sharkey clay, which exhibited strongest affinity for arsenic, an additional irreversible reaction phase was required to predict As(V) desorption or release with time.	Arsenic	66-73	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	141-146
16039940-0	2005	Molecular events associated with arsenic-induced malignant transformation of human prostatic epithelial cells: aberrant genomic DNA methylation and K-ras oncogene activation.	Arsenic	33-40	KRAS proto-oncogene, GTPase	Homo sapiens	148-153
16087744-9	2005	We conclude that the toxic effects of arsenic are not strongly connected to oxidative stress and that although Spc1 is activated by arsenic exposure, the basal activity of Spc1 is largely sufficient for the survival of arsenic.	Arsenic	132-139	signal peptidase complex subunit 1	Homo sapiens	111-115
16084973-8	2005	In contrast, during the warm season, desorption from As-rich sediment occurs which results in an increase of As(V) and As(III) concentrations along Amous river flow until they reach up to approximately 20 microg/l each.	Arsenic	53-55	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	109-114
16240177-8	2005	The MT1 knockdown plant lines were all hypersensitive to Cd and accumulated several fold lower levels of As, Cd, and Zn than wildtype, while Cu and Fe levels were unaffected.	Arsenic	105-107	metallothionein 1A	Arabidopsis thaliana	4-7
15893845-5	2005	RESULTS: AS group exhibited a significant decrease in total beta-catenin at 24 h. A significant decrease in liver/body weight ratio was also observed in the AS group at 24 h and 7 days that was due to decreased proliferation.	Arsenic	9-11	catenin beta 1	Rattus norvegicus	60-72
15761015-6	2005	We further explored the mechanisms by which ROS affects gene regulation and found that the Sp1 transcription factor was oxidized by arsenic treatment, with a corresponding decrease in its in situ binding on the promoters of 3 genes, hTERT, C17, and c-Myc, whose expressions were significantly suppressed.	Arsenic	132-139	telomerase reverse transcriptase	Homo sapiens	233-238
15761015-6	2005	We further explored the mechanisms by which ROS affects gene regulation and found that the Sp1 transcription factor was oxidized by arsenic treatment, with a corresponding decrease in its in situ binding on the promoters of 3 genes, hTERT, C17, and c-Myc, whose expressions were significantly suppressed.	Arsenic	132-139	cytokine like 1	Homo sapiens	240-243
15761015-6	2005	We further explored the mechanisms by which ROS affects gene regulation and found that the Sp1 transcription factor was oxidized by arsenic treatment, with a corresponding decrease in its in situ binding on the promoters of 3 genes, hTERT, C17, and c-Myc, whose expressions were significantly suppressed.	Arsenic	132-139	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	249-254
16394429-0	2005	Cryptic exposure to arsenic.	Arsenic	20-27	cripto, FRL-1, cryptic family 1	Homo sapiens	0-7
15665045-3	2005	This report describes the differential abilities of CS and AS to directly upregulate the early inflammatory mediator COX-2, the recently identified prostaglandin E (PGE) synthase and the downstream mediator PGE2 in primary human lung fibroblasts.	Arsenic	59-61	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	117-122
15954786-3	2005	XRD data reveal that all as-deposited CYO thin films are phase-pure and polycrystalline, with features assignable to a cubic CdO-type crystal structure.	Arsenic	25-27	cell adhesion associated, oncogene regulated	Homo sapiens	125-128
15665045-3	2005	This report describes the differential abilities of CS and AS to directly upregulate the early inflammatory mediator COX-2, the recently identified prostaglandin E (PGE) synthase and the downstream mediator PGE2 in primary human lung fibroblasts.	Arsenic	59-61	prostaglandin E synthase	Homo sapiens	148-178
15929903-7	2005	The existence of a strong, developmentally regulated genetic association between CYT19 and arsenic metabolism carries import for both arsenic pharmacogenetics and arsenic toxicology, as well as for public health and governmental regulatory officials.	Arsenic	91-98	arsenite methyltransferase	Homo sapiens	81-86
15761769-0	2005	Elimination of the differential chemoresistance between the murine B-cell lymphoma LY-ar and LY-as cell lines after arsenic (As2O3) exposure via the overexpression of gsto1 (p28).	Arsenic	116-123	glutathione S-transferase omega 1	Mus musculus	167-172
15761769-4	2005	GSTO1, a member of the glutathione S-transferase superfamily omega, has recently been shown to be identical to the rate-limiting enzyme, monomethyl arsenous (MMA(V)) reductase which catalyzes methylarsonate (MMA(V)) to methylarsenous acid (MMA(III)) during arsenic biotransformation.	Arsenic	257-264	glutathione S-transferase omega 1	Mus musculus	0-5
15761769-4	2005	GSTO1, a member of the glutathione S-transferase superfamily omega, has recently been shown to be identical to the rate-limiting enzyme, monomethyl arsenous (MMA(V)) reductase which catalyzes methylarsonate (MMA(V)) to methylarsenous acid (MMA(III)) during arsenic biotransformation.	Arsenic	257-264	glutathione S-transferase omega 1	Mus musculus	158-175
15761769-6	2005	METHODS: The cytotoxicity of arsenic in the gsto1- and bcl-2-expressing chemoresistant and radioresistant LY-ar mouse lymphoma cell line, was compared with that of the LY-ar"s parental cell line, LY-as.	Arsenic	29-36	glutathione S-transferase omega 1	Mus musculus	44-49
15761769-6	2005	METHODS: The cytotoxicity of arsenic in the gsto1- and bcl-2-expressing chemoresistant and radioresistant LY-ar mouse lymphoma cell line, was compared with that of the LY-ar"s parental cell line, LY-as.	Arsenic	29-36	B cell leukemia/lymphoma 2	Mus musculus	55-60
15761769-18	2005	Gsto1 and its human homolog, GSTO1, may serve as a marker for arsenic sensitivity, particularly in cells that are resistant to other chemotherapeutic agents.	Arsenic	62-69	glutathione S-transferase omega 1	Homo sapiens	0-5
15761769-18	2005	Gsto1 and its human homolog, GSTO1, may serve as a marker for arsenic sensitivity, particularly in cells that are resistant to other chemotherapeutic agents.	Arsenic	62-69	glutathione S-transferase omega 1	Homo sapiens	29-34
15929903-7	2005	The existence of a strong, developmentally regulated genetic association between CYT19 and arsenic metabolism carries import for both arsenic pharmacogenetics and arsenic toxicology, as well as for public health and governmental regulatory officials.	Arsenic	134-141	arsenite methyltransferase	Homo sapiens	81-86
15929903-7	2005	The existence of a strong, developmentally regulated genetic association between CYT19 and arsenic metabolism carries import for both arsenic pharmacogenetics and arsenic toxicology, as well as for public health and governmental regulatory officials.	Arsenic	134-141	arsenite methyltransferase	Homo sapiens	81-86
15735709-0	2005	Arsenic trioxide (As(2)O(3)) induces apoptosis through activation of Bax in hematopoietic cells.	Arsenic	18-20	BCL2 associated X, apoptosis regulator	Homo sapiens	69-72
15820720-3	2005	Arsenic intake from drinking water was estimated from analysis of tap water samples, plus 24-h dietary recall and food frequency questionnaires.	Arsenic	0-7	nuclear RNA export factor 1	Homo sapiens	66-69
15815728-6	2005	We further demonstrate that apoptosis was restricted to dividing cells, whereas nonproliferating BCR/ABL(+) CD34(+) cells were resistant to apoptosis induced by imatinib, Ara-C or arsenic, either alone or in combination.	Arsenic	180-187	CD34 molecule	Homo sapiens	108-112
15804455-5	2005	Striatum had the greatest percentage of decreased activities of total SOD and Mn SOD, whereas cortex had the greatest percentage decrease in the activity of Cu/Zn SOD in arsenic-alone treated rats.	Arsenic	170-177	superoxide dismutase 1	Rattus norvegicus	157-166
15804455-9	2005	SOD, CAT, GSH-Px activities were upregulated in arsenic plus lipoic acid treated versus arsenic-only treated rats.	Arsenic	48-55	superoxide dismutase 1	Rattus norvegicus	0-3
15804455-9	2005	SOD, CAT, GSH-Px activities were upregulated in arsenic plus lipoic acid treated versus arsenic-only treated rats.	Arsenic	48-55	catalase	Rattus norvegicus	5-8
16117113-0	2005	Arsenic and mercury tolerance and cadmium sensitivity in Arabidopsis plants expressing bacterial gamma-glutamylcysteine synthetase.	Arsenic	0-7	glutamate-cysteine ligase	Arabidopsis thaliana	97-130
15919540-6	2005	The results revealed that the acid mine drainage originating mainly during winter along the upper part of the Tinto River course causes high inorganic concentrations of dissolved arsenic, up to 600 microg l(-1) of As(III) and 200 microg l(-1) of As(V).	Arsenic	179-186	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	246-251
15896821-6	2005	More than 0.5 mmol/g of As(V) and As(III) was adsorbed by the TiO(2) at an equilibrium arsenic concentration of 0.6mM.	Arsenic	87-94	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	24-29
16012082-0	2005	CYP1A1 and GSTM1 genetic polymorphisms in lung cancer populations exposed to arsenic in drinking water.	Arsenic	77-84	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	0-6
16012082-0	2005	CYP1A1 and GSTM1 genetic polymorphisms in lung cancer populations exposed to arsenic in drinking water.	Arsenic	77-84	glutathione S-transferase mu 1	Homo sapiens	11-16
15806612-6	2005	Present experiments demonstrate that Ure2 possesses a far broader protection specificity, being required to avoid the toxic effects of As(III), As(V), Cr(III), Cr(VI), Se(IV), as well as Cd(II) and Ni(II), and to varying lesser degrees Co(II), Cu(II), Fe(II), Ag(I), Hg(II), cumene and t-butyl hydroperoxides.	Arsenic	135-137	glutathione peroxidase	Saccharomyces cerevisiae S288C	37-41
15806612-6	2005	Present experiments demonstrate that Ure2 possesses a far broader protection specificity, being required to avoid the toxic effects of As(III), As(V), Cr(III), Cr(VI), Se(IV), as well as Cd(II) and Ni(II), and to varying lesser degrees Co(II), Cu(II), Fe(II), Ag(I), Hg(II), cumene and t-butyl hydroperoxides.	Arsenic	144-146	glutathione peroxidase	Saccharomyces cerevisiae S288C	37-41
15781290-7	2005	RESULTS: Significant increase of lipid peroxidation and protein oxidation in the liver associated with depletion of hepatic thiols (GSH, PSH), and antioxidant enzymes (GPx, Catalase) occurred in mice due to prolonged arsenic exposure in a dose-dependent manner.	Arsenic	217-224	catalase	Mus musculus	173-181
15808521-7	2005	The null phenotype for inorganic arsenic methylation in the chimpanzee is likely due to the deletion in the gene for arsenic (+3 oxidation state) methyltransferase that yields an inactive truncated protein.	Arsenic	33-40	arsenite methyltransferase	Pan troglodytes	117-163
15526190-0	2005	A new metabolic pathway of arsenite: arsenic-glutathione complexes are substrates for human arsenic methyltransferase Cyt19.	Arsenic	37-44	arsenite methyltransferase	Homo sapiens	100-123
15526190-1	2005	The metabolism of arsenic is generally accepted to proceed by repetitive reduction and oxidative methylation; the latter is mediated by arsenic methyltransferase (Cyt19).	Arsenic	18-25	arsenite methyltransferase	Homo sapiens	163-168
15526190-6	2005	Human recombinant Cyt19 catalyzed transfer of a methyl group from S-adenosyl-L-methionine to arsenic and produced monomethyl and dimethyl arsenicals.	Arsenic	93-100	arsenite methyltransferase	Homo sapiens	18-23
15526190-7	2005	The methylation of arsenic was catalyzed by Cyt19 only when ATG was present in the reaction mixture.	Arsenic	19-26	arsenite methyltransferase	Homo sapiens	44-49
15846091-4	2005	At clinically achievable concentrations, arsenic stimulated cytochrome c release and apoptosis via a Bax/Bak-dependent mechanism.	Arsenic	41-48	BCL2-associated X protein	Mus musculus	101-104
15846091-4	2005	At clinically achievable concentrations, arsenic stimulated cytochrome c release and apoptosis via a Bax/Bak-dependent mechanism.	Arsenic	41-48	BCL2-antagonist/killer 1	Mus musculus	105-108
16003583-4	2005	More than 99% of dissolved As existed as As(V) in biotic slurries in contrast to sterile controls (less than 50% of total dissolved As), which indicated that indigenous bacteria transformed some dissolved As(III) to As(V).	Arsenic	27-29	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	41-46
16705804-0	2005	Serum acetyl cholinesterase as a biomarker of arsenic induced neurotoxicity in sprague-dawley rats.	Arsenic	46-53	butyrylcholinesterase	Rattus norvegicus	13-27
16705804-11	2005	Acetyl cholinesterase activities of 6895 +/- 822, 5697 +/- 468, 5069 +/- 624, 4054 +/- 980, and 3158 +/- 648 U/L were recorded for 0, 5, 10, 15, and 20 mg/kg, respectively; indicating a gradual decrease in acetyl cholinesterase activity with increasing doses of arsenic.	Arsenic	262-269	butyrylcholinesterase	Rattus norvegicus	7-21
16705804-12	2005	These findings indicate that acetyl cholinesterase is a candidate biomarker for arsenic-induced neurotoxicity in Sprague-Dawley rats.	Arsenic	80-87	butyrylcholinesterase	Rattus norvegicus	36-50
15689486-2	2005	Here, we show that the yeast ubiquitin ligase SCF(Met30) plays a central role in the response to two of the most toxic environmental heavy metal contaminants, namely, cadmium and arsenic.	Arsenic	179-186	ubiquitin-binding SDF ubiquitin ligase complex subunit MET30	Saccharomyces cerevisiae S288C	50-55
15689486-9	2005	Both cadmium and arsenic induced phosphorylation of the cell cycle checkpoint protein Rad53.	Arsenic	17-24	serine/threonine/tyrosine protein kinase RAD53	Saccharomyces cerevisiae S288C	86-91
15811667-5	2005	When an aqueous solution of As(III) was stirred with a mixed suspension of TiO2 and an adsorbent for As(V) (activated alumina) under sunlight irradiation, the arsenic removal reached 89% after 24 h. By use of the same photocatalyst-adsorbent system, 98% of MMA and 97% of DMA were removed.	Arsenic	159-166	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	101-106
15871236-3	2005	Arsenic present is either As(V) or As(O); we found no evidence for As(III).	Arsenic	0-7	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	26-31
15781290-10	2005	There was a positive correlation between the hepatic arsenic level and collagen content (r = 0.8007), LPx (r = 0.779) and IL-6 (r = 0.7801).	Arsenic	53-60	interleukin 6	Mus musculus	122-126
15819251-1	2005	Oxidation of arsenite, As(III), to arsenate, As(V), is required for the efficient removal of arsenic by many water treatment technologies.	Arsenic	93-100	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	45-50
15819251-12	2005	The selective use of hydroxyl radical quenchers and superoxide dismutase demonstrated that superoxide, O2-, plays a major role in the oxidation of As(III) to As(V).	Arsenic	147-149	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	158-163
15708576-1	2005	Many environmental factors, such as ultraviolet (UV) and arsenic, can induce the clustering of cell surface receptors, including epidermal growth factor receptor (EGFR).	Arsenic	57-64	epidermal growth factor receptor	Homo sapiens	129-161
15945355-2	2005	As and Ae registration during several days revealed strong negative correlation between an index, Ae/As, and serum albumin As in 51% of the patients.	Arsenic	0-2	albumin	Homo sapiens	115-122
15708576-1	2005	Many environmental factors, such as ultraviolet (UV) and arsenic, can induce the clustering of cell surface receptors, including epidermal growth factor receptor (EGFR).	Arsenic	57-64	epidermal growth factor receptor	Homo sapiens	163-167
15601678-0	2005	Glutathione reductase inhibition and methylated arsenic distribution in Cd1 mice brain and liver.	Arsenic	48-55	CD1 antigen complex	Mus musculus	72-75
15758100-6	2005	Desorption of As(V) (the most dominant arsenic species in aerated soils) was therefore investigated using batch and flow-through desorption experiments.	Arsenic	39-46	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	14-19
15805732-8	2005	In this study, we demonstrated that the rate of reduction in the milk yield in cows affected by Akabane disease was -11.4 +/- 14.9%, but values as high as -26.6 +/- 24.7% were reached in the comparison with the milk yield obtained after normal parturition.	Arsenic	108-110	Weaning weight-maternal milk	Bos taurus	65-69
15601678-3	2005	Glutathione (GSH) is extensively involved in the metabolism of inorganic arsenic, and both arsenite and its methylated metabolites have been shown to be potent inhibitors of glutathione reductase (GR) in vitro.	Arsenic	73-80	glutathione reductase	Mus musculus	197-199
15694460-1	2005	Previous studies have demonstrated that mice lacking a functional folate binding protein 2 gene (Folbp2-/-) were significantly more sensitive to in utero arsenic exposure than were the wild-type mice similarly exposed.	Arsenic	154-161	folate receptor 2 (fetal)	Mus musculus	66-90
15664430-6	2005	Glucose 6-phosphatase activity in liver tissue was also significantly decreased after arsenic treatment.	Arsenic	86-93	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	0-21
15694464-7	2005	Thus, MRP-1 is crucially involved in arsenic efflux and eventually prevention of acute renal injury upon acute exposure to NaAs.	Arsenic	37-44	ATP-binding cassette, sub-family C (CFTR/MRP), member 1	Mus musculus	6-11
15743620-6	2005	The removal of the arsenic species by Fe(0) was attributed to electrochemical reduction of As(III) to sparsely soluble As(0) and adsorption of As(III) and As(V) to iron hydroxides formed on the Fe(0) surface under anoxic conditions.	Arsenic	19-26	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	155-160
18969883-0	2005	Preconcentration and determination of ultra trace amounts of arsenic(III) and arsenic(V) in tap water and total arsenic in biological samples by cloud point extraction and electrothermal atomic absorption spectrometry.	Arsenic	61-68	nuclear RNA export factor 1	Homo sapiens	92-95
18969883-0	2005	Preconcentration and determination of ultra trace amounts of arsenic(III) and arsenic(V) in tap water and total arsenic in biological samples by cloud point extraction and electrothermal atomic absorption spectrometry.	Arsenic	78-85	nuclear RNA export factor 1	Homo sapiens	92-95
18969883-0	2005	Preconcentration and determination of ultra trace amounts of arsenic(III) and arsenic(V) in tap water and total arsenic in biological samples by cloud point extraction and electrothermal atomic absorption spectrometry.	Arsenic	78-85	nuclear RNA export factor 1	Homo sapiens	92-95
18969883-11	2005	The method was successfully applied to the determination of As(III) and As(V) in tap water and total arsenic in biological samples (hair and nail).	Arsenic	60-62	nuclear RNA export factor 1	Homo sapiens	81-84
18969883-11	2005	The method was successfully applied to the determination of As(III) and As(V) in tap water and total arsenic in biological samples (hair and nail).	Arsenic	72-74	nuclear RNA export factor 1	Homo sapiens	81-84
15694460-1	2005	Previous studies have demonstrated that mice lacking a functional folate binding protein 2 gene (Folbp2-/-) were significantly more sensitive to in utero arsenic exposure than were the wild-type mice similarly exposed.	Arsenic	154-161	folate receptor 2 (fetal)	Mus musculus	97-103
15592527-10	2005	These results suggest that BNIP3 plays a central role in As(2)O(3)-induced autophagic cell death in malignant glioma cells.	Arsenic	57-59	BCL2 interacting protein 3	Homo sapiens	27-32
15492012-0	2005	Cdc42 regulates arsenic-induced NADPH oxidase activation and cell migration through actin filament reorganization.	Arsenic	16-23	cell division cycle 42	Mus musculus	0-5
15492012-2	2005	The present study reports that exposure to arsenic induced actin filament reorganization, resulting in lamellipodia and filopodia structures through the activation of Cdc42 in SVEC4-10 endothelial cells.	Arsenic	43-50	cell division cycle 42	Mus musculus	167-172
15492012-4	2005	Immunoprecipitation and Western blotting analysis demonstrated that arsenic stimulation induced serine phosphorylation of p47phox, a key component of NADPH oxidase, indicating that arsenic induces O2* formation through NADPH oxidase activation.	Arsenic	68-75	neutrophil cytosolic factor 1	Mus musculus	122-129
15492012-4	2005	Immunoprecipitation and Western blotting analysis demonstrated that arsenic stimulation induced serine phosphorylation of p47phox, a key component of NADPH oxidase, indicating that arsenic induces O2* formation through NADPH oxidase activation.	Arsenic	181-188	neutrophil cytosolic factor 1	Mus musculus	122-129
15492012-5	2005	Inhibition of arsenic-induced actin filament reorganization by either overexpression of a dominant negative Cdc42 or pretreatment of an actin filament stabilizing regent, jasplakinolide, abrogated arsenic-induced NADPH oxidase activation, showing that the activation of NADPH oxidase was regulated by Cdc42-mediated actin filament reorganization.	Arsenic	14-21	cell division cycle 42	Mus musculus	108-113
15492012-5	2005	Inhibition of arsenic-induced actin filament reorganization by either overexpression of a dominant negative Cdc42 or pretreatment of an actin filament stabilizing regent, jasplakinolide, abrogated arsenic-induced NADPH oxidase activation, showing that the activation of NADPH oxidase was regulated by Cdc42-mediated actin filament reorganization.	Arsenic	14-21	cell division cycle 42	Mus musculus	301-306
15492012-5	2005	Inhibition of arsenic-induced actin filament reorganization by either overexpression of a dominant negative Cdc42 or pretreatment of an actin filament stabilizing regent, jasplakinolide, abrogated arsenic-induced NADPH oxidase activation, showing that the activation of NADPH oxidase was regulated by Cdc42-mediated actin filament reorganization.	Arsenic	197-204	cell division cycle 42	Mus musculus	108-113
15492012-6	2005	This study also showed that overexpression of a dominant negative Rac1 was sufficient to abolish arsenic-induced O2*- production, implying that Rac1 activities are required for Cdc42-mediated NADPH oxidase activation in response to arsenic stimulation.	Arsenic	97-104	Rac family small GTPase 1	Mus musculus	66-70
15492012-6	2005	This study also showed that overexpression of a dominant negative Rac1 was sufficient to abolish arsenic-induced O2*- production, implying that Rac1 activities are required for Cdc42-mediated NADPH oxidase activation in response to arsenic stimulation.	Arsenic	97-104	Rac family small GTPase 1	Mus musculus	144-148
15492012-6	2005	This study also showed that overexpression of a dominant negative Rac1 was sufficient to abolish arsenic-induced O2*- production, implying that Rac1 activities are required for Cdc42-mediated NADPH oxidase activation in response to arsenic stimulation.	Arsenic	97-104	cell division cycle 42	Mus musculus	177-182
15492012-6	2005	This study also showed that overexpression of a dominant negative Rac1 was sufficient to abolish arsenic-induced O2*- production, implying that Rac1 activities are required for Cdc42-mediated NADPH oxidase activation in response to arsenic stimulation.	Arsenic	232-239	Rac family small GTPase 1	Mus musculus	66-70
15492012-6	2005	This study also showed that overexpression of a dominant negative Rac1 was sufficient to abolish arsenic-induced O2*- production, implying that Rac1 activities are required for Cdc42-mediated NADPH oxidase activation in response to arsenic stimulation.	Arsenic	232-239	Rac family small GTPase 1	Mus musculus	144-148
15492012-6	2005	This study also showed that overexpression of a dominant negative Rac1 was sufficient to abolish arsenic-induced O2*- production, implying that Rac1 activities are required for Cdc42-mediated NADPH oxidase activation in response to arsenic stimulation.	Arsenic	232-239	cell division cycle 42	Mus musculus	177-182
15492012-7	2005	Furthermore, arsenic stimulation induced cell migration, which can be inhibited by the inactivation of either Cdc42 or NADPH oxidase.	Arsenic	13-20	cell division cycle 42	Mus musculus	110-115
15492012-8	2005	Taken together, the results indicate that arsenic is able to activate NADPH oxidase through Cdc42-mediated actin filament reorganization, leading to the induction of an increase in cell migration in SVEC4-10 endothelial cells.	Arsenic	42-49	cell division cycle 42	Mus musculus	92-97
15538402-4	2005	We isolated an arsenic-resistant NB4 subline (NB4-As(R)), which showed stronger ERK1/2 activity (2.7-fold increase) and Bad phosphorylation (2.4-fold increase) compared to parental NB4 cells in response to ATO treatment.	Arsenic	15-22	mitogen-activated protein kinase 3	Homo sapiens	80-86
15843154-3	2005	Using this effect, we have measured the enthalpy (DeltaH) of loop cleavage and insertion for plasminogen activator inhibitor 1 (PAI-1) as -38 kcal/mol.	Arsenic	29-31	serpin family E member 1	Homo sapiens	93-126
15843154-3	2005	Using this effect, we have measured the enthalpy (DeltaH) of loop cleavage and insertion for plasminogen activator inhibitor 1 (PAI-1) as -38 kcal/mol.	Arsenic	29-31	serpin family E member 1	Homo sapiens	128-133
15748426-15	2005	Combination of Gleevec and arsenic agents in treating chronic myeloid leukemia has already make a figure both in clinical and laboratory research, aiming at counteracting the abnormal tyrosine kinase activity of ABL and the degradating BCR-ABL fusion protein.	Arsenic	27-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-215
15748426-15	2005	Combination of Gleevec and arsenic agents in treating chronic myeloid leukemia has already make a figure both in clinical and laboratory research, aiming at counteracting the abnormal tyrosine kinase activity of ABL and the degradating BCR-ABL fusion protein.	Arsenic	27-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	240-243
16121039-5	2005	The goal of this study was to investigate the effects of trivalent arsenic (arsenite), a known transcriptional activator of Pgp, on CFTR expression.	Arsenic	67-74	ATP binding cassette subfamily B member 1	Homo sapiens	124-127
16121039-5	2005	The goal of this study was to investigate the effects of trivalent arsenic (arsenite), a known transcriptional activator of Pgp, on CFTR expression.	Arsenic	67-74	CF transmembrane conductance regulator	Homo sapiens	132-136
15604884-6	2005	The mechanism of arsenic cytotoxicity is thought to involve posttranslational modification followed by degradation of the PML-retinoic acid receptor-alpha (PML-RARalpha) fusion protein; targeting of PML to nuclear bodies with restoration of its physiologic functions; and production of reactive oxygen species (ROS) by NADPH oxidase in leukemic cells or collapse of the mitochondrial transmembrane potential.	Arsenic	17-24	PML nuclear body scaffold	Homo sapiens	122-125
15604884-6	2005	The mechanism of arsenic cytotoxicity is thought to involve posttranslational modification followed by degradation of the PML-retinoic acid receptor-alpha (PML-RARalpha) fusion protein; targeting of PML to nuclear bodies with restoration of its physiologic functions; and production of reactive oxygen species (ROS) by NADPH oxidase in leukemic cells or collapse of the mitochondrial transmembrane potential.	Arsenic	17-24	PML nuclear body scaffold	Homo sapiens	156-159
15604884-6	2005	The mechanism of arsenic cytotoxicity is thought to involve posttranslational modification followed by degradation of the PML-retinoic acid receptor-alpha (PML-RARalpha) fusion protein; targeting of PML to nuclear bodies with restoration of its physiologic functions; and production of reactive oxygen species (ROS) by NADPH oxidase in leukemic cells or collapse of the mitochondrial transmembrane potential.	Arsenic	17-24	PML nuclear body scaffold	Homo sapiens	156-159
21783469-8	2005	Exposure to arsenic led to a significant inhibition of blood delta-aminolevulinic acid dehydratase (ALAD), depletion of glutathione (GSH) level and marginal elevations of zinc protoporphyrin (ZPP).	Arsenic	12-19	aminolevulinate, delta-, dehydratase	Mus musculus	61-98
21783469-8	2005	Exposure to arsenic led to a significant inhibition of blood delta-aminolevulinic acid dehydratase (ALAD), depletion of glutathione (GSH) level and marginal elevations of zinc protoporphyrin (ZPP).	Arsenic	12-19	aminolevulinate, delta-, dehydratase	Mus musculus	100-104
21783456-1	2005	Folate binding protein-2 (Folbp2(-/-)) knockout mice have been previously shown to be highly susceptible to the teratogenic effects of arsenic.	Arsenic	135-142	folate receptor 2 (fetal)	Mus musculus	0-24
21783456-1	2005	Folate binding protein-2 (Folbp2(-/-)) knockout mice have been previously shown to be highly susceptible to the teratogenic effects of arsenic.	Arsenic	135-142	folate receptor 2 (fetal)	Mus musculus	26-32
21783456-5	2005	No genotype-specific effects were observed in arsenic speciation thereby negating altered biotransformation of arsenic as the mechanism of the enhanced teratogenicity seen in Folbp2(-/-) mice.	Arsenic	111-118	folate receptor 2 (fetal)	Mus musculus	175-181
21783469-10	2005	Concomitant administration of zinc with arsenic provided significant protection to blood ALAD activity while, GSH and ZPP levels remained unaltered.	Arsenic	40-47	aminolevulinate, delta-, dehydratase	Mus musculus	89-93
21783469-13	2005	Interestingly, post-arsenic exposure treatment with MiADMSA provided significant recovery in blood ALAD activity while, zinc supplementation alone had no effect.	Arsenic	20-27	aminolevulinate, delta-, dehydratase	Mus musculus	99-103
16050262-9	2005	Arsenic interferes with the formation of hERG/chaperone complexes and inhibits hERG maturation causing ECG abnormalities.	Arsenic	0-7	ETS transcription factor ERG	Homo sapiens	79-83
16217917-7	2005	We observed differences in the risk estimates for the MTHFR polymorphisms by arsenic exposure, but they were not statistically significant (P = 0.67 for MTHFR 677C &gt; T and P = 0.12 for MTHFR 1298A&gt;C).	Arsenic	77-84	methylenetetrahydrofolate reductase	Homo sapiens	54-59
16319020-0	2005	Sorption kinetics of As(V) with iron-oxide-coated cement-a new adsorbent and its application in the removal of arsenic from real-life groundwater samples.	Arsenic	111-118	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	21-26
16319020-7	2005	The efficiency of this adsorbent was also checked for the removal of arsenic from three real ground water samples containing both As(III) and As(V) with total arsenic in the range of 0.33-1.2 mg/L.	Arsenic	69-76	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	142-147
16319020-7	2005	The efficiency of this adsorbent was also checked for the removal of arsenic from three real ground water samples containing both As(III) and As(V) with total arsenic in the range of 0.33-1.2 mg/L.	Arsenic	159-166	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	142-147
15715267-12	2005	The heating of As(V) in the presence of gluconate, glucose, ascorbic acid, methionine, isoleucine, sodium chloride, and pure water, in autoclave for 15 minutes, showed that, whereas no As(III) was found in pure water and sodium chloride solution, approximately 50% of As(V) was converted into As(III) in the remainder of the solutions.	Arsenic	15-17	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	268-273
16050262-9	2005	Arsenic interferes with the formation of hERG/chaperone complexes and inhibits hERG maturation causing ECG abnormalities.	Arsenic	0-7	ETS transcription factor ERG	Homo sapiens	41-45
15831085-7	2005	We also evaluated the role of tea in inducing antioxidant enzymes such as superoxide dismutase and catalase to provide protection against the oxidative stress induced by As.	Arsenic	170-172	catalase	Cricetulus griseus	99-107
16050262-8	2005	hERG/chaperone complexes represent novel targets for therapeutic compounds with cardiac liability such as arsenic, which is used in the treatment of leukaemias.	Arsenic	106-113	ETS transcription factor ERG	Homo sapiens	0-4
15513899-5	2004	Activation of JNK by SAAD or As, but not that of p38 kinase or ERK1/2, was inhibited by treatment of cells with deprenyl.	Arsenic	29-31	mitogen-activated protein kinase 8	Rattus norvegicus	14-17
16416669-0	2005	Chronic exposure to arsenic sensitizes CD3+ and CD56+ human cells to sodium arsenite-mediated apoptosis.	Arsenic	20-27	neural cell adhesion molecule 1	Homo sapiens	48-52
15544921-6	2004	The combination of emodin and arsenic promoted the major apoptotic signaling events, i.e., the collapse of the mitochondrial transmembrane potential, the release of cytochrome c, and the activation of caspases 9 and 3.	Arsenic	30-37	caspase 9	Mus musculus	201-217
15544921-7	2004	Meanwhile a combination of emodin and arsenic suppressed the activation of transcription factor NF-kappaB and downregulated the expression of a NF-kappaB-specific antiapoptotic protein, survivin.	Arsenic	38-45	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	96-105
15544921-7	2004	Meanwhile a combination of emodin and arsenic suppressed the activation of transcription factor NF-kappaB and downregulated the expression of a NF-kappaB-specific antiapoptotic protein, survivin.	Arsenic	38-45	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	144-153
15544921-7	2004	Meanwhile a combination of emodin and arsenic suppressed the activation of transcription factor NF-kappaB and downregulated the expression of a NF-kappaB-specific antiapoptotic protein, survivin.	Arsenic	38-45	baculoviral IAP repeat-containing 5	Mus musculus	186-194
15534382-1	2004	Recently lithium bis(oxalato)borate, LiB(C2O4)2, has been proposed as an alternative lithium salt for the electrolyte in rechargeable batteries that do not contain explosive perchlorate, reactive fluoride or toxic arsenic.	Arsenic	214-221	leucine rich repeat containing 15	Homo sapiens	37-40
15513899-6	2004	The cells that had been exposed to As or SAAD exhibited decreases in mitochondrial permeability to rhodamine 123, which was restored by deprenyl treatment or transfection with the plasmid encoding a dominant negative mutant of JNK [JNK1( )].	Arsenic	35-37	mitogen-activated protein kinase 8	Rattus norvegicus	227-230
15342953-3	2004	Arsenic caused induction of multidrug resistance-associated protein 2 (MRP2), and changes of glutathione (GSH) levels in the liver and bile were also determined.	Arsenic	0-7	ATP binding cassette subfamily C member 2	Rattus norvegicus	28-69
15653797-0	2004	Overexpression of phytochelatin synthase in Arabidopsis leads to enhanced arsenic tolerance and cadmium hypersensitivity.	Arsenic	74-81	phytochelatin synthase 1 (PCS1)	Arabidopsis thaliana	18-40
15653797-3	2004	When AtPCS1 was overexpressed in Arabidopsis from a strong constitutive Arabidopsis actin regulatory sequence (A2), the A2::AtPCS1 plants were highly resistant to arsenic, accumulating 20-100 times more biomass on 250 and 300 microM arsenate than wild type (WT); however, they were hypersensitive to Cd(II).	Arsenic	163-170	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	5-11
15653797-3	2004	When AtPCS1 was overexpressed in Arabidopsis from a strong constitutive Arabidopsis actin regulatory sequence (A2), the A2::AtPCS1 plants were highly resistant to arsenic, accumulating 20-100 times more biomass on 250 and 300 microM arsenate than wild type (WT); however, they were hypersensitive to Cd(II).	Arsenic	163-170	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	124-130
15653797-4	2004	After exposure to cadmium and arsenic, the overall accumulation of thiol-peptides increased to 10-fold higher levels in the A2::AtPCS1 plants compared with WT, as determined by fluorescent HPLC.	Arsenic	30-37	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	128-134
15653797-8	2004	The potential for AtPCS1 overexpression to be useful in strategies for phytoremediating arsenic and to compound the negative effects of cadmium are discussed.	Arsenic	88-95	Eukaryotic aspartyl protease family protein	Arabidopsis thaliana	18-24
15342953-3	2004	Arsenic caused induction of multidrug resistance-associated protein 2 (MRP2), and changes of glutathione (GSH) levels in the liver and bile were also determined.	Arsenic	0-7	ATP binding cassette subfamily C member 2	Rattus norvegicus	71-75
15570009-7	2004	AS-4625 treatment of BT474 cells decreased both Bcl-2 and Bcl-XL expression, resulting in a 21 +/- 7% net apoptosis induction; the combination of AS-4625 followed by trastuzumab resulted in a significantly stronger induction of apoptosis (37 +/- 6%, P &lt;0.01) that was not observed with the reverse treatment sequence (trastuzumab followed by AS-4625).	Arsenic	0-2	BCL2 apoptosis regulator	Homo sapiens	48-53
15570009-7	2004	AS-4625 treatment of BT474 cells decreased both Bcl-2 and Bcl-XL expression, resulting in a 21 +/- 7% net apoptosis induction; the combination of AS-4625 followed by trastuzumab resulted in a significantly stronger induction of apoptosis (37 +/- 6%, P &lt;0.01) that was not observed with the reverse treatment sequence (trastuzumab followed by AS-4625).	Arsenic	0-2	BCL2 like 1	Homo sapiens	58-64
15610608-5	2004	VLP was able to package and deliver an antisense oligodeoxynucleotide (AS-ODN) against simian virus 40 (SV40) large tumor antigen (LT) into SV40-transformed human fetal glial (SVG) cells in order to inhibit expression of the oncoprotein.	Arsenic	71-73	VHL like	Homo sapiens	0-3
15519606-5	2004	In addition, there is a significant increase in the 5-lipoxygenase (5-LO) product, leukotriene E4 (LTE4), in the serum of arsenic-treated mice.	Arsenic	122-129	arachidonate 5-lipoxygenase	Mus musculus	52-66
15485279-7	2004	The transition observed with increasing P is the continuation at high T of the black P to arsenic (A17) structure observed in the solid state, and also corresponds to a semiconductor to metal transition.	Arsenic	90-97	immunoglobulin kappa variable 2-30	Homo sapiens	99-102
15504454-12	2004	Stimulation of MAP kinase cascades by arsenic and subsequent regulation of genes including c-fos, c-jun, and the matrix degrading proteases may play an important role in arsenic-induced skin carcinogenesis.	Arsenic	170-177	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	91-96
15504454-12	2004	Stimulation of MAP kinase cascades by arsenic and subsequent regulation of genes including c-fos, c-jun, and the matrix degrading proteases may play an important role in arsenic-induced skin carcinogenesis.	Arsenic	170-177	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	98-103
15314284-0	2004	RIP kinase is involved in arsenic-induced apoptosis in multiple myeloma cells.	Arsenic	26-33	receptor interacting serine/threonine kinase 1	Homo sapiens	0-3
15486292-1	2004	Arsenate [As(V)]-respiring bacteria affect the speciation and mobilization of arsenic in the environment.	Arsenic	78-85	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	10-15
15486292-3	2004	Using molecular genetics, we show that the functional gene for As(V) respiration, arrA, is highly conserved; that it is required for As(V) reduction to arsenite when arsenic is sorbed onto iron minerals; and that it can be used to identify the presence and activity of As(V)-respiring bacteria in arsenic-contaminated iron-rich sediments.	Arsenic	166-173	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	63-68
15486292-3	2004	Using molecular genetics, we show that the functional gene for As(V) respiration, arrA, is highly conserved; that it is required for As(V) reduction to arsenite when arsenic is sorbed onto iron minerals; and that it can be used to identify the presence and activity of As(V)-respiring bacteria in arsenic-contaminated iron-rich sediments.	Arsenic	166-173	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	133-138
15486292-3	2004	Using molecular genetics, we show that the functional gene for As(V) respiration, arrA, is highly conserved; that it is required for As(V) reduction to arsenite when arsenic is sorbed onto iron minerals; and that it can be used to identify the presence and activity of As(V)-respiring bacteria in arsenic-contaminated iron-rich sediments.	Arsenic	166-173	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	133-138
15486292-3	2004	Using molecular genetics, we show that the functional gene for As(V) respiration, arrA, is highly conserved; that it is required for As(V) reduction to arsenite when arsenic is sorbed onto iron minerals; and that it can be used to identify the presence and activity of As(V)-respiring bacteria in arsenic-contaminated iron-rich sediments.	Arsenic	297-304	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	63-68
15486292-4	2004	The expression of arrA thus can be used to monitor sites in which As(V)-respiring bacteria may be controlling arsenic geochemistry.	Arsenic	110-117	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	66-71
15314284-5	2004	Arsenic also activated caspase-3 resulting in the cleavage of poly (ADP-ribose) polymerase (PARP) and Fas/TNF alpha related receptor interacting protein (RIP).	Arsenic	0-7	caspase 3	Homo sapiens	23-32
15314284-5	2004	Arsenic also activated caspase-3 resulting in the cleavage of poly (ADP-ribose) polymerase (PARP) and Fas/TNF alpha related receptor interacting protein (RIP).	Arsenic	0-7	poly(ADP-ribose) polymerase 1	Homo sapiens	62-90
16381491-0	2004	Reduction in kidney cancer mortality following installation of a tap water supply system in an arsenic-endemic area of Taiwan.	Arsenic	95-102	nuclear RNA export factor 1	Homo sapiens	65-68
15314284-5	2004	Arsenic also activated caspase-3 resulting in the cleavage of poly (ADP-ribose) polymerase (PARP) and Fas/TNF alpha related receptor interacting protein (RIP).	Arsenic	0-7	poly(ADP-ribose) polymerase 1	Homo sapiens	92-96
15314284-5	2004	Arsenic also activated caspase-3 resulting in the cleavage of poly (ADP-ribose) polymerase (PARP) and Fas/TNF alpha related receptor interacting protein (RIP).	Arsenic	0-7	tumor necrosis factor	Homo sapiens	106-115
15314284-5	2004	Arsenic also activated caspase-3 resulting in the cleavage of poly (ADP-ribose) polymerase (PARP) and Fas/TNF alpha related receptor interacting protein (RIP).	Arsenic	0-7	receptor interacting serine/threonine kinase 1	Homo sapiens	154-157
15314284-7	2004	This study first shows that arsenic induces apoptotic signaling in MM through the cleavage of TNF alpha related receptor interacting protein (RIP).	Arsenic	28-35	tumor necrosis factor	Homo sapiens	94-103
15314284-7	2004	This study first shows that arsenic induces apoptotic signaling in MM through the cleavage of TNF alpha related receptor interacting protein (RIP).	Arsenic	28-35	receptor interacting serine/threonine kinase 1	Homo sapiens	142-145
15073043-9	2004	RT-PCR and immunohistochemistry confirmed arsenic-induced increases in hepatic ER-alpha and cyclin D1 transcription and translation products, respectively.	Arsenic	42-49	estrogen receptor 1 (alpha)	Mus musculus	79-87
15073043-9	2004	RT-PCR and immunohistochemistry confirmed arsenic-induced increases in hepatic ER-alpha and cyclin D1 transcription and translation products, respectively.	Arsenic	42-49	cyclin D1	Mus musculus	92-101
15073043-11	2004	Arsenic also markedly reduced the methylation within the ER-alpha gene promoter region, as assessed by methylation-specific PCR, and this reduction was statistically significant in 8 of 13 CpG sites within the promoter region.	Arsenic	0-7	estrogen receptor 1 (alpha)	Mus musculus	57-65
15073043-13	2004	Thus, long-term exposure of mice to arsenic in the drinking water can induce aberrant gene expression, global DNA hypomethylation, and the hypomethylation of the ER-alpha gene promoter, all of which could potentially contribute to arsenic hepatocarcinogenesis.	Arsenic	36-43	estrogen receptor 1 (alpha)	Mus musculus	162-170
15176048-2	2004	In this study, we tested whether interruption of MDM2 function using antisense MDM2 oligonucleotide (AS) affects the apoptotic response of prostate cancer cells to AD.	Arsenic	101-103	MDM2 proto-oncogene	Homo sapiens	49-53
15377153-9	2004	The caspase-3, -8, and -9 relative activities were all increased in the UVB group; however, arsenic significantly enhanced caspase-8 and -3 relative activities in UVB-irradiated keratinocytes (the UVB-As group).	Arsenic	92-99	caspase 8	Homo sapiens	123-139
15377153-11	2004	Our findings revealed that arsenic enhances UVB-induced keratinocyte apoptosis via suppression of Bcl-2 expression and stimulation of caspase-8 activity.	Arsenic	27-34	BCL2 apoptosis regulator	Homo sapiens	98-103
15377153-11	2004	Our findings revealed that arsenic enhances UVB-induced keratinocyte apoptosis via suppression of Bcl-2 expression and stimulation of caspase-8 activity.	Arsenic	27-34	caspase 8	Homo sapiens	134-143
15450189-5	2004	Different mechanisms of regulation of ARR1 genes expression may therefore explain the increased tolerance of S. douglasii to arsenic in comparison with S. cerevisiae.	Arsenic	125-132	Arr1p	Saccharomyces cerevisiae S288C	38-42
15310238-0	2004	Arsenic at very low concentrations alters glucocorticoid receptor (GR)-mediated gene activation but not GR-mediated gene repression: complex dose-response effects are closely correlated with levels of activated GR and require a functional GR DNA binding domain.	Arsenic	0-7	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	42-65
15310238-0	2004	Arsenic at very low concentrations alters glucocorticoid receptor (GR)-mediated gene activation but not GR-mediated gene repression: complex dose-response effects are closely correlated with levels of activated GR and require a functional GR DNA binding domain.	Arsenic	0-7	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	67-69
15310238-9	2004	Point mutations located within the DBD that have known structural consequences significantly altered the GR response to As.	Arsenic	120-122	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	105-107
15276028-10	2004	Mutations of the KCNJ2 gene should be considered in genetic subclassification of LQTS patients, even in the absence of overt manifestations of AS.	Arsenic	143-145	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	17-22
15176048-2	2004	In this study, we tested whether interruption of MDM2 function using antisense MDM2 oligonucleotide (AS) affects the apoptotic response of prostate cancer cells to AD.	Arsenic	101-103	MDM2 proto-oncogene	Homo sapiens	79-83
15176048-3	2004	METHODS: Wild type LNCaP cells and MDM2-overexpressing (LNCaP-MST) cells were treated with AS alone or in combination with AD.	Arsenic	91-93	MDM2 proto-oncogene	Homo sapiens	35-39
15276425-4	2004	Consistent with these data, arsenic accelerates atherosclerosis in apolipoprotein E (ApoE) deficient mice, a model of human atherosclerosis.	Arsenic	28-35	apolipoprotein E	Mus musculus	67-83
15276407-1	2004	We evaluated in Mexican children environmentally exposed to arsenic and lead monocyte nitric oxide (NO) and superoxide anion production in response to direct activation with interferon-gamma (IFN-gamma) + lipopolysaccharide (LPS).	Arsenic	60-67	interferon gamma	Homo sapiens	174-190
15276425-4	2004	Consistent with these data, arsenic accelerates atherosclerosis in apolipoprotein E (ApoE) deficient mice, a model of human atherosclerosis.	Arsenic	28-35	apolipoprotein E	Mus musculus	85-89
15276422-6	2004	Arsenic-induced cell proliferation in the bladder epithelium was correlated with activation of the MAP kinase pathway, leading to extracellular signal-regulated kinase (ERK) kinase activity, AP-1 activation, and expression of AP-1-associated genes involved in cell proliferation.	Arsenic	0-7	mitogen-activated protein kinase 1	Mus musculus	130-167
15276426-4	2004	Decreased availability of biologically active NO in the endothelium is implicated in the pathophysiology of several vascular diseases and inhibition of eNOS by arsenic is one of the proposed mechanism s for arsenic-induced vascular diseases.	Arsenic	160-167	nitric oxide synthase 3	Homo sapiens	152-156
15276422-6	2004	Arsenic-induced cell proliferation in the bladder epithelium was correlated with activation of the MAP kinase pathway, leading to extracellular signal-regulated kinase (ERK) kinase activity, AP-1 activation, and expression of AP-1-associated genes involved in cell proliferation.	Arsenic	0-7	mitogen-activated protein kinase 1	Mus musculus	169-172
15276423-0	2004	Inhibition of insulin-dependent glucose uptake by trivalent arsenicals: possible mechanism of arsenic-induced diabetes.	Arsenic	60-67	insulin	Homo sapiens	14-21
15276426-4	2004	Decreased availability of biologically active NO in the endothelium is implicated in the pathophysiology of several vascular diseases and inhibition of eNOS by arsenic is one of the proposed mechanism s for arsenic-induced vascular diseases.	Arsenic	207-214	nitric oxide synthase 3	Homo sapiens	152-156
15276427-10	2004	N-acetyl-l-cysteine (NAC) reduced cellular arsenic content in DMA(V)-exposed cells and also decreased the cytotoxicity of DMA(V), whereas it changed neither cellular arsenic content nor the viability in MMA(V)-exposed cells.	Arsenic	43-50	X-linked Kx blood group	Homo sapiens	21-24
15089098-0	2004	Signaling pathways for arsenic-stimulated vascular endothelial growth factor-a expression in primary vascular smooth muscle cells.	Arsenic	23-30	vascular endothelial growth factor A	Homo sapiens	42-78
15280248-3	2004	CRY2 DNA sequences reveal strong LD and the existence of two highly differentiated haplogroups (A and B) across the gene; in addition, a haplotype possessing a radical glutamine-to-serine replacement (AS) occurs within the more common haplogroup.	Arsenic	201-203	cryptochrome 2	Arabidopsis thaliana	0-4
15359896-3	2004	Some reports, including our findings, showed that MT-I/II null mice have an increased sensitivity to harmful metals such as cadmium, mercury, zinc and arsenic.	Arsenic	151-158	metallothionein 3	Mus musculus	50-57
15169625-7	2004	The significant dispersion of depressed mRNA abundance of RyR2 and SERCA2 was associated with an increase in AS in Isop group, and it was much depressed in the left than the right ventricle.	Arsenic	109-111	ryanodine receptor 2	Rattus norvegicus	58-62
15169625-7	2004	The significant dispersion of depressed mRNA abundance of RyR2 and SERCA2 was associated with an increase in AS in Isop group, and it was much depressed in the left than the right ventricle.	Arsenic	109-111	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2	Rattus norvegicus	67-73
15163543-9	2004	Induction of oxidative stress and interferences in signal transduction or gene expression by arsenic or by its methylated metabolites are the most possible causes to arsenic-induced diabetes mellitus through mechanisms of induction of insulin resistance and beta cell dysfunction.	Arsenic	93-100	insulin	Homo sapiens	235-242
15163543-9	2004	Induction of oxidative stress and interferences in signal transduction or gene expression by arsenic or by its methylated metabolites are the most possible causes to arsenic-induced diabetes mellitus through mechanisms of induction of insulin resistance and beta cell dysfunction.	Arsenic	166-173	insulin	Homo sapiens	235-242
15163543-10	2004	Recent studies have shown that, in subjects with chronic arsenic exposure, oxidative stress is increased and the expression of tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) is upregulated.	Arsenic	57-64	tumor necrosis factor	Homo sapiens	127-154
15163543-10	2004	Recent studies have shown that, in subjects with chronic arsenic exposure, oxidative stress is increased and the expression of tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) is upregulated.	Arsenic	57-64	tumor necrosis factor	Homo sapiens	156-164
15163543-10	2004	Recent studies have shown that, in subjects with chronic arsenic exposure, oxidative stress is increased and the expression of tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) is upregulated.	Arsenic	57-64	interleukin 6	Homo sapiens	170-183
15163543-10	2004	Recent studies have shown that, in subjects with chronic arsenic exposure, oxidative stress is increased and the expression of tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) is upregulated.	Arsenic	57-64	interleukin 6	Homo sapiens	185-189
15163543-14	2004	Although without supportive data, superoxide production induced by arsenic exposure can theoretically impair insulin secretion by interaction with uncoupling protein 2 (UCP2), and oxidative stress can also cause amyloid formation in the pancreas, which could progressively destroy the insulin-secreting beta cells.	Arsenic	67-74	uncoupling protein 2	Homo sapiens	147-167
15163543-14	2004	Although without supportive data, superoxide production induced by arsenic exposure can theoretically impair insulin secretion by interaction with uncoupling protein 2 (UCP2), and oxidative stress can also cause amyloid formation in the pancreas, which could progressively destroy the insulin-secreting beta cells.	Arsenic	67-74	uncoupling protein 2	Homo sapiens	169-173
15163543-14	2004	Although without supportive data, superoxide production induced by arsenic exposure can theoretically impair insulin secretion by interaction with uncoupling protein 2 (UCP2), and oxidative stress can also cause amyloid formation in the pancreas, which could progressively destroy the insulin-secreting beta cells.	Arsenic	67-74	insulin	Homo sapiens	109-116
15163543-16	2004	In conclusions, insulin resistance and beta cell dysfunction can be induced by chronic arsenic exposure.	Arsenic	87-94	insulin	Homo sapiens	16-23
15138027-9	2004	In a second study, the same doses of arsenic were used and the skin tumor promoting phorbol ester, TPA, was applied to the skin after birth in an effort to promote skin tumors potentially initiated by arsenic in utero.	Arsenic	201-208	promotion susceptibility QTL 1	Mus musculus	99-102
15138027-14	2004	In addition, it appears gestational arsenic can act as a tumor initiator in the female mouse liver, inducing liver lesions that can be promoted by TPA.	Arsenic	36-43	promotion susceptibility QTL 1	Mus musculus	147-150
15212268-11	2004	Once this Fe/As precipitate was removed from solution using a 0.45 and 0.2 microm filter, the resulting arsenic concentration (As(III) + As(V)) was relatively constant (the largest LLS slope was -1.4 x 10(-2) (ng As g water(-1)) day(-1)).	Arsenic	104-111	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	137-142
15198077-7	2004	Arsenic also enhanced the liver lactate dehydrogenase activity whereas glucose 6-phosphatase activity in both liver and kidney decreased significantly following arsenic treatment.	Arsenic	161-168	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	71-92
15198077-11	2004	Arsenic-induced alteration of glucose 6-phosphatase activity in both liver and kidney was also counteracted by NAC.	Arsenic	0-7	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	30-51
14578163-1	2004	Concomitant exposures to arsenic and polycyclic aromatic hydrocarbons (PAHs) such as benzo[a]pyrene (BaP) are widespread.	Arsenic	25-32	prohibitin 2	Mus musculus	101-104
14578163-4	2004	A previous in vitro study showed that arsenic potentiated the formation of DNA adducts at low doses of BaP and arsenic.	Arsenic	38-45	prohibitin 2	Mus musculus	103-106
14578163-5	2004	The present study was conducted to test the effect of arsenic on BaP-DNA adduct formation in vivo.	Arsenic	54-61	prohibitin 2	Mus musculus	65-68
14578163-6	2004	We hypothesized that arsenic co-treatment would significantly increase BaP adduct levels in C57BL/6 mouse target organs: skin and lung.	Arsenic	21-28	prohibitin 2	Mus musculus	71-74
14578163-12	2004	Arsenic co-treatment increased average BaP adduct levels in both lung and skin; the increase was statistically significant in the lung (P = 0.038).	Arsenic	0-7	prohibitin 2	Mus musculus	39-42
14578163-13	2004	BaP adduct levels in the skin of individual animals were positively related to skin arsenic concentrations.	Arsenic	84-91	prohibitin 2	Mus musculus	0-3
15355704-7	2004	The expression of MRP2 was correlated with total arsenic content in bile (r = 0.713, P &lt; 0.05).	Arsenic	49-56	ATP binding cassette subfamily C member 2	Rattus norvegicus	18-22
15161912-0	2004	Arsenic transport by the human multidrug resistance protein 1 (MRP1/ABCC1).	Arsenic	0-7	ATP binding cassette subfamily B member 1	Homo sapiens	31-61
15161912-0	2004	Arsenic transport by the human multidrug resistance protein 1 (MRP1/ABCC1).	Arsenic	0-7	ATP binding cassette subfamily C member 1	Homo sapiens	63-67
15161912-0	2004	Arsenic transport by the human multidrug resistance protein 1 (MRP1/ABCC1).	Arsenic	0-7	ATP binding cassette subfamily C member 1	Homo sapiens	68-73
15161912-4	2004	MRP1 also confers resistance to arsenic in association with GSH; however, the mechanism and the species of arsenic transported are unknown.	Arsenic	32-39	ATP binding cassette subfamily C member 1	Homo sapiens	0-4
15161912-4	2004	MRP1 also confers resistance to arsenic in association with GSH; however, the mechanism and the species of arsenic transported are unknown.	Arsenic	107-114	ATP binding cassette subfamily C member 1	Homo sapiens	0-4
15161912-13	2004	As(GS)(3) transport experiments using MRP1 mutants with substrate specificities differing from wild-type MRP1 suggested a commonality in the substrate binding pockets of As(GS)(3) and leukotriene C(4).	Arsenic	0-2	ATP binding cassette subfamily C member 1	Homo sapiens	38-42
15161912-13	2004	As(GS)(3) transport experiments using MRP1 mutants with substrate specificities differing from wild-type MRP1 suggested a commonality in the substrate binding pockets of As(GS)(3) and leukotriene C(4).	Arsenic	0-2	ATP binding cassette subfamily C member 1	Homo sapiens	105-109
15764300-2	2004	A preliminary case-control study was conducted to explore the association between genetic polymorphisms of GSTT1, p53 codon 72 and bladder cancer in southern Taiwan, a former high arsenic exposure area.	Arsenic	180-187	glutathione S-transferase theta 1	Homo sapiens	107-112
15764300-2	2004	A preliminary case-control study was conducted to explore the association between genetic polymorphisms of GSTT1, p53 codon 72 and bladder cancer in southern Taiwan, a former high arsenic exposure area.	Arsenic	180-187	tumor protein p53	Homo sapiens	114-117
15203256-8	2004	In plasma BNP levels, there was only significant difference between MS and AS group (MS 67.5+/-9.7 vs. AS 314.3+/-112.0 pg/ml, P=0.04).	Arsenic	75-77	natriuretic peptide B	Homo sapiens	10-13
15103387-3	2004	PML/RARalpha is the central leukemia-inducing lesion in APL and is directly targeted by all trans retinoic acid (t-RA) as well as by arsenic, both compounds able to induce complete remissions.	Arsenic	133-140	PML nuclear body scaffold	Homo sapiens	0-3
15103387-3	2004	PML/RARalpha is the central leukemia-inducing lesion in APL and is directly targeted by all trans retinoic acid (t-RA) as well as by arsenic, both compounds able to induce complete remissions.	Arsenic	133-140	retinoic acid receptor alpha	Homo sapiens	4-12
15147786-3	2004	Arsenic susceptibility of lymphocyte subpopulations (T helper (Th), CD4+; T cytotoxic (Tc), CD8+) and whether arsenic effects are gender related are still to be determined.	Arsenic	0-7	CD4 molecule	Homo sapiens	68-71
15056798-1	2004	Based on evidence that arsenic modulates proinflammatory events that are involved in skin carcinogenecity, we hypothesized that in normal human epidermal keratinocytes (NHEK) arsenic increases expression of the procarcinogenic enzyme cyclooxygenase-2 (COX-2) and that this occurs via specific mitogen and stress signaling pathways.	Arsenic	175-182	prostaglandin-endoperoxide synthase 2	Homo sapiens	234-250
15056798-1	2004	Based on evidence that arsenic modulates proinflammatory events that are involved in skin carcinogenecity, we hypothesized that in normal human epidermal keratinocytes (NHEK) arsenic increases expression of the procarcinogenic enzyme cyclooxygenase-2 (COX-2) and that this occurs via specific mitogen and stress signaling pathways.	Arsenic	175-182	prostaglandin-endoperoxide synthase 2	Homo sapiens	252-257
15147884-0	2004	Yap8p activation in Saccharomyces cerevisiae under arsenic conditions.	Arsenic	51-58	Arr1p	Saccharomyces cerevisiae S288C	0-5
15147884-1	2004	Yap8p, a member of the Saccharomyces cerevisiae Yap family, is activated in response to arsenic.	Arsenic	88-95	Arr1p	Saccharomyces cerevisiae S288C	0-5
14701702-8	2004	Together, these data support an essential role for JNK signaling in the induction of growth inhibition and apoptosis by As(2)O(3) and suggest that activating JNK may provide a therapeutic advantage in the treatment of cancers that do not respond to arsenic alone.	Arsenic	249-256	mitogen-activated protein kinase 8	Homo sapiens	158-161
14978214-4	2004	Using chromatin immunoprecipitation assays, we show that Yap8p is associated with the ACR3 promoter in untreated as well as arsenic-exposed cells.	Arsenic	124-131	Arr1p	Saccharomyces cerevisiae S288C	57-62
14978214-4	2004	Using chromatin immunoprecipitation assays, we show that Yap8p is associated with the ACR3 promoter in untreated as well as arsenic-exposed cells.	Arsenic	124-131	Arr3p	Saccharomyces cerevisiae S288C	86-90
15604672-2	2004	Our earlier work has shown that tobacco cellular as-1-binding complex SARP (salicylic acid responsive protein) is primarily comprised of bZIP protein TGA2.2 and of minor amounts of a protein that cross-reacts with an antibody directed against related bZIP factor TGA2.1.	Arsenic	18-20	ABSCISIC ACID-INSENSITIVE 5-like protein 2	Nicotiana tabacum	137-141
15604672-2	2004	Our earlier work has shown that tobacco cellular as-1-binding complex SARP (salicylic acid responsive protein) is primarily comprised of bZIP protein TGA2.2 and of minor amounts of a protein that cross-reacts with an antibody directed against related bZIP factor TGA2.1.	Arsenic	18-20	transcription factor TGA2-like	Nicotiana tabacum	150-156
15604672-2	2004	Our earlier work has shown that tobacco cellular as-1-binding complex SARP (salicylic acid responsive protein) is primarily comprised of bZIP protein TGA2.2 and of minor amounts of a protein that cross-reacts with an antibody directed against related bZIP factor TGA2.1.	Arsenic	18-20	ABSCISIC ACID-INSENSITIVE 5-like protein 2	Nicotiana tabacum	251-255
15604672-2	2004	Our earlier work has shown that tobacco cellular as-1-binding complex SARP (salicylic acid responsive protein) is primarily comprised of bZIP protein TGA2.2 and of minor amounts of a protein that cross-reacts with an antibody directed against related bZIP factor TGA2.1.	Arsenic	18-20	TGACG-sequence-specific DNA-binding protein TGA-2.1	Nicotiana tabacum	263-269
15093537-0	2004	Death by arsenic: implications of PML sumoylation.	Arsenic	9-16	PML nuclear body scaffold	Homo sapiens	34-37
15089098-2	2004	Arsenic causes blood vessel growth and remodeling in vivo and cell specific, dose-dependent induction vascular endothelial growth factor-A (VEGF), which is essential for both processes.	Arsenic	0-7	vascular endothelial growth factor A	Homo sapiens	102-138
15089098-2	2004	Arsenic causes blood vessel growth and remodeling in vivo and cell specific, dose-dependent induction vascular endothelial growth factor-A (VEGF), which is essential for both processes.	Arsenic	0-7	vascular endothelial growth factor A	Homo sapiens	140-144
15089098-3	2004	The current study examined the hypothesis that low, environmentally relevant levels of trivalent arsenic (AsIII) activate discrete signaling pathways in vascular smooth muscle cells (SMC) to induce expression of VEGF.	Arsenic	97-104	vascular endothelial growth factor A	Homo sapiens	212-216
15074691-11	2004	In the Eaglehawk soil higher concentrations of As were again due to conversion of exchangeable forms of As(V) into less strongly sorbed As(III) species.	Arsenic	47-49	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	104-109
15026472-10	2004	Specifically, overexpression of ER-alpha, potentially through promoter region hypomethylation, in livers of such mice may be linked to the hepatocarcinogenicity of arsenic.	Arsenic	164-171	estrogen receptor 1 (alpha)	Mus musculus	32-40
15202869-1	2004	OBJECTIVE: The objective of this study was to investigate arsenic induced changes in blood delta-aminolevulinic acid dehydratase (ALAD) after in vitro and in vivo exposure to this element and its response to co-administration of meso 2,3-dimercaptosuccinic acid (DMSA) and monoisoamyl DMSA (MiADMSA) either individually or in combination.	Arsenic	58-65	aminolevulinate dehydratase	Rattus norvegicus	91-128
15202869-1	2004	OBJECTIVE: The objective of this study was to investigate arsenic induced changes in blood delta-aminolevulinic acid dehydratase (ALAD) after in vitro and in vivo exposure to this element and its response to co-administration of meso 2,3-dimercaptosuccinic acid (DMSA) and monoisoamyl DMSA (MiADMSA) either individually or in combination.	Arsenic	58-65	aminolevulinate dehydratase	Rattus norvegicus	130-134
15202869-10	2004	CONCLUSIONS: The results thus suggest that arsenic has a distinct effect on ALAD activity.	Arsenic	43-50	aminolevulinate dehydratase	Rattus norvegicus	76-80
15202869-8	2004	Similarly, MiADMSA at a lower concentration (0.1 mmol/L) was partially effective in the turnover of ALAD activity against 0.5 mmol/L arsenic (III), but at two higher concentrations (0.5 and 1.0 mmol/L) a complete restoration of ALAD activity was observed.	Arsenic	133-140	aminolevulinate dehydratase	Rattus norvegicus	100-104
14967012-5	2004	Rodents deficient in three known ABC family transporters (MRP1, MRP2, and MDR1a/1b) exhibited urinary arsenic levels similar or greater than those in wild-type rodents; however, administration of MK571, an MRP inhibitor, reduced urinary arsenic excretion by almost 50%.	Arsenic	102-109	prolactin family 2, subfamily c, member 2	Mus musculus	58-62
14967012-5	2004	Rodents deficient in three known ABC family transporters (MRP1, MRP2, and MDR1a/1b) exhibited urinary arsenic levels similar or greater than those in wild-type rodents; however, administration of MK571, an MRP inhibitor, reduced urinary arsenic excretion by almost 50%.	Arsenic	102-109	prolactin family 2, subfamily c, member 3	Mus musculus	64-68
14967012-5	2004	Rodents deficient in three known ABC family transporters (MRP1, MRP2, and MDR1a/1b) exhibited urinary arsenic levels similar or greater than those in wild-type rodents; however, administration of MK571, an MRP inhibitor, reduced urinary arsenic excretion by almost 50%.	Arsenic	102-109	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	74-79
14967012-5	2004	Rodents deficient in three known ABC family transporters (MRP1, MRP2, and MDR1a/1b) exhibited urinary arsenic levels similar or greater than those in wild-type rodents; however, administration of MK571, an MRP inhibitor, reduced urinary arsenic excretion by almost 50%.	Arsenic	102-109	ATP-binding cassette, sub-family C (CFTR/MRP), member 1	Mus musculus	58-61
14967012-7	2004	These findings suggest that arsenic excretion is in part dependent on GSH and on an MRP transporter other than MRP1 or 2.	Arsenic	28-35	ATP-binding cassette, sub-family C (CFTR/MRP), member 1	Mus musculus	84-87
14968884-9	2004	The maximum uptake of As(V) by MA was found to be 7 times higher [121 mg of As(V)/g and 47 mg of As(III)/ g] than that of conventional AA, and the kinetics of adsorption were also rapid with complete adsorption in less than 5 h as compared to the conventional AA (about 2 d to reach half of the equilibrium value).	Arsenic	22-24	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	76-81
15045037-12	2004	Recombinant human erythropoietin appears to be effective whether it is given as 300 units/kg of body weight subcutaneously every other day or as 40,000 units subcutaneously every week.	Arsenic	77-79	erythropoietin	Homo sapiens	18-32
14691202-7	2004	Overexpression of alpha-fetoprotein, c-myc, cyclin D1, proliferation-associated protein PAG, and cytokeratin-18 were more dramatic in arsenic-induced HCC than spontaneous tumors.	Arsenic	134-141	alpha fetoprotein	Mus musculus	18-35
15032863-0	2004	Arsenic uptake, translocation and speciation in pho1 and pho2 mutants of Arabidopsis thaliana.	Arsenic	0-7	phosphate 1	Arabidopsis thaliana	48-52
15032863-0	2004	Arsenic uptake, translocation and speciation in pho1 and pho2 mutants of Arabidopsis thaliana.	Arsenic	0-7	phosphate 2	Arabidopsis thaliana	57-61
15032863-5	2004	Both pho2 and the wild type contained mainly As (III) in roots and shoot (67-90% of total As).	Arsenic	45-47	phosphate 2	Arabidopsis thaliana	5-9
15032863-6	2004	Arsenic was likely to be translocated by a different pathway to P (V) in the pho2 and pho1 mutants.	Arsenic	0-7	phosphate 2	Arabidopsis thaliana	77-81
15032863-6	2004	Arsenic was likely to be translocated by a different pathway to P (V) in the pho2 and pho1 mutants.	Arsenic	0-7	phosphate 1	Arabidopsis thaliana	86-90
15028000-0	2004	Children"s exposure to arsenic from CCA-treated wooden decks and playground structures.	Arsenic	23-30	fibrillin 2	Homo sapiens	36-39
15028000-2	2004	Because arsenic can be removed from the surface of CCA-treated wood both by physical contact and by leaching, it is important to determine whether children who play on such structures may ingest arsenic in quantities sufficient to be of public health concern.	Arsenic	8-15	fibrillin 2	Homo sapiens	51-54
15028000-2	2004	Because arsenic can be removed from the surface of CCA-treated wood both by physical contact and by leaching, it is important to determine whether children who play on such structures may ingest arsenic in quantities sufficient to be of public health concern.	Arsenic	195-202	fibrillin 2	Homo sapiens	51-54
15028000-3	2004	Based on a review of existing studies, it is estimated that arsenic doses in amounts of tens of micrograms per day may be incurred by children having realistic levels of exposure to CCA-treated decks and playground structures.	Arsenic	60-67	fibrillin 2	Homo sapiens	182-185
14691202-7	2004	Overexpression of alpha-fetoprotein, c-myc, cyclin D1, proliferation-associated protein PAG, and cytokeratin-18 were more dramatic in arsenic-induced HCC than spontaneous tumors.	Arsenic	134-141	cyclin D1	Mus musculus	44-53
14691202-7	2004	Overexpression of alpha-fetoprotein, c-myc, cyclin D1, proliferation-associated protein PAG, and cytokeratin-18 were more dramatic in arsenic-induced HCC than spontaneous tumors.	Arsenic	134-141	keratin 18	Mus musculus	97-111
14691202-8	2004	In nontumorous liver samples of arsenic-exposed animals, 60 genes (10%) were differentially expressed, including the increased expression of alpha-fetoprotein, c-myc, insulin-like growth factor binding protein-1, superoxide dismutase, glutathione S-transferases, and CYP2A4, and the depressed expression of CYP7B1.	Arsenic	32-39	alpha fetoprotein	Mus musculus	141-158
15028000-6	2004	Considerable uncertainty, however, is associated with quantitative estimates of children"s arsenic exposure from CCA-treated wood.	Arsenic	91-98	fibrillin 2	Homo sapiens	113-116
14691202-8	2004	In nontumorous liver samples of arsenic-exposed animals, 60 genes (10%) were differentially expressed, including the increased expression of alpha-fetoprotein, c-myc, insulin-like growth factor binding protein-1, superoxide dismutase, glutathione S-transferases, and CYP2A4, and the depressed expression of CYP7B1.	Arsenic	32-39	insulin-like growth factor binding protein 1	Mus musculus	167-211
15028000-7	2004	Priorities for refining estimates of arsenic dose include detailed studies of the hand-to-mouth transfer of arsenic, studies of the dermal and gastrointestinal absorption of dislodgeable arsenic, and studies in which doses of arsenic to children playing in contact with CCA-treated wood are directly determined by measurement of arsenic in their urine, hair, and nails.	Arsenic	37-44	fibrillin 2	Homo sapiens	270-273
14691202-8	2004	In nontumorous liver samples of arsenic-exposed animals, 60 genes (10%) were differentially expressed, including the increased expression of alpha-fetoprotein, c-myc, insulin-like growth factor binding protein-1, superoxide dismutase, glutathione S-transferases, and CYP2A4, and the depressed expression of CYP7B1.	Arsenic	32-39	cytochrome P450, family 2, subfamily a, polypeptide 4	Mus musculus	267-273
14691202-8	2004	In nontumorous liver samples of arsenic-exposed animals, 60 genes (10%) were differentially expressed, including the increased expression of alpha-fetoprotein, c-myc, insulin-like growth factor binding protein-1, superoxide dismutase, glutathione S-transferases, and CYP2A4, and the depressed expression of CYP7B1.	Arsenic	32-39	cytochrome P450, family 7, subfamily b, polypeptide 1	Mus musculus	307-313
15161340-4	2004	Imatinib mesylate was also effective in patients with chronic-phase CML refractory to or intolerant of treatment with IFNalpha (as 400 mg/day) and in those with blast-crisis or accelerated-phase CML (600 mg/day).	Arsenic	19-21	interferon alpha 1	Homo sapiens	118-126
15575969-8	2004	We also carried out transcriptional profiling of specific deletion strains, confirming that the transcription factors Yap1, Arr1 (Yap8), and Rpn4 strongly mediate the cell"s adaptation to arsenic-induced stress but that Cad1 has negligible impact.	Arsenic	188-195	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	118-122
14514659-2	2004	Many studies have demonstrated the activation of mitogen-activated protein kinase (MAPK) in several cell types by using lethal concentrations of arsenic in the range of 50-500 micro M. Since the exposure of humans to arsenic is normally at a much lower level in the workplace or in daily life, it is more relevant to study the effects of arsenic at this lower exposure level.	Arsenic	145-152	mitogen-activated protein kinase 1	Homo sapiens	83-87
14514659-2	2004	Many studies have demonstrated the activation of mitogen-activated protein kinase (MAPK) in several cell types by using lethal concentrations of arsenic in the range of 50-500 micro M. Since the exposure of humans to arsenic is normally at a much lower level in the workplace or in daily life, it is more relevant to study the effects of arsenic at this lower exposure level.	Arsenic	217-224	mitogen-activated protein kinase 1	Homo sapiens	83-87
14514659-2	2004	Many studies have demonstrated the activation of mitogen-activated protein kinase (MAPK) in several cell types by using lethal concentrations of arsenic in the range of 50-500 micro M. Since the exposure of humans to arsenic is normally at a much lower level in the workplace or in daily life, it is more relevant to study the effects of arsenic at this lower exposure level.	Arsenic	217-224	mitogen-activated protein kinase 1	Homo sapiens	83-87
15575969-8	2004	We also carried out transcriptional profiling of specific deletion strains, confirming that the transcription factors Yap1, Arr1 (Yap8), and Rpn4 strongly mediate the cell"s adaptation to arsenic-induced stress but that Cad1 has negligible impact.	Arsenic	188-195	Arr1p	Saccharomyces cerevisiae S288C	124-128
15575969-8	2004	We also carried out transcriptional profiling of specific deletion strains, confirming that the transcription factors Yap1, Arr1 (Yap8), and Rpn4 strongly mediate the cell"s adaptation to arsenic-induced stress but that Cad1 has negligible impact.	Arsenic	188-195	Arr1p	Saccharomyces cerevisiae S288C	130-134
15575969-8	2004	We also carried out transcriptional profiling of specific deletion strains, confirming that the transcription factors Yap1, Arr1 (Yap8), and Rpn4 strongly mediate the cell"s adaptation to arsenic-induced stress but that Cad1 has negligible impact.	Arsenic	188-195	stress-regulated transcription factor RPN4	Saccharomyces cerevisiae S288C	141-145
15461930-1	2004	The use of arsenic-containing compounds in cancer therapy is currently being re-considered, after the recent approval of arsenic trioxide (Trisenox) for the treatment of relapsed promyelocytic leukemia (PML).	Arsenic	11-18	PML nuclear body scaffold	Homo sapiens	203-206
14962100-0	2004	Arsenic induces human keratinocyte apoptosis by the FAS/FAS ligand pathway, which correlates with alterations in nuclear factor-kappa B and activator protein-1 activity.	Arsenic	0-7	Fas ligand	Homo sapiens	56-66
14962100-0	2004	Arsenic induces human keratinocyte apoptosis by the FAS/FAS ligand pathway, which correlates with alterations in nuclear factor-kappa B and activator protein-1 activity.	Arsenic	0-7	nuclear factor kappa B subunit 1	Homo sapiens	113-135
14962100-0	2004	Arsenic induces human keratinocyte apoptosis by the FAS/FAS ligand pathway, which correlates with alterations in nuclear factor-kappa B and activator protein-1 activity.	Arsenic	0-7	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	140-159
14962100-4	2004	To investigate the mechanism of arsenic-induced apoptosis and related alterations in NF-kappa B and AP-1 activity, we exposed cultured human foreskin keratinocytes to different concentrations of sodium arsenite.	Arsenic	32-39	nuclear factor kappa B subunit 1	Homo sapiens	85-95
14962100-4	2004	To investigate the mechanism of arsenic-induced apoptosis and related alterations in NF-kappa B and AP-1 activity, we exposed cultured human foreskin keratinocytes to different concentrations of sodium arsenite.	Arsenic	32-39	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	100-104
14962100-5	2004	At lower concentrations (&lt; or =1 microM), arsenic induced keratinocyte proliferation and enhanced both NF-kappa B and AP-1 activity.	Arsenic	45-52	nuclear factor kappa B subunit 1	Homo sapiens	106-116
14962100-5	2004	At lower concentrations (&lt; or =1 microM), arsenic induced keratinocyte proliferation and enhanced both NF-kappa B and AP-1 activity.	Arsenic	45-52	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	121-125
14971641-0	2004	Toxicokinetic and genomic analysis of chronic arsenic exposure in multidrug-resistance mdr1a/1b(-/-) double knockout mice.	Arsenic	46-53	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	87-92
14962100-6	2004	At higher concentrations (&gt; or =5 microM), arsenic induced keratinocyte apoptosis by the Fas/Fas ligand (FasL) pathway.	Arsenic	46-53	Fas ligand	Homo sapiens	96-106
14962100-6	2004	At higher concentrations (&gt; or =5 microM), arsenic induced keratinocyte apoptosis by the Fas/Fas ligand (FasL) pathway.	Arsenic	46-53	Fas ligand	Homo sapiens	108-112
14962100-8	2004	These results indicated that upregulation of NF-kappa B at lower arsenic concentrations was correlated with keratinocyte proliferation.	Arsenic	65-72	nuclear factor kappa B subunit 1	Homo sapiens	45-55
14962100-9	2004	In contrast, higher concentrations of arsenic enhanced AP-1 and induced Fas/FasL-associated apoptosis.	Arsenic	38-45	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	55-59
14962100-9	2004	In contrast, higher concentrations of arsenic enhanced AP-1 and induced Fas/FasL-associated apoptosis.	Arsenic	38-45	Fas ligand	Homo sapiens	76-80
15620040-8	2004	RESULTS AND CONCLUSIONS: The study allowed to establish a strong positive correlation between urine arsenic concentration, blood cadmium concentration and some serum neoplastic markers (CEA, SCC-Ag, PSA).	Arsenic	100-107	serpin family B member 3	Homo sapiens	191-194
15620040-8	2004	RESULTS AND CONCLUSIONS: The study allowed to establish a strong positive correlation between urine arsenic concentration, blood cadmium concentration and some serum neoplastic markers (CEA, SCC-Ag, PSA).	Arsenic	100-107	aminopeptidase puromycin sensitive	Homo sapiens	199-202
14971641-5	2004	Arsenic induced pathological changes, elevated LPO levels and enhanced glutathione S-transferase (GST) activity, in the liver to a greater extent in mdr1a/1b(-/-) than in WT mice.	Arsenic	0-7	hematopoietic prostaglandin D synthase	Mus musculus	71-96
15633628-1	2004	In vitro studies have suggested that arsenic can modify the activity of macrophages in the mouse producing an over-regulation of the COX-2 and increased concentrations of PGE2 in endothelial cells.	Arsenic	37-44	cytochrome c oxidase II, mitochondrial	Mus musculus	133-138
14971641-5	2004	Arsenic induced pathological changes, elevated LPO levels and enhanced glutathione S-transferase (GST) activity, in the liver to a greater extent in mdr1a/1b(-/-) than in WT mice.	Arsenic	0-7	hematopoietic prostaglandin D synthase	Mus musculus	98-101
14971641-5	2004	Arsenic induced pathological changes, elevated LPO levels and enhanced glutathione S-transferase (GST) activity, in the liver to a greater extent in mdr1a/1b(-/-) than in WT mice.	Arsenic	0-7	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	149-154
14971641-6	2004	Arsenic also decreased Cu/Zn superoxide dismutase activity in both mdr1a/1b(-/-) and WT mice.	Arsenic	0-7	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	67-72
14971641-7	2004	The expressions of certain genes, such as those encoding cell proliferation, GST, acute-phase proteins and metabolic enzymes, were modestly altered in arsenic-exposed mice.	Arsenic	151-158	hematopoietic prostaglandin D synthase	Mus musculus	77-80
14971641-8	2004	The expression of cyclin D1, a potential hepatic oncogene, was enhanced in arsenic-exposed mdr1a/1b(-/-) mice only.	Arsenic	75-82	cyclin D1	Mus musculus	18-27
14971641-8	2004	The expression of cyclin D1, a potential hepatic oncogene, was enhanced in arsenic-exposed mdr1a/1b(-/-) mice only.	Arsenic	75-82	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	91-96
14971641-9	2004	At the highest level of exposure, hepatic arsenic content was higher in mdr1a/1b(-/-) than in WT mice, suggesting that enhanced accumulation due to transport deficiency may, in part, account for the enhanced toxicity in these mice.	Arsenic	42-49	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	72-77
14971641-10	2004	In summary, this study shows that chronic arsenic toxicity, including liver pathology and oxidative stress, is enhanced in mdr1a/1b(-/-) mice, possibly due to enhanced accumulation of arsenic as a result of transport system deficiency.	Arsenic	42-49	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	123-128
14971643-0	2004	p53 expression in circulating lymphocytes of non-melanoma skin cancer patients from an arsenic contaminated region in Mexico.	Arsenic	87-94	tumor protein p53	Homo sapiens	0-3
15029704-1	2004	Gene constructions rendering bacteria resistant to arsenic and capable of dissolving phosphates and/or arsenates were created by cloning ars operon and the gene of citrate synthase from a chromosome of the strain Pseudomonas aeruginosa PAO1.	Arsenic	51-58	citrate synthase	Pseudomonas aeruginosa PAO1	164-180
14713550-4	2004	A 1-month exposure to arsenic significantly increased hepatic mRNA levels of cyclin D1 (10 ppm), ILK (1 ppm), and p27(Kip1) (10 ppm), whereas it reduced mRNA levels of PTEN (1 ppm) and beta-catenin (100 ppm).	Arsenic	22-29	cyclin D1	Rattus norvegicus	77-86
14713550-4	2004	A 1-month exposure to arsenic significantly increased hepatic mRNA levels of cyclin D1 (10 ppm), ILK (1 ppm), and p27(Kip1) (10 ppm), whereas it reduced mRNA levels of PTEN (1 ppm) and beta-catenin (100 ppm).	Arsenic	22-29	integrin-linked kinase	Rattus norvegicus	97-100
14713550-4	2004	A 1-month exposure to arsenic significantly increased hepatic mRNA levels of cyclin D1 (10 ppm), ILK (1 ppm), and p27(Kip1) (10 ppm), whereas it reduced mRNA levels of PTEN (1 ppm) and beta-catenin (100 ppm).	Arsenic	22-29	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	114-117
14713550-4	2004	A 1-month exposure to arsenic significantly increased hepatic mRNA levels of cyclin D1 (10 ppm), ILK (1 ppm), and p27(Kip1) (10 ppm), whereas it reduced mRNA levels of PTEN (1 ppm) and beta-catenin (100 ppm).	Arsenic	22-29	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	118-122
14713550-4	2004	A 1-month exposure to arsenic significantly increased hepatic mRNA levels of cyclin D1 (10 ppm), ILK (1 ppm), and p27(Kip1) (10 ppm), whereas it reduced mRNA levels of PTEN (1 ppm) and beta-catenin (100 ppm).	Arsenic	22-29	phosphatase and tensin homolog	Rattus norvegicus	168-172
14713550-4	2004	A 1-month exposure to arsenic significantly increased hepatic mRNA levels of cyclin D1 (10 ppm), ILK (1 ppm), and p27(Kip1) (10 ppm), whereas it reduced mRNA levels of PTEN (1 ppm) and beta-catenin (100 ppm).	Arsenic	22-29	catenin beta 1	Rattus norvegicus	185-197
14713550-5	2004	In contrast, a 4-month arsenic exposure showed increased mRNA expression of cyclin D1 (100 ppm), ILK (1 ppm), and p27(Kip1) (1 and 10 ppm), and decreased expression of both PTEN and beta-catenin at all 3 doses.	Arsenic	23-30	cyclin D1	Rattus norvegicus	76-85
14713550-5	2004	In contrast, a 4-month arsenic exposure showed increased mRNA expression of cyclin D1 (100 ppm), ILK (1 ppm), and p27(Kip1) (1 and 10 ppm), and decreased expression of both PTEN and beta-catenin at all 3 doses.	Arsenic	23-30	integrin-linked kinase	Rattus norvegicus	97-100
14713550-5	2004	In contrast, a 4-month arsenic exposure showed increased mRNA expression of cyclin D1 (100 ppm), ILK (1 ppm), and p27(Kip1) (1 and 10 ppm), and decreased expression of both PTEN and beta-catenin at all 3 doses.	Arsenic	23-30	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	114-117
14713550-5	2004	In contrast, a 4-month arsenic exposure showed increased mRNA expression of cyclin D1 (100 ppm), ILK (1 ppm), and p27(Kip1) (1 and 10 ppm), and decreased expression of both PTEN and beta-catenin at all 3 doses.	Arsenic	23-30	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	118-122
14713550-5	2004	In contrast, a 4-month arsenic exposure showed increased mRNA expression of cyclin D1 (100 ppm), ILK (1 ppm), and p27(Kip1) (1 and 10 ppm), and decreased expression of both PTEN and beta-catenin at all 3 doses.	Arsenic	23-30	phosphatase and tensin homolog	Rattus norvegicus	173-177
14713550-5	2004	In contrast, a 4-month arsenic exposure showed increased mRNA expression of cyclin D1 (100 ppm), ILK (1 ppm), and p27(Kip1) (1 and 10 ppm), and decreased expression of both PTEN and beta-catenin at all 3 doses.	Arsenic	23-30	catenin beta 1	Rattus norvegicus	182-194
14668793-9	2003	Synergism by IFNgamma and arsenic on IRF-1 expression is mediated by a composite element in the IRF-1 promoter that includes an IFNgamma-activation site (GAS) overlapped by a nonconsensus site for nuclear factor kappa B (NFkappaB).	Arsenic	26-33	interferon regulatory factor 1	Homo sapiens	37-42
14744017-2	2003	Using a mini-Tn mutagenized yeast pool, we isolated a chromate-tolerant mutant, CrT9, that displayed metal-specific tolerance since it was only tolerant to Cr(VI), not to Cr(III), Cd, As, or Fe.	Arsenic	184-186	thymidylate synthase	Saccharomyces cerevisiae S288C	80-84
14668793-9	2003	Synergism by IFNgamma and arsenic on IRF-1 expression is mediated by a composite element in the IRF-1 promoter that includes an IFNgamma-activation site (GAS) overlapped by a nonconsensus site for nuclear factor kappa B (NFkappaB).	Arsenic	26-33	interferon regulatory factor 1	Homo sapiens	96-101
14668793-0	2003	Arsenic enhances the activation of Stat1 by interferon gamma leading to synergistic expression of IRF-1.	Arsenic	0-7	signal transducer and activator of transcription 1	Homo sapiens	35-40
14668793-0	2003	Arsenic enhances the activation of Stat1 by interferon gamma leading to synergistic expression of IRF-1.	Arsenic	0-7	interferon gamma	Homo sapiens	44-60
14668793-9	2003	Synergism by IFNgamma and arsenic on IRF-1 expression is mediated by a composite element in the IRF-1 promoter that includes an IFNgamma-activation site (GAS) overlapped by a nonconsensus site for nuclear factor kappa B (NFkappaB).	Arsenic	26-33	interferon gamma	Homo sapiens	128-136
14668793-0	2003	Arsenic enhances the activation of Stat1 by interferon gamma leading to synergistic expression of IRF-1.	Arsenic	0-7	interferon regulatory factor 1	Homo sapiens	98-103
14668793-9	2003	Synergism by IFNgamma and arsenic on IRF-1 expression is mediated by a composite element in the IRF-1 promoter that includes an IFNgamma-activation site (GAS) overlapped by a nonconsensus site for nuclear factor kappa B (NFkappaB).	Arsenic	26-33	nuclear factor kappa B subunit 1	Homo sapiens	197-219
14668793-9	2003	Synergism by IFNgamma and arsenic on IRF-1 expression is mediated by a composite element in the IRF-1 promoter that includes an IFNgamma-activation site (GAS) overlapped by a nonconsensus site for nuclear factor kappa B (NFkappaB).	Arsenic	26-33	nuclear factor kappa B subunit 1	Homo sapiens	221-229
14668793-10	2003	Arsenic has no effect on NFkappaB, whereas it enhances the activation of Stat1 by IFNgamma in NB4 cells leading to an increase in IRF-1 expression.	Arsenic	0-7	signal transducer and activator of transcription 1	Homo sapiens	73-78
14668793-10	2003	Arsenic has no effect on NFkappaB, whereas it enhances the activation of Stat1 by IFNgamma in NB4 cells leading to an increase in IRF-1 expression.	Arsenic	0-7	interferon gamma	Homo sapiens	82-90
14668793-10	2003	Arsenic has no effect on NFkappaB, whereas it enhances the activation of Stat1 by IFNgamma in NB4 cells leading to an increase in IRF-1 expression.	Arsenic	0-7	interferon regulatory factor 1	Homo sapiens	130-135
14563695-0	2003	Genetic predisposition to the cytotoxicity of arsenic: the role of DNA damage and ATM.	Arsenic	46-53	ATM serine/threonine kinase	Homo sapiens	82-85
14680363-2	2003	To understand this variability, we studied the relationship between polymorphisms in the gene for human monomethylarsonic acid (MMA(V)) reductase/hGSTO1 and the urinary arsenic profiles of individuals chronically exposed to arsenic in their drinking water.	Arsenic	169-176	glutathione S-transferase omega 1	Homo sapiens	128-145
14680363-2	2003	To understand this variability, we studied the relationship between polymorphisms in the gene for human monomethylarsonic acid (MMA(V)) reductase/hGSTO1 and the urinary arsenic profiles of individuals chronically exposed to arsenic in their drinking water.	Arsenic	224-231	glutathione S-transferase omega 1	Homo sapiens	128-145
14563695-5	2003	The protective role of the ATM protein was confirmed by the normal response to arsenic displayed by AT cells expressing wild-type ATM.	Arsenic	79-86	ATM serine/threonine kinase	Homo sapiens	27-30
14563695-8	2003	Our data suggest that the ATM protein functions in an important but different capacity in the cellular response to arsenic toxicity than it does in response to agents that generate double-strand breaks, such as ionizing radiation.	Arsenic	115-122	ATM serine/threonine kinase	Homo sapiens	26-29
14669219-2	2003	METHODS: After the process of extracting genomic DNA from blood of 94 health smokers and 88 COPD smokers by use of phenol-chloroform-isoamyl alcohol, three single nucleotide polymorphism (SNP) sites in IL-10 gene promoter marked as -1082G/A,-819C/T,-592C/A were determined by polymerase chain reaction/restriction fragment length polymorphism analysis.	Arsenic	229-231	interleukin 10	Homo sapiens	202-207
14617642-15	2003	SynArsC and pI258 ArsC thus appear to represent alternative branches in the evolution of their shared phosphohydrolytic ancestor into an agent of arsenic detoxification.	Arsenic	146-153	arsenate reductase	Staphylococcus aureus	3-7
14633691-4	2003	By using wild-type and Ikkbeta gene knockout (Ikkbeta(-/-)) mouse embryo fibroblasts, we found that IKKbeta deficiency results in prolongation of arsenic-induced JNK activation, which was not due to the decreased expression of GADD45beta or X-linked Inhibitor of Apoptosis (XIAP), as suggested previously for RelA(-/-) cells treated with tumor necrosis factor alpha.	Arsenic	146-153	inhibitor of kappaB kinase beta	Mus musculus	23-30
14633691-4	2003	By using wild-type and Ikkbeta gene knockout (Ikkbeta(-/-)) mouse embryo fibroblasts, we found that IKKbeta deficiency results in prolongation of arsenic-induced JNK activation, which was not due to the decreased expression of GADD45beta or X-linked Inhibitor of Apoptosis (XIAP), as suggested previously for RelA(-/-) cells treated with tumor necrosis factor alpha.	Arsenic	146-153	inhibitor of kappaB kinase beta	Mus musculus	46-53
14633691-4	2003	By using wild-type and Ikkbeta gene knockout (Ikkbeta(-/-)) mouse embryo fibroblasts, we found that IKKbeta deficiency results in prolongation of arsenic-induced JNK activation, which was not due to the decreased expression of GADD45beta or X-linked Inhibitor of Apoptosis (XIAP), as suggested previously for RelA(-/-) cells treated with tumor necrosis factor alpha.	Arsenic	146-153	mitogen-activated protein kinase 8	Mus musculus	162-165
14633691-4	2003	By using wild-type and Ikkbeta gene knockout (Ikkbeta(-/-)) mouse embryo fibroblasts, we found that IKKbeta deficiency results in prolongation of arsenic-induced JNK activation, which was not due to the decreased expression of GADD45beta or X-linked Inhibitor of Apoptosis (XIAP), as suggested previously for RelA(-/-) cells treated with tumor necrosis factor alpha.	Arsenic	146-153	growth arrest and DNA-damage-inducible 45 beta	Mus musculus	227-237
14633691-4	2003	By using wild-type and Ikkbeta gene knockout (Ikkbeta(-/-)) mouse embryo fibroblasts, we found that IKKbeta deficiency results in prolongation of arsenic-induced JNK activation, which was not due to the decreased expression of GADD45beta or X-linked Inhibitor of Apoptosis (XIAP), as suggested previously for RelA(-/-) cells treated with tumor necrosis factor alpha.	Arsenic	146-153	X-linked inhibitor of apoptosis	Mus musculus	241-272
14633691-4	2003	By using wild-type and Ikkbeta gene knockout (Ikkbeta(-/-)) mouse embryo fibroblasts, we found that IKKbeta deficiency results in prolongation of arsenic-induced JNK activation, which was not due to the decreased expression of GADD45beta or X-linked Inhibitor of Apoptosis (XIAP), as suggested previously for RelA(-/-) cells treated with tumor necrosis factor alpha.	Arsenic	146-153	X-linked inhibitor of apoptosis	Mus musculus	274-278
14633691-4	2003	By using wild-type and Ikkbeta gene knockout (Ikkbeta(-/-)) mouse embryo fibroblasts, we found that IKKbeta deficiency results in prolongation of arsenic-induced JNK activation, which was not due to the decreased expression of GADD45beta or X-linked Inhibitor of Apoptosis (XIAP), as suggested previously for RelA(-/-) cells treated with tumor necrosis factor alpha.	Arsenic	146-153	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	309-313
14633691-4	2003	By using wild-type and Ikkbeta gene knockout (Ikkbeta(-/-)) mouse embryo fibroblasts, we found that IKKbeta deficiency results in prolongation of arsenic-induced JNK activation, which was not due to the decreased expression of GADD45beta or X-linked Inhibitor of Apoptosis (XIAP), as suggested previously for RelA(-/-) cells treated with tumor necrosis factor alpha.	Arsenic	146-153	tumor necrosis factor	Mus musculus	338-365
14633691-7	2003	Inhibition of CYP1B1 reduced both oxidative stress and arsenic-stimulated JNK activation.	Arsenic	55-62	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	14-20
14633691-7	2003	Inhibition of CYP1B1 reduced both oxidative stress and arsenic-stimulated JNK activation.	Arsenic	55-62	mitogen-activated protein kinase 8	Mus musculus	74-77
14581169-4	2003	Compared to normal folate intake, folate deficiency caused lower amounts of arsenic to be excreted in the urine of both the wildtype controls and Folbp1(-/-) mice.	Arsenic	76-83	folate receptor 1 (adult)	Mus musculus	146-152
14580687-0	2003	Susceptibility to arsenic-induced hyperkeratosis and oxidative stress genes myeloperoxidase and catalase.	Arsenic	18-25	myeloperoxidase	Homo sapiens	76-91
14580687-0	2003	Susceptibility to arsenic-induced hyperkeratosis and oxidative stress genes myeloperoxidase and catalase.	Arsenic	18-25	catalase	Homo sapiens	96-104
14580687-3	2003	Carriers of the susceptible MPO and CAT genotypes were at elevated risk (OR 2.1 and 95% CI 0.7-6.2 for MPO; OR 1.9 and 95% CI 0.8-4.7 for CAT) of hyperkeratosis after adjustment for arsenic exposure and other covariates.	Arsenic	182-189	myeloperoxidase	Homo sapiens	28-31
14580687-3	2003	Carriers of the susceptible MPO and CAT genotypes were at elevated risk (OR 2.1 and 95% CI 0.7-6.2 for MPO; OR 1.9 and 95% CI 0.8-4.7 for CAT) of hyperkeratosis after adjustment for arsenic exposure and other covariates.	Arsenic	182-189	catalase	Homo sapiens	36-39
14580687-4	2003	Subjects carrying the high-risk MPO genotype and with high arsenic exposure were at almost six times (OR 5.8; 95% CI 1.1-30.1) elevated risk of developing hyperkeratosis as compared to those carrying the low-risk genotype and with low arsenic exposure.	Arsenic	59-66	myeloperoxidase	Homo sapiens	32-35
14580687-4	2003	Subjects carrying the high-risk MPO genotype and with high arsenic exposure were at almost six times (OR 5.8; 95% CI 1.1-30.1) elevated risk of developing hyperkeratosis as compared to those carrying the low-risk genotype and with low arsenic exposure.	Arsenic	235-242	myeloperoxidase	Homo sapiens	32-35
14580687-5	2003	Similarly, highly exposed subjects carrying the high-risk CAT genotype were at more than four times (OR 4.6; 95% CI 1.4-15.6) elevated risk of developing hyperkeratosis as compared to those carrying the low-risk genotype and with low arsenic exposure.	Arsenic	234-241	catalase	Homo sapiens	58-61
14580687-6	2003	Our findings, although based on small numbers, suggest that the oxidative stress genes MPO and CAT may influence the risk of arsenic-induced premalignant hyperkeratotic skin lesions.	Arsenic	125-132	myeloperoxidase	Homo sapiens	87-90
14580687-6	2003	Our findings, although based on small numbers, suggest that the oxidative stress genes MPO and CAT may influence the risk of arsenic-induced premalignant hyperkeratotic skin lesions.	Arsenic	125-132	catalase	Homo sapiens	95-98
14594625-0	2003	Arsenic exposure accelerates atherogenesis in apolipoprotein E(-/-) mice.	Arsenic	0-7	apolipoprotein E	Mus musculus	46-62
12919957-0	2003	P53 alterations in bladder tumors from arsenic and tobacco exposed patients.	Arsenic	39-46	tumor protein p53	Homo sapiens	0-3
12919957-2	2003	A case-case study was conducted to compare p53 mutations in 147 bladder tumors from South American patients by tobacco and arsenic exposure.	Arsenic	123-130	tumor protein p53	Homo sapiens	43-46
12919957-4	2003	The prevalence of p53 mutations and protein expression was examined in relation to tumor stage, grade, patient age, gender, tobacco and arsenic exposure.	Arsenic	136-143	tumor protein p53	Homo sapiens	18-21
14594625-4	2003	As assessed morphometrically, the size of grossly discernible lesions covering the intimal area of aorta were increased significantly in arsenic-treated ApoE-deficient mice compared with nontreated transgenic mice.	Arsenic	137-144	apolipoprotein E	Mus musculus	153-157
14594625-9	2003	Arsenic treatment does not modulate endothelial cell-mediated lipid oxidation or smooth muscle cell proliferation but induced the expression of genes coding inflammatory mediators, including interleukin-8.	Arsenic	0-7	chemokine (C-X-C motif) ligand 15	Mus musculus	191-204
14567983-5	2003	We found, for the first time, that arsenic enhanced cellular expression of Nrf2 at the transcriptional and protein levels and activated expression of Nrf2-related genes in these cells.	Arsenic	35-42	NFE2 like bZIP transcription factor 2	Homo sapiens	75-79
14567983-12	2003	Taken together, these data clearly show that arsenic increases Nrf2 expression and activity at multiple levels and that H(2)O(2) is one of the mediators of this process.	Arsenic	45-52	NFE2 like bZIP transcription factor 2	Homo sapiens	63-67
12883650-11	2003	Our results suggested that the morphological changes of arsenic-induced apoptosis of human esophageal epithelial cells were initiated by ezrin and actin-cytoskeletal aberrance.	Arsenic	56-63	ezrin	Homo sapiens	137-142
14581378-8	2003	CONCLUSIONS: A combination of EGFR AS and docetaxel may be effective in the treatment of SCCHN with a reduced toxicity profile compared with standard chemotherapy regimens.	Arsenic	35-37	epidermal growth factor receptor	Mus musculus	30-34
14507663-4	2003	Quantitative real-time polymerase chain reaction normalized to beta-actin revealed expression of the MRP5 gene in all samples (LV, 38.5 +/- 12.9; AS, 12.7 +/- 5.6; P &lt; 0.001).	Arsenic	146-148	ATP binding cassette subfamily C member 5	Homo sapiens	101-105
14567983-5	2003	We found, for the first time, that arsenic enhanced cellular expression of Nrf2 at the transcriptional and protein levels and activated expression of Nrf2-related genes in these cells.	Arsenic	35-42	NFE2 like bZIP transcription factor 2	Homo sapiens	150-154
14567983-6	2003	In addition, arsenic exposure caused nuclear accumulation of Nrf2 in association with downstream activation of Nrf2-mediated oxidative response genes.	Arsenic	13-20	NFE2 like bZIP transcription factor 2	Homo sapiens	61-65
14567983-6	2003	In addition, arsenic exposure caused nuclear accumulation of Nrf2 in association with downstream activation of Nrf2-mediated oxidative response genes.	Arsenic	13-20	NFE2 like bZIP transcription factor 2	Homo sapiens	111-115
14567983-7	2003	Arsenic simultaneously increased the expression of Keap1, a regulator of Nrf2 activity.	Arsenic	0-7	kelch like ECH associated protein 1	Homo sapiens	51-56
14567983-7	2003	Arsenic simultaneously increased the expression of Keap1, a regulator of Nrf2 activity.	Arsenic	0-7	NFE2 like bZIP transcription factor 2	Homo sapiens	73-77
14567983-8	2003	The coordinated induction of Keap1 expression and nuclear Nrf2 accumulation induced by arsenic suggests that Keap1 is important to arsenic-induced Nrf2 activation.	Arsenic	87-94	kelch like ECH associated protein 1	Homo sapiens	29-34
14567983-8	2003	The coordinated induction of Keap1 expression and nuclear Nrf2 accumulation induced by arsenic suggests that Keap1 is important to arsenic-induced Nrf2 activation.	Arsenic	87-94	NFE2 like bZIP transcription factor 2	Homo sapiens	58-62
14567983-8	2003	The coordinated induction of Keap1 expression and nuclear Nrf2 accumulation induced by arsenic suggests that Keap1 is important to arsenic-induced Nrf2 activation.	Arsenic	87-94	kelch like ECH associated protein 1	Homo sapiens	109-114
14567983-8	2003	The coordinated induction of Keap1 expression and nuclear Nrf2 accumulation induced by arsenic suggests that Keap1 is important to arsenic-induced Nrf2 activation.	Arsenic	87-94	NFE2 like bZIP transcription factor 2	Homo sapiens	147-151
14567983-8	2003	The coordinated induction of Keap1 expression and nuclear Nrf2 accumulation induced by arsenic suggests that Keap1 is important to arsenic-induced Nrf2 activation.	Arsenic	131-138	kelch like ECH associated protein 1	Homo sapiens	29-34
14567983-8	2003	The coordinated induction of Keap1 expression and nuclear Nrf2 accumulation induced by arsenic suggests that Keap1 is important to arsenic-induced Nrf2 activation.	Arsenic	131-138	NFE2 like bZIP transcription factor 2	Homo sapiens	58-62
14567983-8	2003	The coordinated induction of Keap1 expression and nuclear Nrf2 accumulation induced by arsenic suggests that Keap1 is important to arsenic-induced Nrf2 activation.	Arsenic	131-138	kelch like ECH associated protein 1	Homo sapiens	109-114
14567983-8	2003	The coordinated induction of Keap1 expression and nuclear Nrf2 accumulation induced by arsenic suggests that Keap1 is important to arsenic-induced Nrf2 activation.	Arsenic	131-138	NFE2 like bZIP transcription factor 2	Homo sapiens	147-151
12931215-4	2003	C-Jun-terminal kinase (JNK) was activated only in NKM-1 cells and arsenic-sensitive NB4 cells, but not in arsenic-insensitive HL-60 cells.	Arsenic	66-73	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-5
12931215-4	2003	C-Jun-terminal kinase (JNK) was activated only in NKM-1 cells and arsenic-sensitive NB4 cells, but not in arsenic-insensitive HL-60 cells.	Arsenic	66-73	mitogen-activated protein kinase 8	Homo sapiens	23-26
14621283-9	2003	MPO activity increased significantly, starting at 3 h in both AP and AS (P &lt; 0.05).	Arsenic	69-71	myeloperoxidase	Rattus norvegicus	0-3
12915149-2	2003	The inorganic forms of arsenic occurring as As(III) and As(V) are toxic and may pose a health risk to human population.	Arsenic	23-30	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	56-61
12903988-1	2003	A study was carried out to determine arsenic species in Porphyra seaweed originating from the China Sea.	Arsenic	37-44	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	100-103
12909714-4	2003	Adh::TaPCS1/cad1-3 and 35S::TaPCS1/cad1-3 complemented the cadmium, mercury, and arsenic sensitivities of the cad1-3 mutant.	Arsenic	81-88	glutathione gamma-glutamylcysteinyltransferase 1	Triticum aestivum	28-34
12909714-4	2003	Adh::TaPCS1/cad1-3 and 35S::TaPCS1/cad1-3 complemented the cadmium, mercury, and arsenic sensitivities of the cad1-3 mutant.	Arsenic	81-88	cinnamyl-alcohol dehydrogenase	Arabidopsis thaliana	35-39
12909714-4	2003	Adh::TaPCS1/cad1-3 and 35S::TaPCS1/cad1-3 complemented the cadmium, mercury, and arsenic sensitivities of the cad1-3 mutant.	Arsenic	81-88	cinnamyl-alcohol dehydrogenase	Arabidopsis thaliana	35-39
12676792-6	2003	Furthermore, arsenic treatment down-regulated NF-kappaB target genes, including tumor necrosis factor-alphareceptor-associated factor 1 (TRAF1), c-IAP2, interleukin-13 (IL-13), and CCR7.	Arsenic	13-20	TNF receptor associated factor 1	Homo sapiens	80-135
12660146-8	2003	In conclusion, in this article we provide a protocol for an optimized AS-mediated knockdown, representing a specific and efficient instrument for blocking of iNOS formation and allowing for studying the impact of iNOS expression on endothelial function.	Arsenic	70-72	nitric oxide synthase 2	Rattus norvegicus	158-162
12660146-8	2003	In conclusion, in this article we provide a protocol for an optimized AS-mediated knockdown, representing a specific and efficient instrument for blocking of iNOS formation and allowing for studying the impact of iNOS expression on endothelial function.	Arsenic	70-72	nitric oxide synthase 2	Rattus norvegicus	213-217
12676792-6	2003	Furthermore, arsenic treatment down-regulated NF-kappaB target genes, including tumor necrosis factor-alphareceptor-associated factor 1 (TRAF1), c-IAP2, interleukin-13 (IL-13), and CCR7.	Arsenic	13-20	TNF receptor associated factor 1	Homo sapiens	137-142
12676792-6	2003	Furthermore, arsenic treatment down-regulated NF-kappaB target genes, including tumor necrosis factor-alphareceptor-associated factor 1 (TRAF1), c-IAP2, interleukin-13 (IL-13), and CCR7.	Arsenic	13-20	baculoviral IAP repeat containing 3	Homo sapiens	145-151
12676792-6	2003	Furthermore, arsenic treatment down-regulated NF-kappaB target genes, including tumor necrosis factor-alphareceptor-associated factor 1 (TRAF1), c-IAP2, interleukin-13 (IL-13), and CCR7.	Arsenic	13-20	interleukin 13	Homo sapiens	153-167
12676792-6	2003	Furthermore, arsenic treatment down-regulated NF-kappaB target genes, including tumor necrosis factor-alphareceptor-associated factor 1 (TRAF1), c-IAP2, interleukin-13 (IL-13), and CCR7.	Arsenic	13-20	interleukin 13	Homo sapiens	169-174
12676792-6	2003	Furthermore, arsenic treatment down-regulated NF-kappaB target genes, including tumor necrosis factor-alphareceptor-associated factor 1 (TRAF1), c-IAP2, interleukin-13 (IL-13), and CCR7.	Arsenic	13-20	C-C motif chemokine receptor 7	Homo sapiens	181-185
12928150-0	2003	Genetic variation in genes associated with arsenic metabolism: glutathione S-transferase omega 1-1 and purine nucleoside phosphorylase polymorphisms in European and indigenous Americans.	Arsenic	43-50	glutathione S-transferase omega 1	Homo sapiens	63-98
14686617-0	2003	Toxicity and metabolism of subcytotoxic inorganic arsenic in human renal proximal tubule epithelial cells (HK-2).	Arsenic	50-57	hexokinase 2	Homo sapiens	107-111
14686617-3	2003	This study investigates the potential of an immortalized human proximal tubular epithelial cell line, HK-2, to serve as a representative model for low level exposures of the human kidney to arsenic.	Arsenic	190-197	hexokinase 2	Homo sapiens	102-106
14686617-10	2003	When compared to the activities of these enzymes in other animal tissues, the specific activities of HK-2 cells were indicative of a robust capacity to metabolize arsenic.	Arsenic	163-170	hexokinase 2	Homo sapiens	101-105
12864797-7	2003	Gly533Cys-TPO was located on the endoplasmic reticulum (ER) and nuclear envelope but not on the plasma membrane, whereas Asp574/Leu575del-TPO was located not only on the ER and nuclear envelope but also on the plasma membrane, as wild-type TPO.	Arsenic	15-17	thyroid peroxidase	Homo sapiens	10-13
12928150-0	2003	Genetic variation in genes associated with arsenic metabolism: glutathione S-transferase omega 1-1 and purine nucleoside phosphorylase polymorphisms in European and indigenous Americans.	Arsenic	43-50	purine nucleoside phosphorylase	Homo sapiens	103-134
12928150-4	2003	We screened two genes responsible for arsenic metabolism, human purine nucleoside phosphorylase (hNP), which functions as an arsenate reductase converting arsenate to arsenite, and human glutathione S-transferase omega 1-1 (hGSTO1-1), which functions as a monomethylarsonic acid (MMA) reductase, converting MMA(V) to MMA(III), to develop a comprehensive catalog of commonly occurring genetic polymorphisms in these genes.	Arsenic	38-45	purine nucleoside phosphorylase	Homo sapiens	64-95
12928150-4	2003	We screened two genes responsible for arsenic metabolism, human purine nucleoside phosphorylase (hNP), which functions as an arsenate reductase converting arsenate to arsenite, and human glutathione S-transferase omega 1-1 (hGSTO1-1), which functions as a monomethylarsonic acid (MMA) reductase, converting MMA(V) to MMA(III), to develop a comprehensive catalog of commonly occurring genetic polymorphisms in these genes.	Arsenic	38-45	kallikrein related peptidase 8	Homo sapiens	97-100
12928150-4	2003	We screened two genes responsible for arsenic metabolism, human purine nucleoside phosphorylase (hNP), which functions as an arsenate reductase converting arsenate to arsenite, and human glutathione S-transferase omega 1-1 (hGSTO1-1), which functions as a monomethylarsonic acid (MMA) reductase, converting MMA(V) to MMA(III), to develop a comprehensive catalog of commonly occurring genetic polymorphisms in these genes.	Arsenic	38-45	glutathione S-transferase omega 1	Homo sapiens	187-222
12928150-4	2003	We screened two genes responsible for arsenic metabolism, human purine nucleoside phosphorylase (hNP), which functions as an arsenate reductase converting arsenate to arsenite, and human glutathione S-transferase omega 1-1 (hGSTO1-1), which functions as a monomethylarsonic acid (MMA) reductase, converting MMA(V) to MMA(III), to develop a comprehensive catalog of commonly occurring genetic polymorphisms in these genes.	Arsenic	38-45	glutathione S-transferase omega 1	Homo sapiens	224-232
12877744-3	2003	A survey of GenBank shows that arsC appears to be phylogenetically widespread both in organisms with known arsenic resistance and those organisms that have been sequenced as part of whole genome projects.	Arsenic	107-114	steroid sulfatase	Homo sapiens	31-35
12928150-4	2003	We screened two genes responsible for arsenic metabolism, human purine nucleoside phosphorylase (hNP), which functions as an arsenate reductase converting arsenate to arsenite, and human glutathione S-transferase omega 1-1 (hGSTO1-1), which functions as a monomethylarsonic acid (MMA) reductase, converting MMA(V) to MMA(III), to develop a comprehensive catalog of commonly occurring genetic polymorphisms in these genes.	Arsenic	38-45	glutathione S-transferase omega 1	Homo sapiens	256-294
12928151-8	2003	Multivariate analyses on 64 study subjects of varying arsenic exposure levels showed that the association of CCL2/MCP1 plasma protein level with blood arsenic remained significant after adjustment for other risk factors of cardiovascular diseases.	Arsenic	54-61	C-C motif chemokine ligand 2	Homo sapiens	109-113
12928151-8	2003	Multivariate analyses on 64 study subjects of varying arsenic exposure levels showed that the association of CCL2/MCP1 plasma protein level with blood arsenic remained significant after adjustment for other risk factors of cardiovascular diseases.	Arsenic	54-61	C-C motif chemokine ligand 2	Homo sapiens	114-118
12928151-8	2003	Multivariate analyses on 64 study subjects of varying arsenic exposure levels showed that the association of CCL2/MCP1 plasma protein level with blood arsenic remained significant after adjustment for other risk factors of cardiovascular diseases.	Arsenic	151-158	C-C motif chemokine ligand 2	Homo sapiens	109-113
12928151-8	2003	Multivariate analyses on 64 study subjects of varying arsenic exposure levels showed that the association of CCL2/MCP1 plasma protein level with blood arsenic remained significant after adjustment for other risk factors of cardiovascular diseases.	Arsenic	151-158	C-C motif chemokine ligand 2	Homo sapiens	114-118
12971693-13	2003	Arsenic has been found in at least 1,014 current or former NPL sites.	Arsenic	0-7	N-acetylneuraminate pyruvate lyase	Homo sapiens	59-62
14743630-8	2003	The concentration of IL-5 in the serum of AR and AS was both significantly higher than that of Con.	Arsenic	49-51	interleukin 5	Rattus norvegicus	21-25
12883267-8	2003	Arsenic increased expression of the P21 protein and decreased levels of cyclin A, cyclin B1 and cyclin D1, but expression of CDK2, CDK4, CDK6, and cyclin E were not affected.	Arsenic	0-7	H3 histone pseudogene 16	Homo sapiens	36-39
12883267-8	2003	Arsenic increased expression of the P21 protein and decreased levels of cyclin A, cyclin B1 and cyclin D1, but expression of CDK2, CDK4, CDK6, and cyclin E were not affected.	Arsenic	0-7	cyclin A2	Homo sapiens	72-80
12883267-8	2003	Arsenic increased expression of the P21 protein and decreased levels of cyclin A, cyclin B1 and cyclin D1, but expression of CDK2, CDK4, CDK6, and cyclin E were not affected.	Arsenic	0-7	cyclin B1	Homo sapiens	82-91
12883267-8	2003	Arsenic increased expression of the P21 protein and decreased levels of cyclin A, cyclin B1 and cyclin D1, but expression of CDK2, CDK4, CDK6, and cyclin E were not affected.	Arsenic	0-7	cyclin D1	Homo sapiens	96-105
12642121-5	2003	It is now apparent that the nature of the RARalpha-fusion partner is a critical determinant of response to ATRA and arsenic, underlining the importance of cytogenetic and molecular characterisation of patients with suspected APL to determine the most appropriate treatment approach.	Arsenic	116-123	retinoic acid receptor alpha	Homo sapiens	42-50
12669191-12	2003	In the 40-h time-course study, CRP levels peaked at 25-40 h post-dosing, to approximately 120% of control (as 100%).	Arsenic	107-109	C-reactive protein	Rattus norvegicus	31-34
12916849-4	2003	Effect of LPRM/(As(V) solution) volumetric ratio on the removal of As(V) by co-precipitation arsenic together with aluminum present as aluminate in the LPRM were studied.	Arsenic	93-100	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	67-72
12915223-4	2003	Co-administration of arsenic treated rats with ascorbic acid and alpha-tocopherol showed significant reduction in the level of lipid peroxidation and elevation in the levels of ascorbic acid, alpha-tocopherol, glutathione and total sulfhydryls and in the activities of isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, NADH-dehydrogenase and cytochrome c oxidase.	Arsenic	21-28	oxoglutarate dehydrogenase	Rattus norvegicus	295-328
12749816-0	2003	DNA repair gene XPD and susceptibility to arsenic-induced hyperkeratosis.	Arsenic	42-49	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	16-19
12749816-3	2003	We undertook the first study to examine whether genetic susceptibility, as determined by the codon 751 SNP (A--&gt;C) of the DNA repair gene XPD, influences the risk of arsenic-induced hyperkeratotic skin lesions, precursors of skin cancer, in a case-control study of 29 hyperkeratosis cases and 105 healthy controls from the same community in an area of Bangladesh.	Arsenic	169-176	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	141-144
12749816-5	2003	However, the increase in hyperkeratosis risk in relation to urinary arsenic measures genotype was borderline significant for urinary total arsenic (P for trend=0.06) and statistically significant for urinary creatinine adjusted arsenic (P for trend=0.01) among subjects with the XPD A allele (AA) but not among subjects with the other XPD genotypes.	Arsenic	68-75	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	279-282
12749816-5	2003	However, the increase in hyperkeratosis risk in relation to urinary arsenic measures genotype was borderline significant for urinary total arsenic (P for trend=0.06) and statistically significant for urinary creatinine adjusted arsenic (P for trend=0.01) among subjects with the XPD A allele (AA) but not among subjects with the other XPD genotypes.	Arsenic	68-75	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	335-338
12749816-7	2003	In conclusion, our findings suggest that the DNA repair gene XPD may influence the risk of arsenic-induced premalignant hyperkeratotic skin lesions.	Arsenic	91-98	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	61-64
12717832-21	2003	In the arsenic groups, the expression of bcl-2 in the renal tubular epithelium was increased (P=0.005), no obvious changes happened to PCNA LI.	Arsenic	7-14	BCL2, apoptosis regulator	Rattus norvegicus	41-46
12745069-0	2003	Activation of Nrf2 and accumulation of ubiquitinated A170 by arsenic in osteoblasts.	Arsenic	61-68	sequestosome 1	Homo sapiens	53-57
12745069-2	2003	We here report for the first time that inorganic arsenic activates the transcription factor Nrf2, which controls the expression of oxidative stress-induced proteins.	Arsenic	49-56	NFE2 like bZIP transcription factor 2	Homo sapiens	92-96
12745069-7	2003	These results provide the first direct evidence that toxic arsenics impair the normal function of A170.	Arsenic	59-67	sequestosome 1	Homo sapiens	98-102
12711313-5	2003	Remarkably, heterologous expression of PCS sensitizes S. cerevisiae to arsenate, while ACR3 confers much higher arsenic resistance in pcsDelta than in wild-type S. pombe.	Arsenic	112-119	Arr3p	Saccharomyces cerevisiae S288C	87-91
12732551-9	2003	These results suggest that ArsB and ArsC may be useful for As(V)-respiring bacteria in environments where As concentrations are high, but that neither is required for respiration.	Arsenic	59-61	arsenate reductase (glutaredoxin)	Shewanella oneidensis MR-1	36-40
12757736-4	2003	Since arsenic induces cytoskeleton alterations, which in turn may affect protein transport of the cell, we assumed that NaAsO(2) induced an accumulation of IL-2 inside the cells, and thus a reduction in the secretion of IL-2.	Arsenic	6-13	interleukin 2	Homo sapiens	156-160
12652554-8	2003	An example is given from an ongoing study of cancer and exposure to arsenic as measured by toenail concentrations and tap water samples.	Arsenic	68-75	nuclear RNA export factor 1	Homo sapiens	118-121
12826625-6	2003	Analyses of arsenic accumulation and release revealed that PTB1-disrupted cells show arsenate resistance due to low arsenate uptake.	Arsenic	12-19	uncharacterized protein	Chlamydomonas reinhardtii	59-63
12731862-2	2003	MRP1 overexpression in tumor cells results in an ATP-dependent efflux of many oncolytic agents and arsenic and antimony oxyanions.	Arsenic	99-106	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
12750708-5	2003	Despite being approximately 10-fold more resistant to arsenic than their parental cell line, PML/RARalpha protein was still degraded by As(2)O(3) in these cells, providing further evidence that loss of expression of the oncoprotein does not confer arsenic sensitivity.	Arsenic	248-255	PML nuclear body scaffold	Homo sapiens	93-96
12704230-10	2003	Arterial plasma CGRP rose 3-fold with AS but was unaltered by DEA/NO or NTG, supporting a proposed role of this peptide to HNO/NO(-) cardiotropic action.	Arsenic	38-40	calcitonin related polypeptide alpha	Homo sapiens	16-20
12519079-0	2003	Identification of galectin I and thioredoxin peroxidase II as two arsenic-binding proteins in Chinese hamster ovary cells.	Arsenic	66-73	peroxiredoxin-1	Cricetulus griseus	33-58
12547826-8	2003	Our results strongly suggest that arsenic-triggered alterations in chromatin structure perturb specific gene transcription, including that of proto-oncogenes c-jun and c-fos, and may thereby contribute to the carcinogenic process.	Arsenic	34-41	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	158-163
12547826-8	2003	Our results strongly suggest that arsenic-triggered alterations in chromatin structure perturb specific gene transcription, including that of proto-oncogenes c-jun and c-fos, and may thereby contribute to the carcinogenic process.	Arsenic	34-41	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	168-173
12569548-5	2003	Toenail arsenic levels were inversely correlated with expression of critical members of the nucleotide excision repair complex, ERCC1 (r(2) = 0.82, p &lt; 0.0001), XPF (r(2) = 0.56, p &lt; 0.002), and XPB (r(2) = 0.75, p &lt; 0.0001).	Arsenic	8-15	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	128-133
12569548-5	2003	Toenail arsenic levels were inversely correlated with expression of critical members of the nucleotide excision repair complex, ERCC1 (r(2) = 0.82, p &lt; 0.0001), XPF (r(2) = 0.56, p &lt; 0.002), and XPB (r(2) = 0.75, p &lt; 0.0001).	Arsenic	8-15	ERCC excision repair 4, endonuclease catalytic subunit	Homo sapiens	164-167
12641444-0	2003	Inorganic and dimethylated arsenic species induce cellular p53.	Arsenic	27-34	tumor protein p53	Homo sapiens	59-62
12532412-4	2003	Here we report that poly(ADP-ribosyl)ation, which is predominantly mediated by poly(ADP-ribose) polymerase-1 (PARP-1), is inhibited at concentrations as low as 10 nM in cultured HeLa cells, closely matching arsenic concentrations in blood and urine of the general population.	Arsenic	207-214	poly(ADP-ribose) polymerase 1	Homo sapiens	79-108
12532412-4	2003	Here we report that poly(ADP-ribosyl)ation, which is predominantly mediated by poly(ADP-ribose) polymerase-1 (PARP-1), is inhibited at concentrations as low as 10 nM in cultured HeLa cells, closely matching arsenic concentrations in blood and urine of the general population.	Arsenic	207-214	poly(ADP-ribose) polymerase 1	Homo sapiens	110-116
12703962-0	2003	Low concentrations of arsenic induce vascular endothelial growth factor and nitric oxide release and stimulate angiogenesis in vitro.	Arsenic	22-29	vascular endothelial growth factor A	Homo sapiens	37-71
12864950-6	2003	CONCLUSION: One of the pharmacological mechanisms of As(2)O(3) is to activate the expression of CDKI P15, P16 and P21, and consequently affect cell proliferation cycle.	Arsenic	53-55	cyclin dependent kinase inhibitor 2B	Homo sapiens	101-104
12864950-6	2003	CONCLUSION: One of the pharmacological mechanisms of As(2)O(3) is to activate the expression of CDKI P15, P16 and P21, and consequently affect cell proliferation cycle.	Arsenic	53-55	cyclin dependent kinase inhibitor 2A	Homo sapiens	106-109
12864950-6	2003	CONCLUSION: One of the pharmacological mechanisms of As(2)O(3) is to activate the expression of CDKI P15, P16 and P21, and consequently affect cell proliferation cycle.	Arsenic	53-55	cyclin dependent kinase inhibitor 1A	Homo sapiens	114-117
12614848-7	2003	These results suggested that selective blockade of the arsenite-provoked PI-3 kinase/Akt pathway can promote the arsenite-triggered pathway for caspase activation, and this may open a new study area for wider applications of arsenic as a drug for treating various kinds of leukemia.	Arsenic	225-232	AKT serine/threonine kinase 1	Homo sapiens	85-88
12388546-8	2002	Chromatin immunoprecipitation assays revealed that As(2)O(3) potently enhances histone H3 phosphoacetylation at the CASPASE-10 locus.	Arsenic	51-53	caspase 10	Homo sapiens	116-126
12471029-4	2003	Ribonuclease protection assays revealed that one of these splice variants, RyR3 (AS-8a), which lacks a 29-amino acid fragment (His(4406)-Lys(4434)) encompassing a predicted transmembrane helix, was highly expressed in smooth muscle tissues, but not in skeletal muscle, the heart, or the brain.	Arsenic	81-83	ryanodine receptor 3	Homo sapiens	75-79
12565892-1	2003	Glutathione-S-transferase class Omega (GSTO 1-1) belongs to a new subfamily of GSTs, which is identical with human monomethylarsonic acid (MMA(V)) reductase, the rate limiting enzyme for biotransformation of inorganic arsenic, environmental carcinogen.	Arsenic	218-225	glutathione S-transferase omega 1	Homo sapiens	39-47
12565892-1	2003	Glutathione-S-transferase class Omega (GSTO 1-1) belongs to a new subfamily of GSTs, which is identical with human monomethylarsonic acid (MMA(V)) reductase, the rate limiting enzyme for biotransformation of inorganic arsenic, environmental carcinogen.	Arsenic	218-225	glutathione S-transferase omega 1	Homo sapiens	79-83
12565892-1	2003	Glutathione-S-transferase class Omega (GSTO 1-1) belongs to a new subfamily of GSTs, which is identical with human monomethylarsonic acid (MMA(V)) reductase, the rate limiting enzyme for biotransformation of inorganic arsenic, environmental carcinogen.	Arsenic	218-225	glutathione S-transferase omega 1	Homo sapiens	115-156
18365053-8	2003	The human MRP1, a member of this family, is frequently amplified in cancer cells and it is well-documented that MRPl-overexpressing cells poorly accumulate arsenic and antimony because of enhanced cellular effiux which depends on the presence of GSH.	Arsenic	156-163	ATP binding cassette subfamily C member 1	Homo sapiens	10-14
12461767-6	2003	Interestingly, by using a SAX2 chip, we were able to detect several protein peaks that increased their expression in lung epithelial cells (LEC) treated with only B[a]P. Identification and characterization of these proteins may reveal the molecular basis of As-induced cell transformation and provide insight into the mechanisms by which arsenic induces carcinogenesis.	Arsenic	338-345	NK1 homeobox 1	Homo sapiens	26-30
15000836-2	2003	The introduction of 0.1-0.5 microM PEG-AS-ACHE or 0.5 microM AS-ACHE into methylcellulose bone marrow (BM) cultures produced a doubling in number of colony-forming unit-granulocyte-erythrocyte-macrophage-megakaryocyte (CFU-GEMM) and a 5-fold increase in cell number of the PEG-ODN.	Arsenic	39-41	acetylcholinesterase (Cartwright blood group)	Homo sapiens	42-46
12465798-1	2003	A fixed-bed sorption process can be very effective in removing trace concentrations of arsenic from contaminated groundwater provided: the sorbent is very selective toward both As(III) and As(V) species; the influent and treated water do not warrant any additional pre- or post- treatment; pH and composition of the raw water with respect to other electrolytes remain unchanged besides arsenic removal, and the sorbent is durable with excellent attrition resistance properties.	Arsenic	87-94	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	189-194
12669407-4	2003	Administration of steroid and low dose chemotherapy (DNR 60 mg x day 1-2, BH-AC 250 mg x day 1-2) with arsenic was effective for APL syndrome, and complete remission (CR) was obtained at day 35 and PML-RAR mRNA became negative.	Arsenic	103-110	PML-RARA regulated adaptor molecule 1	Homo sapiens	198-205
12723893-6	2003	Ascorbic acid and alpha-tocopherol treatment decreases the activity of haem oxygenase, whereas it increases the levels/ activity of cytochrome P450, cytochrome b5 and NADPH-cytochrome P450 reductase in arsenic-intoxicated rats.	Arsenic	202-209	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	132-162
12723893-6	2003	Ascorbic acid and alpha-tocopherol treatment decreases the activity of haem oxygenase, whereas it increases the levels/ activity of cytochrome P450, cytochrome b5 and NADPH-cytochrome P450 reductase in arsenic-intoxicated rats.	Arsenic	202-209	cytochrome p450 oxidoreductase	Rattus norvegicus	167-198
12733083-6	2003	CONCLUSION: A synergistic action of As on the tubular effects of Cd is observed in women moderately exposed to these elements and leads to RBP urinary excretion slightly above normal values.	Arsenic	36-38	retinol binding protein 4	Homo sapiens	139-142
12635821-0	2003	Pattern of excretion of arsenic compounds [arsenite, arsenate, MMA(V), DMA(V)] in urine of children compared to adults from an arsenic exposed area in Bangladesh.	Arsenic	24-31	monocyte to macrophage differentiation associated	Homo sapiens	63-66
12635821-9	2003	For arsenic species between adults and children, it has been observed that inorganic arsenic (In-As) in average is 2.36% and MMA is 6.55% lower for children than adults while DMA is 8.91% (average) higher in children than adults.	Arsenic	4-11	monocyte to macrophage differentiation associated	Homo sapiens	125-128
12635821-12	2003	Results show the values of the MMA/In-As ratio for adults and children are 0.93 and 0.74 respectively.	Arsenic	38-40	monocyte to macrophage differentiation associated	Homo sapiens	31-34
12635833-4	2003	Arsenic safe drinking water is provided for adopted villages by constructing shallow, concrete dugwells designed to tap the water of the unconfined aquifer, 20-30 feet below ground level, that contains low levels (&lt; 0.05 mg/L) of arsenic in the target region.	Arsenic	0-7	nuclear RNA export factor 1	Homo sapiens	116-119
12239215-4	2002	Interestingly, pharmacological inhibition of p38 potentiates arsenic-dependent apoptosis and suppression of growth of leukemia cell lines, suggesting that this signaling cascade negatively regulates induction of antileukemic responses by arsenic trioxide.	Arsenic	61-68	mitogen-activated protein kinase 14	Homo sapiens	45-48
12540038-5	2002	Administration of alpha-tocopherol and ascorbic acid to arsenic-exposed rats showed a decrease in the level of lipid peroxidation (LPO) and enhanced levels of total sulfhydryls, reduced glutathione, ascorbic acid and alpha-tocopherol and so do the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase to near normal.	Arsenic	56-63	catalase	Rattus norvegicus	284-292
12540038-5	2002	Administration of alpha-tocopherol and ascorbic acid to arsenic-exposed rats showed a decrease in the level of lipid peroxidation (LPO) and enhanced levels of total sulfhydryls, reduced glutathione, ascorbic acid and alpha-tocopherol and so do the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase to near normal.	Arsenic	56-63	glutathione-disulfide reductase	Rattus norvegicus	318-339
12540038-5	2002	Administration of alpha-tocopherol and ascorbic acid to arsenic-exposed rats showed a decrease in the level of lipid peroxidation (LPO) and enhanced levels of total sulfhydryls, reduced glutathione, ascorbic acid and alpha-tocopherol and so do the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase to near normal.	Arsenic	56-63	glucose-6-phosphate dehydrogenase	Rattus norvegicus	344-377
12523593-1	2002	BACKGROUND: The effects of cyclooxygenase-2 (cox-2) inhibition by a cox-2 selective antisense phosphorothioated oligonucleotide (AS) and meloxicam were examined in experimental colitis.	Arsenic	129-131	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	68-73
12523593-10	2002	The colitis-induced changes were significantly suppressed by the treatment of the test compounds but not by the CO. Cox-2 mRNA but not cox-1 was decreased by the AS, but not by meloxicam or in CO-treated colitic animals.	Arsenic	162-164	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	116-121
12239215-6	2002	To further define the relevance of activation of the Rac1/p38 MAP kinase pathway in the induction of arsenic-dependent antileukemic effects, studies were performed using bone marrows from patients with chronic myelogenous leukemia.	Arsenic	101-108	Rac family small GTPase 1	Homo sapiens	53-57
12239215-6	2002	To further define the relevance of activation of the Rac1/p38 MAP kinase pathway in the induction of arsenic-dependent antileukemic effects, studies were performed using bone marrows from patients with chronic myelogenous leukemia.	Arsenic	101-108	mitogen-activated protein kinase 14	Homo sapiens	58-61
12368812-0	2002	Engineering tolerance and hyperaccumulation of arsenic in plants by combining arsenate reductase and gamma-glutamylcysteine synthetase expression.	Arsenic	47-54	Arsenate reductase	Escherichia coli	78-96
12513685-7	2002	HSP70 mRNA is strongly induced by arsenic.	Arsenic	34-41	heat shock 70kDa protein L homeolog	Xenopus laevis	0-5
12530527-3	2002	Trivalent arsenic compounds increased intracellular oxidized glutathione (GSSG) and total glutathione (GSH) and cellular glutathione peroxidase (cGPX) and glutathione S-transferase (GST) activity, but not glutathione reductase activity.	Arsenic	10-17	glutathione peroxidase 1	Homo sapiens	112-143
12530527-3	2002	Trivalent arsenic compounds increased intracellular oxidized glutathione (GSSG) and total glutathione (GSH) and cellular glutathione peroxidase (cGPX) and glutathione S-transferase (GST) activity, but not glutathione reductase activity.	Arsenic	10-17	glutathione peroxidase 1	Homo sapiens	145-149
12530527-3	2002	Trivalent arsenic compounds increased intracellular oxidized glutathione (GSSG) and total glutathione (GSH) and cellular glutathione peroxidase (cGPX) and glutathione S-transferase (GST) activity, but not glutathione reductase activity.	Arsenic	10-17	glutathione S-transferase kappa 1	Homo sapiens	155-180
12530527-3	2002	Trivalent arsenic compounds increased intracellular oxidized glutathione (GSSG) and total glutathione (GSH) and cellular glutathione peroxidase (cGPX) and glutathione S-transferase (GST) activity, but not glutathione reductase activity.	Arsenic	10-17	glutathione S-transferase kappa 1	Homo sapiens	182-185
12530527-7	2002	The increased GST activity implies that the elevated intracellular GSH level responding to the oxidative stress may be used to conjugate arsenic in PAECs and facilitate arsenic efflux.	Arsenic	137-144	glutathione S-transferase kappa 1	Homo sapiens	14-17
12530527-7	2002	The increased GST activity implies that the elevated intracellular GSH level responding to the oxidative stress may be used to conjugate arsenic in PAECs and facilitate arsenic efflux.	Arsenic	169-176	glutathione S-transferase kappa 1	Homo sapiens	14-17
12425634-0	2002	Peculiar antiaromatic inorganic molecules of tetrapnictogen in Na+Pn4- (Pn = P, As, Sb) and important consequences for hydrocarbons.	Arsenic	80-82	sodium voltage-gated channel alpha subunit 8	Homo sapiens	66-69
12368812-5	2002	However, plants expressing SRS1p/ArsC and ACT2p/gamma-ECS together showed substantially greater arsenic tolerance than gamma-ECS or wild-type plants.	Arsenic	96-103	SRS1	Glycine max	27-32
12368812-5	2002	However, plants expressing SRS1p/ArsC and ACT2p/gamma-ECS together showed substantially greater arsenic tolerance than gamma-ECS or wild-type plants.	Arsenic	96-103	Arsenate reductase	Escherichia coli	33-37
12406325-0	2002	Arsenic induces tumor necrosis factor alpha release and tumor necrosis factor receptor 1 signaling in T helper cell apoptosis.	Arsenic	0-7	tumor necrosis factor	Homo sapiens	16-43
12426127-9	2002	Arsenic also induced AP-1 and nuclear factor kappa B (NF-kappaB) activation.	Arsenic	0-7	nuclear factor kappa B subunit 1	Homo sapiens	30-52
12426127-9	2002	Arsenic also induced AP-1 and nuclear factor kappa B (NF-kappaB) activation.	Arsenic	0-7	nuclear factor kappa B subunit 1	Homo sapiens	54-63
12426127-10	2002	Blocking NF-kappaB activation by dominant-negative inhibitory kappa Balpha inhibited arsenic-induced apoptosis and enhanced arsenic-induced cell transformation.	Arsenic	85-92	nuclear factor kappa B subunit 1	Homo sapiens	9-18
12426127-10	2002	Blocking NF-kappaB activation by dominant-negative inhibitory kappa Balpha inhibited arsenic-induced apoptosis and enhanced arsenic-induced cell transformation.	Arsenic	124-131	nuclear factor kappa B subunit 1	Homo sapiens	9-18
12426127-14	2002	In contrast, arsenic-induced apoptosis was almost totally blocked by expression of a dominant-negative mutant of JNK.	Arsenic	13-20	mitogen-activated protein kinase 8	Homo sapiens	113-116
12426127-15	2002	Taken together with previous findings that p53 mutations are involved in approximately 50% of all human cancers and nearly all chemotherapeutic agents kill cancer cells mainly by apoptotic induction, we suggest that arsenic may be a useful agent for the treatment of cancers with p53 mutations.	Arsenic	216-223	tumor protein p53	Homo sapiens	43-46
12426127-15	2002	Taken together with previous findings that p53 mutations are involved in approximately 50% of all human cancers and nearly all chemotherapeutic agents kill cancer cells mainly by apoptotic induction, we suggest that arsenic may be a useful agent for the treatment of cancers with p53 mutations.	Arsenic	216-223	tumor protein p53	Homo sapiens	280-283
12426127-16	2002	These results suggest that the activation of Erks is required for arsenic-induced cell transformation, whereas the activation of JNKs and NF-kappaB is involved in arsenic-induced apoptosis of JB6 cells.	Arsenic	66-73	mitogen-activated protein kinase 1	Homo sapiens	45-49
12426127-16	2002	These results suggest that the activation of Erks is required for arsenic-induced cell transformation, whereas the activation of JNKs and NF-kappaB is involved in arsenic-induced apoptosis of JB6 cells.	Arsenic	163-170	nuclear factor kappa B subunit 1	Homo sapiens	138-147
12363309-3	2002	It was found that the arsenic speciation using an ion exchange method was effective to separate As(III) and As(V) in leachate of mine tailings.	Arsenic	22-29	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	108-113
12363309-4	2002	The concentration of As(V) was found to be 63-99% in the leachate, indicating that As(V) would be the major arsenic species in the mine tailings and the tailings were under oxic conditions.	Arsenic	108-115	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	21-26
12363309-4	2002	The concentration of As(V) was found to be 63-99% in the leachate, indicating that As(V) would be the major arsenic species in the mine tailings and the tailings were under oxic conditions.	Arsenic	108-115	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	83-88
12406325-5	2002	Arsenic concentrations higher than 1 micro M induced tumor necrosis factor alpha release from mononuclear cells and caused a cytotoxic effect on T cells.	Arsenic	0-7	tumor necrosis factor	Homo sapiens	53-80
12153718-0	2002	Interactions of arsenic with human metallothionein-2.	Arsenic	16-23	metallothionein 2A	Homo sapiens	35-52
12210687-3	2002	RESULTS: A significant increase in the excretion of penta and uroporphyrins was demonstrated for workers exposed to As; As3 was the species best correlated with urinary porphyrin excretion.	Arsenic	116-118	PDS5 cohesin associated factor B	Homo sapiens	120-123
12392964-0	2002	Arsenic induces peroxynitrite generation and cyclooxygenase-2 protein expression in aortic endothelial cells: possible role in atherosclerosis.	Arsenic	0-7	prostaglandin-endoperoxide synthase 2	Bos taurus	45-61
12392964-5	2002	The increase in COX-2 protein was time dependent with highest levels at 30 min and 48 h. This result was supported by an increase in the generation of prostaglandin E(2) following exposure to arsenic.	Arsenic	192-199	prostaglandin-endoperoxide synthase 2	Bos taurus	16-21
12392964-8	2002	Nitration of COX-2 was detected in arsenic-treated cells, but not in untreated control cells.	Arsenic	35-42	prostaglandin-endoperoxide synthase 2	Bos taurus	13-18
12387749-0	2002	Chronic arsenic-exposed human prostate epithelial cells exhibit stable arsenic tolerance: mechanistic implications of altered cellular glutathione and glutathione S-transferase.	Arsenic	8-15	glutathione S-transferase kappa 1	Homo sapiens	151-176
12387749-9	2002	Arsenic tolerance was also abolished by treatment with inhibitors of the Mdr1 and Mrp1 transporters, although no increases in mdr1 or mrp1 gene expression were observed.	Arsenic	0-7	ATP binding cassette subfamily B member 1	Homo sapiens	73-77
12387749-9	2002	Arsenic tolerance was also abolished by treatment with inhibitors of the Mdr1 and Mrp1 transporters, although no increases in mdr1 or mrp1 gene expression were observed.	Arsenic	0-7	ATP binding cassette subfamily C member 1	Homo sapiens	82-86
12387749-10	2002	Our results indicate that this tolerance in human cells involves increases in GSH levels and GST activity that allow for more efficient arsenic efflux by MRP1 and MDR1.	Arsenic	136-143	ATP binding cassette subfamily C member 1	Homo sapiens	154-158
12387749-10	2002	Our results indicate that this tolerance in human cells involves increases in GSH levels and GST activity that allow for more efficient arsenic efflux by MRP1 and MDR1.	Arsenic	136-143	ATP binding cassette subfamily B member 1	Homo sapiens	163-167
12153718-3	2002	MALDI-TOF-MS revealed that the structure of the adduct formed by arsenic and hMT-2 (As-hMT-2) was not homogeneous.	Arsenic	65-72	metallothionein 2A	Homo sapiens	87-92
12153718-4	2002	The maximum molar ratio of arsenic to hMT-2 was found to be more than 6:1 on ICP-AES, UV absorption spectroscopy and MALDI-TOF-MS.	Arsenic	27-34	metallothionein 2A	Homo sapiens	38-43
12153718-5	2002	The ratio of the number of sulfhydryl groups in hMT-2 that bound arsenic was 3:1, which is the same as the ratios reported previously for arsenic-glutathione and arsenic-phytochelatin complexes.	Arsenic	65-72	metallothionein 2A	Homo sapiens	48-53
12153718-5	2002	The ratio of the number of sulfhydryl groups in hMT-2 that bound arsenic was 3:1, which is the same as the ratios reported previously for arsenic-glutathione and arsenic-phytochelatin complexes.	Arsenic	138-145	metallothionein 2A	Homo sapiens	48-53
12153718-5	2002	The ratio of the number of sulfhydryl groups in hMT-2 that bound arsenic was 3:1, which is the same as the ratios reported previously for arsenic-glutathione and arsenic-phytochelatin complexes.	Arsenic	138-145	metallothionein 2A	Homo sapiens	48-53
12140762-7	2002	The implications of these findings to a specific cellular role of AS-p53 are discussed.	Arsenic	66-68	transformation related protein 53, pseudogene	Mus musculus	69-72
12115560-9	2002	Hepatic microsome cytochrome P-450 content was markedly increased with all 3 arsenic treatments.	Arsenic	77-84	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	18-34
12095348-0	2002	Comparison of the binding of cadmium(II), mercury(II), and arsenic(III) to the de novo designed peptides TRI L12C and TRI L16C.	Arsenic	59-66	immunoglobulin kappa variable 3D-15	Homo sapiens	122-126
12076508-0	2002	Effect of arsenic on transcription factor AP-1 and NF-kappaB DNA binding activity and related gene expression.	Arsenic	10-17	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	42-46
12076508-0	2002	Effect of arsenic on transcription factor AP-1 and NF-kappaB DNA binding activity and related gene expression.	Arsenic	10-17	nuclear factor kappa B subunit 1	Homo sapiens	51-60
12176006-1	2002	Measurement of in vitro percutaneous absorption of As(III) and As(V) by artificial human skin shows a strong affinity of arsenic for the human keratinocytes, with 1-10% of the applied arsenic dose retained by the artificial skin per hour.	Arsenic	121-128	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	63-68
12176006-1	2002	Measurement of in vitro percutaneous absorption of As(III) and As(V) by artificial human skin shows a strong affinity of arsenic for the human keratinocytes, with 1-10% of the applied arsenic dose retained by the artificial skin per hour.	Arsenic	184-191	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	63-68
12016150-11	2002	Significantly reduced methylation at a key regulatory region of Ha-ras in the mouse liver may have relevance to understanding arsenic-induced perturbations in the methylation patterns of cellular growth genes involved in the formation of tumors.	Arsenic	126-133	Harvey rat sarcoma virus oncogene	Mus musculus	64-70
12171393-6	2002	Rogaska, Donat Mg even had an average As(V) concentration around the permittable level of 50 microgl(-1) for arsenic in minerals waters, viz.	Arsenic	109-116	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	38-43
12115494-12	2002	Experiments using the methylation-sensitive restriction endonuclease isoschizomers HpaII and MspI revealed hypomethylation of c-myc and c-Ha-ras in the 5"-CCGG sequence of arsenic-exposed cell lines but not in the parental SHE cells or a spontaneously transformed cell line.	Arsenic	172-179	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	126-131
12146911-15	2002	An acid hydrolysis mechanism was proposed for the formation of As(254) from each of the native arsenosugars by hydrolysis at the C-1 carbon on the ribose ring.	Arsenic	63-65	heterogeneous nuclear ribonucleoprotein C	Homo sapiens	129-132
12034312-1	2002	Co-exposures to complex mixtures of arsenic and polycyclic aromatic hydrocarbons such as benzo[a]pyrene (BaP) are common in the environment.	Arsenic	36-43	prohibitin 2	Mus musculus	105-108
12034312-4	2002	We have examined the genotoxicity of BaP-arsenic mixtures.	Arsenic	41-48	prohibitin 2	Mus musculus	37-40
11943669-9	2002	In summary, exposure to As, Zn, and V initiated EGFR signaling and Ras-dependent activation of MEK1/2 and ERK1/2, but only V induced Ras-dependent NF-kappaB nuclear translocation.	Arsenic	24-26	epidermal growth factor receptor	Homo sapiens	48-52
11943669-9	2002	In summary, exposure to As, Zn, and V initiated EGFR signaling and Ras-dependent activation of MEK1/2 and ERK1/2, but only V induced Ras-dependent NF-kappaB nuclear translocation.	Arsenic	24-26	mitogen-activated protein kinase kinase 1	Homo sapiens	95-101
11943669-9	2002	In summary, exposure to As, Zn, and V initiated EGFR signaling and Ras-dependent activation of MEK1/2 and ERK1/2, but only V induced Ras-dependent NF-kappaB nuclear translocation.	Arsenic	24-26	mitogen-activated protein kinase 3	Homo sapiens	106-112
11943669-9	2002	In summary, exposure to As, Zn, and V initiated EGFR signaling and Ras-dependent activation of MEK1/2 and ERK1/2, but only V induced Ras-dependent NF-kappaB nuclear translocation.	Arsenic	24-26	nuclear factor kappa B subunit 1	Homo sapiens	147-156
12429934-1	2002	Arsenic trioxide (As(2)O(3)) is highly effective in the treatment of acute promyelocytic leukemias that express the promyelocytic leukemia-retinoic acid receptor-alpha (PML-RARalpha) fusion protein.	Arsenic	18-20	PML nuclear body scaffold	Homo sapiens	169-172
12429934-1	2002	Arsenic trioxide (As(2)O(3)) is highly effective in the treatment of acute promyelocytic leukemias that express the promyelocytic leukemia-retinoic acid receptor-alpha (PML-RARalpha) fusion protein.	Arsenic	18-20	retinoic acid receptor alpha	Homo sapiens	173-181
12162444-0	2002	Arsenic carcinogenicity: relevance of c-Src activation.	Arsenic	0-7	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	38-43
11993874-4	2002	Interaction of As(III) and As(V) with the sulfide surfaces shows primary coordination to four oxygens (As-O: 1.69-1.76 A) with further sulfur (approximately 3.1 A) and iron (3.4-3.5 A) shells suggesting outer sphere complexation.	Arsenic	15-17	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	27-32
11923065-6	2002	Research data strongly suggest that arsenic influences distinct signaling pathways involved in mediating proliferation or apoptosis, including mitogen-activated protein kinases, p53, activator protein-1 or nuclear factor kappa B.	Arsenic	36-43	tumor protein p53	Homo sapiens	178-181
11993874-2	2002	Arsenic species retain original oxidation states and occupy similar environments on the oxyhydroxide substrates, with first-shell coordination to four oxygens at 1.78 A for As(III) and 1.69 A for As(V).	Arsenic	0-7	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	196-201
11923065-6	2002	Research data strongly suggest that arsenic influences distinct signaling pathways involved in mediating proliferation or apoptosis, including mitogen-activated protein kinases, p53, activator protein-1 or nuclear factor kappa B.	Arsenic	36-43	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	183-228
12012315-10	2002	It has been proposed that ATO acts through activation of Jun N-terminal kinase (JNK), activator protein-1, and inhibition of dual-specificity phosphatases, and evidence is accumulating that JNK activation is an important event in arsenic-induced apoptosis.	Arsenic	230-237	mitogen-activated protein kinase 8	Homo sapiens	190-193
12018890-0	2002	The MRP1-mediated effluxes of arsenic and antimony do not require arsenic-glutathione and antimony-glutathione complex formation.	Arsenic	30-37	ATP binding cassette subfamily C member 1	Homo sapiens	4-8
12509260-0	2002	Arsenic-induced Mre11 phosphorylation is cell cycle-dependent and defective in NBS cells.	Arsenic	0-7	MRE11 homolog, double strand break repair nuclease	Homo sapiens	16-21
12509260-3	2002	To dissect the repair mechanism of As-induced DSB, wild type, AT and NBS cells were treated with sodium arsenite to study the complex formation and post-translational modification of Rad50/NBS1/Mre11 repair proteins.	Arsenic	35-37	RAD50 double strand break repair protein	Homo sapiens	183-188
12509260-3	2002	To dissect the repair mechanism of As-induced DSB, wild type, AT and NBS cells were treated with sodium arsenite to study the complex formation and post-translational modification of Rad50/NBS1/Mre11 repair proteins.	Arsenic	35-37	nibrin	Homo sapiens	189-193
12509260-3	2002	To dissect the repair mechanism of As-induced DSB, wild type, AT and NBS cells were treated with sodium arsenite to study the complex formation and post-translational modification of Rad50/NBS1/Mre11 repair proteins.	Arsenic	35-37	MRE11 homolog, double strand break repair nuclease	Homo sapiens	194-199
21315017-11	2002	Mutated p53 protein in parent cell line 801D was positive and in PEGFP-p53(AS)-801D was negative with immunochemical stain.	Arsenic	75-77	tumor protein p53	Homo sapiens	71-74
11911489-1	2002	Both simultaneous and sequential exposure to arsenite and benzo[a]pyrene (BaP) potentially occur in human populations drinking arsenic-contaminated water or burning arsenic-contaminated coal.	Arsenic	127-134	prohibitin 2	Homo sapiens	74-77
11911489-1	2002	Both simultaneous and sequential exposure to arsenite and benzo[a]pyrene (BaP) potentially occur in human populations drinking arsenic-contaminated water or burning arsenic-contaminated coal.	Arsenic	165-172	prohibitin 2	Homo sapiens	74-77
11857507-9	2002	Arsenic increased the frequency of NTDs and embryonic death in the Splotch, LM/Bc and SWV litters and folinic acid failed to ameliorate the teratogenic effect of this metal.	Arsenic	0-7	paired box 3	Mus musculus	67-74
11812925-6	2002	Arsenic also blocks upregulation of p21(Cip1/Waf1), a factor whose expression is tightly regulated during adipogenesis.	Arsenic	0-7	cyclin dependent kinase inhibitor 1A	Homo sapiens	36-39
11812925-6	2002	Arsenic also blocks upregulation of p21(Cip1/Waf1), a factor whose expression is tightly regulated during adipogenesis.	Arsenic	0-7	cyclin dependent kinase inhibitor 1A	Homo sapiens	40-44
11723127-0	2002	c-Src-dependent activation of the epidermal growth factor receptor and mitogen-activated protein kinase pathway by arsenic.	Arsenic	115-122	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	0-5
11812925-6	2002	Arsenic also blocks upregulation of p21(Cip1/Waf1), a factor whose expression is tightly regulated during adipogenesis.	Arsenic	0-7	cyclin dependent kinase inhibitor 1A	Homo sapiens	45-49
11812925-7	2002	The differentiating effect of pioglitazone, which induces adipogenesis by activating PPAR gamma, is inhibited by arsenic, suggesting that arsenic interferes with adipogenic signaling at or below the level of PPAR gamma.	Arsenic	138-145	peroxisome proliferator activated receptor gamma	Homo sapiens	85-95
11812925-8	2002	Because C/EBP alpha is important in the expression of certain keratinocyte-specific genes, the negative effect of arsenic on C/EBP alpha might also contribute to the development of skin cancer.	Arsenic	114-121	CCAAT enhancer binding protein alpha	Homo sapiens	125-136
11723127-0	2002	c-Src-dependent activation of the epidermal growth factor receptor and mitogen-activated protein kinase pathway by arsenic.	Arsenic	115-122	epidermal growth factor receptor	Homo sapiens	34-66
11723127-5	2002	In the current studies, we demonstrate that arsenic activates EGFR and ERK in a human uroepithelial cell line.	Arsenic	44-51	epidermal growth factor receptor	Homo sapiens	62-66
11723127-5	2002	In the current studies, we demonstrate that arsenic activates EGFR and ERK in a human uroepithelial cell line.	Arsenic	44-51	mitogen-activated protein kinase 1	Homo sapiens	71-74
11723127-6	2002	The EGFR phosphorylation by arsenic is ligand-independent and does not involve the major autophosphorylation site Tyr(1173).	Arsenic	28-35	epidermal growth factor receptor	Homo sapiens	4-8
11723127-7	2002	c-Src activity is also induced by arsenic and is a prerequisite for the EGFR and ERK activation.	Arsenic	34-41	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	0-5
11723127-7	2002	c-Src activity is also induced by arsenic and is a prerequisite for the EGFR and ERK activation.	Arsenic	34-41	epidermal growth factor receptor	Homo sapiens	72-76
11723127-7	2002	c-Src activity is also induced by arsenic and is a prerequisite for the EGFR and ERK activation.	Arsenic	34-41	mitogen-activated protein kinase 1	Homo sapiens	81-84
11723127-8	2002	Consistent with these in vitro observations, exposure of mice to arsenic in drinking water, which has been found previously to be associated with AP-1 activation and epithelial proliferation, induces EGFR and ERK activation in the urinary bladder.	Arsenic	65-72	epidermal growth factor receptor	Mus musculus	200-204
11723127-8	2002	Consistent with these in vitro observations, exposure of mice to arsenic in drinking water, which has been found previously to be associated with AP-1 activation and epithelial proliferation, induces EGFR and ERK activation in the urinary bladder.	Arsenic	65-72	mitogen-activated protein kinase 1	Mus musculus	209-212
12189281-9	2002	Furthermore, arsenic caused myocardial apoptosis, as determined by a terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay, which was confirmed by caspase-3 activation detected by enzymatic assay.	Arsenic	13-20	caspase 3	Homo sapiens	169-178
11748063-4	2002	With the use of miniosmotic pumps, phosphate-buffered saline, VEGF, or VEGF combined with AS-Flk-1, AS-Flt-1, or AS-scrambled oligonucleotides were released in mouse testis for 14 days.	Arsenic	90-92	kinase insert domain protein receptor	Mus musculus	93-98
11756236-0	2002	Acquisition of apoptotic resistance in arsenic-induced malignant transformation: role of the JNK signal transduction pathway.	Arsenic	39-46	mitogen-activated protein kinase 8	Rattus norvegicus	93-96
11756236-12	2002	Thus, during arsenic-induced malignant transformation resistance to apoptosis develops, possibly due to perturbation of the JNK pathway.	Arsenic	13-20	mitogen-activated protein kinase 8	Rattus norvegicus	124-127
11750083-0	2002	Multidrug-resistance mdr1a/1b double knockout mice are more sensitive than wild type mice to acute arsenic toxicity, with higher arsenic accumulation in tissues.	Arsenic	99-106	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	21-26
11750083-10	2002	The mdr1a/1b(-/-) mice accumulated more arsenic in the liver (15.3 vs. 5.2 microg/g), kidney (7.23 vs. 3.22 microg/g), small intestine (3.98 vs. 1.57 microg/g) and brain (0.45 vs. 0.17 microg/g), as compared with wild-type mice 24 h after sodium arsenite (14 mg/kg, s.c.) administration.	Arsenic	40-47	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	4-9
11750083-11	2002	In summary, this study demonstrated that the mdr1a/1b(-/-) mice were more sensitive to acute arsenic toxicity and accumulated more arsenic than wild-type mice, suggesting that P-glycoproteins are involved, at least in part, in arsenic efflux in mammalians.	Arsenic	93-100	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	45-50
11750083-11	2002	In summary, this study demonstrated that the mdr1a/1b(-/-) mice were more sensitive to acute arsenic toxicity and accumulated more arsenic than wild-type mice, suggesting that P-glycoproteins are involved, at least in part, in arsenic efflux in mammalians.	Arsenic	131-138	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	45-50
12510962-5	2002	It is postulated that arsenic-induced mitogen-activated protein kinases (MAPKs) signal transduction, which leads to activation of transcription factors such as activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB) (which in turn alter gene expression), is associated with the carcinogenicity of arsenic.	Arsenic	307-314	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	160-179
11862551-1	2002	Arsenate reductase (ArsC) encoded by Staphylococcus aureus arsenic-resistance plasmid pI258 reduces intracellular arsenate(V) to the more toxic arsenite(III), which is subsequently extruded from the cell.	Arsenic	59-66	Arsenate reductase	Staphylococcus aureus	0-18
11862551-1	2002	Arsenate reductase (ArsC) encoded by Staphylococcus aureus arsenic-resistance plasmid pI258 reduces intracellular arsenate(V) to the more toxic arsenite(III), which is subsequently extruded from the cell.	Arsenic	59-66	Arsenate reductase	Staphylococcus aureus	20-24
12210719-6	2002	Our data demonstrated that arsenic induced the heavy subunit of gamma-GCS (gamma-GCS-HS) mRNA levels as early as 4 h as compared to the control level.	Arsenic	27-34	glutamate-cysteine ligase catalytic subunit	Homo sapiens	64-73
12210719-6	2002	Our data demonstrated that arsenic induced the heavy subunit of gamma-GCS (gamma-GCS-HS) mRNA levels as early as 4 h as compared to the control level.	Arsenic	27-34	glutamate-cysteine ligase catalytic subunit	Homo sapiens	75-87
12210719-9	2002	Significant elevations in c-fos and c-jun mRNA levels were observed within 30 min after exposure to arsenic and by enhancement of AP-1 DNA binding activity and transactivation activity.	Arsenic	100-107	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	26-31
12210719-9	2002	Significant elevations in c-fos and c-jun mRNA levels were observed within 30 min after exposure to arsenic and by enhancement of AP-1 DNA binding activity and transactivation activity.	Arsenic	100-107	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	36-41
12210719-12	2002	The NF-kappa B DNA binding activities increased more than twofold 30 min after exposure to arsenic and returned to control levels after 4 h of treatment.	Arsenic	91-98	nuclear factor kappa B subunit 1	Homo sapiens	4-14
12210719-13	2002	It remains to be determined whether NF-kappa B plays a role in the As-induced apoptosis or alternatively in attempting to protect the cells from As-induced cell death by upregulating the expression of resistance factors.	Arsenic	67-69	nuclear factor kappa B subunit 1	Homo sapiens	36-46
12210719-13	2002	It remains to be determined whether NF-kappa B plays a role in the As-induced apoptosis or alternatively in attempting to protect the cells from As-induced cell death by upregulating the expression of resistance factors.	Arsenic	145-147	nuclear factor kappa B subunit 1	Homo sapiens	36-46
12510962-5	2002	It is postulated that arsenic-induced mitogen-activated protein kinases (MAPKs) signal transduction, which leads to activation of transcription factors such as activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB) (which in turn alter gene expression), is associated with the carcinogenicity of arsenic.	Arsenic	22-29	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	160-179
12510962-5	2002	It is postulated that arsenic-induced mitogen-activated protein kinases (MAPKs) signal transduction, which leads to activation of transcription factors such as activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB) (which in turn alter gene expression), is associated with the carcinogenicity of arsenic.	Arsenic	22-29	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	181-185
12510962-5	2002	It is postulated that arsenic-induced mitogen-activated protein kinases (MAPKs) signal transduction, which leads to activation of transcription factors such as activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB) (which in turn alter gene expression), is associated with the carcinogenicity of arsenic.	Arsenic	22-29	nuclear factor kappa B subunit 1	Homo sapiens	191-213
12510962-5	2002	It is postulated that arsenic-induced mitogen-activated protein kinases (MAPKs) signal transduction, which leads to activation of transcription factors such as activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB) (which in turn alter gene expression), is associated with the carcinogenicity of arsenic.	Arsenic	22-29	nuclear factor kappa B subunit 1	Homo sapiens	215-224
12510962-5	2002	It is postulated that arsenic-induced mitogen-activated protein kinases (MAPKs) signal transduction, which leads to activation of transcription factors such as activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB) (which in turn alter gene expression), is associated with the carcinogenicity of arsenic.	Arsenic	307-314	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	181-185
12510962-5	2002	It is postulated that arsenic-induced mitogen-activated protein kinases (MAPKs) signal transduction, which leads to activation of transcription factors such as activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB) (which in turn alter gene expression), is associated with the carcinogenicity of arsenic.	Arsenic	307-314	nuclear factor kappa B subunit 1	Homo sapiens	215-224
12510962-6	2002	In this article, we review the recent findings in arsenic-induced MAPKs, AP-1 and NF-kappaB activation, and aberrant gene expression; their implications in arsenic carcinogenesis are discussed.	Arsenic	50-57	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	73-77
12510962-6	2002	In this article, we review the recent findings in arsenic-induced MAPKs, AP-1 and NF-kappaB activation, and aberrant gene expression; their implications in arsenic carcinogenesis are discussed.	Arsenic	50-57	nuclear factor kappa B subunit 1	Homo sapiens	82-91
11769802-0	2001	Speciation and oxidation kinetics of arsenic in the thermal springs of Wiesbaden spa, Germany.	Arsenic	37-44	surfactant protein A2	Homo sapiens	81-84
11852569-0	2002	[Effect of arsenic on bacterial growth and plasma membrane atpase activity].	Arsenic	11-18	dynein axonemal heavy chain 8	Homo sapiens	59-65
11775163-6	2001	The major arsenic species in a water extract of a poultry litter sample was identified as ROX by all three methods with trace concentrations of DMA and As(V) also detected.	Arsenic	10-17	ribosomal oxygenase 1	Homo sapiens	90-93
11952183-7	2002	The maximum removals are 96.52% for As(V) and 87.54% for As(III) for solutions with a final pH of 7.25 and 3.50, respectively, for the initial arsenic concentration of 133.5 micromol l(-1) (10 mg l(-1)), activated red mud dosage of 20 g l(-1), contact time of 60 min and temperature of 25 degrees C. The adsorption data obtained follow a first-order rate expression and fit the Langmuir isotherm well.	Arsenic	143-150	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	36-41
11890656-1	2001	Anti-TNFalpha treatment seems to be highly effective in AS.	Arsenic	56-58	tumor necrosis factor	Homo sapiens	5-13
11826741-1	2001	Anti-TNF therapy seems to be highly effective in AS.	Arsenic	49-51	tumor necrosis factor	Homo sapiens	5-8
11507245-0	2001	ATM status confers sensitivity to arsenic cytotoxic effects.	Arsenic	34-41	ATM serine/threonine kinase	Homo sapiens	0-3
11760813-11	2001	The mode of responses of GPx and GR activities as well as the unaltered G6PDH activity might result in arsenic-induced GSH depletion and increase in lipid peroxidation.	Arsenic	103-110	glutathione-disulfide reductase	Rattus norvegicus	33-35
11760813-11	2001	The mode of responses of GPx and GR activities as well as the unaltered G6PDH activity might result in arsenic-induced GSH depletion and increase in lipid peroxidation.	Arsenic	103-110	glucose-6-phosphate dehydrogenase	Rattus norvegicus	72-77
11704854-4	2001	Each drug targets a specific moiety of the fusion protein (RARalpha for retinoic acid, PML for arsenic) to the proteasome.	Arsenic	95-102	PML nuclear body scaffold	Homo sapiens	87-90
11704854-6	2001	Specific molecular determinants (the AF2 transactivator domain of RARalpha for retinoic acid and the K160 SUMO-binding site in PML for arsenic) are respectively implicated in RA- or arsenic-triggered catabolism.	Arsenic	135-142	PML nuclear body scaffold	Homo sapiens	127-130
11704854-6	2001	Specific molecular determinants (the AF2 transactivator domain of RARalpha for retinoic acid and the K160 SUMO-binding site in PML for arsenic) are respectively implicated in RA- or arsenic-triggered catabolism.	Arsenic	182-189	retinoic acid receptor alpha	Homo sapiens	66-74
11704854-6	2001	Specific molecular determinants (the AF2 transactivator domain of RARalpha for retinoic acid and the K160 SUMO-binding site in PML for arsenic) are respectively implicated in RA- or arsenic-triggered catabolism.	Arsenic	182-189	PML nuclear body scaffold	Homo sapiens	127-130
11714746-5	2001	We found that arsenic inhibits transcription of the hTERT gene, which encodes the reverse transcriptase subunit of human telomerase.	Arsenic	14-21	telomerase reverse transcriptase	Homo sapiens	52-57
11507245-9	2001	Paradoxically, ATM heterozygous cells were more sensitive to As, leading us to propose that this might be related to activation of apoptosis and removal of non-repairable cells.	Arsenic	61-63	ATM serine/threonine kinase	Homo sapiens	15-18
11507245-10	2001	In contrast, in AT cells in which ATM is absent or mutated activation of P53 and its target genes is abrogated, allowing cells to replicate with damage in the presence of As, with cell death ensuing by a pathway different from P53.	Arsenic	171-173	tumor protein p53	Homo sapiens	73-76
11446828-0	2001	Arsenic induces apoptosis in rat cerebellar neurons via activation of JNK3 and p38 MAP kinases.	Arsenic	0-7	mitogen activated protein kinase 10	Rattus norvegicus	70-74
11485391-0	2001	Keratinocyte differentiation marker suppression by arsenic: mediation by AP1 response elements and antagonism by tetradecanoylphorbol acetate.	Arsenic	51-58	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	73-76
11591116-6	2001	Finally, we examined whether lym-Spo11 antisense S-oligonucleotide (AS) can inhibit CSR reactions in three in vitro CSR systems, IgA,IgG1, and IgE.	Arsenic	68-70	SPO11 initiator of meiotic double stranded breaks	Mus musculus	33-38
11455017-10	2001	Thus, acquired tolerance to arsenic is associated with increased expression GST-Pi, Mrp1/Mrp2 and P-glycoprotein, which function together to reduce cellular arsenic accumulation.	Arsenic	28-35	ATP binding cassette subfamily C member 1	Rattus norvegicus	84-88
11455017-10	2001	Thus, acquired tolerance to arsenic is associated with increased expression GST-Pi, Mrp1/Mrp2 and P-glycoprotein, which function together to reduce cellular arsenic accumulation.	Arsenic	28-35	ATP binding cassette subfamily C member 2	Rattus norvegicus	89-93
11455017-10	2001	Thus, acquired tolerance to arsenic is associated with increased expression GST-Pi, Mrp1/Mrp2 and P-glycoprotein, which function together to reduce cellular arsenic accumulation.	Arsenic	157-164	ATP binding cassette subfamily C member 1	Rattus norvegicus	84-88
11455017-10	2001	Thus, acquired tolerance to arsenic is associated with increased expression GST-Pi, Mrp1/Mrp2 and P-glycoprotein, which function together to reduce cellular arsenic accumulation.	Arsenic	157-164	ATP binding cassette subfamily C member 2	Rattus norvegicus	89-93
11446828-0	2001	Arsenic induces apoptosis in rat cerebellar neurons via activation of JNK3 and p38 MAP kinases.	Arsenic	0-7	mitogen activated protein kinase 14	Rattus norvegicus	79-82
11419606-0	2001	Inhibition of human plasmin activity using humic acids with arsenic.	Arsenic	60-67	plasminogen	Homo sapiens	20-27
11408366-2	2001	The effect on PAH-mediated CYP1A induction of arsenic, lead, mercury, or cadmium (ranked as the most hazardous environmental metals by the Environmental Protection Agency and the Agency for Toxic Substances and Disease Registry) has thus been investigated.	Arsenic	46-53	phenylalanine hydroxylase	Homo sapiens	14-17
11408366-8	2001	With BAP as inducer decreases in induction were arsenic, 57%; cadmium, 82%; mercury, 4%; and lead, 20%.	Arsenic	48-55	prohibitin 2	Homo sapiens	5-8
11408547-0	2001	Arsenic induces expression of the multidrug resistance-associated protein 2 (MRP2) gene in primary rat and human hepatocytes.	Arsenic	0-7	ATP binding cassette subfamily C member 2	Rattus norvegicus	34-75
11408547-0	2001	Arsenic induces expression of the multidrug resistance-associated protein 2 (MRP2) gene in primary rat and human hepatocytes.	Arsenic	0-7	ATP binding cassette subfamily C member 2	Rattus norvegicus	77-81
11419606-3	2001	Organometallic complexes composed of HA and arsenic show enhanced inhibition of plasmin activity as compared with either HA or arsenic alone.	Arsenic	44-51	plasminogen	Homo sapiens	80-87
11419606-3	2001	Organometallic complexes composed of HA and arsenic show enhanced inhibition of plasmin activity as compared with either HA or arsenic alone.	Arsenic	127-134	plasminogen	Homo sapiens	80-87
11459200-1	2001	PURPOSE: Arsenic compounds have been found to be effective in the treatment of acute promyelocytic leukemia through the downregulation of bcl-2 expression.	Arsenic	9-16	BCL2 apoptosis regulator	Homo sapiens	138-143
11331074-1	2001	The human multidrug-resistance protein (MRP1) confers resistance to some heavy metals such as arsenic and antimony, mainly through mediating an increased cellular efflux of metal.	Arsenic	94-101	ATP binding cassette subfamily C member 1	Homo sapiens	40-44
11430827-4	2001	In the presence of arsenic, PML is sequestered in the nucleus, and the efficiency of HIV-mediated transduction is markedly increased.	Arsenic	19-26	PML nuclear body scaffold	Homo sapiens	28-31
11312036-0	2001	Potentiation of arsenic-induced cytotoxicity by sulfur amino acid deprivation (SAAD) through activation of ERK1/2, p38 kinase and JNK1: the distinct role of JNK1 in SAAD-potentiated mercury toxicity.	Arsenic	16-23	mitogen activated protein kinase 3	Rattus norvegicus	107-113
11678593-2	2001	Tumor promotion effects of arsenic are believed to be associated with its transactivational activities on transcription factors, such as AP-1 and NFkappaB, while the induction of cell apoptosis and differentiation by arsenic is considered to be a mechanism for the chemotherapeutic effects of arsenic.	Arsenic	27-34	nuclear factor kappa B subunit 1	Homo sapiens	146-154
11678607-0	2001	Arsenic-induced NFkappaB transactivation through Erks- and JNKs-dependent pathways in mouse epidermal JB6 cells.	Arsenic	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	16-24
11678607-1	2001	Tumor promoting effects of arsenic are believed to be associated with its transactivation activity on transcription factors, such as AP-1 and NFkappaB.	Arsenic	27-34	nuclear factor kappa B subunit 1	Homo sapiens	142-150
11678607-2	2001	However, the results from different groups studying the effects of arsenic on NFkappaB activation are contradictory in different cell models.	Arsenic	67-74	nuclear factor kappa B subunit 1	Homo sapiens	78-86
11678607-3	2001	Since arsenic is a strong skin carcinogen, we have investigated the activation of NFkappaB by arsenic in a mouse skin epidermal cell line, JB6 cells.	Arsenic	94-101	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	82-90
11678607-5	2001	This induction of NFkappaB activity by arsenic was dose- and time-dependent.	Arsenic	39-46	nuclear factor kappa B subunit 1	Homo sapiens	18-26
11678607-6	2001	The transactivation of NFkappaB by arsenic appeared to be through activation of Erks and JNKs pathways because increased NFkappaB activity by arsenic could be dramatically inhibited by either pre-treatment of cells with PD98059 or overexpression of dominant negative JNK1.	Arsenic	35-42	nuclear factor kappa B subunit 1	Homo sapiens	23-31
11678607-6	2001	The transactivation of NFkappaB by arsenic appeared to be through activation of Erks and JNKs pathways because increased NFkappaB activity by arsenic could be dramatically inhibited by either pre-treatment of cells with PD98059 or overexpression of dominant negative JNK1.	Arsenic	35-42	nuclear factor kappa B subunit 1	Homo sapiens	121-129
11678607-6	2001	The transactivation of NFkappaB by arsenic appeared to be through activation of Erks and JNKs pathways because increased NFkappaB activity by arsenic could be dramatically inhibited by either pre-treatment of cells with PD98059 or overexpression of dominant negative JNK1.	Arsenic	35-42	mitogen-activated protein kinase 8	Homo sapiens	267-271
11678607-6	2001	The transactivation of NFkappaB by arsenic appeared to be through activation of Erks and JNKs pathways because increased NFkappaB activity by arsenic could be dramatically inhibited by either pre-treatment of cells with PD98059 or overexpression of dominant negative JNK1.	Arsenic	142-149	nuclear factor kappa B subunit 1	Homo sapiens	23-31
11678607-6	2001	The transactivation of NFkappaB by arsenic appeared to be through activation of Erks and JNKs pathways because increased NFkappaB activity by arsenic could be dramatically inhibited by either pre-treatment of cells with PD98059 or overexpression of dominant negative JNK1.	Arsenic	142-149	nuclear factor kappa B subunit 1	Homo sapiens	121-129
11678607-6	2001	The transactivation of NFkappaB by arsenic appeared to be through activation of Erks and JNKs pathways because increased NFkappaB activity by arsenic could be dramatically inhibited by either pre-treatment of cells with PD98059 or overexpression of dominant negative JNK1.	Arsenic	142-149	mitogen-activated protein kinase 8	Homo sapiens	267-271
11678607-7	2001	That Erks activation is required for arsenic-induced NFkappaB transactivation was further supported by the findings that arsenic-induced NFkappaB transactivation was impaired in JB6 30.7b cells, which were deficient in Erks.	Arsenic	37-44	nuclear factor kappa B subunit 1	Homo sapiens	53-61
11678607-7	2001	That Erks activation is required for arsenic-induced NFkappaB transactivation was further supported by the findings that arsenic-induced NFkappaB transactivation was impaired in JB6 30.7b cells, which were deficient in Erks.	Arsenic	37-44	nuclear factor kappa B subunit 1	Homo sapiens	137-145
11678607-7	2001	That Erks activation is required for arsenic-induced NFkappaB transactivation was further supported by the findings that arsenic-induced NFkappaB transactivation was impaired in JB6 30.7b cells, which were deficient in Erks.	Arsenic	121-128	nuclear factor kappa B subunit 1	Homo sapiens	53-61
11678607-7	2001	That Erks activation is required for arsenic-induced NFkappaB transactivation was further supported by the findings that arsenic-induced NFkappaB transactivation was impaired in JB6 30.7b cells, which were deficient in Erks.	Arsenic	121-128	nuclear factor kappa B subunit 1	Homo sapiens	137-145
11353140-7	2001	Expression of heme oxygenase 1 (HO-1), a hallmark for arsenic-induced stress, was increased 10-fold, along with increases in heat shock protein-60 (HSP60), DNA damage inducible protein GADD45, and the DNA excision repair protein ERCC1.	Arsenic	54-61	heme oxygenase 1	Mus musculus	14-30
11353140-7	2001	Expression of heme oxygenase 1 (HO-1), a hallmark for arsenic-induced stress, was increased 10-fold, along with increases in heat shock protein-60 (HSP60), DNA damage inducible protein GADD45, and the DNA excision repair protein ERCC1.	Arsenic	54-61	heme oxygenase 1	Mus musculus	32-36
11353140-9	2001	Multiprobe RNase protection assay revealed the activation of the c-Jun/AP-1 transcription complex after arsenic treatments.	Arsenic	104-111	jun proto-oncogene	Mus musculus	65-70
11353140-10	2001	Western blot analysis further confirmed the enhanced production of arsenic-induced stress proteins such as HO-1, HSP70, HSP90, metallothionein, the metal-responsive transcription factor MTF-1, nuclear factor kappa B and c-Jun/AP-1.	Arsenic	67-74	heme oxygenase 1	Mus musculus	107-111
11353140-10	2001	Western blot analysis further confirmed the enhanced production of arsenic-induced stress proteins such as HO-1, HSP70, HSP90, metallothionein, the metal-responsive transcription factor MTF-1, nuclear factor kappa B and c-Jun/AP-1.	Arsenic	67-74	heat shock protein 1B	Mus musculus	113-118
11353140-10	2001	Western blot analysis further confirmed the enhanced production of arsenic-induced stress proteins such as HO-1, HSP70, HSP90, metallothionein, the metal-responsive transcription factor MTF-1, nuclear factor kappa B and c-Jun/AP-1.	Arsenic	67-74	heat shock protein, 2	Mus musculus	120-125
11353140-10	2001	Western blot analysis further confirmed the enhanced production of arsenic-induced stress proteins such as HO-1, HSP70, HSP90, metallothionein, the metal-responsive transcription factor MTF-1, nuclear factor kappa B and c-Jun/AP-1.	Arsenic	67-74	metal response element binding transcription factor 1	Mus musculus	186-215
11353140-10	2001	Western blot analysis further confirmed the enhanced production of arsenic-induced stress proteins such as HO-1, HSP70, HSP90, metallothionein, the metal-responsive transcription factor MTF-1, nuclear factor kappa B and c-Jun/AP-1.	Arsenic	67-74	jun proto-oncogene	Mus musculus	220-225
11312036-13	2001	These results demonstrated that SAAD potentiated cytotoxicity induced by arsenic or mercury and that activation of ERK1/2, p38 kinase and JNK1 was responsible for the potentiated arsenic toxicity, whereas the mercury toxicity enhanced by SAAD was mediated with the activity of JNK1.	Arsenic	179-186	mitogen activated protein kinase 3	Rattus norvegicus	115-121
11348091-6	2001	No As(III) was detected by X-ray photoelectron spectroscopy (XPS) on Peerless Fe0 at 5 days when As(V) was the initial arsenic species in the solution.	Arsenic	119-126	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	97-102
11348091-7	2001	As(III) was detected by XPS at 30 and 60 days present on Peerless Fe0, when As(V) was the initial arsenic species in the solution.	Arsenic	98-105	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	76-81
11348091-11	2001	The desorption of As(V) and As(III) by phosphate extraction decreased as the residence time of interaction between the sorbents and arsenic increased from 1 to 60 days.	Arsenic	132-139	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	18-23
11357877-0	2001	Immunosuppression by arsenic: a comparison of cathepsin L inhibition and apoptosis.	Arsenic	21-28	cathepsin L	Homo sapiens	46-57
11298321-5	2001	All of the HIV-1 sequence-specific AS-P-OdN"s inhibited intracellular p24 antigen expression in a time- and dose-dependent manner; although, blocking p24 expression alone was not sufficient to modulate TCR/CD3 surface density.	Arsenic	35-37	transmembrane p24 trafficking protein 2	Homo sapiens	150-153
11298321-5	2001	All of the HIV-1 sequence-specific AS-P-OdN"s inhibited intracellular p24 antigen expression in a time- and dose-dependent manner; although, blocking p24 expression alone was not sufficient to modulate TCR/CD3 surface density.	Arsenic	35-37	transmembrane p24 trafficking protein 2	Homo sapiens	70-73
11248451-3	2001	Poisoning with organophosphate pesticides and arsenic (ingestion) showed a second grade SP-A score.	Arsenic	46-53	surfactant protein A2	Homo sapiens	88-92
11357877-3	2001	In this study, we show that trivalent arsenic inhibits enzymatic activity of the lysosomal protease cathepsin L (CathL) in the murine antigen-presenting B cell line TA3.	Arsenic	38-45	cathepsin L	Homo sapiens	100-111
11357877-3	2001	In this study, we show that trivalent arsenic inhibits enzymatic activity of the lysosomal protease cathepsin L (CathL) in the murine antigen-presenting B cell line TA3.	Arsenic	38-45	cathepsin L	Homo sapiens	113-118
11357877-3	2001	In this study, we show that trivalent arsenic inhibits enzymatic activity of the lysosomal protease cathepsin L (CathL) in the murine antigen-presenting B cell line TA3.	Arsenic	38-45	trace amine associated receptor 9	Homo sapiens	165-168
11248140-3	2001	In the present studies, dose-response relationships and recovery studies employing a cancer precursor marker, i.e., activating protein (AP)-1 DNA-binding activity, were examined in bladders of mice exposed to arsenic in drinking water and compared to histopathological changes and arsenic tissue levels in the same tissue.	Arsenic	209-216	jun proto-oncogene	Mus musculus	116-141
11333185-0	2001	Arsenic alters the function of the glucocorticoid receptor as a transcription factor.	Arsenic	0-7	nuclear receptor subfamily 3 group C member 1	Homo sapiens	35-58
11258980-3	2001	Because MAs(III) is produced in the biomethylation of As, it was postulated that the extent of inhibition of TR in cultured rat hepatocytes would correlate with the intracellular concentration of methyl As.	Arsenic	9-11	peroxiredoxin 5	Rattus norvegicus	109-111
11257063-6	2001	Among individuals with toenail arsenic concentrations above the 97th percentile, the adjusted odds ratios were 2.07 (95% confidence interval (CI): 0.92, 4.66) for SCC and 1.44 (95% CI: 0.74, 2.81) for BCC, compared with those with concentrations at or below the median.	Arsenic	31-38	serpin family B member 3	Homo sapiens	163-166
11321952-2	2001	The results showed that the spotaneous oxidation of As(III) to As(V) was very slow and could not be enhanced by aerating for 24 h. The removal rate of As(III) could reach that of As(V) when pre-aerating water samples with ozone for 60 s, putting 7.5 ml/L hydrogen peroxide solution, adding 2.5 mg/L javelle water (sodium hypochlorite) or 15 mg/L bleaching powder(numerated by chlorine).	Arsenic	52-54	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	63-68
11512994-3	2001	In the blackfoot disease area, arsenic with a high oxidation state (As(V)) was also observed in the contaminated soil.	Arsenic	31-38	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	68-73
11321952-2	2001	The results showed that the spotaneous oxidation of As(III) to As(V) was very slow and could not be enhanced by aerating for 24 h. The removal rate of As(III) could reach that of As(V) when pre-aerating water samples with ozone for 60 s, putting 7.5 ml/L hydrogen peroxide solution, adding 2.5 mg/L javelle water (sodium hypochlorite) or 15 mg/L bleaching powder(numerated by chlorine).	Arsenic	52-54	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	179-184
11321952-2	2001	The results showed that the spotaneous oxidation of As(III) to As(V) was very slow and could not be enhanced by aerating for 24 h. The removal rate of As(III) could reach that of As(V) when pre-aerating water samples with ozone for 60 s, putting 7.5 ml/L hydrogen peroxide solution, adding 2.5 mg/L javelle water (sodium hypochlorite) or 15 mg/L bleaching powder(numerated by chlorine).	Arsenic	63-65	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	179-184
11269692-9	2001	The relative quantity of hepatic apo B mRNA in the AS group was 1.2 times higher than that in the CS group, and the hepatic LDL receptor mRNA levels in the AS and TS groups were 1.8-2.0 times higher than that in the CS group.	Arsenic	156-158	low density lipoprotein receptor	Rattus norvegicus	124-136
11269692-10	2001	The results of this study demonstrate that AS, KS, and TS lowered the serum total cholesterol level by enhancing the hepatic LDL receptor mRNA level.	Arsenic	43-45	low density lipoprotein receptor	Rattus norvegicus	125-137
11114829-8	2000	Declines of CD8+ percentage were significantly higher in the ES (-18%) than in the AS group (-2%).	Arsenic	83-85	CD8a molecule	Homo sapiens	12-15
11162773-2	2001	The effect of As, Pb, Hg, or Cd (ranked as the most hazardous environmental metals by EPA and ATSDR) on CYP1A1 and 1A2 induction by benzo[a]pyrene (BaP), benzo[b]fluoranthene (BbF), dibenzo[a,h]anthracene (DBahA), benzo[a]anthracene (BaA), and benzo[k]fluoranthene (BkF) has thus been investigated in fresh human hepatocyte cultures.	Arsenic	14-16	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	104-110
11548067-3	2001	In the current study, we specifically evaluated the long-term reproducibility of tap water and toenail concentrations of arsenic, and the relation between water, toenail, and urinary measurement.	Arsenic	121-128	nuclear RNA export factor 1	Homo sapiens	81-84
11548067-6	2001	Tap water arsenic concentrations ranged from undetectable (&lt;0.01 microg/L) to 66.6 microg/L.	Arsenic	10-17	nuclear RNA export factor 1	Homo sapiens	0-3
11778665-3	2001	RESULTS: Following chronic arsenic (III) exposure, delta-aminolevulinic acid dehydratase activity in blood showed a significant reduction as did the total cell counts (RBC and WBC) and reduced glutathione with increased urinary delta-aminolevulinic acid.	Arsenic	27-34	aminolevulinate dehydratase	Rattus norvegicus	51-88
11778665-5	2001	The hepatic delta-aminolevulinic acid dehydratase and delta-aminolevulinic acid synthetase activity increased in chronic arsenic (III) exposure in rats and guinea pigs.	Arsenic	121-128	aminolevulinate dehydratase	Rattus norvegicus	12-49
11414427-1	2000	Ron Phibun district in southern Thailand has been known as an endemic area for arsenic contamination.	Arsenic	79-86	macrophage stimulating 1 receptor	Homo sapiens	0-3
10967126-6	2000	The affinity of IKKbeta for trivalent arsenic was verified in vitro by the ability of IKKbeta to enhance the fluorescence of an arsenic-substituted fluorescein dye.	Arsenic	38-45	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	16-23
10967126-6	2000	The affinity of IKKbeta for trivalent arsenic was verified in vitro by the ability of IKKbeta to enhance the fluorescence of an arsenic-substituted fluorescein dye.	Arsenic	38-45	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	86-93
10967126-6	2000	The affinity of IKKbeta for trivalent arsenic was verified in vitro by the ability of IKKbeta to enhance the fluorescence of an arsenic-substituted fluorescein dye.	Arsenic	128-135	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	16-23
10967126-6	2000	The affinity of IKKbeta for trivalent arsenic was verified in vitro by the ability of IKKbeta to enhance the fluorescence of an arsenic-substituted fluorescein dye.	Arsenic	128-135	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	86-93
11798837-9	2000	CONCLUSION: After introduced into GLC-82 cells, Ad-p53 shows enhanced therapeutic efficiency for GLC-82 cells when combined with CDDP or As(2)O(3).	Arsenic	137-139	tumor protein p53	Homo sapiens	51-54
11033234-1	2000	We studied the effects of chronic arsenic exposure on brain monoamines and plasma levels of adrenocorticotropic hormone (ACTH) of mice.	Arsenic	34-41	pro-opiomelanocortin-alpha	Mus musculus	92-119
11033234-1	2000	We studied the effects of chronic arsenic exposure on brain monoamines and plasma levels of adrenocorticotropic hormone (ACTH) of mice.	Arsenic	34-41	pro-opiomelanocortin-alpha	Mus musculus	121-125
11068345-8	2000	Alb-30-fed arsenic-intoxicated mice showed revival and restoration in both liver and testis as revealed by gel patterns and quantitative assay of DNA and RNA.	Arsenic	11-18	albumin	Mus musculus	0-3
11068345-10	2000	Alb-30 in reducing arsenic-induced damage to protein and nucleic acids is substantiated and the mechanism of action of the homeopathic drug through expression of regulatory genes inferred.	Arsenic	19-26	albumin	Mus musculus	0-3
10938093-0	2000	The MRP2/cMOAT transporter and arsenic-glutathione complex formation are required for biliary excretion of arsenic.	Arsenic	107-114	ATP binding cassette subfamily C member 2	Homo sapiens	4-8
10938093-2	2000	Here we show that transport of arsenic into bile depends on the MRP2/cMOAT transporter and that glutathione is obligatory for such transport.	Arsenic	31-38	ATP binding cassette subfamily C member 2	Homo sapiens	64-68
11035063-7	2000	This Thy-1 aggregation and subsequent activation of MAP family kinase and c-Jun and the degradation of PARP induced by NaAsO(2) were all inhibited by DTT, suggesting the requirement of interaction between arsenic and protein sulfhydryl groups for those effects.	Arsenic	205-212	thymus cell antigen 1, theta	Mus musculus	5-10
11035063-7	2000	This Thy-1 aggregation and subsequent activation of MAP family kinase and c-Jun and the degradation of PARP induced by NaAsO(2) were all inhibited by DTT, suggesting the requirement of interaction between arsenic and protein sulfhydryl groups for those effects.	Arsenic	205-212	jun proto-oncogene	Mus musculus	74-79
11035063-7	2000	This Thy-1 aggregation and subsequent activation of MAP family kinase and c-Jun and the degradation of PARP induced by NaAsO(2) were all inhibited by DTT, suggesting the requirement of interaction between arsenic and protein sulfhydryl groups for those effects.	Arsenic	205-212	poly (ADP-ribose) polymerase family, member 1	Mus musculus	103-107
10785545-2	2000	We have investigated the action of AS-35 on the enzyme activities which are involved in the synthesis of LTC(4) and LTB(4) (LT-synthesizing enzymes); cytosolic phospholipase A(2) (cPLA(2)), 5-lipoxygenase (5-LO), leukotriene (LT)C(4) synthase and LTA(4) hydrolase.	Arsenic	35-37	arachidonate 5-lipoxygenase	Homo sapiens	190-204
10972992-3	2000	Cadmium or arsenic did not change Cyp1a1 mRNA levels but did enhance TCDD-inducible levels of Nqo1 mRNA, an effect that paralleled the ability of these metals to activate a beta-galactosidase gene reporter system regulated by an electrophile response promoter element.	Arsenic	11-18	NAD(P)H dehydrogenase, quinone 1	Mus musculus	94-98
10785545-2	2000	We have investigated the action of AS-35 on the enzyme activities which are involved in the synthesis of LTC(4) and LTB(4) (LT-synthesizing enzymes); cytosolic phospholipase A(2) (cPLA(2)), 5-lipoxygenase (5-LO), leukotriene (LT)C(4) synthase and LTA(4) hydrolase.	Arsenic	35-37	leukotriene A4 hydrolase	Homo sapiens	247-263
10775461-9	2000	These studies demonstrate that high levels of arsenic may inhibit NF-kappaB-mediated gene transcription by specifically blocking IKK activity, thereby limiting the phosphorylation and subsequent degradation of the NF-kappaB inhibitor, IkappaBalpha.	Arsenic	46-53	nuclear factor kappa B subunit 1	Homo sapiens	66-75
10996542-4	2000	Following arsenic treatment, liver showed significantly enhanced concentration of glutathione and increased activities of glutathione reductase and glutathione-S-transferase on either of the dietary protein levels.	Arsenic	10-17	glutathione-disulfide reductase	Rattus norvegicus	122-143
10996542-4	2000	Following arsenic treatment, liver showed significantly enhanced concentration of glutathione and increased activities of glutathione reductase and glutathione-S-transferase on either of the dietary protein levels.	Arsenic	10-17	hematopoietic prostaglandin D synthase	Rattus norvegicus	148-173
10996542-7	2000	On the other hand, kidney of arsenic-treated rats receiving either of the dietary protein levels showed significantly increased lipid peroxidation and decreased superoxide dismutase and catalase activities.	Arsenic	29-36	catalase	Rattus norvegicus	186-194
10996542-8	2000	Kidney glutathione content and glutathione reductase activity remained unaltered while glutathione peroxidase activity increased and glutathione-S-transferase activity decreased significantly on a low-protein diet following exposure to arsenic.	Arsenic	236-243	hematopoietic prostaglandin D synthase	Rattus norvegicus	133-158
10775461-0	2000	Arsenic inhibits NF-kappaB-mediated gene transcription by blocking IkappaB kinase activity and IkappaBalpha phosphorylation and degradation.	Arsenic	0-7	nuclear factor kappa B subunit 1	Homo sapiens	17-26
10775461-0	2000	Arsenic inhibits NF-kappaB-mediated gene transcription by blocking IkappaB kinase activity and IkappaBalpha phosphorylation and degradation.	Arsenic	0-7	NFKB inhibitor alpha	Homo sapiens	95-107
10996542-9	2000	On an adequate protein diet glucose-6-phosphate dehydrogenase activity in kidney, however, became significantly elevated following arsenic treatment.	Arsenic	131-138	glucose-6-phosphate dehydrogenase	Rattus norvegicus	28-61
10828279-8	2000	Chronic As exposures produced 2-10 fold elevation of serum interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha levels, with greater increases seen by repeated injections than by oral exposure, and again, MT-null mice had higher serum cytokines than WT mice after As exposure.	Arsenic	8-10	interleukin 1 beta	Mus musculus	59-76
10828279-8	2000	Chronic As exposures produced 2-10 fold elevation of serum interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha levels, with greater increases seen by repeated injections than by oral exposure, and again, MT-null mice had higher serum cytokines than WT mice after As exposure.	Arsenic	8-10	interleukin 6	Mus musculus	78-124
10775461-2	2000	Here, we investigated whether arsenic, which has been shown to inhibit the ubiquitin-proteasome pathway, could inhibit TNF-alpha-mediated increases in IL-8 expression.	Arsenic	30-37	tumor necrosis factor	Homo sapiens	119-128
10775461-9	2000	These studies demonstrate that high levels of arsenic may inhibit NF-kappaB-mediated gene transcription by specifically blocking IKK activity, thereby limiting the phosphorylation and subsequent degradation of the NF-kappaB inhibitor, IkappaBalpha.	Arsenic	46-53	nuclear factor kappa B subunit 1	Homo sapiens	214-223
10775461-2	2000	Here, we investigated whether arsenic, which has been shown to inhibit the ubiquitin-proteasome pathway, could inhibit TNF-alpha-mediated increases in IL-8 expression.	Arsenic	30-37	C-X-C motif chemokine ligand 8	Homo sapiens	151-155
10775461-9	2000	These studies demonstrate that high levels of arsenic may inhibit NF-kappaB-mediated gene transcription by specifically blocking IKK activity, thereby limiting the phosphorylation and subsequent degradation of the NF-kappaB inhibitor, IkappaBalpha.	Arsenic	46-53	NFKB inhibitor alpha	Homo sapiens	235-247
10764629-5	2000	Analysis of positive proliferative regulators revealed an increase in the expression of c-myc and E2F-1, thereby supporting the hypothesis that arsenic increases activity of positive growth modulators.	Arsenic	144-151	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	88-93
10764629-5	2000	Analysis of positive proliferative regulators revealed an increase in the expression of c-myc and E2F-1, thereby supporting the hypothesis that arsenic increases activity of positive growth modulators.	Arsenic	144-151	E2F transcription factor 1	Homo sapiens	98-103
10764629-7	2000	When negative regulators of proliferation were examined, expression levels of MAP kinase phosphatase-1 and p27(Kip1) were found to be lower in arsenic-treated cells compared to control cells; this result supports a model in which arsenic disinhibits normal regulation of cell proliferation.	Arsenic	143-150	dual specificity phosphatase 1	Homo sapiens	78-102
10764629-7	2000	When negative regulators of proliferation were examined, expression levels of MAP kinase phosphatase-1 and p27(Kip1) were found to be lower in arsenic-treated cells compared to control cells; this result supports a model in which arsenic disinhibits normal regulation of cell proliferation.	Arsenic	143-150	interferon alpha inducible protein 27	Homo sapiens	107-110
10764629-7	2000	When negative regulators of proliferation were examined, expression levels of MAP kinase phosphatase-1 and p27(Kip1) were found to be lower in arsenic-treated cells compared to control cells; this result supports a model in which arsenic disinhibits normal regulation of cell proliferation.	Arsenic	143-150	cyclin dependent kinase inhibitor 1B	Homo sapiens	111-115
10821403-2	2000	Four arsenic species [arsenite As(III), arsenate As(V), monomethylarsonate (MMA), and dimethylarsinate (DMA)] present in the urine samples of patients treated intravenously with arsenite, were analyzed separately by HPLC-HG-ICP-AES using a non-polar C18 column.	Arsenic	5-12	Bardet-Biedl syndrome 9	Homo sapiens	250-253
10721144-2	2000	Conversion of As(III), which constituted over 70% of dissolved arsenic in the samples, to As(V) was fast with ozone, but sluggish with pure oxygen and air.	Arsenic	63-70	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	90-95
10721769-6	2000	The arsenic-induced apoptosis in neuroblastoma cell lines was mediated by the activation of caspase 3 in all cases tested.	Arsenic	4-11	caspase 3	Homo sapiens	92-101
18967861-7	2000	The separation and quantification of arsenic compounds in the microwave digests and extracts, were carried out in anion (PRP-X100) and cation (LC-SCX) exchange columns using ICP-MS as arsenic specific detector.	Arsenic	37-44	scleraxis bHLH transcription factor	Homo sapiens	146-149
11498362-2	2000	Arsenic may be effective in counteracting drug resistance because it appears to induce apoptosis in tumor cells independently of p53 activation, thereby allowing it to be directed against p53-defective cancers.	Arsenic	0-7	tumor protein p53	Homo sapiens	129-132
10677095-0	2000	Expression of p53 in arsenic-related and sporadic basal cell carcinoma.	Arsenic	21-28	tumor protein p53	Homo sapiens	14-17
10677095-3	2000	Arsenic treatment has been shown to cause hypermethylation of the TP53 gene in lung carcinoma cell lines, but it is not known if this occurs in vivo in arsenic-related BCCs.	Arsenic	0-7	tumor protein p53	Homo sapiens	66-70
10677095-9	2000	RESULTS: Arsenic-related BCCs express p53 less often and at a lower intensity than sporadic BCCs (P = .001; 2-tailed test).	Arsenic	9-16	tumor protein p53	Homo sapiens	38-41
10677095-10	2000	The BCCs from sun-exposed sites, whether arsenic related or sporadic, more frequently showed overexpression of p53 than those from less-exposed areas (P = .004; 2-tailed test).	Arsenic	41-48	tumor protein p53	Homo sapiens	111-114
10677095-12	2000	CONCLUSIONS: These results are consistent with the hypothesis that the TP53 gene is down-regulated by methylation in arsenic-related BCC, particularly those from less-exposed sites.	Arsenic	117-124	tumor protein p53	Homo sapiens	71-75
10648417-0	2000	Arsenic induces apoptosis of multidrug-resistant human myeloid leukemia cells that express Bcr-Abl or overexpress MDR, MRP, Bcl-2, or Bcl-x(L).	Arsenic	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
10648417-0	2000	Arsenic induces apoptosis of multidrug-resistant human myeloid leukemia cells that express Bcr-Abl or overexpress MDR, MRP, Bcl-2, or Bcl-x(L).	Arsenic	0-7	ATP binding cassette subfamily C member 1	Homo sapiens	119-122
10648417-0	2000	Arsenic induces apoptosis of multidrug-resistant human myeloid leukemia cells that express Bcr-Abl or overexpress MDR, MRP, Bcl-2, or Bcl-x(L).	Arsenic	0-7	BCL2 apoptosis regulator	Homo sapiens	124-129
10648417-0	2000	Arsenic induces apoptosis of multidrug-resistant human myeloid leukemia cells that express Bcr-Abl or overexpress MDR, MRP, Bcl-2, or Bcl-x(L).	Arsenic	0-7	BCL2 like 1	Homo sapiens	134-142
11498362-2	2000	Arsenic may be effective in counteracting drug resistance because it appears to induce apoptosis in tumor cells independently of p53 activation, thereby allowing it to be directed against p53-defective cancers.	Arsenic	0-7	tumor protein p53	Homo sapiens	188-191
10635991-0	1999	Effects of arsenic exposure on the frequency of HPRT-mutant lymphocytes in a population of copper roasters in Antofagasta, Chile: a pilot study.	Arsenic	11-18	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	48-52
10662863-3	2000	In the electrophoretic mobility shift assay, NPR1 substantially increased the binding of TGA2 to its cognate promoter element (as-1) as well as to a positive salicylic acid-inducible element (LS7) and a negative element (LS5) in the promoter of the pathogenesis-related PR-1 gene.	Arsenic	38-40	regulatory protein (NPR1)	Arabidopsis thaliana	45-49
10662863-3	2000	In the electrophoretic mobility shift assay, NPR1 substantially increased the binding of TGA2 to its cognate promoter element (as-1) as well as to a positive salicylic acid-inducible element (LS7) and a negative element (LS5) in the promoter of the pathogenesis-related PR-1 gene.	Arsenic	38-40	bZIP transcription factor family protein	Arabidopsis thaliana	89-93
10662863-3	2000	In the electrophoretic mobility shift assay, NPR1 substantially increased the binding of TGA2 to its cognate promoter element (as-1) as well as to a positive salicylic acid-inducible element (LS7) and a negative element (LS5) in the promoter of the pathogenesis-related PR-1 gene.	Arsenic	38-40	pathogenesis-related protein 1	Arabidopsis thaliana	270-274
10685512-7	2000	In conclusion, these findings demonstrated that MRP1 likely handled some, but not all, cytotoxic metals such as arsenic and mercuric ions in addition to antimony, therefore resulting in reduced toxicity of these compounds towards MRP1-overexpressing cells.	Arsenic	112-119	ATP binding cassette subfamily C member 1	Homo sapiens	48-52
10685512-7	2000	In conclusion, these findings demonstrated that MRP1 likely handled some, but not all, cytotoxic metals such as arsenic and mercuric ions in addition to antimony, therefore resulting in reduced toxicity of these compounds towards MRP1-overexpressing cells.	Arsenic	112-119	ATP binding cassette subfamily C member 1	Homo sapiens	230-234
11314982-0	2000	Effect of arsenic trioxide on metallothionein and its conversion to different arsenic metabolites in hen liver.	Arsenic	10-17	metallothionein 4	Gallus gallus	30-45
10712745-0	2000	Arsenic[III] and heavy metal ions induce intrachromosomal homologous recombination in the hprt gene of V79 Chinese hamster cells.	Arsenic	0-7	hypoxanthine-guanine phosphoribosyltransferase	Cricetulus griseus	90-94
11671301-1	1999	Dimethyltrithiocarbonate reacts with the superacidic systems HF/MF(5) and DF/MF(5) (M = As, Sb) to form (MeS)(2)CSX(+)MF(6)(-) (X = H, D).	Arsenic	88-90	MKS transition zone complex subunit 1	Homo sapiens	105-108
11671301-6	1999	The Raman, IR, and (1)H, (75)As, (19)F, and (13)C NMR spectra of (MeS)(2)CSX(+)SbF(6)(-) and (MeS)(2)CSX(+)As(2)F(11)(-) (X = H, D) are reported.	Arsenic	29-31	MKS transition zone complex subunit 1	Homo sapiens	66-69
10635991-1	1999	A pilot biomarker study was conducted to investigate the feasibility of using the hypoxanthine guanine phosphoribosyltransferase (HPRT) gene in peripheral blood lymphocytes as a biomarker for detecting genetic effects of arsenic exposure.	Arsenic	221-228	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	82-128
10635991-1	1999	A pilot biomarker study was conducted to investigate the feasibility of using the hypoxanthine guanine phosphoribosyltransferase (HPRT) gene in peripheral blood lymphocytes as a biomarker for detecting genetic effects of arsenic exposure.	Arsenic	221-228	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	130-134
10604879-0	1999	Enzymatic reduction of arsenic compounds in mammalian systems: the rate-limiting enzyme of rabbit liver arsenic biotransformation is MMA(V) reductase.	Arsenic	23-30	glutathione S-transferase omega 2	Homo sapiens	133-149
10658539-8	1999	The best correlations between As in air and its urinary species were found for total iAs and As3 + As5.	Arsenic	30-32	PDS5 cohesin associated factor B	Homo sapiens	93-96
10555748-7	1999	Multidrug-resistant cancer cells that were cross-resistant to arsenic contained higher levels of GSH or multidrug-resistance-associated protein 1 than their drug-sensitive parental cells.	Arsenic	62-69	ATP binding cassette subfamily C member 1	Homo sapiens	104-145
10564177-2	1999	To study the mechanisms responsible for metal-induced activation of ERK, we examined the effect of noncytotoxic exposures to As, Cu, V, or Zn on the kinases upstream of ERK in the epidermal growth factor (EGF) receptor signaling pathway.	Arsenic	125-127	mitogen-activated protein kinase 1	Homo sapiens	169-172
10564177-10	1999	Together, these data demonstrate that As, Cu, V, and Zn can activate the EGF receptor signaling pathway in BEAS cells and suggest that this mechanism may be involved in pulmonary responses to metal inhalation.	Arsenic	38-40	epidermal growth factor receptor	Homo sapiens	73-85
10444232-9	1999	The recommended dose of fexofenadine HC1 is 120 mg daily for SAR (either as 120 mg once daily or 60 mg twice daily) or 180 mg once daily for CIU.	Arsenic	73-75	CYCS pseudogene 39	Homo sapiens	37-40
10491313-0	1999	Arsenic disrupts cellular levels of p53 and mdm2: a potential mechanism of carcinogenesis.	Arsenic	0-7	tumor protein p53	Homo sapiens	36-39
10491313-0	1999	Arsenic disrupts cellular levels of p53 and mdm2: a potential mechanism of carcinogenesis.	Arsenic	0-7	MDM2 proto-oncogene	Homo sapiens	44-48
10491313-5	1999	We propose the disruption of the p53-mdm2 loop regulating cell cycle arrest as a model for arsenic-related skin carcinogenesis and it may be important in tumors with elevated mdm2 levels.	Arsenic	91-98	tumor protein p53	Homo sapiens	33-36
10491313-5	1999	We propose the disruption of the p53-mdm2 loop regulating cell cycle arrest as a model for arsenic-related skin carcinogenesis and it may be important in tumors with elevated mdm2 levels.	Arsenic	91-98	MDM2 proto-oncogene	Homo sapiens	37-41
10491313-5	1999	We propose the disruption of the p53-mdm2 loop regulating cell cycle arrest as a model for arsenic-related skin carcinogenesis and it may be important in tumors with elevated mdm2 levels.	Arsenic	91-98	MDM2 proto-oncogene	Homo sapiens	175-179
10397243-0	1999	Arsenic induces apoptosis through a c-Jun NH2-terminal kinase-dependent, p53-independent pathway.	Arsenic	0-7	tumor protein p53	Homo sapiens	73-76
10397243-5	1999	In contrast, arsenic-induced apoptosis was almost totally blocked by expression of a dominant-negative mutant of JNK1.	Arsenic	13-20	mitogen-activated protein kinase 8	Homo sapiens	113-117
10397243-7	1999	Taken together with previous findings that p53 mutations are involved in approximately 50% of all human cancers and nearly all chemotherapeutic agents kill cancer cells mainly by apoptotic induction, we suggest that arsenic may be a useful agent for the treatment of cancers with p53 mutation.	Arsenic	216-223	tumor protein p53	Homo sapiens	43-46
10397243-7	1999	Taken together with previous findings that p53 mutations are involved in approximately 50% of all human cancers and nearly all chemotherapeutic agents kill cancer cells mainly by apoptotic induction, we suggest that arsenic may be a useful agent for the treatment of cancers with p53 mutation.	Arsenic	216-223	tumor protein p53	Homo sapiens	280-283
10598025-1	1999	We previously found that 72-kDa heat shock protein (Hsp72) was induced and accumulated in the nuclei, together with DNA damage, in human alveolar epithelial (L-132) cells by exposure to dimethylarsinic acid (DMAA), which is a main metabolite of inorganic arsenics in mammals.	Arsenic	255-263	heat shock protein family A (Hsp70) member 1A	Homo sapiens	52-57
10571731-4	1999	First, we observed that sodium arsenate induced a concentration-dependent production of interleukin-1alpha and a significant increase in cell proliferation, that could be suppressed by the addition of a neutralizing antibody against murine interleukin-1alpha, confirming the ability of arsenic to induce keratinocyte growth-promoting cytokines.	Arsenic	286-293	interleukin 1 alpha	Mus musculus	240-258
10571731-7	1999	Arsenic induced a concentration- and time-dependent increase in cellular oxidative activity, which was followed by activation of redox-sensitive transcription factors such as nuclear factor-kappaB and activator protein-1, that are essential for interleukin-1alpha synthesis.	Arsenic	0-7	interleukin 1 alpha	Mus musculus	245-263
11783229-1	1999	OBJECTIVE: To observe the effect of heart preservation of Astragalus saponins (AS) in modified Euro-Collins solution (mEC) containing AS.	Arsenic	79-81	chemokine (C-C motif) ligand 28	Mus musculus	118-121
11783229-1	1999	OBJECTIVE: To observe the effect of heart preservation of Astragalus saponins (AS) in modified Euro-Collins solution (mEC) containing AS.	Arsenic	134-136	chemokine (C-C motif) ligand 28	Mus musculus	118-121
10411148-4	1999	We examined the effects of non-cytotoxic and cytotoxic doses of arsenic(III) and chromium(VI) on nuclear binding of the transcription factors AP-1, NF-kappaB, Sp1, and YB-1 in human MDA-MB-435 breast cancer and rat H4IIE hepatoma cells.	Arsenic	64-71	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	142-146
10445212-9	1999	The decreased renal reduction of As(V) led to a decrease in As(III) and an increase of As(V) and the associated As(V)-transferrin binding in plasma.	Arsenic	33-35	serotransferrin	Oryctolagus cuniculus	118-129
10411148-4	1999	We examined the effects of non-cytotoxic and cytotoxic doses of arsenic(III) and chromium(VI) on nuclear binding of the transcription factors AP-1, NF-kappaB, Sp1, and YB-1 in human MDA-MB-435 breast cancer and rat H4IIE hepatoma cells.	Arsenic	64-71	Y-box binding protein 1	Homo sapiens	168-172
10407497-4	1999	h apo A-I in sera of tg mice was 429 +/- 18 and 308 +/- 10 mg/dl in male and female mice, the ratio of phospholipid (PL) to apo A-I was 0.94 in tg and 2.4 and 1.9 in male and female controls, taking mouse apo A-I as 100 mg/dl.	Arsenic	30-32	apolipoprotein A1	Homo sapiens	2-9
10445755-2	1999	Based on the hypothesis that arsenic sensitizes cells to mitogenic stimulation by affecting the receptor tyrosine kinase (RTK) signal transduction pathway, these studies first examined the response of fibroblasts to specific mitogens using a defined media system.	Arsenic	29-36	ret proto-oncogene	Homo sapiens	96-120
10445755-2	1999	Based on the hypothesis that arsenic sensitizes cells to mitogenic stimulation by affecting the receptor tyrosine kinase (RTK) signal transduction pathway, these studies first examined the response of fibroblasts to specific mitogens using a defined media system.	Arsenic	29-36	ret proto-oncogene	Homo sapiens	122-125
10445755-4	1999	This effect is observed for up to 32 h after removal of arsenic, suggesting that the RTK pathway is affected in a sustained manner.	Arsenic	56-63	ret proto-oncogene	Homo sapiens	85-88
10328340-1	1999	Biotransformation of inorganic arsenic in mammals is catalyzed by three serial enzyme activities: arsenate reductase, arsenite methyltransferase, and monomethylarsonate methyltransferase.	Arsenic	31-38	arsenite methyltransferase	Homo sapiens	118-186
10362120-1	1999	To understand the role of p53 tumour suppressor gene in the carcinogenesis of arsenic-related skin cancers from the blackfoot disease endemic area of Taiwan, we collected tumour samples from 23 patients with Bowen"s disease, seven patients with basal cell carcinomas (BCC) and nine patients with squamous cell carcinomas (SCC).	Arsenic	78-85	tumor protein p53	Homo sapiens	26-29
10362120-8	1999	These findings showed that p53 gene mutation rate in arsenic-related skin cancers from the blackfoot disease endemic area of Taiwan is high and that the mutation types are different from those in UV-induced skin cancers.	Arsenic	53-60	tumor protein p53	Homo sapiens	27-30
9935161-3	1999	Anti-sense phosphorothioate oligodeoxynucleotides (AS S-oligos) directed against either CR or TGF-alpha inhibit the proliferation of both cell lines.	Arsenic	51-53	teratocarcinoma-derived growth factor 1	Homo sapiens	88-90
10190895-4	1999	Using syngenic grafts of leukemic blasts from PML/RARalpha transgenic mice as a model for APL, we demonstrate that arsenic induces apoptosis and modest differentiation, and prolongs mouse survival.	Arsenic	115-122	promyelocytic leukemia	Mus musculus	46-49
10190895-4	1999	Using syngenic grafts of leukemic blasts from PML/RARalpha transgenic mice as a model for APL, we demonstrate that arsenic induces apoptosis and modest differentiation, and prolongs mouse survival.	Arsenic	115-122	retinoic acid receptor, alpha	Mus musculus	50-58
10363626-6	1999	The LDLr promoter activity assay showed that treatment with 100 micromol/ of diltiazem and verapamil increased LDLr promoter activity by 126.72 +/- 10.68%, and 166.41 +/- 11.41%, respectively, at 24 hours (control as 100%), while treatment with 100 micromol/l of nifedipine had an inhibitory effect on LDLr promoter activity.	Arsenic	27-29	low density lipoprotein receptor	Homo sapiens	4-8
10363626-6	1999	The LDLr promoter activity assay showed that treatment with 100 micromol/ of diltiazem and verapamil increased LDLr promoter activity by 126.72 +/- 10.68%, and 166.41 +/- 11.41%, respectively, at 24 hours (control as 100%), while treatment with 100 micromol/l of nifedipine had an inhibitory effect on LDLr promoter activity.	Arsenic	27-29	low density lipoprotein receptor	Homo sapiens	111-115
10363626-6	1999	The LDLr promoter activity assay showed that treatment with 100 micromol/ of diltiazem and verapamil increased LDLr promoter activity by 126.72 +/- 10.68%, and 166.41 +/- 11.41%, respectively, at 24 hours (control as 100%), while treatment with 100 micromol/l of nifedipine had an inhibitory effect on LDLr promoter activity.	Arsenic	27-29	low density lipoprotein receptor	Homo sapiens	111-115
10340400-7	1999	Induction of apoptosis in arsenic-treated Meg-01 and UT7 cells was accompanied by a dose-response decrease of Bcl-2 protein, whereas As2O3 had no effect on this measurement in HL60, ZR75, and MCF7 cell lines.	Arsenic	26-33	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	42-45
10340400-7	1999	Induction of apoptosis in arsenic-treated Meg-01 and UT7 cells was accompanied by a dose-response decrease of Bcl-2 protein, whereas As2O3 had no effect on this measurement in HL60, ZR75, and MCF7 cell lines.	Arsenic	26-33	BCL2 apoptosis regulator	Homo sapiens	110-115
10319276-6	1999	Proliferative inhibition was due to a suboptimal levels of IL-2 secreted by lymphocytes, since the addition of recombinant IL-2 to the cultures reversed in a dose-dependent fashion the inhibitory effect of As.	Arsenic	206-208	interleukin 2	Homo sapiens	123-127
10374879-3	1999	This apoptosis did not require the activation of classical retinoid receptors and like arsenic (As)-induced apoptosis was preceded by the rapid activation of a caspase-3-like enzymatic activity as indicated by the increase of DEVD-pNA hydrolytic activity, by the processing of procaspase-3 protein and by the cleavage of poly(ADP-ribose) polymerase (PARP).	Arsenic	87-94	caspase 3	Homo sapiens	160-169
10374879-3	1999	This apoptosis did not require the activation of classical retinoid receptors and like arsenic (As)-induced apoptosis was preceded by the rapid activation of a caspase-3-like enzymatic activity as indicated by the increase of DEVD-pNA hydrolytic activity, by the processing of procaspase-3 protein and by the cleavage of poly(ADP-ribose) polymerase (PARP).	Arsenic	87-94	caspase 3	Homo sapiens	277-289
10374879-3	1999	This apoptosis did not require the activation of classical retinoid receptors and like arsenic (As)-induced apoptosis was preceded by the rapid activation of a caspase-3-like enzymatic activity as indicated by the increase of DEVD-pNA hydrolytic activity, by the processing of procaspase-3 protein and by the cleavage of poly(ADP-ribose) polymerase (PARP).	Arsenic	87-94	poly(ADP-ribose) polymerase 1	Homo sapiens	321-348
10374879-3	1999	This apoptosis did not require the activation of classical retinoid receptors and like arsenic (As)-induced apoptosis was preceded by the rapid activation of a caspase-3-like enzymatic activity as indicated by the increase of DEVD-pNA hydrolytic activity, by the processing of procaspase-3 protein and by the cleavage of poly(ADP-ribose) polymerase (PARP).	Arsenic	87-94	poly(ADP-ribose) polymerase 1	Homo sapiens	350-354
10374879-3	1999	This apoptosis did not require the activation of classical retinoid receptors and like arsenic (As)-induced apoptosis was preceded by the rapid activation of a caspase-3-like enzymatic activity as indicated by the increase of DEVD-pNA hydrolytic activity, by the processing of procaspase-3 protein and by the cleavage of poly(ADP-ribose) polymerase (PARP).	Arsenic	96-99	caspase 3	Homo sapiens	160-169
10374879-3	1999	This apoptosis did not require the activation of classical retinoid receptors and like arsenic (As)-induced apoptosis was preceded by the rapid activation of a caspase-3-like enzymatic activity as indicated by the increase of DEVD-pNA hydrolytic activity, by the processing of procaspase-3 protein and by the cleavage of poly(ADP-ribose) polymerase (PARP).	Arsenic	96-99	caspase 3	Homo sapiens	277-289
10374879-3	1999	This apoptosis did not require the activation of classical retinoid receptors and like arsenic (As)-induced apoptosis was preceded by the rapid activation of a caspase-3-like enzymatic activity as indicated by the increase of DEVD-pNA hydrolytic activity, by the processing of procaspase-3 protein and by the cleavage of poly(ADP-ribose) polymerase (PARP).	Arsenic	96-99	poly(ADP-ribose) polymerase 1	Homo sapiens	321-348
10374879-3	1999	This apoptosis did not require the activation of classical retinoid receptors and like arsenic (As)-induced apoptosis was preceded by the rapid activation of a caspase-3-like enzymatic activity as indicated by the increase of DEVD-pNA hydrolytic activity, by the processing of procaspase-3 protein and by the cleavage of poly(ADP-ribose) polymerase (PARP).	Arsenic	96-99	poly(ADP-ribose) polymerase 1	Homo sapiens	350-354
10605884-0	1999	Optimization of the solubilization, extraction and determination of inorganic arsenic [As(III) + (As(V)] in seafood products by acid digestion, solvent extraction and hydride generation atomic absorption spectrometry.	Arsenic	78-85	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	97-103
9935161-3	1999	Anti-sense phosphorothioate oligodeoxynucleotides (AS S-oligos) directed against either CR or TGF-alpha inhibit the proliferation of both cell lines.	Arsenic	51-53	transforming growth factor alpha	Homo sapiens	94-103
9806544-6	1998	Arsenic enhances targeting of PML, BAX and p27KIP1 to NBs and synergizes with PML and IFN to induce cell death.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	30-33
10549161-3	1999	There was increased lipid peroxidation at all doses of arsenic, including the "permissible limit", decrease in glutathione level, superoxide dismutase and glutathione reductase activities, indicating the free-radical-mediated degeneration of brain.	Arsenic	55-62	glutathione-disulfide reductase	Rattus norvegicus	155-176
9846968-6	1998	Consistent with earlier in vitro findings, increases in granulocyte/macrophage colony-stimulating factor (GM-CSF) and TGF-alpha mRNA transcripts were found in the epidermis at clinically normal sites within 10 weeks after arsenic treatment.	Arsenic	222-229	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	56-104
9846968-6	1998	Consistent with earlier in vitro findings, increases in granulocyte/macrophage colony-stimulating factor (GM-CSF) and TGF-alpha mRNA transcripts were found in the epidermis at clinically normal sites within 10 weeks after arsenic treatment.	Arsenic	222-229	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	106-112
9846968-6	1998	Consistent with earlier in vitro findings, increases in granulocyte/macrophage colony-stimulating factor (GM-CSF) and TGF-alpha mRNA transcripts were found in the epidermis at clinically normal sites within 10 weeks after arsenic treatment.	Arsenic	222-229	transforming growth factor alpha	Mus musculus	118-127
9879838-0	1998	Defective IL-2 receptor expression in lymphocytes of patients with arsenic-induced Bowen"s disease.	Arsenic	67-74	interleukin 2 receptor subunit beta	Homo sapiens	10-23
9820195-0	1998	Inhibition of hsp70-1 and hsp70-3 expression disrupts preimplantation embryogenesis and heightens embryo sensitivity to arsenic.	Arsenic	120-127	heat shock protein 1B	Mus musculus	14-21
9820195-0	1998	Inhibition of hsp70-1 and hsp70-3 expression disrupts preimplantation embryogenesis and heightens embryo sensitivity to arsenic.	Arsenic	120-127	heat shock protein 1A	Mus musculus	26-33
9820195-7	1998	Limiting expression of Hsp70-1/3 with 5 microM A070-1/3 also heightened embryo sensitivity to arsenic, resulting in less than 5% in vitro development to blastocyst in the presence of the subtoxic dose of 0.4 microM sodium arsenite.	Arsenic	94-101	heat shock protein 1A	Mus musculus	23-32
9852896-10	1998	Maximal and high-affinity binding sites for IGF-I receptor in the HOCM were greater (P &lt; 0.01 and P &lt; 0.05) than the levels in AS, SA, and TM.	Arsenic	133-135	insulin like growth factor 1 receptor	Homo sapiens	44-58
10667331-1	1999	In HepG2 cells phosphorothioate modified antisense oligonucleotides against a sequence in the Ca2+ binding domain (AS-Ca2+) of type II sPLA2 mRNA restrained IL-6-induced synthesis of sPLA2 protein, sPLA2 mRNA (northern blot), and abolished IL-6 stimulated PGE2 release.	Arsenic	115-117	phospholipase A2 group IIA	Homo sapiens	135-140
10667331-1	1999	In HepG2 cells phosphorothioate modified antisense oligonucleotides against a sequence in the Ca2+ binding domain (AS-Ca2+) of type II sPLA2 mRNA restrained IL-6-induced synthesis of sPLA2 protein, sPLA2 mRNA (northern blot), and abolished IL-6 stimulated PGE2 release.	Arsenic	115-117	interleukin 6	Homo sapiens	157-161
10667331-1	1999	In HepG2 cells phosphorothioate modified antisense oligonucleotides against a sequence in the Ca2+ binding domain (AS-Ca2+) of type II sPLA2 mRNA restrained IL-6-induced synthesis of sPLA2 protein, sPLA2 mRNA (northern blot), and abolished IL-6 stimulated PGE2 release.	Arsenic	115-117	phospholipase A2 group IIA	Homo sapiens	183-188
10667331-1	1999	In HepG2 cells phosphorothioate modified antisense oligonucleotides against a sequence in the Ca2+ binding domain (AS-Ca2+) of type II sPLA2 mRNA restrained IL-6-induced synthesis of sPLA2 protein, sPLA2 mRNA (northern blot), and abolished IL-6 stimulated PGE2 release.	Arsenic	115-117	phospholipase A2 group IIA	Homo sapiens	183-188
10667331-1	1999	In HepG2 cells phosphorothioate modified antisense oligonucleotides against a sequence in the Ca2+ binding domain (AS-Ca2+) of type II sPLA2 mRNA restrained IL-6-induced synthesis of sPLA2 protein, sPLA2 mRNA (northern blot), and abolished IL-6 stimulated PGE2 release.	Arsenic	115-117	interleukin 6	Homo sapiens	240-244
9831507-2	1998	The AsD2 radical was generated in a free-space cell by dc-glow discharge of a gaseous mixture of D2 and He over arsenic powder.	Arsenic	112-119	GATA binding protein 4	Homo sapiens	4-8
9831507-3	1998	Fifty fine and hyperfine components of nine rotational transitions were measured and analyzed by least-squares methods determining the detailed molecular constants of AsD2: the rotational constants, the centrifugal distortion constants, the spin-rotation coupling constant with the centrifugal distortion terms, and the hyperfine coupling constants associated with the arsenic and deuterium nuclei.	Arsenic	369-376	GATA binding protein 4	Homo sapiens	167-171
9844570-5	1998	The concentration of As(V) was calculated by difference (the total inorganic arsenic and As(III)).	Arsenic	77-84	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	21-26
9806544-6	1998	Arsenic enhances targeting of PML, BAX and p27KIP1 to NBs and synergizes with PML and IFN to induce cell death.	Arsenic	0-7	BCL2 associated X, apoptosis regulator	Homo sapiens	35-38
9806544-6	1998	Arsenic enhances targeting of PML, BAX and p27KIP1 to NBs and synergizes with PML and IFN to induce cell death.	Arsenic	0-7	cyclin dependent kinase inhibitor 1B	Homo sapiens	43-50
9806544-6	1998	Arsenic enhances targeting of PML, BAX and p27KIP1 to NBs and synergizes with PML and IFN to induce cell death.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	78-81
9806544-6	1998	Arsenic enhances targeting of PML, BAX and p27KIP1 to NBs and synergizes with PML and IFN to induce cell death.	Arsenic	0-7	interferon alpha 1	Homo sapiens	86-89
9848127-2	1998	In rodent cells, arsenic has been reported to induce aberrant gene expression, including activation of the proto-oncogene c-myc.	Arsenic	17-24	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	107-127
9817078-7	1998	The main findings of this study were the predominantly conjugated hyperbilirubinemia and increased serum ALP activity which were related to the concentration of total arsenic (TAs) in urine, suggesting the presence of cholestasis in As-exposed individuals.	Arsenic	167-174	alkaline phosphatase, placental	Homo sapiens	105-108
9821074-5	1998	The constant expression of bcl-2 i early dysplastic cells of BD and the earliest expression of P53 in the basal cells of perilesional normal skin indicate that the initial step of arsenic-induced carcinogenesis is from the basal germinative cells.	Arsenic	180-187	BCL2 apoptosis regulator	Homo sapiens	27-32
9821074-5	1998	The constant expression of bcl-2 i early dysplastic cells of BD and the earliest expression of P53 in the basal cells of perilesional normal skin indicate that the initial step of arsenic-induced carcinogenesis is from the basal germinative cells.	Arsenic	180-187	tumor protein p53	Homo sapiens	95-98
9784401-0	1998	Human lymphocyte heme oxygenase 1 as a response biomarker to inorganic arsenic.	Arsenic	71-78	heme oxygenase 1	Homo sapiens	17-33
11939045-1	1998	The authors observed the joint effects of arsenic and lead on lipid peroxidation(LPO) in vitro and in vivo.	Arsenic	42-49	lactoperoxidase	Rattus norvegicus	81-84
11939045-6	1998	The results show that there is interaction between As and Pb on LPO of erythrocyte membrane.	Arsenic	51-53	lactoperoxidase	Rattus norvegicus	64-67
9784401-7	1998	We suggest that circulating lymphocyte HO1 levels may be useful in assessing the biological activity of arsenic exposure in vivo under properly controlled conditions of simultaneous urinalysis for arsenic, cadmium, and mercury.	Arsenic	104-111	heme oxygenase 1	Homo sapiens	39-42
9784401-7	1998	We suggest that circulating lymphocyte HO1 levels may be useful in assessing the biological activity of arsenic exposure in vivo under properly controlled conditions of simultaneous urinalysis for arsenic, cadmium, and mercury.	Arsenic	197-204	heme oxygenase 1	Homo sapiens	39-42
9784401-1	1998	We propose the use of human lymphocyte heme oxygenase 1 (HO1) as a biomarker of response to environmental arsenic exposure.	Arsenic	106-113	heme oxygenase 1	Homo sapiens	39-55
9784401-1	1998	We propose the use of human lymphocyte heme oxygenase 1 (HO1) as a biomarker of response to environmental arsenic exposure.	Arsenic	106-113	heme oxygenase 1	Homo sapiens	57-60
10420077-7	1998	The percentages of activated CD41 and CD63 surface antigen expression were significantly increased in the AS+ compared to AS- subjects.	Arsenic	106-109	integrin subunit alpha 2b	Homo sapiens	29-33
9728050-6	1998	Similarly, the transcription factors c-Jun and ATF-2, substrates of JNK and P38, respectively, were markedly phosphorylated in BEAS cells treated with As, Cr, Cu, V, and Zn.	Arsenic	151-153	activating transcription factor 2	Homo sapiens	47-52
9728050-6	1998	Similarly, the transcription factors c-Jun and ATF-2, substrates of JNK and P38, respectively, were markedly phosphorylated in BEAS cells treated with As, Cr, Cu, V, and Zn.	Arsenic	151-153	mitogen-activated protein kinase 8	Homo sapiens	68-71
9728050-6	1998	Similarly, the transcription factors c-Jun and ATF-2, substrates of JNK and P38, respectively, were markedly phosphorylated in BEAS cells treated with As, Cr, Cu, V, and Zn.	Arsenic	151-153	mitogen-activated protein kinase 14	Homo sapiens	76-79
9728050-7	1998	The same acute exposure to As, V, or Zn that activated MAPK was sufficient to induce a subsequent increase in IL-8 protein expression in BEAS cells.	Arsenic	27-29	C-X-C motif chemokine ligand 8	Homo sapiens	110-114
9806419-5	1998	We have measured the dose-response for arsenic inhibition of several purified human DNA repair enzymes, including DNA polymerase beta, DNA ligase I and DNA ligase III and have found that most enzymes, even those with critical SH groups, are very insensitive to As.	Arsenic	39-46	DNA polymerase beta	Homo sapiens	114-133
9728050-4	1998	Activity assays confirmed marked activation of ERK, JNK, and P38 in BEAS cells exposed to As, V, and Zn.	Arsenic	90-92	mitogen-activated protein kinase 8	Homo sapiens	52-55
9728050-4	1998	Activity assays confirmed marked activation of ERK, JNK, and P38 in BEAS cells exposed to As, V, and Zn.	Arsenic	90-92	mitogen-activated protein kinase 14	Homo sapiens	61-64
9728050-6	1998	Similarly, the transcription factors c-Jun and ATF-2, substrates of JNK and P38, respectively, were markedly phosphorylated in BEAS cells treated with As, Cr, Cu, V, and Zn.	Arsenic	151-153	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	37-42
9734658-0	1998	Arsenic induces apoptosis in B-cell leukaemic cell lines in vitro: activation of caspases and down-regulation of Bcl-2 protein.	Arsenic	0-7	BCL2 apoptosis regulator	Homo sapiens	113-118
9734658-6	1998	We concluded that combined activation of the caspases and down-regulation of Bcl-2 could determine the fate of B-cell leukaemic cells in response to arsenic.	Arsenic	149-156	BCL2 apoptosis regulator	Homo sapiens	77-82
9741595-1	1998	The effects of arsenic on the expression of the antioxidant genes encoding superoxide dismutase, catalase, and glutathione S-transferase, as well as the activity of SOD and CAT enzymes, were examined at different developmental stages and in different tissues.	Arsenic	15-22	superoxide dismutase	Zea mays	75-95
9741595-4	1998	Cat1 transcript increased in response to arsenic in developing and germinating embryos and in young leaves.	Arsenic	41-48	catalase isozyme 1	Zea mays	0-4
9741595-5	1998	Conversely, Cat2 increased at low concentrations of arsenic only in germinating embryos.	Arsenic	52-59	catalase isozyme 2	Zea mays	12-16
9741595-6	1998	Cat3 transcript levels increased in response to low concentrations of arsenic only in developing embryos.	Arsenic	70-77	catalase isozyme 3	Zea mays	0-4
9741595-7	1998	Sod3 transcript increased at low concentrations of arsenic in developing, germinating embryos and in leaves.	Arsenic	51-58	superoxide dismutase [Mn] 3.1, mitochondrial	Zea mays	0-4
9741595-8	1998	The cytosolic Sod4 and Sod4A increased in response to arsenic in germinating embryos, while only Sod4 transcript increased in response to arsenic in leaves.	Arsenic	54-61	superoxide dismutase [Cu-Zn] 4AP	Zea mays	14-18
9741595-8	1998	The cytosolic Sod4 and Sod4A increased in response to arsenic in germinating embryos, while only Sod4 transcript increased in response to arsenic in leaves.	Arsenic	54-61	superoxide dismutase [Cu-Zn] 4A	Zea mays	23-28
9741595-8	1998	The cytosolic Sod4 and Sod4A increased in response to arsenic in germinating embryos, while only Sod4 transcript increased in response to arsenic in leaves.	Arsenic	54-61	superoxide dismutase [Cu-Zn] 4AP	Zea mays	23-27
10420077-7	1998	The percentages of activated CD41 and CD63 surface antigen expression were significantly increased in the AS+ compared to AS- subjects.	Arsenic	106-109	CD63 molecule	Homo sapiens	38-42
10420077-7	1998	The percentages of activated CD41 and CD63 surface antigen expression were significantly increased in the AS+ compared to AS- subjects.	Arsenic	106-108	integrin subunit alpha 2b	Homo sapiens	29-33
10420077-7	1998	The percentages of activated CD41 and CD63 surface antigen expression were significantly increased in the AS+ compared to AS- subjects.	Arsenic	106-108	CD63 molecule	Homo sapiens	38-42
9678064-5	1998	In one series of substrates, based on a known hotspot for frameshift mutations in the hypoxanthine-guanine phosphoribosyltransferase gene, in which different length G, A, C or T tracts were flanked by closely similar sequences, an A loop was bound preferentially in the absence of adjacent As and a C loop in the absence of adjacent Cs.	Arsenic	290-292	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	86-132
9703486-6	1998	Arsenic(III) and chromium(VI) each significantly altered both basal and hormone-inducible expression of a model inducible gene, phosphoenolpyruvate carboxykinase (PEPCK), at nonovertly toxic doses in the chick embryo in vivo and rat hepatoma H411E cells in culture.	Arsenic	0-7	phosphoenolpyruvate carboxykinase 1	Gallus gallus	128-161
9703486-6	1998	Arsenic(III) and chromium(VI) each significantly altered both basal and hormone-inducible expression of a model inducible gene, phosphoenolpyruvate carboxykinase (PEPCK), at nonovertly toxic doses in the chick embryo in vivo and rat hepatoma H411E cells in culture.	Arsenic	0-7	phosphoenolpyruvate carboxykinase 1	Gallus gallus	163-168
29710901-2	1998	The structures of the new antimony- and arsenic-containing compounds 2 b and 2 c have been determined-this is the first structural characterization of complexes with mu,eta2 -PE heteroligands from elements of Group 15.	Arsenic	40-47	DNA polymerase iota	Homo sapiens	169-173
9793363-2	1998	METHODS: In this work, considering the high toxicity of low quantity of Arsenic ion, a comparative research has been made in order to determine, by using high level liquid Cromatography (HPCL), the quantity in ppm of As hydro- and acid soluble given by five ionomeric products, in water and in nitric acid concentrated solution.	Arsenic	72-79	2-hydroxyacyl-CoA lyase 1	Homo sapiens	187-191
9578589-6	1998	We found that the carboxy-terminal 10-residue region of peptide A encompassing Arg681-Leu690 (peptide As-10; s, skeletal muscle-type sequence) activated ryanodine binding in a RyR1-specific manner and induced calcium release even more efficiently than the 20-residue peptide A.	Arsenic	102-104	ryanodine receptor 1	Homo sapiens	176-180
9679562-5	1998	AS-ONs directed to the A--&gt;G and C--&gt;T transitions, unique to hGSTP1*C, were more RNAse H-dependent than AS-ONs directed against the translation initiation site, indicating a greater involvement of RNAse H-dependent mRNA cleavage in the mechanism of translational inhibition by AS-ON at the polymorphic site.	Arsenic	0-2	glutathione S-transferase pi 1	Homo sapiens	68-74
9590144-5	1998	Prophylactic G-CSF was given in 57 courses (Group B) as 200 microg/m2/d SC started one day after the completion of HD C/T and continued until the neutrophil recovery was maintained.	Arsenic	20-22	colony stimulating factor 3	Homo sapiens	13-18
9581013-8	1998	The inorganic As species in serum were bound to proteins, mainly transferrin (about 5-6% of total As in serum).	Arsenic	14-16	transferrin	Homo sapiens	65-76
21644729-6	1998	The accuracy of the ETA-LIF approaches was demonstrated by determining the As and Se content of aqueous reference samples.	Arsenic	75-77	endothelin receptor type A	Homo sapiens	20-23
21644729-6	1998	The accuracy of the ETA-LIF approaches was demonstrated by determining the As and Se content of aqueous reference samples.	Arsenic	75-77	LIF interleukin 6 family cytokine	Homo sapiens	24-27
9568746-4	1998	Currently, the cause of BFD is believed to be artesian drinking water containing a high concentration of arsenic and/or humic substances, although the mechanism of EC destruction is not entirely understood.	Arsenic	105-112	complement factor properdin	Homo sapiens	24-27
9486671-17	1998	Patients with SCC were significantly older at the start of arsenic exposure and had significantly more palmar arsenical keratoses than those without SCC.	Arsenic	59-66	serpin family B member 3	Homo sapiens	14-17
9219559-8	1997	Consistent with that observed in human keratinocyte cultures, increases in GM-CSF and TGF-alpha mRNA transcripts were found within the epidermis of arsenic-treated mice when compared to controls within 6 weeks of treatment.	Arsenic	148-155	colony stimulating factor 2	Homo sapiens	75-81
9523453-10	1998	The arsenic resistance system transports arsenite [As(III)], alternatively with the ArsB polypeptide functioning as a chemiosmotic efflux transporter or with two polypeptides, ArsB and ArsA, functioning as an ATPase.	Arsenic	4-11	arylsulfatase B	Homo sapiens	84-88
9523453-10	1998	The arsenic resistance system transports arsenite [As(III)], alternatively with the ArsB polypeptide functioning as a chemiosmotic efflux transporter or with two polypeptides, ArsB and ArsA, functioning as an ATPase.	Arsenic	4-11	arylsulfatase B	Homo sapiens	176-180
9523453-10	1998	The arsenic resistance system transports arsenite [As(III)], alternatively with the ArsB polypeptide functioning as a chemiosmotic efflux transporter or with two polypeptides, ArsB and ArsA, functioning as an ATPase.	Arsenic	4-11	arylsulfatase A	Homo sapiens	185-189
9523453-10	1998	The arsenic resistance system transports arsenite [As(III)], alternatively with the ArsB polypeptide functioning as a chemiosmotic efflux transporter or with two polypeptides, ArsB and ArsA, functioning as an ATPase.	Arsenic	4-11	dynein axonemal heavy chain 8	Homo sapiens	209-215
9389570-10	1997	Furthermore, AS-c-myc RNA expression caused a 1.4-fold increased cDDP sensitivity but no change in doxorubicin or vincristine sensitivity in GLC4cDDP/AS cells.	Arsenic	13-15	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	16-21
9314418-10	1997	However, the antihypertensive effect lasted less than 24 hours in losartan-treated SHR compared with 90 days in LNSV-AT1R-AS-treated SHR.	Arsenic	122-124	angiotensin II receptor, type 1a	Rattus norvegicus	117-121
18966874-5	1997	Precision of the proposed method was very good (RSD=2-0.6% at 1-5 ppb) and a relatively good accuracy determined by analysis of certified reference seawater (CASS-1) and seawater samples spiked with an arsenic standard solution, was also obtained.	Arsenic	202-209	BCAR1 scaffold protein, Cas family member	Homo sapiens	158-164
9224745-9	1997	This study showed that significant overexpression of p53 protein was higher in BD with chronic arsenic exposure.	Arsenic	95-102	tumor protein p53	Homo sapiens	53-56
10223623-0	1998	Infrequent p53 mutations in arsenic-related skin lesions.	Arsenic	28-35	tumor protein p53	Homo sapiens	11-14
10223623-6	1998	Accumulation of the p53 protein was detected (with a monoclonal DO-7 antibody) in 78% of the lesions from cases with arsenic exposure.	Arsenic	117-124	tumor protein p53	Homo sapiens	20-23
10223623-7	1998	Two of the six (30%) arsenic-related premalignant lesions and in addition one UV related carcinoma in situ lesion were clearly and repeatedly positive when p53 exons 5 to 8 were screened by a nonradioactive single-strand conformation polymorphism (SSCP) analysis.	Arsenic	21-28	tumor protein p53	Homo sapiens	156-159
10223623-10	1998	Our results suggest that the frequent accumulation of p53 protein in arsenic-related skin lesions is not due to p53 mutations.	Arsenic	69-76	tumor protein p53	Homo sapiens	54-57
9434882-7	1997	In addition, we transfected Jurkat cells and human lymphocytes with wild-type and mutated p53 genes; lymphocytes and Jurkat cells that received the mutated p53 showed increased sensitivity to arsenic cytotoxicity.	Arsenic	192-199	tumor protein p53	Homo sapiens	90-93
9434882-7	1997	In addition, we transfected Jurkat cells and human lymphocytes with wild-type and mutated p53 genes; lymphocytes and Jurkat cells that received the mutated p53 showed increased sensitivity to arsenic cytotoxicity.	Arsenic	192-199	tumor protein p53	Homo sapiens	156-159
9434882-8	1997	Data obtained indicate that arsenic induces p53 expression and that cells with a functional p53 contend better with damage induced by this metalloid.	Arsenic	28-35	tumor protein p53	Homo sapiens	44-47
9434882-8	1997	Data obtained indicate that arsenic induces p53 expression and that cells with a functional p53 contend better with damage induced by this metalloid.	Arsenic	28-35	tumor protein p53	Homo sapiens	92-95
9224745-0	1997	p53 expression and proliferative activity in Bowen"s disease with or without chronic arsenic exposure.	Arsenic	85-92	tumor protein p53	Homo sapiens	0-3
9234670-0	1997	Isolation of three contiguous genes, ACR1, ACR2 and ACR3, involved in resistance to arsenic compounds in the yeast Saccharomyces cerevisiae.	Arsenic	84-91	Arr1p	Saccharomyces cerevisiae S288C	37-41
9234670-0	1997	Isolation of three contiguous genes, ACR1, ACR2 and ACR3, involved in resistance to arsenic compounds in the yeast Saccharomyces cerevisiae.	Arsenic	84-91	Arr2p	Saccharomyces cerevisiae S288C	43-47
9234670-0	1997	Isolation of three contiguous genes, ACR1, ACR2 and ACR3, involved in resistance to arsenic compounds in the yeast Saccharomyces cerevisiae.	Arsenic	84-91	Arr3p	Saccharomyces cerevisiae S288C	52-56
9219559-8	1997	Consistent with that observed in human keratinocyte cultures, increases in GM-CSF and TGF-alpha mRNA transcripts were found within the epidermis of arsenic-treated mice when compared to controls within 6 weeks of treatment.	Arsenic	148-155	transforming growth factor alpha	Homo sapiens	86-95
9219564-0	1997	Arsenic alters cytosine methylation patterns of the promoter of the tumor suppressor gene p53 in human lung cells: a model for a mechanism of carcinogenesis.	Arsenic	0-7	tumor protein p53	Homo sapiens	90-93
9088000-9	1997	In situ hybridization experiments using an [35S]-labeled antisense MR probe showed that hippocampal MR mRNA levels were increased in MR-AS-treated rats.	Arsenic	136-138	nuclear receptor subfamily 3, group C, member 2	Rattus norvegicus	67-69
10325626-3	1997	Experimental results showed there was a dose-response relationship between arsenic level and iNOS expression (P &lt; 0.05).	Arsenic	75-82	nitric oxide synthase 2, inducible	Mus musculus	93-97
9118521-9	1997	A dose-response study showed inhibition of the increase in HSP 72 with as little as 5 micrograms (1.24 mumol/L) of AS.	Arsenic	115-117	heat shock protein family A (Hsp70) member 1A	Homo sapiens	59-65
9073392-6	1997	Analysis of IL-10 and TNF alpha RNA levels using semiquantitative PCR reveals that AS-101 blocks the transcription of IL-10 mRNA, but does not significantly affect TNF alpha mRNA.	Arsenic	83-85	interleukin 10	Homo sapiens	12-17
9073392-6	1997	Analysis of IL-10 and TNF alpha RNA levels using semiquantitative PCR reveals that AS-101 blocks the transcription of IL-10 mRNA, but does not significantly affect TNF alpha mRNA.	Arsenic	83-85	tumor necrosis factor	Homo sapiens	22-31
9073392-6	1997	Analysis of IL-10 and TNF alpha RNA levels using semiquantitative PCR reveals that AS-101 blocks the transcription of IL-10 mRNA, but does not significantly affect TNF alpha mRNA.	Arsenic	83-85	interleukin 10	Homo sapiens	118-123
9108090-0	1997	Arsenic-induced PML targeting onto nuclear bodies: implications for the treatment of acute promyelocytic leukemia.	Arsenic	0-7	PML nuclear body scaffold	Homo sapiens	16-19
9108090-6	1997	We demonstrate that in non-APL cells, arsenic recruits the nucleoplasmic form of several NB antigens onto NB, but induces the degradation of PML only, identifying a powerful tool to approach NB function.	Arsenic	38-45	PML nuclear body scaffold	Homo sapiens	141-144
9108090-7	1997	In APL cells, arsenic targets PML and PML/RAR alpha onto NB and induces their degradation.	Arsenic	14-21	PML nuclear body scaffold	Homo sapiens	30-33
9108090-7	1997	In APL cells, arsenic targets PML and PML/RAR alpha onto NB and induces their degradation.	Arsenic	14-21	PML nuclear body scaffold	Homo sapiens	38-51
9108090-8	1997	Thus, RA and arsenic target RAR alpha and PML, respectively, but both induce the degradation of the PML/RAR alpha fusion protein, which should contribute to their therapeutic effects.	Arsenic	13-20	retinoic acid receptor alpha	Homo sapiens	28-37
9108090-8	1997	Thus, RA and arsenic target RAR alpha and PML, respectively, but both induce the degradation of the PML/RAR alpha fusion protein, which should contribute to their therapeutic effects.	Arsenic	13-20	PML nuclear body scaffold	Homo sapiens	42-45
9108090-8	1997	Thus, RA and arsenic target RAR alpha and PML, respectively, but both induce the degradation of the PML/RAR alpha fusion protein, which should contribute to their therapeutic effects.	Arsenic	13-20	retinoic acid receptor alpha	Homo sapiens	100-113
9145211-1	1997	The induction and subsequent intracellular distribution of the 72-kDa heat shock (stress) protein (Hsp72) by exposure of cultured human alveolar (L-132) cells to dimethylarsinic acid (DMAA), a main metabolite of inorganic arsenics in mammals, were examined.	Arsenic	222-230	heat shock protein family A (Hsp70) member 1A	Homo sapiens	99-104
9088000-9	1997	In situ hybridization experiments using an [35S]-labeled antisense MR probe showed that hippocampal MR mRNA levels were increased in MR-AS-treated rats.	Arsenic	136-138	nuclear receptor subfamily 3, group C, member 2	Rattus norvegicus	100-102
9088000-9	1997	In situ hybridization experiments using an [35S]-labeled antisense MR probe showed that hippocampal MR mRNA levels were increased in MR-AS-treated rats.	Arsenic	136-138	nuclear receptor subfamily 3, group C, member 2	Rattus norvegicus	100-102
8986606-0	1996	The PML and PML/RARalpha domains: from autoimmunity to molecular oncology and from retinoic acid to arsenic.	Arsenic	100-107	PML nuclear body scaffold	Homo sapiens	4-7
9027627-0	1997	The inhibitory effect of UVB irradiation on the expression of p53 and Ki-67 proteins in arsenic-induced Bowen"s disease.	Arsenic	88-95	tumor protein p53	Homo sapiens	62-65
12321049-0	1997	Arsenic on tap.	Arsenic	0-7	nuclear RNA export factor 1	Homo sapiens	11-14
8986606-0	1996	The PML and PML/RARalpha domains: from autoimmunity to molecular oncology and from retinoic acid to arsenic.	Arsenic	100-107	PML nuclear body scaffold	Homo sapiens	12-15
8986606-0	1996	The PML and PML/RARalpha domains: from autoimmunity to molecular oncology and from retinoic acid to arsenic.	Arsenic	100-107	retinoic acid receptor alpha	Homo sapiens	16-24
8755166-8	1996	Significant suppression of peroxidase expression in the range of 40-80% was seen in the T0 and T1 populations carrying 35S-AS, 35S-Rz and tRNA-Rz constructs.	Arsenic	123-125	lignin-forming anionic peroxidase-like	Nicotiana tabacum	27-37
8917704-5	1996	While a number of cytokine regulatory networks exist in the skin, studies utilizing neutralizing antibodies against the growth factors of interest indicate that inhibition of the arsenic-induced increase in TGF alpha results in a corresponding decrease in the gene expression and secretion of GM-CSF.	Arsenic	179-186	transforming growth factor alpha	Homo sapiens	207-216
8917704-5	1996	While a number of cytokine regulatory networks exist in the skin, studies utilizing neutralizing antibodies against the growth factors of interest indicate that inhibition of the arsenic-induced increase in TGF alpha results in a corresponding decrease in the gene expression and secretion of GM-CSF.	Arsenic	179-186	colony stimulating factor 2	Homo sapiens	293-299
9984843-0	1996	Electrical transport properties of semimetallic GdX single crystals (X=P, As, Sb, and Bi).	Arsenic	74-76	ubiquitin like 4A	Homo sapiens	48-51
8931876-0	1996	Arsenic induces interleukin-8 expression in cultured keratinocytes.	Arsenic	0-7	C-X-C motif chemokine ligand 8	Homo sapiens	16-29
8884985-3	1996	In the present studies, we demonstrate that increases in AP-1 DNA binding activity, as well as c-jun and c-fos mRNA levels, occur in human keratinocytes in response to diverse dermatotoxic chemicals, including phenol and arsenic as well as phorbol ester, the latter employed as a positive control.	Arsenic	221-228	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	57-61
8884985-3	1996	In the present studies, we demonstrate that increases in AP-1 DNA binding activity, as well as c-jun and c-fos mRNA levels, occur in human keratinocytes in response to diverse dermatotoxic chemicals, including phenol and arsenic as well as phorbol ester, the latter employed as a positive control.	Arsenic	221-228	PYD and CARD domain containing	Homo sapiens	92-96
11666872-4	1996	For the series (CH(3))(3)As, (CH(3))(2)AsF, CH(3)AsF(2), and AsF(3), both As-C and As-F bond lengths are shortened with increasing numbers of F atoms, but the angles CAsF and FAsF are almost invariant.	Arsenic	25-27	steroid sulfatase	Homo sapiens	74-78
11666872-4	1996	For the series (CH(3))(3)As, (CH(3))(2)AsF, CH(3)AsF(2), and AsF(3), both As-C and As-F bond lengths are shortened with increasing numbers of F atoms, but the angles CAsF and FAsF are almost invariant.	Arsenic	25-27	arylsulfatase F	Homo sapiens	83-87
8991852-7	1996	The arsenic resistance efflux system transports arsenite [As(III)], alternatively using either a double-polypeptide (ArsA and ArsB) ATPase or a single-polypeptide (ArsB) functioning as a chemiosmotic transporter.	Arsenic	4-11	arylsulfatase A	Homo sapiens	117-121
8991852-7	1996	The arsenic resistance efflux system transports arsenite [As(III)], alternatively using either a double-polypeptide (ArsA and ArsB) ATPase or a single-polypeptide (ArsB) functioning as a chemiosmotic transporter.	Arsenic	4-11	arylsulfatase B	Homo sapiens	126-130
8991852-7	1996	The arsenic resistance efflux system transports arsenite [As(III)], alternatively using either a double-polypeptide (ArsA and ArsB) ATPase or a single-polypeptide (ArsB) functioning as a chemiosmotic transporter.	Arsenic	4-11	dynein axonemal heavy chain 8	Homo sapiens	132-138
8991852-7	1996	The arsenic resistance efflux system transports arsenite [As(III)], alternatively using either a double-polypeptide (ArsA and ArsB) ATPase or a single-polypeptide (ArsB) functioning as a chemiosmotic transporter.	Arsenic	4-11	arylsulfatase B	Homo sapiens	164-168
8991852-8	1996	The third gene in the arsenic resistance system, arsC, encodes an enzyme that converts intracellular arsenate [As(V)] to arsenite [As(III)], the substrate of the efflux system.	Arsenic	22-29	steroid sulfatase	Homo sapiens	49-53
8949908-2	1996	Arsenic also interferes with the activities of several enzymes of the heme biosynthesis pathway, such as aminolevulinate synthase (ALA-S), porphobilinogen deaminase (PBGD), uroporphyrinogen III synthase (Uro III S), uroporphyrinogen decarboxylase (URO-D), coproporphyrinogen oxidase (COPRO-O), ferrochelatase and heme oxygenase (H-O).	Arsenic	0-7	5'-aminolevulinate synthase 1	Homo sapiens	131-136
8949908-2	1996	Arsenic also interferes with the activities of several enzymes of the heme biosynthesis pathway, such as aminolevulinate synthase (ALA-S), porphobilinogen deaminase (PBGD), uroporphyrinogen III synthase (Uro III S), uroporphyrinogen decarboxylase (URO-D), coproporphyrinogen oxidase (COPRO-O), ferrochelatase and heme oxygenase (H-O).	Arsenic	0-7	hydroxymethylbilane synthase	Homo sapiens	139-164
8949908-2	1996	Arsenic also interferes with the activities of several enzymes of the heme biosynthesis pathway, such as aminolevulinate synthase (ALA-S), porphobilinogen deaminase (PBGD), uroporphyrinogen III synthase (Uro III S), uroporphyrinogen decarboxylase (URO-D), coproporphyrinogen oxidase (COPRO-O), ferrochelatase and heme oxygenase (H-O).	Arsenic	0-7	hydroxymethylbilane synthase	Homo sapiens	166-170
8949908-2	1996	Arsenic also interferes with the activities of several enzymes of the heme biosynthesis pathway, such as aminolevulinate synthase (ALA-S), porphobilinogen deaminase (PBGD), uroporphyrinogen III synthase (Uro III S), uroporphyrinogen decarboxylase (URO-D), coproporphyrinogen oxidase (COPRO-O), ferrochelatase and heme oxygenase (H-O).	Arsenic	0-7	uroporphyrinogen III synthase	Homo sapiens	173-202
8949908-2	1996	Arsenic also interferes with the activities of several enzymes of the heme biosynthesis pathway, such as aminolevulinate synthase (ALA-S), porphobilinogen deaminase (PBGD), uroporphyrinogen III synthase (Uro III S), uroporphyrinogen decarboxylase (URO-D), coproporphyrinogen oxidase (COPRO-O), ferrochelatase and heme oxygenase (H-O).	Arsenic	0-7	uroporphyrinogen III synthase	Homo sapiens	204-213
8949908-2	1996	Arsenic also interferes with the activities of several enzymes of the heme biosynthesis pathway, such as aminolevulinate synthase (ALA-S), porphobilinogen deaminase (PBGD), uroporphyrinogen III synthase (Uro III S), uroporphyrinogen decarboxylase (URO-D), coproporphyrinogen oxidase (COPRO-O), ferrochelatase and heme oxygenase (H-O).	Arsenic	0-7	uroporphyrinogen decarboxylase	Homo sapiens	216-246
8949908-2	1996	Arsenic also interferes with the activities of several enzymes of the heme biosynthesis pathway, such as aminolevulinate synthase (ALA-S), porphobilinogen deaminase (PBGD), uroporphyrinogen III synthase (Uro III S), uroporphyrinogen decarboxylase (URO-D), coproporphyrinogen oxidase (COPRO-O), ferrochelatase and heme oxygenase (H-O).	Arsenic	0-7	uroporphyrinogen decarboxylase	Homo sapiens	248-253
8949908-2	1996	Arsenic also interferes with the activities of several enzymes of the heme biosynthesis pathway, such as aminolevulinate synthase (ALA-S), porphobilinogen deaminase (PBGD), uroporphyrinogen III synthase (Uro III S), uroporphyrinogen decarboxylase (URO-D), coproporphyrinogen oxidase (COPRO-O), ferrochelatase and heme oxygenase (H-O).	Arsenic	0-7	coproporphyrinogen oxidase	Homo sapiens	256-282
8949908-2	1996	Arsenic also interferes with the activities of several enzymes of the heme biosynthesis pathway, such as aminolevulinate synthase (ALA-S), porphobilinogen deaminase (PBGD), uroporphyrinogen III synthase (Uro III S), uroporphyrinogen decarboxylase (URO-D), coproporphyrinogen oxidase (COPRO-O), ferrochelatase and heme oxygenase (H-O).	Arsenic	0-7	ferrochelatase	Homo sapiens	294-308
8755166-14	1996	Although peroxidase levels were significantly reduced in transgenic plants carrying 35S-AS, 35S-Rz and tRNA-Rz constructs, no significant difference in lignin levels was observed.	Arsenic	88-90	lignin-forming anionic peroxidase-like	Nicotiana tabacum	9-19
8658531-8	1996	ICR conceptuses were more sensitive than CD1s with regard to perturbation in embryonic growth by both forms of arsenic.	Arsenic	111-118	CD1 antigen complex	Mus musculus	41-44
8902524-0	1996	Arsenic induces oxidant stress and NF-kappa B activation in cultured aortic endothelial cells.	Arsenic	0-7	nuclear factor kappa B subunit 1	Homo sapiens	35-45
8905098-10	1996	The arsenic resistance efflux system transports arsenite, using alternatively either a two-component (ArsA and ArsB) ATPase or a single polypeptide (ArsB) functioning as a chemiosmotic transporter.	Arsenic	4-11	arylsulfatase A	Homo sapiens	102-106
8905098-10	1996	The arsenic resistance efflux system transports arsenite, using alternatively either a two-component (ArsA and ArsB) ATPase or a single polypeptide (ArsB) functioning as a chemiosmotic transporter.	Arsenic	4-11	arylsulfatase B	Homo sapiens	111-115
8905098-10	1996	The arsenic resistance efflux system transports arsenite, using alternatively either a two-component (ArsA and ArsB) ATPase or a single polypeptide (ArsB) functioning as a chemiosmotic transporter.	Arsenic	4-11	arylsulfatase B	Homo sapiens	149-153
8905098-11	1996	The third gene in the arsenic resistance system, arsC, encodes an enzyme that converts intracellular arsenate [As (V)] to arsenite [As (III)], the substrate of the efflux system.	Arsenic	22-29	steroid sulfatase	Homo sapiens	49-53
8987103-4	1996	Insulin (INS) concentrations measured by RIA-INS test were highest in the colostrum (701 microU/mL as 100%) of the does, and in the blood (82 microU/mL) of newborn rabbits during the first day postpartum.	Arsenic	31-33	insulin	Oryctolagus cuniculus	0-7
8597097-7	1995	Treatment of human keratinocyte cultures with arsenic, a human skin carcinogen, resulted in a unique cytokine profile characterized by induction of growth factors, including transforming growth factor-alpha and granulocyte-macrophage colony stimulating factor.	Arsenic	46-53	colony stimulating factor 2	Homo sapiens	211-259
8676296-7	1995	The best accuracy was obtained with the combined formula F12 ([(DSc x DAPc x DT x 0.523) + (DT x AS)]/2).	Arsenic	97-99	coagulation factor XII	Homo sapiens	57-60
8083219-2	1994	Two alleles of the cystatin D gene (CST5), encoding protein variants with either Cys or Arg as residue 26 in their 122-residue polypeptide chains, are present in the population.	Arsenic	92-94	cystatin D	Homo sapiens	19-29
8659090-4	1995	G-6-PD activity was evaluated in the erythrocytes of sheep kept in the region contaminated by heavy metals with mercury dominating among them, and in the same animals after administration of a feed mixture containing Hg, Pb Cd, Zn Cr, Cu, Fe and As (Fig.	Arsenic	246-248	glucose-6-phosphate 1-dehydrogenase	Ovis aries	0-6
7645022-1	1995	Most mammals methylate inorganic arsenic (As) to methylarsonic acid (MMA) and dimethylarsinic acid, which are rapidly excreted in the urine.	Arsenic	33-40	monocyte to macrophage differentiation associated	Homo sapiens	69-72
7882325-4	1995	A dose-response relationship was observed between the long-term arsenic exposure from drinking artesian well water and the incidence of lung cancer, bladder cancer, and cancers of all sites combined after adjustment for age, sex, and cigarette smoking through Cox"s proportional hazards regression analysis.	Arsenic	64-71	cytochrome c oxidase subunit 8A	Homo sapiens	260-263
7776969-6	1995	The mitogenic effect of TGF-beta was abolished in cells cultured in the presence of AS, whereas S had no effect, showing that c-fos is required for TGF beta-induced osteoblast cell growth.	Arsenic	84-86	transforming growth factor, beta 1	Rattus norvegicus	24-32
7776969-6	1995	The mitogenic effect of TGF-beta was abolished in cells cultured in the presence of AS, whereas S had no effect, showing that c-fos is required for TGF beta-induced osteoblast cell growth.	Arsenic	84-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
7776969-6	1995	The mitogenic effect of TGF-beta was abolished in cells cultured in the presence of AS, whereas S had no effect, showing that c-fos is required for TGF beta-induced osteoblast cell growth.	Arsenic	84-86	transforming growth factor, beta 1	Rattus norvegicus	148-156
7982393-9	1994	In vivo exposure to either oxidative form of arsenic decreased basal and lipopolysaccharide (LPS)-induced release of TNF-alpha production by PAM, but did not suppress LPS-induced production of PGE2.	Arsenic	45-52	tumor necrosis factor	Rattus norvegicus	117-126
7954356-4	1994	Interestingly, a silent change at codon 27 of H-ras in one allele was detected in all 4 paraquat manufacturing workers and in 2 of 16 arsenic-related Bowen"s disease patients.	Arsenic	134-141	HRas proto-oncogene, GTPase	Homo sapiens	46-51
8519522-11	1995	The decrease in renal URO-D activity may help to explain the inversion in the coproporphyrin/uroporphyrin ratio previously reported in humans chronically exposed to As; however, there were differences between the urinary porphyrin profiles found in both species.	Arsenic	165-167	uroporphyrinogen decarboxylase	Homo sapiens	22-27
8083219-2	1994	Two alleles of the cystatin D gene (CST5), encoding protein variants with either Cys or Arg as residue 26 in their 122-residue polypeptide chains, are present in the population.	Arsenic	92-94	cystatin D	Homo sapiens	36-40
8195079-4	1994	In this report, we demonstrate that mutations within the periplasmic domain but outside the predicted ChvE binding region can drastically alter the sensitivity of VirA to As.	Arsenic	171-173	two-component VirA-like sensor kinase	Agrobacterium tumefaciens	163-167
8003493-1	1994	Arsenate reductase encoded by Staphylococcus aureus arsenic-resistance plasmid pI258 was overproduced in Escherichia coli and purified.	Arsenic	52-59	Arsenate reductase	Staphylococcus aureus	0-18
8020109-4	1994	By immunostaining and light microscopy the AS-treated neurons appeared smaller, more rounded, and less intensely stained for MAP-2 than the untreated or the MAP-2 sense-treated cultures.	Arsenic	43-45	microtubule-associated protein 2	Rattus norvegicus	125-130
8021910-1	1994	Nineteen patients with essential hypertension on regular treatment with nifedipine tablets 20 mg twice daily and whose DBP was &lt; 95 mmHg on at least two occasions two weeks apart were entered in a double-blind randomised crossover study of three weeks treatment with nifedipine coat core (new formulation) either as 30 mg one daily or as 60 mg once daily dose.	Arsenic	124-126	D-box binding PAR bZIP transcription factor	Homo sapiens	119-122
18965955-7	1994	Complete separation of the five arsenic compounds is achieved on a reversed phase C18 column by using sodium heptanesulfonate as ion pair reagent.	Arsenic	32-39	Bardet-Biedl syndrome 9	Homo sapiens	82-85
8057250-7	1994	In perforated-patch recordings employing cation-selective ionophores, GABAA receptor activation depolarized 123 of 132 cells to membrane potentials as depolarized as -33 mV (mean -50 mV in all 132 cells, +12 mV above resting potential).	Arsenic	148-150	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	70-75
8155694-1	1994	Four maleylated derivatives of goat serum albumin having percent modification as 40%, 46%, 84% and 98% were prepared using varying molar ratio of maleic anhydride over protein.	Arsenic	78-80	albumin	Homo sapiens	42-49
8344231-2	1993	Arsenic and cadmium were found in the environment (air, soil, and household dust, and tap water) as well as in the urine and hair from children.	Arsenic	0-7	nuclear RNA export factor 1	Homo sapiens	86-89
8394790-1	1993	A method has been developed for the determination of inorganic arsenic [As(III) and As(V)] and its organic metabolites (monomethylarsenic and dimethylarsenic) in urine by flow-injection hydride generation atomic absorption spectrometry.	Arsenic	63-70	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	84-89
1299273-6	1992	Addition of CaCl2 or purified SPARC to the Ca(2+)-deficient medium resulted in spreading of the AS and control lines and a reappearance of the altered morphologies.	Arsenic	96-98	secreted protein acidic and cysteine rich	Homo sapiens	30-35
8501052-5	1993	Efflux of arsenic originating as arsenate required the presence of the arsC gene and occurred more rapidly with the addition of arsB.	Arsenic	10-17	arsenate reductase	Staphylococcus aureus	71-75
8501052-5	1993	Efflux of arsenic originating as arsenate required the presence of the arsC gene and occurred more rapidly with the addition of arsB.	Arsenic	10-17	arsenic efflux pump protein	Staphylococcus aureus	128-132
8270282-1	1993	Pseudomonas strain MR1 isolated from the coastal waters of Bay of Bengal was found to resist Hg, As, Cd, Cu, Zn and Pb.	Arsenic	97-99	major histocompatibility complex, class I-related	Homo sapiens	19-22
1409657-0	1992	Reduction of arsenate to arsenite by the ArsC protein of the arsenic resistance operon of Staphylococcus aureus plasmid pI258.	Arsenic	61-68	arsenate reductase	Staphylococcus aureus	41-45
1409657-1	1992	The arsenic resistance operon of Staphylococcus aureus plasmid pI258 consists of three genes, arsR (encoding the repressor regulatory protein), arsB (the determinant of the membrane efflux protein that confers resistance by pumping arsenic from the cells), and arsC (the small gene whose protein product is required for arsenate resistance only, not for arsenite resistance).	Arsenic	4-11	arsenate reductase	Staphylococcus aureus	261-265
1456170-1	1992	Chronic ethanol feeding as 12% or 36% of total calories caused a dose-dependent diminution of diamine oxidase activity in rat liver.	Arsenic	24-26	amine oxidase, copper containing 1	Rattus norvegicus	94-109
1588354-3	1992	The questionnaire responses were obtained in 1979 from the four exposed communities and compared to those of a Wyoming community whose tap water levels of arsenic were less than 0.001 mg/l in 1979.	Arsenic	155-162	nuclear RNA export factor 1	Homo sapiens	135-138
1425931-0	1992	5-HT3 receptor antagonist effects of DAT-582, (R) enantiomer of AS-5370.	Arsenic	64-66	5-hydroxytryptamine receptor 3A	Rattus norvegicus	0-14
1425931-0	1992	5-HT3 receptor antagonist effects of DAT-582, (R) enantiomer of AS-5370.	Arsenic	64-66	solute carrier family 6 member 3	Rattus norvegicus	37-40
1425931-11	1992	These results suggest that DAT-582, the (R) enantiomer of AS-5370, potently and selectively blocks 5-HT3 receptors.	Arsenic	58-60	solute carrier family 6 member 3	Rattus norvegicus	27-30
1335858-6	1992	As arsenic is detoxified by methylation, we suggest that the MTHFR deficiency in this girl might explain the fact that of all family members exposed to arsenic, only she developed severe clinical signs and symptoms of arsenic poisoning.	Arsenic	3-10	methylenetetrahydrofolate reductase	Homo sapiens	61-66
1737056-2	1992	Addition of iron (as 200 micrograms/ml saturated transferrin) or retinoic acid (1 microM) both caused approx.	Arsenic	18-20	transferrin	Homo sapiens	49-60
10001637-0	1992	Identification of the isolated arsenic antisite defect in electron-irradiated gallium arsenide and its relation to the EL2 defect.	Arsenic	31-38	spectrin alpha, erythrocytic 1	Homo sapiens	119-122
1335858-6	1992	As arsenic is detoxified by methylation, we suggest that the MTHFR deficiency in this girl might explain the fact that of all family members exposed to arsenic, only she developed severe clinical signs and symptoms of arsenic poisoning.	Arsenic	152-159	methylenetetrahydrofolate reductase	Homo sapiens	61-66
1596480-12	1992	Also some correlations were found between K, Ca, Zn, Br, Sr, Pb, Ca/Sr, Zn/Cu and Ca/K ratios with some of the variables of the AS in each coronary artery.	Arsenic	128-130	calcium sensing receptor	Homo sapiens	65-84
1578049-3	1992	BAL therapy has been criticized because of its delayed action, its own toxicity and its possible influence on arsenic clearance during hemodialysis.	Arsenic	110-117	poly(ADP-ribose) polymerase family member 9	Homo sapiens	0-3
1808840-3	1991	Chemical (atomic absorption spectrometry, AAS) and physical (electron dispersion spectrometry, EDS) examination of the work environment showed long-term deposition of high levels of arsenic in a cleaning bath.	Arsenic	182-189	FYVE, RhoGEF and PH domain containing 1	Homo sapiens	42-45
2050385-2	1991	In a search for the genotoxic mechanism we have studied the effects of the oxygen-radical-scavenging enzymes superoxide dismutase (SOD) and catalase (CAT) on arsenic-induced SCEs in cultured human lymphocytes.	Arsenic	158-165	catalase	Homo sapiens	150-153
1752205-9	1991	Milk and muscle produced in a metal polluted and not polluted areas were very low in cadmium, lead and arsenic.	Arsenic	103-110	Weaning weight-maternal milk	Bos taurus	0-4
1707002-10	1991	It is concluded that an MBP peptide-specific disease can be induced in three different haplotypes and it is possible that shared structures between the As, Aq and Ar molecules are of importance for the trigger of encephalitogenic T cells with different TcR V elements.	Arsenic	152-154	myelin basic protein	Mus musculus	24-27
1707002-10	1991	It is concluded that an MBP peptide-specific disease can be induced in three different haplotypes and it is possible that shared structures between the As, Aq and Ar molecules are of importance for the trigger of encephalitogenic T cells with different TcR V elements.	Arsenic	152-154	T cell receptor alpha variable 6-3	Mus musculus	253-256
1993145-5	1991	A positive correlation was observed between the development of SCC and the total UVA dosage, the age of the patient at the start of the PUVA treatment and a history of arsenic use.	Arsenic	168-175	serpin family B member 3	Homo sapiens	63-66
2050385-3	1991	The results indicate that SOD and possibly also CAT have a protective effect against arsenic-induced DNA damage.	Arsenic	85-92	catalase	Homo sapiens	48-51
1773747-5	1991	Arm SBP was 62.3 +/- 1.6 mmHg and DBP 35.5 +/- 1.0 mmHg on day 1 in AS and QS.	Arsenic	68-70	D-box binding PAR bZIP transcription factor	Bos taurus	34-37
1897930-10	1991	The low abundance of the high molecular weight form of SCP-2 from hepatoma peroxisomes and the lower amounts of SCP-2 detected in the AS-30D peroxisomes may be related to the accumulation of cholesterol in the cells.	Arsenic	134-136	sterol carrier protein 2	Rattus norvegicus	112-117
2050385-2	1991	In a search for the genotoxic mechanism we have studied the effects of the oxygen-radical-scavenging enzymes superoxide dismutase (SOD) and catalase (CAT) on arsenic-induced SCEs in cultured human lymphocytes.	Arsenic	158-165	catalase	Homo sapiens	140-148
2005667-2	1991	Female balb/c mice injected with arsanilic acid conjugated to a carrier protein (ovalbumin) were shown to produce antibodies (arsenic reactive serum, ARS) reactive with arsanilic acid and sodium arsenite.	Arsenic	126-133	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	81-90
2357455-4	1990	For the most exposed groups, the ranges in the average urinary arsenic speciation pattern were 1-6% As (V), 11-14% As (III), 14-18% MMAA, and 63-70% DMAA.	Arsenic	63-70	metabolism of cobalamin associated A	Homo sapiens	132-136
1700974-3	1990	In addition, inhibitors of protein and RNA synthesis interfere markedly with bacteriolysis, as do ionophores and the ATPase inhibitor DCCD, suggesting the participation of an internal messenger in autolysin activation in the presence of AS-48.	Arsenic	237-239	ATPase	Enterococcus faecalis	117-123
2143602-0	1990	Arsenic as a promoter in the effect of humic substances on plasma prothrombin time in vitro.	Arsenic	0-7	coagulation factor II, thrombin	Homo sapiens	66-77
2148901-4	1990	These results demonstrate that this spa water, despite its high arsenic content, is not toxic and does not interfere with the immune system of healthy mice.	Arsenic	64-71	surfactant associated protein A1	Mus musculus	36-39
2169719-10	1990	The efficacy of BAL, DMPS, and DMSA in reducing the tissue content of arsenic following acute As2O3 poisoning was investigated in mice (n = 6/group) and guinea pigs (n = 3-4/group).	Arsenic	70-77	desmoglein 3	Mus musculus	16-19
33774247-6	2021	The arsenic and trace metals released via oxidation of the sulfide phases (particularly Fe sulfides) were almost entirely sequestered by the Fe(III) (oxyhydr)oxides, but acidification during the oxidation stage of the incubation resulted in the pH-dependent release of the As and trace metals (Co, Cu, Ni) (especially in the Fe-rich/organic-low soil).	Arsenic	4-11	general transcription factor IIE subunit 1	Homo sapiens	141-148
33768354-7	2021	These adverse health effects are in part associated with the production of methylated trivalent arsenic species, methylarsonous acid (MAsIII) and dimethylarsinous acid (DMAsIII), during AS3MT-catalyzed methylation of iAs.	Arsenic	96-103	arsenite methyltransferase	Homo sapiens	186-191
33033900-4	2021	However, it stays unclear regarding how the mechanism of MEG3 regulates arsenic-induced apoptosis.	Arsenic	72-79	maternally expressed 3	Homo sapiens	57-61
33823236-0	2021	Cooperation between NRF2-mediated transcription and MDIG-dependent epigenetic modifications in arsenic-induced carcinogenesis and cancer stem cells.	Arsenic	95-102	NFE2 like bZIP transcription factor 2	Homo sapiens	20-24
33823236-0	2021	Cooperation between NRF2-mediated transcription and MDIG-dependent epigenetic modifications in arsenic-induced carcinogenesis and cancer stem cells.	Arsenic	95-102	ribosomal oxygenase 2	Homo sapiens	52-56
33823236-3	2021	In this review, we discuss some recent discoveries showing how the transcription factor NRF2 and an epigenetic regulator, MDIG, contribute to the arsenic-induced generation of cancer stem-like cells (CSCs) as determined by applying CRISPR-Cas9 gene editing and chromosome immunoprecipitation followed by DNA sequencing (ChIP-seq).	Arsenic	146-153	NFE2 like bZIP transcription factor 2	Homo sapiens	88-92
33823236-3	2021	In this review, we discuss some recent discoveries showing how the transcription factor NRF2 and an epigenetic regulator, MDIG, contribute to the arsenic-induced generation of cancer stem-like cells (CSCs) as determined by applying CRISPR-Cas9 gene editing and chromosome immunoprecipitation followed by DNA sequencing (ChIP-seq).	Arsenic	146-153	ribosomal oxygenase 2	Homo sapiens	122-126
33774797-0	2021	Arsenic-induced uterine apoptotic damage is protected by ethyl acetate fraction of Camellia sinensis (green tea) via Bcl-2-BAX through NF-kappaB regulations in Wistar rats.	Arsenic	0-7	BCL2, apoptosis regulator	Rattus norvegicus	117-122
33819377-12	2021	CONCLUSIONS: DPP-4Is can alleviate the development of AS in T2DM patients to a certain extent by reducing CIMT.	Arsenic	54-56	dipeptidyl peptidase 4	Homo sapiens	13-18
32890875-0	2021	Arsenic-induced HER2 promotes proliferation, migration and angiogenesis of bladder epithelial cells via activation of multiple signaling pathways in vitro and in vivo.	Arsenic	0-7	erb-b2 receptor tyrosine kinase 2	Homo sapiens	16-20
32890875-3	2021	Human epidermal growth factor receptor 2 (HER2) is an oncogenic factor that is overexpressed in bladder cancer, but its role in the initiation and progression of As-induced bladder cancer has not been elucidated.	Arsenic	162-164	erb-b2 receptor tyrosine kinase 2	Homo sapiens	6-40
32890875-3	2021	Human epidermal growth factor receptor 2 (HER2) is an oncogenic factor that is overexpressed in bladder cancer, but its role in the initiation and progression of As-induced bladder cancer has not been elucidated.	Arsenic	162-164	erb-b2 receptor tyrosine kinase 2	Homo sapiens	42-46
32890875-8	2021	These findings indicate that HER2 mediates the oncogenic effects of As on bladder epithelial cells by activating the MAPK, PI3K/AKT and Src/STAT3 signaling pathways, and is therefore a promising biomarker.	Arsenic	68-70	erb-b2 receptor tyrosine kinase 2	Homo sapiens	29-33
32890875-8	2021	These findings indicate that HER2 mediates the oncogenic effects of As on bladder epithelial cells by activating the MAPK, PI3K/AKT and Src/STAT3 signaling pathways, and is therefore a promising biomarker.	Arsenic	68-70	AKT serine/threonine kinase 1	Homo sapiens	128-131
32890875-8	2021	These findings indicate that HER2 mediates the oncogenic effects of As on bladder epithelial cells by activating the MAPK, PI3K/AKT and Src/STAT3 signaling pathways, and is therefore a promising biomarker.	Arsenic	68-70	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	136-139
32890875-8	2021	These findings indicate that HER2 mediates the oncogenic effects of As on bladder epithelial cells by activating the MAPK, PI3K/AKT and Src/STAT3 signaling pathways, and is therefore a promising biomarker.	Arsenic	68-70	signal transducer and activator of transcription 3	Homo sapiens	140-145
33033900-5	2021	Our focus was to explore the effects of MEG3 on arsenic-induced apoptosis.	Arsenic	48-55	maternally expressed 3	Homo sapiens	40-44
33033900-8	2021	Our results demonstrated that MEG3 expression was positively correlated with the concentration of three arsenic species (inorganic arsenic (iAs), monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA)) (p < 0.05).	Arsenic	104-111	maternally expressed 3	Homo sapiens	30-34
33033900-10	2021	In addition, our experiments confirmed that MEG3 knockdown increased cell viability and arsenic-induced apoptosis, but cell viability decreased after iAs treatment.	Arsenic	88-95	maternally expressed 3	Homo sapiens	44-48
33033900-12	2021	It is further proved that arsenic-induced apoptosis increased after the knockdown of MEG3, which regulates these genes.	Arsenic	26-33	maternally expressed 3	Homo sapiens	85-89
34865739-2	2022	The physico-chemical features of as-prepared samples were evaluated via XRD, FTIR, UV-vis, BET, XPS, FESEM and EDS analysis.	Arsenic	33-35	delta/notch like EGF repeat containing	Homo sapiens	91-94
33034807-1	2021	Biochar derived from food waste was modified with Fe to enhance its adsorption capacity for As(III), which is the most toxic form of As.	Arsenic	92-94	general transcription factor IIE subunit 1	Homo sapiens	50-52
31150806-0	2019	Arsenic inhibited cholesterol efflux of THP-1 macrophages via ROS-mediated ABCA1 hypermethylation.	Arsenic	0-7	ATP binding cassette subfamily A member 1	Homo sapiens	75-80
31150806-4	2019	In the present study, we analyzed the effect of arsenic on oxidative stress, ABCA1 promoter methylation and cholesterol efflux of THP-1 macrophages.	Arsenic	48-55	ATP binding cassette subfamily A member 1	Homo sapiens	77-82
31150806-5	2019	Results showed that arsenic could induce ROS-mediated DNA methyltransferase 1 (DNMT1) transcription and activity up-regulation, causing ABCA1 promoter to be hypermethylated with repressed expression.	Arsenic	20-27	DNA methyltransferase 1	Homo sapiens	54-77
31150806-5	2019	Results showed that arsenic could induce ROS-mediated DNA methyltransferase 1 (DNMT1) transcription and activity up-regulation, causing ABCA1 promoter to be hypermethylated with repressed expression.	Arsenic	20-27	DNA methyltransferase 1	Homo sapiens	79-84
31150806-5	2019	Results showed that arsenic could induce ROS-mediated DNA methyltransferase 1 (DNMT1) transcription and activity up-regulation, causing ABCA1 promoter to be hypermethylated with repressed expression.	Arsenic	20-27	ATP binding cassette subfamily A member 1	Homo sapiens	136-141
31150806-7	2019	Arsenic inhibited cholesterol efflux of THP-1 macrophages, which could be attenuated after pretreatment with NAC or DNMT inhibitor 5-Aza-2"-deoxycytidine, but not with SAM.	Arsenic	0-7	X-linked Kx blood group	Homo sapiens	109-112
31150806-7	2019	Arsenic inhibited cholesterol efflux of THP-1 macrophages, which could be attenuated after pretreatment with NAC or DNMT inhibitor 5-Aza-2"-deoxycytidine, but not with SAM.	Arsenic	0-7	DNA methyltransferase 1	Homo sapiens	116-120
31150806-8	2019	All of the findings suggest that arsenic inhibit cholesterol efflux of THP-1 macrophages via ROS-mediated ABCA1 hypermethylation.	Arsenic	33-40	ATP binding cassette subfamily A member 1	Homo sapiens	106-111
23970802-2	2013	The organic anion transporter coded by the gene SLCO1B1 may transport arsenic species, but its association with arsenic metabolites in human urine has not yet been studied.	Arsenic	70-77	solute carrier organic anion transporter family member 1B1	Homo sapiens	48-55
23970802-2	2013	The organic anion transporter coded by the gene SLCO1B1 may transport arsenic species, but its association with arsenic metabolites in human urine has not yet been studied.	Arsenic	112-119	solute carrier organic anion transporter family member 1B1	Homo sapiens	48-55
23970802-3	2013	The objective of this study is to evaluate associations of urine arsenic metabolites with variants in the candidate gene SLCO1B1 in adults from the Strong Heart Family Study.	Arsenic	65-72	solute carrier organic anion transporter family member 1B1	Homo sapiens	121-128
23970802-4	2013	We estimated associations between % arsenic species biomarker traits and 5 single-nucleotide polymorphisms (SNPs) in the SLCO1B1 gene in 157 participants, assuming additive genetics.	Arsenic	36-43	solute carrier organic anion transporter family member 1B1	Homo sapiens	121-128
23970802-10	2013	Common variants in SLCO1B1 were associated with differences in arsenic metabolites in a preliminary candidate gene study.	Arsenic	63-70	solute carrier organic anion transporter family member 1B1	Homo sapiens	19-26
7843081-6	1994	The arsenic-resistance system of gram-negative bacteria functions as an oxyanion efflux ATPase for arsenite and presumably antimonite.	Arsenic	4-11	dynein axonemal heavy chain 8	Homo sapiens	88-94
34757104-2	2022	The results showed that compared with OP2018-2019, the concentrations of V, Ni, As, Pb, and Cd in PM1 in OP2019-2020 decreased by 61.9%, 31.4%, 49.2%, 25.4%, and 27.1%, respectively.	Arsenic	80-82	transmembrane protein 11	Homo sapiens	98-101
34800529-10	2022	For PC1 (partly reflecting metals such as Pb, As, Cu or Cd), we observed a strongly suggestive positive association with all-cause cardiovascular diseases mortality.	Arsenic	46-48	proprotein convertase subtilisin/kexin type 1	Homo sapiens	4-7
34609586-10	2022	In the exposed group a positive correlation between serum copper, arsenic and serum ICAM and IL8 was found.	Arsenic	66-73	C-X-C motif chemokine ligand 8	Homo sapiens	93-96
34953952-7	2022	However, around 56% groundwater samples were decreases in arsenic concentrations because of increased NO3- levels in these samples in 2020.	Arsenic	58-65	NBL1, DAN family BMP antagonist	Homo sapiens	102-105
34609586-13	2022	CONCLUSION: Occupational exposure to copper and arsenic was associated with ventilatory and radiological impairment, with a corresponding increase in the serum level of ICAM-1 and IL8, which can be used as biomarkers for pulmonary impairment among copper smelter workers.	Arsenic	48-55	intercellular adhesion molecule 1	Homo sapiens	169-175
34609586-13	2022	CONCLUSION: Occupational exposure to copper and arsenic was associated with ventilatory and radiological impairment, with a corresponding increase in the serum level of ICAM-1 and IL8, which can be used as biomarkers for pulmonary impairment among copper smelter workers.	Arsenic	48-55	C-X-C motif chemokine ligand 8	Homo sapiens	180-183
34619203-8	2022	The ratio of As5+/As3+ significantly varied within 1.08-32.5 and the percentages of soluble arsenic in total arsenic varied within 50%-93%, implying that arsenic in TSP of Taiyuan has multiple sources and none of them stably dominated during 2018.	Arsenic	154-161	PDS5 cohesin associated factor B	Homo sapiens	18-21
34741939-4	2022	The followed multi-omics analyses of mice revealed that As exposure inhibited ATP production by decreasing the expression of proteins HK1, and GAPDHS, and the enzymatic activities of PDH and SDH.	Arsenic	56-58	hexokinase 1	Mus musculus	134-137
34953944-0	2022	The role of Fas-FasL-FADD signaling pathway in arsenic-mediated neuronal apoptosis in vivo and in vitro.	Arsenic	47-54	Fas ligand	Homo sapiens	16-20
34953944-0	2022	The role of Fas-FasL-FADD signaling pathway in arsenic-mediated neuronal apoptosis in vivo and in vitro.	Arsenic	47-54	Fas associated via death domain	Homo sapiens	21-25
34953944-2	2022	Our study aimed to determine the role of the Fas-FasL-FADD signaling pathway in arsenic-mediated neuronal apoptosis.	Arsenic	80-87	Fas ligand	Homo sapiens	49-53
34953944-2	2022	Our study aimed to determine the role of the Fas-FasL-FADD signaling pathway in arsenic-mediated neuronal apoptosis.	Arsenic	80-87	Fas associated via death domain	Homo sapiens	54-58
34953944-5	2022	Mechanistically, arsenic activated the Fas-FasL-FADD signaling pathway and the downstream caspases both in vivo and in vitro.	Arsenic	17-24	Fas ligand	Homo sapiens	43-47
34953944-5	2022	Mechanistically, arsenic activated the Fas-FasL-FADD signaling pathway and the downstream caspases both in vivo and in vitro.	Arsenic	17-24	Fas associated via death domain	Homo sapiens	48-52
34953944-7	2022	Taken together, arsenic induces neurotoxicity by activating the Fas-FasL-FADD signaling pathway.	Arsenic	16-23	Fas ligand	Homo sapiens	68-72
34953944-7	2022	Taken together, arsenic induces neurotoxicity by activating the Fas-FasL-FADD signaling pathway.	Arsenic	16-23	Fas associated via death domain	Homo sapiens	73-77
34810009-10	2022	The impacts of environmental factors such as pH and co-existing ions on As(III)/As(V) removal, have been discussed.	Arsenic	72-74	phenylalanine hydroxylase	Homo sapiens	45-47
34741939-4	2022	The followed multi-omics analyses of mice revealed that As exposure inhibited ATP production by decreasing the expression of proteins HK1, and GAPDHS, and the enzymatic activities of PDH and SDH.	Arsenic	56-58	glyceraldehyde-3-phosphate dehydrogenase, spermatogenic	Mus musculus	143-149
34968464-0	2022	Leptin and adiponectin synthesis and secretion in mature 3T3-L1 adipocytes are differentially down-regulated by arsenic and palmitic acid exposure throughout different stages of adipogenesis.	Arsenic	112-119	leptin	Homo sapiens	0-6
34741939-4	2022	The followed multi-omics analyses of mice revealed that As exposure inhibited ATP production by decreasing the expression of proteins HK1, and GAPDHS, and the enzymatic activities of PDH and SDH.	Arsenic	56-58	serine dehydratase	Mus musculus	191-194
34879548-9	2022	500 mg L-1 SGO prevented the radical over-accumulation produced by AS via the regeneration of AsA and peroxidase (POX) activity rather than GSH regeneration.	Arsenic	67-69	peroxidase-like	Triticum aestivum	102-112
34879548-9	2022	500 mg L-1 SGO prevented the radical over-accumulation produced by AS via the regeneration of AsA and peroxidase (POX) activity rather than GSH regeneration.	Arsenic	67-69	peroxidase-like	Triticum aestivum	114-117
34968464-0	2022	Leptin and adiponectin synthesis and secretion in mature 3T3-L1 adipocytes are differentially down-regulated by arsenic and palmitic acid exposure throughout different stages of adipogenesis.	Arsenic	112-119	adiponectin, C1Q and collagen domain containing	Homo sapiens	11-22
34763015-0	2022	Anthocyanin-mediated arsenic tolerance in plants.	Arsenic	21-28	DDB1 and CUL4 associated factor 7	Homo sapiens	0-11
34920032-0	2022	Ubiquitinated gasdermin D mediates arsenic-induced pyroptosis and hepatic insulin resistance in rat liver.	Arsenic	35-42	gasdermin D	Rattus norvegicus	14-25
34920032-8	2022	In summary, we demonstrated that GSDMD participated in arsenic-induced hepatic IR.	Arsenic	55-62	gasdermin D	Rattus norvegicus	33-38
34798141-0	2022	Corrigendum to "Nrf2 deficiency aggravates the increase in osteoclastogenesis and bone loss induced by inorganic arsenic" (Toxicology and applied pharmacology 367 (2019) 62-70).	Arsenic	113-120	NFE2 like bZIP transcription factor 2	Homo sapiens	16-20
34844335-0	2022	Sea-level-rise-induced flooding drives arsenic release from coastal sediments.	Arsenic	39-46	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	0-3
34953898-0	2022	The mechanism underlying arsenic-induced PD-L1 upregulation in BEAS-2B cells.	Arsenic	25-32	CD274 molecule	Homo sapiens	41-46
34953898-5	2022	More recently our study further showed that arsenic induced PD-L1 up-regulation, inhibited T cell effector function, and enhanced lung tumor formation in the mice.	Arsenic	44-51	CD274 antigen	Mus musculus	60-65
34953898-6	2022	In the current study, using arsenic-induced BEAS-2B transformation as a model system we investigated the mechanism underlying PD-L1 up-regulation by arsenic.	Arsenic	149-156	CD274 antigen	Mus musculus	126-131
34953898-7	2022	Our data suggests that Lnc-DC, a long non-coding RNA, and signal transducer and activator of transcription 3 (STAT3) mediates PD-L1 up-regulation by arsenic.	Arsenic	149-156	WAP four-disulfide core domain 21, pseudogene	Homo sapiens	23-29
34953898-7	2022	Our data suggests that Lnc-DC, a long non-coding RNA, and signal transducer and activator of transcription 3 (STAT3) mediates PD-L1 up-regulation by arsenic.	Arsenic	149-156	signal transducer and activator of transcription 3	Homo sapiens	58-108
34953898-7	2022	Our data suggests that Lnc-DC, a long non-coding RNA, and signal transducer and activator of transcription 3 (STAT3) mediates PD-L1 up-regulation by arsenic.	Arsenic	149-156	signal transducer and activator of transcription 3	Homo sapiens	110-115
34953898-7	2022	Our data suggests that Lnc-DC, a long non-coding RNA, and signal transducer and activator of transcription 3 (STAT3) mediates PD-L1 up-regulation by arsenic.	Arsenic	149-156	CD274 antigen	Mus musculus	126-131
34786856-0	2022	Recent Developments in the Chemistry of Pn(I) (Pn = N, P, As, Sb, Bi) Cations.	Arsenic	58-60	serpin family E member 2	Homo sapiens	40-45
34786856-1	2022	The Group 15 Pn(I) cations (Pn = N, P, As, Sb and Bi), which are isoelectronic with the donor-stabilized carbones, have emerged recently.	Arsenic	39-41	serpin family E member 2	Homo sapiens	13-18
34388870-7	2022	This review collates knowledge regarding the fate of As in multicomponent As-DOM-Fe systems, including ternary complexes involving both Fe and DOM.	Arsenic	53-55	general transcription factor IIE subunit 1	Homo sapiens	81-83
34388870-7	2022	This review collates knowledge regarding the fate of As in multicomponent As-DOM-Fe systems, including ternary complexes involving both Fe and DOM.	Arsenic	53-55	general transcription factor IIE subunit 1	Homo sapiens	136-138
34388870-8	2022	Additionally, the release mechanisms of As from sediments into groundwater in the presence of both Fe and DOM have been discussed.	Arsenic	40-42	general transcription factor IIE subunit 1	Homo sapiens	99-101
34619179-12	2022	Most importantly, we provide here the first evidence of As-associated DNA methylation in relation with gene expression of ATR, ATF7IP, TPM3, UBE2J2.	Arsenic	56-58	ATR serine/threonine kinase	Homo sapiens	122-125
34619179-12	2022	Most importantly, we provide here the first evidence of As-associated DNA methylation in relation with gene expression of ATR, ATF7IP, TPM3, UBE2J2.	Arsenic	56-58	activating transcription factor 7 interacting protein	Homo sapiens	127-133
34619179-12	2022	Most importantly, we provide here the first evidence of As-associated DNA methylation in relation with gene expression of ATR, ATF7IP, TPM3, UBE2J2.	Arsenic	56-58	tropomyosin 3	Homo sapiens	135-139
34619179-12	2022	Most importantly, we provide here the first evidence of As-associated DNA methylation in relation with gene expression of ATR, ATF7IP, TPM3, UBE2J2.	Arsenic	56-58	ubiquitin conjugating enzyme E2 J2	Homo sapiens	141-147
34763015-12	2022	Our analysis proposes that anthocyanin manipulation in crop plants may ensure sustainable crop yield and food safety in the marginal lands prone to arsenic pollution.	Arsenic	148-155	DDB1 and CUL4 associated factor 7	Homo sapiens	27-38
34963605-11	2022	The younger channel belts (<1 ka BP) and old Holocene aquifers below undisturbed floodplain environments deposited during a period with high sea level host groundwater enriched in As.	Arsenic	180-182	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	141-144
34757248-12	2022	CONCLUSION: Exposure to As and Cd was associated with BDNF gene DNA methylation BDNF gene and serum BDNF, respectively.	Arsenic	24-26	brain derived neurotrophic factor	Homo sapiens	54-58
34757248-12	2022	CONCLUSION: Exposure to As and Cd was associated with BDNF gene DNA methylation BDNF gene and serum BDNF, respectively.	Arsenic	24-26	brain derived neurotrophic factor	Homo sapiens	80-84
34757248-12	2022	CONCLUSION: Exposure to As and Cd was associated with BDNF gene DNA methylation BDNF gene and serum BDNF, respectively.	Arsenic	24-26	brain derived neurotrophic factor	Homo sapiens	100-104
34952004-5	2022	Here we investigated a novel regulatory mechanism of CD200R1 expression following exposure to an environmental stressor, arsenic, combining in silico analysis, in vitro, and in vivo experiments, as well as validation in human samples.	Arsenic	121-128	CD200 receptor 1	Homo sapiens	53-60
34952004-6	2022	The in silico analysis and in vitro studies with primary neonatal microglia and BV2 microglia revealed that arsenic demethylates the promoter of a microRNA, miR-129-5p, thereby increasing its expression, which subsequently represses CD200R1 by binding to its 3 - untranslated region and shuttling the CD200R1 mRNA to the cytoplasmic-processing body in mouse microglia.	Arsenic	108-115	CD200 receptor 1	Mus musculus	233-240
34952004-6	2022	The in silico analysis and in vitro studies with primary neonatal microglia and BV2 microglia revealed that arsenic demethylates the promoter of a microRNA, miR-129-5p, thereby increasing its expression, which subsequently represses CD200R1 by binding to its 3 - untranslated region and shuttling the CD200R1 mRNA to the cytoplasmic-processing body in mouse microglia.	Arsenic	108-115	CD200 receptor 1	Mus musculus	301-308
34798142-3	2022	Arsenic exposure leads to oxidation of zinc coordinating cysteine residues, zinc loss and decreased activity of the DNA repair protein poly(ADP)ribose polymerase (PARP)-1.	Arsenic	0-7	damage specific DNA binding protein 1	Mus musculus	116-134
34798142-3	2022	Arsenic exposure leads to oxidation of zinc coordinating cysteine residues, zinc loss and decreased activity of the DNA repair protein poly(ADP)ribose polymerase (PARP)-1.	Arsenic	0-7	poly (ADP-ribose) polymerase family, member 1	Mus musculus	135-170
34798142-4	2022	Because arsenic stimulates NADPH oxidase (NOX) activity leading to generation of reactive oxygen species (ROS), the goal of this study was to investigate the role of NOX in arsenic-induced inhibition of PARP activity and retention of DNA damage.	Arsenic	8-15	poly (ADP-ribose) polymerase family, member 1	Mus musculus	203-207
34798142-4	2022	Because arsenic stimulates NADPH oxidase (NOX) activity leading to generation of reactive oxygen species (ROS), the goal of this study was to investigate the role of NOX in arsenic-induced inhibition of PARP activity and retention of DNA damage.	Arsenic	173-180	poly (ADP-ribose) polymerase family, member 1	Mus musculus	203-207
34798143-0	2022	Up-regulation of PUMA caused the activation of p53 phosphorylation and acetylation, enhancing the interaction between PUMA and Bcl-X and mediating arsenic-induced apoptosis.	Arsenic	147-154	BCL2 binding component 3	Homo sapiens	17-21
34798143-0	2022	Up-regulation of PUMA caused the activation of p53 phosphorylation and acetylation, enhancing the interaction between PUMA and Bcl-X and mediating arsenic-induced apoptosis.	Arsenic	147-154	tumor protein p53	Homo sapiens	47-50
34798143-3	2022	The purpose of this work was to determine whether inorganic arsenic (NaAsO2) and its metabolites influenced the expression of PUMA in vivo and vitro, followed by investigating the mechanisms.	Arsenic	60-67	BCL2 binding component 3	Homo sapiens	126-130
34959015-0	2021	Arsenic causes mitochondrial biogenesis obstacles by inhibiting the AMPK/PGC-1alpha signaling pathway and also induces apoptosis and dysregulated mitophagy in the duck liver.	Arsenic	0-7	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	68-72
34959015-0	2021	Arsenic causes mitochondrial biogenesis obstacles by inhibiting the AMPK/PGC-1alpha signaling pathway and also induces apoptosis and dysregulated mitophagy in the duck liver.	Arsenic	0-7	PPARG coactivator 1 alpha	Homo sapiens	73-83
34959015-6	2021	Furthermore, arsenic-exposure significantly inhibited AMPK/PGC-1alpha-mediated mitochondrial biogenesis, determined by the ultrastructure observation and down-regulation of p-AMPKalpha/AMPKalpha, PGC-1alpha, NRF1, NRF2, TFAM, TFB1M, TFB2M and COX-IV expression levels.	Arsenic	13-20	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	54-58
34959015-6	2021	Furthermore, arsenic-exposure significantly inhibited AMPK/PGC-1alpha-mediated mitochondrial biogenesis, determined by the ultrastructure observation and down-regulation of p-AMPKalpha/AMPKalpha, PGC-1alpha, NRF1, NRF2, TFAM, TFB1M, TFB2M and COX-IV expression levels.	Arsenic	13-20	PPARG coactivator 1 alpha	Homo sapiens	59-69
34959015-6	2021	Furthermore, arsenic-exposure significantly inhibited AMPK/PGC-1alpha-mediated mitochondrial biogenesis, determined by the ultrastructure observation and down-regulation of p-AMPKalpha/AMPKalpha, PGC-1alpha, NRF1, NRF2, TFAM, TFB1M, TFB2M and COX-IV expression levels.	Arsenic	13-20	PPARG coactivator 1 alpha	Homo sapiens	196-206
34959015-6	2021	Furthermore, arsenic-exposure significantly inhibited AMPK/PGC-1alpha-mediated mitochondrial biogenesis, determined by the ultrastructure observation and down-regulation of p-AMPKalpha/AMPKalpha, PGC-1alpha, NRF1, NRF2, TFAM, TFB1M, TFB2M and COX-IV expression levels.	Arsenic	13-20	nuclear respiratory factor 1	Homo sapiens	208-212
34959015-6	2021	Furthermore, arsenic-exposure significantly inhibited AMPK/PGC-1alpha-mediated mitochondrial biogenesis, determined by the ultrastructure observation and down-regulation of p-AMPKalpha/AMPKalpha, PGC-1alpha, NRF1, NRF2, TFAM, TFB1M, TFB2M and COX-IV expression levels.	Arsenic	13-20	NFE2 like bZIP transcription factor 2	Homo sapiens	214-218
34959015-6	2021	Furthermore, arsenic-exposure significantly inhibited AMPK/PGC-1alpha-mediated mitochondrial biogenesis, determined by the ultrastructure observation and down-regulation of p-AMPKalpha/AMPKalpha, PGC-1alpha, NRF1, NRF2, TFAM, TFB1M, TFB2M and COX-IV expression levels.	Arsenic	13-20	transcription factor A, mitochondrial	Homo sapiens	220-224
34863900-5	2022	Strikingly, Atf6 activation in the zebrafish liver by transgenic nAtf6 overexpression, ethanol and arsenic exposure resulted in a distinct CPAT signature for each; with only 34 CPATs differentially expressed in all conditions.	Arsenic	99-106	activating transcription factor 6	Danio rerio	12-16
34959015-6	2021	Furthermore, arsenic-exposure significantly inhibited AMPK/PGC-1alpha-mediated mitochondrial biogenesis, determined by the ultrastructure observation and down-regulation of p-AMPKalpha/AMPKalpha, PGC-1alpha, NRF1, NRF2, TFAM, TFB1M, TFB2M and COX-IV expression levels.	Arsenic	13-20	transcription factor B1, mitochondrial	Homo sapiens	226-231
34959015-6	2021	Furthermore, arsenic-exposure significantly inhibited AMPK/PGC-1alpha-mediated mitochondrial biogenesis, determined by the ultrastructure observation and down-regulation of p-AMPKalpha/AMPKalpha, PGC-1alpha, NRF1, NRF2, TFAM, TFB1M, TFB2M and COX-IV expression levels.	Arsenic	13-20	transcription factor B2, mitochondrial	Homo sapiens	233-238
34897760-8	2022	The study demonstrates for the first time kisspeptin"s potential to mitigate the biochemical and histotoxic effects of arsenic on male reproductive system.	Arsenic	119-126	KiSS-1 metastasis-suppressor	Mus musculus	42-52
34959015-6	2021	Furthermore, arsenic-exposure significantly inhibited AMPK/PGC-1alpha-mediated mitochondrial biogenesis, determined by the ultrastructure observation and down-regulation of p-AMPKalpha/AMPKalpha, PGC-1alpha, NRF1, NRF2, TFAM, TFB1M, TFB2M and COX-IV expression levels.	Arsenic	13-20	cytochrome c oxidase subunit 4I1	Homo sapiens	243-249
34959015-7	2021	Besides, arsenic-treatment obviously increased the levels of mitophagy (PINK1, Parkin, LC3, P62) and pro-apoptotic (Caspase-3, Caspase-9, Cleaved Caspase-3, Cytc, Bax, P53) indexes, and simultaneously resulted in reductions in anti-apoptosis index (Bcl-2).	Arsenic	9-16	PTEN induced kinase 1	Homo sapiens	72-77
34959015-7	2021	Besides, arsenic-treatment obviously increased the levels of mitophagy (PINK1, Parkin, LC3, P62) and pro-apoptotic (Caspase-3, Caspase-9, Cleaved Caspase-3, Cytc, Bax, P53) indexes, and simultaneously resulted in reductions in anti-apoptosis index (Bcl-2).	Arsenic	9-16	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	87-90
34959015-7	2021	Besides, arsenic-treatment obviously increased the levels of mitophagy (PINK1, Parkin, LC3, P62) and pro-apoptotic (Caspase-3, Caspase-9, Cleaved Caspase-3, Cytc, Bax, P53) indexes, and simultaneously resulted in reductions in anti-apoptosis index (Bcl-2).	Arsenic	9-16	nucleoporin 62	Homo sapiens	92-95
34959015-7	2021	Besides, arsenic-treatment obviously increased the levels of mitophagy (PINK1, Parkin, LC3, P62) and pro-apoptotic (Caspase-3, Caspase-9, Cleaved Caspase-3, Cytc, Bax, P53) indexes, and simultaneously resulted in reductions in anti-apoptosis index (Bcl-2).	Arsenic	9-16	caspase 3	Homo sapiens	116-125
34959015-7	2021	Besides, arsenic-treatment obviously increased the levels of mitophagy (PINK1, Parkin, LC3, P62) and pro-apoptotic (Caspase-3, Caspase-9, Cleaved Caspase-3, Cytc, Bax, P53) indexes, and simultaneously resulted in reductions in anti-apoptosis index (Bcl-2).	Arsenic	9-16	caspase 9	Homo sapiens	127-136
34959015-7	2021	Besides, arsenic-treatment obviously increased the levels of mitophagy (PINK1, Parkin, LC3, P62) and pro-apoptotic (Caspase-3, Caspase-9, Cleaved Caspase-3, Cytc, Bax, P53) indexes, and simultaneously resulted in reductions in anti-apoptosis index (Bcl-2).	Arsenic	9-16	BCL2 associated X, apoptosis regulator	Homo sapiens	163-166
34959015-7	2021	Besides, arsenic-treatment obviously increased the levels of mitophagy (PINK1, Parkin, LC3, P62) and pro-apoptotic (Caspase-3, Caspase-9, Cleaved Caspase-3, Cytc, Bax, P53) indexes, and simultaneously resulted in reductions in anti-apoptosis index (Bcl-2).	Arsenic	9-16	tumor protein p53	Homo sapiens	168-171
34959015-7	2021	Besides, arsenic-treatment obviously increased the levels of mitophagy (PINK1, Parkin, LC3, P62) and pro-apoptotic (Caspase-3, Caspase-9, Cleaved Caspase-3, Cytc, Bax, P53) indexes, and simultaneously resulted in reductions in anti-apoptosis index (Bcl-2).	Arsenic	9-16	BCL2 apoptosis regulator	Homo sapiens	249-254
34673408-7	2021	Despite no difference on Tet1, Tet2 and Tet3 expression, TET activity was suppressed in As-exposed fetal brain.	Arsenic	88-90	tet methylcytosine dioxygenase 2	Homo sapiens	31-35
34673408-7	2021	Despite no difference on Tet1, Tet2 and Tet3 expression, TET activity was suppressed in As-exposed fetal brain.	Arsenic	88-90	tet methylcytosine dioxygenase 3	Homo sapiens	40-44
34954307-0	2022	Corrigendum to "SFPQ is involved in regulating arsenic-induced oxidative stress by interacting with the miRNA-induced silencing complexes" (Environ.	Arsenic	47-54	splicing factor proline and glutamine rich	Homo sapiens	16-20
34405393-7	2021	In conclusion, the present long-term follow-up study further confirmed the high cure probability of ATRA plus oral arsenic as front-line therapy for non-high-risk APL and showed that the PML-RARA transcript level at the end of induction therapy was associated with relapse.	Arsenic	115-122	retinoic acid receptor alpha	Homo sapiens	191-195
34783632-3	2021	This work was designed to elucidate the biological functions of miR-512-3p in the pathological process of AS and probe into the underlying molecular mechanism.	Arsenic	106-108	microRNA 5123	Mus musculus	64-74
33904385-3	2021	And we found that positive expression of VEGF and VEGF receptor 2 (VEGFR2) was observed by Immunohistochemical staining in the epididymal tissues of arsenic-exposed rats.	Arsenic	149-156	vascular endothelial growth factor A	Rattus norvegicus	41-45
33904385-3	2021	And we found that positive expression of VEGF and VEGF receptor 2 (VEGFR2) was observed by Immunohistochemical staining in the epididymal tissues of arsenic-exposed rats.	Arsenic	149-156	kinase insert domain receptor	Rattus norvegicus	67-73
34217924-8	2021	Moreover, the contribution of PMS5 to arsenic (3+, 5+) bioprocessing under oligotrophic conditions was confirmed in fixed-bed reactors fed with the TDE of the gold factory (R1) and synthetic water containing As5+ (R2).	Arsenic	38-45	PMS1 homolog 2, mismatch repair system component pseudogene 3	Homo sapiens	30-34
34385035-6	2021	In this regard, arsenic interference with endocrine system, leptin and adiponectin hormones as well as thermogenesis is more evidence.	Arsenic	16-23	leptin	Homo sapiens	60-66
34217924-7	2021	PMS5 was also found to cause the volatilization and biotransformation of arsenic oxyanions through their oxidation and reduction.	Arsenic	73-80	PMS1 homolog 2, mismatch repair system component pseudogene 3	Homo sapiens	0-4
34085563-10	2021	Redox imbalance and functional amendment in epididymis have been observed with arsenic revelation as evidenced by altered genomic appearance of SOD, GST, catalase, Ddx3Y, VEGF and VEGFR2.	Arsenic	79-86	superoxide dismutase 1	Homo sapiens	144-147
34085563-10	2021	Redox imbalance and functional amendment in epididymis have been observed with arsenic revelation as evidenced by altered genomic appearance of SOD, GST, catalase, Ddx3Y, VEGF and VEGFR2.	Arsenic	79-86	catalase	Homo sapiens	154-162
34085563-10	2021	Redox imbalance and functional amendment in epididymis have been observed with arsenic revelation as evidenced by altered genomic appearance of SOD, GST, catalase, Ddx3Y, VEGF and VEGFR2.	Arsenic	79-86	DEAD-box helicase 3 Y-linked	Homo sapiens	164-169
34085563-10	2021	Redox imbalance and functional amendment in epididymis have been observed with arsenic revelation as evidenced by altered genomic appearance of SOD, GST, catalase, Ddx3Y, VEGF and VEGFR2.	Arsenic	79-86	vascular endothelial growth factor A	Homo sapiens	171-175
34085563-10	2021	Redox imbalance and functional amendment in epididymis have been observed with arsenic revelation as evidenced by altered genomic appearance of SOD, GST, catalase, Ddx3Y, VEGF and VEGFR2.	Arsenic	79-86	kinase insert domain receptor	Homo sapiens	180-186
34085585-6	2021	Our study provides some limited evidence that Ginkgo biloba L. can increase the expression of NF-AT1 by downregulating the level of miR-155-5p, alleviating immunological dysfunction, and decreasing the expression of EMT biomarkers, thus indirectly improving arsenic-induced skin damage.	Arsenic	258-265	nuclear factor of activated T cells 2	Homo sapiens	94-100
34385035-6	2021	In this regard, arsenic interference with endocrine system, leptin and adiponectin hormones as well as thermogenesis is more evidence.	Arsenic	16-23	adiponectin, C1Q and collagen domain containing	Homo sapiens	71-82
34673086-0	2021	Arsenic-induced lung inflammation and fibrosis in a rat model: Contribution of the HMGB1/RAGE, PI3K/AKT, and TGF-beta1/SMAD pathways.	Arsenic	0-7	AKT serine/threonine kinase 1	Rattus norvegicus	100-103
34624384-3	2021	We investigated the correlation of DNA methylation changes in APOE and ACKR3 genes in MS patients and the possible association with blood concentration of arsenic (As), cadmium (Cd) and lead (Pb) as major heavy metal pollutants.	Arsenic	155-162	apolipoprotein E	Homo sapiens	62-66
34624384-3	2021	We investigated the correlation of DNA methylation changes in APOE and ACKR3 genes in MS patients and the possible association with blood concentration of arsenic (As), cadmium (Cd) and lead (Pb) as major heavy metal pollutants.	Arsenic	164-166	apolipoprotein E	Homo sapiens	62-66
34634286-12	2021	These data suggest that arsenic inhalation during lung development can decrease CC16 expression leading to functional and structural alterations in the adult lung.	Arsenic	24-31	secretoglobin, family 1A, member 1 (uteroglobin)	Mus musculus	80-84
34673086-0	2021	Arsenic-induced lung inflammation and fibrosis in a rat model: Contribution of the HMGB1/RAGE, PI3K/AKT, and TGF-beta1/SMAD pathways.	Arsenic	0-7	transforming growth factor, beta 1	Rattus norvegicus	109-118
34730462-0	2021	Polymorphisms of the AS3MT gene are associated with arsenic methylation capacity and damage to the P21 gene in arsenic trioxide plant workers.	Arsenic	52-59	arsenite methyltransferase	Homo sapiens	21-26
34730462-2	2021	The arsenite methyltransferase (AS3MT) gene plays a key role in As metabolism.	Arsenic	64-66	arsenite methyltransferase	Homo sapiens	32-37
34673086-4	2021	The aim of this study was to investigate whether HMGB1/RAGE and its activated downstream pathways are involved in the process of arsenic exposure-induced lung injury in rats.	Arsenic	129-136	high mobility group box 1	Rattus norvegicus	49-54
34730462-10	2021	The results showed that DNA damage in P21 gene fragments was greater in those individuals exposed to high levels of As.	Arsenic	116-118	H3 histone pseudogene 16	Homo sapiens	38-41
34673086-4	2021	The aim of this study was to investigate whether HMGB1/RAGE and its activated downstream pathways are involved in the process of arsenic exposure-induced lung injury in rats.	Arsenic	129-136	advanced glycosylation end product-specific receptor	Rattus norvegicus	55-59
34730462-15	2021	Our results suggest that rs1191454 and rs7085104 in the AS3MT gene affect the As-induced DNA damage by altering individual metabolic efficiency.	Arsenic	78-80	arsenite methyltransferase	Homo sapiens	56-61
34673086-8	2021	Furthermore, the results confirmed that the expressions of HMGB1 and RAGE in lung tissue were enhanced, and protein expression of PI3K, p-AKT, IL-1beta, IL-18, and MMP-9 was increased in lung homogenates from the arsenic-exposed groups compared to the control group.	Arsenic	213-220	high mobility group box 1	Rattus norvegicus	59-64
34673086-8	2021	Furthermore, the results confirmed that the expressions of HMGB1 and RAGE in lung tissue were enhanced, and protein expression of PI3K, p-AKT, IL-1beta, IL-18, and MMP-9 was increased in lung homogenates from the arsenic-exposed groups compared to the control group.	Arsenic	213-220	advanced glycosylation end product-specific receptor	Rattus norvegicus	69-73
34673086-8	2021	Furthermore, the results confirmed that the expressions of HMGB1 and RAGE in lung tissue were enhanced, and protein expression of PI3K, p-AKT, IL-1beta, IL-18, and MMP-9 was increased in lung homogenates from the arsenic-exposed groups compared to the control group.	Arsenic	213-220	AKT serine/threonine kinase 1	Rattus norvegicus	138-141
34673086-8	2021	Furthermore, the results confirmed that the expressions of HMGB1 and RAGE in lung tissue were enhanced, and protein expression of PI3K, p-AKT, IL-1beta, IL-18, and MMP-9 was increased in lung homogenates from the arsenic-exposed groups compared to the control group.	Arsenic	213-220	interleukin 1 alpha	Rattus norvegicus	143-151
34673086-8	2021	Furthermore, the results confirmed that the expressions of HMGB1 and RAGE in lung tissue were enhanced, and protein expression of PI3K, p-AKT, IL-1beta, IL-18, and MMP-9 was increased in lung homogenates from the arsenic-exposed groups compared to the control group.	Arsenic	213-220	interleukin 18	Rattus norvegicus	153-158
34673086-8	2021	Furthermore, the results confirmed that the expressions of HMGB1 and RAGE in lung tissue were enhanced, and protein expression of PI3K, p-AKT, IL-1beta, IL-18, and MMP-9 was increased in lung homogenates from the arsenic-exposed groups compared to the control group.	Arsenic	213-220	matrix metallopeptidase 9	Rattus norvegicus	164-169
34673086-10	2021	Moreover, a significant increase in key fibrosis factors, including TGF-beta1, p-SMAD2, p-SMAD3, and SMAD4 was observed in the lung homogenates in arsenic-exposed groups.	Arsenic	147-154	transforming growth factor, beta 1	Rattus norvegicus	68-77
34673086-10	2021	Moreover, a significant increase in key fibrosis factors, including TGF-beta1, p-SMAD2, p-SMAD3, and SMAD4 was observed in the lung homogenates in arsenic-exposed groups.	Arsenic	147-154	SMAD family member 2	Rattus norvegicus	81-86
34673086-10	2021	Moreover, a significant increase in key fibrosis factors, including TGF-beta1, p-SMAD2, p-SMAD3, and SMAD4 was observed in the lung homogenates in arsenic-exposed groups.	Arsenic	147-154	SMAD family member 3	Rattus norvegicus	90-95
34673086-10	2021	Moreover, a significant increase in key fibrosis factors, including TGF-beta1, p-SMAD2, p-SMAD3, and SMAD4 was observed in the lung homogenates in arsenic-exposed groups.	Arsenic	147-154	SMAD family member 4	Rattus norvegicus	101-106
34899152-3	2021	Arsenite methyltransferase (AS3MT) catalyzes the biomethylation of arsenic and hence regulates arsenic metabolism.	Arsenic	67-74	arsenite methyltransferase	Homo sapiens	0-26
34841959-8	2021	Plasma insulin concentration AUC was significantly lower after AS (P = 0.019) and trended lower in CON (P = 0.054) compared to following NS.	Arsenic	63-65	insulin	Homo sapiens	7-14
34885804-2	2021	Reactions of EBr3 (E = P, As) with iPr2PAcenapLi (Acenap = acenaphthene-5,6-diyl) afforded the thermally stable peri-substitution supported donor-acceptor complexes, iPr2PAcenapEBr23 and 4.	Arsenic	26-28	EBR3	Homo sapiens	13-17
34899152-3	2021	Arsenite methyltransferase (AS3MT) catalyzes the biomethylation of arsenic and hence regulates arsenic metabolism.	Arsenic	67-74	arsenite methyltransferase	Homo sapiens	28-33
34899152-3	2021	Arsenite methyltransferase (AS3MT) catalyzes the biomethylation of arsenic and hence regulates arsenic metabolism.	Arsenic	95-102	arsenite methyltransferase	Homo sapiens	0-26
34899152-3	2021	Arsenite methyltransferase (AS3MT) catalyzes the biomethylation of arsenic and hence regulates arsenic metabolism.	Arsenic	95-102	arsenite methyltransferase	Homo sapiens	28-33
34830390-7	2021	Primary human TM cells treated with AS.IV decreased TGFbeta2 induced ECM (FN, Col-I) deposition and ER stress (KDEL, ATF4 and CHOP).	Arsenic	36-38	transforming growth factor beta 2	Homo sapiens	52-60
34830390-7	2021	Primary human TM cells treated with AS.IV decreased TGFbeta2 induced ECM (FN, Col-I) deposition and ER stress (KDEL, ATF4 and CHOP).	Arsenic	36-38	activating transcription factor 4	Homo sapiens	117-121
34830390-7	2021	Primary human TM cells treated with AS.IV decreased TGFbeta2 induced ECM (FN, Col-I) deposition and ER stress (KDEL, ATF4 and CHOP).	Arsenic	36-38	DNA damage inducible transcript 3	Homo sapiens	126-130
34869465-6	2021	The correlation between AS and prognosis of IgAN was assessed.	Arsenic	24-26	IGAN1	Homo sapiens	44-48
34426183-5	2021	The mechanisms involved in arsenic-induced diabetes are pancreatic beta-cell dysfunction and death, impaired insulin secretion, insulin resistance and reduced cellular glucose transport.	Arsenic	27-34	insulin	Homo sapiens	128-135
34869235-3	2021	In this research, based on first-principles simulation, we propose CdO/Arsenene (CdO/As) vdW heterostructure as a semiconductor possessing a direct bandgap by 2.179 eV.	Arsenic	85-87	cell adhesion associated, oncogene regulated	Homo sapiens	67-70
34869235-3	2021	In this research, based on first-principles simulation, we propose CdO/Arsenene (CdO/As) vdW heterostructure as a semiconductor possessing a direct bandgap by 2.179 eV.	Arsenic	85-87	cell adhesion associated, oncogene regulated	Homo sapiens	81-84
34714618-7	2021	Compared with Pt nanoparticles, the weaker interaction between arsenic species and Pt1/MoS2 enabled the effortless regeneration and cyclic utilization of active centers, which is more favorable for the oxidation of As(0).	Arsenic	63-70	zinc finger protein 77	Homo sapiens	83-86
34741736-8	2022	The concentrations of P, Fe, Cu, Mn and Ni, and catalase (CAT), ascorbate peroxidase (APX) and superoxide dismutase (SOD) antioxidant activity increased in the As treatment and decreased in the As + AEV treatment.	Arsenic	160-162	peroxidase 1	Zea mays	74-84
34704769-8	2021	Silence of the TrxR expression sensitizes the cells to the arsenic compound treatment, further supporting the critical involvement of TrxR in the cellular actions of compound 10.	Arsenic	59-66	peroxiredoxin 5	Homo sapiens	15-19
34704769-8	2021	Silence of the TrxR expression sensitizes the cells to the arsenic compound treatment, further supporting the critical involvement of TrxR in the cellular actions of compound 10.	Arsenic	59-66	peroxiredoxin 5	Homo sapiens	134-138
34741736-8	2022	The concentrations of P, Fe, Cu, Mn and Ni, and catalase (CAT), ascorbate peroxidase (APX) and superoxide dismutase (SOD) antioxidant activity increased in the As treatment and decreased in the As + AEV treatment.	Arsenic	160-162	ascorbate peroxidase 2	Zea mays	86-89
34741736-8	2022	The concentrations of P, Fe, Cu, Mn and Ni, and catalase (CAT), ascorbate peroxidase (APX) and superoxide dismutase (SOD) antioxidant activity increased in the As treatment and decreased in the As + AEV treatment.	Arsenic	160-162	superoxide dismutase	Zea mays	95-115
34678219-0	2021	Biliary Excretion of Arsenic by Human HepaRG Cells is Stimulated by Selenide and Mediated by the Multidrug Resistance Protein 2 (MRP2/ABCC2).	Arsenic	21-28	ATP binding cassette subfamily C member 2	Homo sapiens	129-133
34638088-0	2021	Zinc antagonizes common carp (Cyprinus carpio) intestinal arsenic poisoning through PI3K/AKT/mTOR signaling cascade and MAPK pathway.	Arsenic	58-65	AKT serine/threonine kinase 1	Homo sapiens	89-92
34638088-0	2021	Zinc antagonizes common carp (Cyprinus carpio) intestinal arsenic poisoning through PI3K/AKT/mTOR signaling cascade and MAPK pathway.	Arsenic	58-65	mechanistic target of rapamycin kinase	Homo sapiens	93-97
34678219-0	2021	Biliary Excretion of Arsenic by Human HepaRG Cells is Stimulated by Selenide and Mediated by the Multidrug Resistance Protein 2 (MRP2/ABCC2).	Arsenic	21-28	ATP binding cassette subfamily C member 2	Homo sapiens	134-139
34678219-12	2021	Knockdown experiments revealed that multidrug resistance protein 2 (MRP2/ABCC2) accounted for all detectable biliary efflux of arsenic (+- selenide).	Arsenic	127-134	ATP binding cassette subfamily C member 2	Homo sapiens	68-72
34678219-12	2021	Knockdown experiments revealed that multidrug resistance protein 2 (MRP2/ABCC2) accounted for all detectable biliary efflux of arsenic (+- selenide).	Arsenic	127-134	ATP binding cassette subfamily C member 2	Homo sapiens	73-78
34678219-13	2021	Overall, the chemical form of selenium and human MRP2 strongly influenced arsenic hepatobiliary transport, information critical for human selenium supplementation in arsenic-endemic regions.	Arsenic	74-81	ATP binding cassette subfamily C member 2	Homo sapiens	49-53
34272803-0	2021	Curcumin functions as an anti-inflammatory and antioxidant agent on arsenic-induced hepatic and kidney injury by inhibiting MAPKs/NF-kappaB and activating Nrf2 pathways.	Arsenic	68-75	nuclear factor, erythroid derived 2, like 2	Mus musculus	155-159
34272803-4	2021	Curcumin treatment (200 mg/kg) not only decreased the deposition of arsenic in liver and kidney, but also relieved the hepatic and nephritic biochemical indexes (Glutamic oxaloacetic transaminase (AST), Alanine aminotransferase (ALT), albumin, and creatinine) altered by arsenic at doses of 10 and 25 mg/L via drinking water.	Arsenic	271-278	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	197-200
34272803-4	2021	Curcumin treatment (200 mg/kg) not only decreased the deposition of arsenic in liver and kidney, but also relieved the hepatic and nephritic biochemical indexes (Glutamic oxaloacetic transaminase (AST), Alanine aminotransferase (ALT), albumin, and creatinine) altered by arsenic at doses of 10 and 25 mg/L via drinking water.	Arsenic	271-278	glutamic pyruvic transaminase, soluble	Mus musculus	203-227
34272803-4	2021	Curcumin treatment (200 mg/kg) not only decreased the deposition of arsenic in liver and kidney, but also relieved the hepatic and nephritic biochemical indexes (Glutamic oxaloacetic transaminase (AST), Alanine aminotransferase (ALT), albumin, and creatinine) altered by arsenic at doses of 10 and 25 mg/L via drinking water.	Arsenic	271-278	glutamic pyruvic transaminase, soluble	Mus musculus	229-232
34272803-7	2021	In conclusion, our results here suggest that curcumin could exert both anti-inflammatory and antioxidant functions on arsenic-induced hepatic and kidney injury by inhibiting MAPKs/NF-kappaB and activating Nrf2 pathways cooperatively.	Arsenic	118-125	nuclear factor, erythroid derived 2, like 2	Mus musculus	205-209
34174665-5	2021	Soil parent materials, pH, organic matter, and clay particle size were the key factors influencing accumulation of arsenic, chromium, and nickel.	Arsenic	115-122	phenylalanine hydroxylase	Homo sapiens	23-25
34599931-2	2021	In our previous study, we observed that when BEAS-2B cells are chronically exposed to arsenic, there is an increase in secreted TGFalpha, as well as an increase in EGFR expression and activity.	Arsenic	86-93	transforming growth factor alpha	Homo sapiens	128-136
34599931-2	2021	In our previous study, we observed that when BEAS-2B cells are chronically exposed to arsenic, there is an increase in secreted TGFalpha, as well as an increase in EGFR expression and activity.	Arsenic	86-93	epidermal growth factor receptor	Homo sapiens	164-168
34599931-4	2021	The overarching goal of this study was to acquire finer resolution of the arsenic-dependent changes in cell migration, as well as to understand the role of increased EGFR expression and activity levels in the underlying mechanisms of cell migration.	Arsenic	74-81	epidermal growth factor receptor	Homo sapiens	166-170
34599931-8	2021	From these data, we were able to isolate both EGFR-dependent and -independent features of cell migration that were enhanced by chronic arsenic exposure.	Arsenic	135-142	epidermal growth factor receptor	Homo sapiens	46-50
34416372-6	2021	Recent studies have demonstrated that some heavy metal carcinogens, including arsenic and nickel, can induce the loss of SLBP and the gain of polyadenylation of canonical histone mRNAs.	Arsenic	78-85	stem-loop binding protein	Homo sapiens	121-125
34768886-6	2021	Fluorescence microscopy analyses of yeast cells expressing fluorescently tagged alpha-synuclein demonstrated that arsenic and cadmium affected the distribution of alpha-synuclein aggregates within the cells, reduced aggregate clearance, and aggravated alpha-synuclein toxicity.	Arsenic	114-121	synuclein alpha	Homo sapiens	80-95
34768886-6	2021	Fluorescence microscopy analyses of yeast cells expressing fluorescently tagged alpha-synuclein demonstrated that arsenic and cadmium affected the distribution of alpha-synuclein aggregates within the cells, reduced aggregate clearance, and aggravated alpha-synuclein toxicity.	Arsenic	114-121	synuclein alpha	Homo sapiens	163-178
34768886-6	2021	Fluorescence microscopy analyses of yeast cells expressing fluorescently tagged alpha-synuclein demonstrated that arsenic and cadmium affected the distribution of alpha-synuclein aggregates within the cells, reduced aggregate clearance, and aggravated alpha-synuclein toxicity.	Arsenic	114-121	synuclein alpha	Homo sapiens	252-267
34332247-0	2021	NAC antagonizes arsenic-induced neurotoxicity through TMEM179 by inhibiting oxidative stress in Oli-neu cells.	Arsenic	16-23	transmembrane protein 179	Mus musculus	54-61
34332247-9	2021	We found that TMEM179 played a critical role in mediating the neurotoxic effects of arsenic and the protective role of NAC.	Arsenic	84-91	transmembrane protein 179	Mus musculus	14-21
34364127-0	2021	NLRP3 inflammasome blocked the glycolytic pathway via targeting to PKLR in arsenic-induced hepatic insulin resistance.	Arsenic	75-82	NLR family pyrin domain containing 3	Homo sapiens	0-5
34364127-0	2021	NLRP3 inflammasome blocked the glycolytic pathway via targeting to PKLR in arsenic-induced hepatic insulin resistance.	Arsenic	75-82	pyruvate kinase L/R	Homo sapiens	67-71
34364127-1	2021	Arsenic exposure is related to insulin resistance (IR).	Arsenic	0-7	insulin	Homo sapiens	31-38
34675983-4	2021	Previous studies have suggested that tumor cell sensitivity to ATO is related to the intracellular arsenic content, and aquaporin 9 (AQP9) is the key factor that determines intracellular arsenic content.	Arsenic	99-106	aquaporin 9	Homo sapiens	133-137
34332247-12	2021	It also identifies a potential molecular target, TMEM179, for the treatment of arsenic-induced neurotoxicity.	Arsenic	79-86	transmembrane protein 179	Mus musculus	49-56
34643861-0	2022	Association of albumin to creatinine ratio with urinary arsenic and metal exposure: evidence from NHANES 2015-2016.	Arsenic	56-63	albumin	Homo sapiens	15-22
34643861-3	2022	The purpose of this study is to assess the association between urinary arsenic and metals and a higher albumin to creatinine ratio (ACR) among adults in the general US population.	Arsenic	71-78	albumin	Homo sapiens	103-110
34675983-4	2021	Previous studies have suggested that tumor cell sensitivity to ATO is related to the intracellular arsenic content, and aquaporin 9 (AQP9) is the key factor that determines intracellular arsenic content.	Arsenic	187-194	aquaporin 9	Homo sapiens	120-131
34675983-4	2021	Previous studies have suggested that tumor cell sensitivity to ATO is related to the intracellular arsenic content, and aquaporin 9 (AQP9) is the key factor that determines intracellular arsenic content.	Arsenic	187-194	aquaporin 9	Homo sapiens	133-137
34675983-16	2021	Curcumin can enhance the killing effects of ATO on U266 by increasing the intracellular arsenic content, which may be related to the upregulation of AQP9 expression.	Arsenic	88-95	aquaporin 9	Homo sapiens	149-153
34333423-6	2021	Regrettably, all of the as-synthesized derivatives exhibited inferior alpha-glucosidase inhibitory activities than those of the parent compounds in both test solvent systems.	Arsenic	24-26	sucrase-isomaltase	Homo sapiens	70-87
34303791-4	2021	Since inorganic arsenic (iAs) targets prostatic stem cells (SCs), we hypothesized that arsenic-transformed SCs (As-CSCs) show an impaired TLR3-associated anti-tumor pathway and, therefore, are unresponsive to PIC activation.	Arsenic	87-94	toll like receptor 3	Homo sapiens	138-142
34380282-1	2021	Naturally occurring goethite commonly undergoes Al-substitution, while how changes in microstructure induced by Al-substitution affect the interactive reaction of Pb(II) or As(V) at the goethite-water interface remains poorly understood.	Arsenic	173-176	submaxillary gland androgen regulated protein 3B	Homo sapiens	163-169
34665768-4	2021	The results of the CPF showed average efficiencies of 91.5% (Hg), 92% (Pb), 50.2% (As) and 78.7% (phenols).	Arsenic	83-85	nuclear receptor subfamily 5 group A member 2	Homo sapiens	19-22
34251737-10	2021	Meanwhile, imbalanced immune response was verified by the notable abnormal ratio of Th17 to Treg cells in peripheral blood as well as the secretion of inflammatory cytokines IL-17A, IL-6, TGF-beta1, and IL-10 in serum and liver of arsenic exposed rats.	Arsenic	231-238	interleukin 17A	Rattus norvegicus	174-180
34251737-10	2021	Meanwhile, imbalanced immune response was verified by the notable abnormal ratio of Th17 to Treg cells in peripheral blood as well as the secretion of inflammatory cytokines IL-17A, IL-6, TGF-beta1, and IL-10 in serum and liver of arsenic exposed rats.	Arsenic	231-238	interleukin 6	Rattus norvegicus	182-186
34251737-10	2021	Meanwhile, imbalanced immune response was verified by the notable abnormal ratio of Th17 to Treg cells in peripheral blood as well as the secretion of inflammatory cytokines IL-17A, IL-6, TGF-beta1, and IL-10 in serum and liver of arsenic exposed rats.	Arsenic	231-238	transforming growth factor, beta 1	Rattus norvegicus	188-197
34251737-10	2021	Meanwhile, imbalanced immune response was verified by the notable abnormal ratio of Th17 to Treg cells in peripheral blood as well as the secretion of inflammatory cytokines IL-17A, IL-6, TGF-beta1, and IL-10 in serum and liver of arsenic exposed rats.	Arsenic	231-238	interleukin 10	Rattus norvegicus	203-208
34265531-7	2021	Meanwhile experiments showed that fluoride and arsenic exposure can modulate autophagic flux, causing increased levels of Beclin1 and LC3 expression and decreased p62 expression.	Arsenic	47-54	beclin 1	Rattus norvegicus	122-129
34265531-7	2021	Meanwhile experiments showed that fluoride and arsenic exposure can modulate autophagic flux, causing increased levels of Beclin1 and LC3 expression and decreased p62 expression.	Arsenic	47-54	annexin A3	Rattus norvegicus	134-137
34265531-7	2021	Meanwhile experiments showed that fluoride and arsenic exposure can modulate autophagic flux, causing increased levels of Beclin1 and LC3 expression and decreased p62 expression.	Arsenic	47-54	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	163-166
34950482-7	2021	Such structurally stabilized composites of As(v)-Fe(iii)-OM may be more widely distributed and allow oxidized As and Fe to persist in other organic-rich, reducing environments.	Arsenic	110-112	oncomodulin 2	Homo sapiens	57-59
34390821-2	2021	Arsenic exerts its pronounced cellular toxicity through its trivalent oxide arsenite (ASN), which directly inhibits numerous proteins including Thioredoxin 1 (Trx1), and causes severe oxidative stress.	Arsenic	0-7	thioredoxin	Homo sapiens	144-157
34390821-2	2021	Arsenic exerts its pronounced cellular toxicity through its trivalent oxide arsenite (ASN), which directly inhibits numerous proteins including Thioredoxin 1 (Trx1), and causes severe oxidative stress.	Arsenic	0-7	thioredoxin	Homo sapiens	159-163
34665768-5	2021	The CPF + GAC-Z showed similar efficiencies for the removal of heavy metals (92.5% Hg, 98.1% Pb and 52.3% As) and a considerably higher efficiency for the removal of phenols (96.4%).	Arsenic	106-108	nuclear receptor subfamily 5 group A member 2	Homo sapiens	4-7
34118311-3	2021	Arsenic treatment altered insulin dose-response curve and reduced maximum insulin response in differentiated human neuroblastoma SH-SY5Y cells, suggesting that arsenic hindered neuronal insulin signaling in a non-competitive like manner.	Arsenic	0-7	insulin	Homo sapiens	26-33
34118311-3	2021	Arsenic treatment altered insulin dose-response curve and reduced maximum insulin response in differentiated human neuroblastoma SH-SY5Y cells, suggesting that arsenic hindered neuronal insulin signaling in a non-competitive like manner.	Arsenic	0-7	insulin	Homo sapiens	74-81
34118311-3	2021	Arsenic treatment altered insulin dose-response curve and reduced maximum insulin response in differentiated human neuroblastoma SH-SY5Y cells, suggesting that arsenic hindered neuronal insulin signaling in a non-competitive like manner.	Arsenic	0-7	insulin	Homo sapiens	186-193
34118311-3	2021	Arsenic treatment altered insulin dose-response curve and reduced maximum insulin response in differentiated human neuroblastoma SH-SY5Y cells, suggesting that arsenic hindered neuronal insulin signaling in a non-competitive like manner.	Arsenic	160-167	insulin	Homo sapiens	26-33
34118311-3	2021	Arsenic treatment altered insulin dose-response curve and reduced maximum insulin response in differentiated human neuroblastoma SH-SY5Y cells, suggesting that arsenic hindered neuronal insulin signaling in a non-competitive like manner.	Arsenic	160-167	insulin	Homo sapiens	74-81
34560123-4	2021	The aim of this study is to investigate molecular mechanisms of arsenic-induced GRP78 expression in BEAS-2B cells model.	Arsenic	64-71	heat shock protein family A (Hsp70) member 5	Homo sapiens	80-85
34118311-3	2021	Arsenic treatment altered insulin dose-response curve and reduced maximum insulin response in differentiated human neuroblastoma SH-SY5Y cells, suggesting that arsenic hindered neuronal insulin signaling in a non-competitive like manner.	Arsenic	160-167	insulin	Homo sapiens	186-193
34118311-4	2021	Mechanistically, arsenic suppressed insulin receptor (IR) kinase activity, as witnessed by a decreased insulin-activated autophosphorylation of IR at Y1150/1151.	Arsenic	17-24	insulin	Homo sapiens	103-110
34118311-5	2021	Arsenic decreased the level of insulin receptor substrate 1 (IRS1) but increased the protein ratio between PI3K regulatory subunit, p85, and PI3K catalytic subunit, p110.	Arsenic	0-7	insulin receptor substrate 1	Homo sapiens	31-59
34118311-5	2021	Arsenic decreased the level of insulin receptor substrate 1 (IRS1) but increased the protein ratio between PI3K regulatory subunit, p85, and PI3K catalytic subunit, p110.	Arsenic	0-7	insulin receptor substrate 1	Homo sapiens	61-65
34118311-5	2021	Arsenic decreased the level of insulin receptor substrate 1 (IRS1) but increased the protein ratio between PI3K regulatory subunit, p85, and PI3K catalytic subunit, p110.	Arsenic	0-7	phosphoinositide-3-kinase regulatory subunit 2	Homo sapiens	132-135
34118311-5	2021	Arsenic decreased the level of insulin receptor substrate 1 (IRS1) but increased the protein ratio between PI3K regulatory subunit, p85, and PI3K catalytic subunit, p110.	Arsenic	0-7	endogenous retrovirus group K member 15	Homo sapiens	165-169
34118311-6	2021	Interestingly, co-immunoprecipitation demonstrated that arsenic did not alter a level of PI3K-p110/PI3K-p85 complex while increased PI3K-p85 levels in a PI3K-p110 depletion supernatant resulted from PI3K-p110 immunoprecipitation.	Arsenic	56-63	phosphoinositide-3-kinase regulatory subunit 2	Homo sapiens	137-140
34118311-6	2021	Interestingly, co-immunoprecipitation demonstrated that arsenic did not alter a level of PI3K-p110/PI3K-p85 complex while increased PI3K-p85 levels in a PI3K-p110 depletion supernatant resulted from PI3K-p110 immunoprecipitation.	Arsenic	56-63	endogenous retrovirus group K member 15	Homo sapiens	158-162
34118311-6	2021	Interestingly, co-immunoprecipitation demonstrated that arsenic did not alter a level of PI3K-p110/PI3K-p85 complex while increased PI3K-p85 levels in a PI3K-p110 depletion supernatant resulted from PI3K-p110 immunoprecipitation.	Arsenic	56-63	endogenous retrovirus group K member 15	Homo sapiens	204-208
34118311-7	2021	These results indicated that arsenic increased PI3K-p85 which was free from PI3K-p110 binding.	Arsenic	29-36	phosphoinositide-3-kinase regulatory subunit 2	Homo sapiens	52-55
34118311-8	2021	In addition, arsenic significantly increased interaction between IRS1 and PI3K-p85 but not PI3K-p110, suggesting that there may be a fraction of free PI3K-p85 interacting with IRS1.	Arsenic	13-20	insulin receptor substrate 1	Homo sapiens	65-69
34118311-8	2021	In addition, arsenic significantly increased interaction between IRS1 and PI3K-p85 but not PI3K-p110, suggesting that there may be a fraction of free PI3K-p85 interacting with IRS1.	Arsenic	13-20	phosphoinositide-3-kinase regulatory subunit 2	Homo sapiens	79-82
34118311-8	2021	In addition, arsenic significantly increased interaction between IRS1 and PI3K-p85 but not PI3K-p110, suggesting that there may be a fraction of free PI3K-p85 interacting with IRS1.	Arsenic	13-20	phosphoinositide-3-kinase regulatory subunit 2	Homo sapiens	155-158
34118311-8	2021	In addition, arsenic significantly increased interaction between IRS1 and PI3K-p85 but not PI3K-p110, suggesting that there may be a fraction of free PI3K-p85 interacting with IRS1.	Arsenic	13-20	insulin receptor substrate 1	Homo sapiens	176-180
34118311-9	2021	In vitro PI3K activity demonstrated that arsenic lowered PI3K activity in both basal and insulin-stimulated conditions.	Arsenic	41-48	insulin	Homo sapiens	89-96
34118311-10	2021	These results suggested that the increase in free PI3K-p85 by arsenic might compete with PI3K heterodimer for the same IRS1 binding site, in turn blocking the activation of its catalytic subunit, PI3K-p110.	Arsenic	62-69	phosphoinositide-3-kinase regulatory subunit 2	Homo sapiens	55-58
34118311-10	2021	These results suggested that the increase in free PI3K-p85 by arsenic might compete with PI3K heterodimer for the same IRS1 binding site, in turn blocking the activation of its catalytic subunit, PI3K-p110.	Arsenic	62-69	insulin receptor substrate 1	Homo sapiens	119-123
34118311-10	2021	These results suggested that the increase in free PI3K-p85 by arsenic might compete with PI3K heterodimer for the same IRS1 binding site, in turn blocking the activation of its catalytic subunit, PI3K-p110.	Arsenic	62-69	endogenous retrovirus group K member 15	Homo sapiens	201-205
34118311-11	2021	Taken together, our results provide additional insights into mechanisms underlying the impairment of neuronal insulin signaling by arsenic through the reduction of IR autophosphorylation, the increase in free PI3K-p85, and the impeding of PI3K activity."	Arsenic	131-138	phosphoinositide-3-kinase regulatory subunit 2	Homo sapiens	214-217
34134382-10	2021	Arsenic has an impact on overall mortality (IRR 1.07; p = 0.01) and death upon the arrival of EMS team (IRR 1.15; p < 0.001).	Arsenic	0-7	insulin receptor related receptor	Homo sapiens	44-47
34134382-10	2021	Arsenic has an impact on overall mortality (IRR 1.07; p = 0.01) and death upon the arrival of EMS team (IRR 1.15; p < 0.001).	Arsenic	0-7	insulin receptor related receptor	Homo sapiens	104-107
34414713-0	2021	(Distribution Characteristics and Seasonal Variations of Arsenic in Atmospheric Aerosols over the Yellow Sea and Bohai Sea).	Arsenic	57-64	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	105-108
34524606-8	2022	Against As-induced oxidative stress, B. oleracea plants mediated an increase in the activities of peroxidase and catalase.	Arsenic	8-10	catalase-2-like	Brassica oleracea	113-121
34574656-7	2021	Subjects" drinking water arsenic concentrations were positively associated with total urinary arsenic concentrations and the percentages of MMA, as well as inversely associated with the percentages of DMA and the secondary methylation index (SMI).	Arsenic	25-32	monocyte to macrophage differentiation associated	Homo sapiens	140-143
34516406-7	2021	In addition, the neuroprotective effects of AS-Exos were abrogated in brain-specific Nrf2-knockout mice subjected to TBI.	Arsenic	44-46	nuclear factor, erythroid derived 2, like 2	Mus musculus	85-89
34414713-6	2021	The highest concentrations of As were observed over the Bohai Sea in winter and the northern Yellow Sea in spring, with an average of 8.8 and 11.3 ng m-3, respectively.	Arsenic	30-32	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	62-65
34414713-7	2021	As concentrations exhibited a relatively uniform spatial pattern in summer over the Yellow Sea and Bohai Sea, which may have been affected by the different sources of As.	Arsenic	167-169	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	91-94
34414713-7	2021	As concentrations exhibited a relatively uniform spatial pattern in summer over the Yellow Sea and Bohai Sea, which may have been affected by the different sources of As.	Arsenic	167-169	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	105-108
34414713-16	2021	The dry deposition flux of As over the Yellow Sea and Bohai Sea was 1.15 mug (m2 d)-1 in winter, 0.77 mug (m2 d)-1 in spring, and 0.97 mug (m2 d)-1 in summer, with an annual mean value of 0.95 mug (m2 d)-1.	Arsenic	27-29	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	46-49
34414713-16	2021	The dry deposition flux of As over the Yellow Sea and Bohai Sea was 1.15 mug (m2 d)-1 in winter, 0.77 mug (m2 d)-1 in spring, and 0.97 mug (m2 d)-1 in summer, with an annual mean value of 0.95 mug (m2 d)-1.	Arsenic	27-29	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	60-63
34229406-0	2021	Microglia-derived IL-1beta promoted neuronal apoptosis through ER stress-mediated signaling pathway PERK/eIF2alpha/ATF4/CHOP upon arsenic exposure.	Arsenic	130-137	interleukin 1 alpha	Homo sapiens	18-26
34087579-8	2021	CONCLUSION: ADIPOQ/rs266729 and FABP2/rs1799883 polymorphisms affect susceptibility to essential hypertension in individuals exposed to high levels of arsenic; there was a clear difference in the urinary arsenic metabolism pattern between hypertensive patients and controls.	Arsenic	151-158	adiponectin, C1Q and collagen domain containing	Homo sapiens	12-18
34087579-8	2021	CONCLUSION: ADIPOQ/rs266729 and FABP2/rs1799883 polymorphisms affect susceptibility to essential hypertension in individuals exposed to high levels of arsenic; there was a clear difference in the urinary arsenic metabolism pattern between hypertensive patients and controls.	Arsenic	151-158	fatty acid binding protein 2	Homo sapiens	32-37
34166680-0	2021	The role of PD-1/PD-L1 checkpoint in arsenic lung tumorigenesis.	Arsenic	37-44	CD274 antigen	Mus musculus	17-22
34166680-11	2021	The results showed that prolonged arsenic exposure up-regulated PD-1/PD-L1, increased regulatory T cells (Tregs), decreased CD8/Treg ratio, inhibited T cell antitumor function in the lungs and enhanced lung tumor formation, while inhibition of PD-1/PD-L1 restored CD8/Treg ratio and T cell anti-tumor effector function, and mitigated arsenic-enhanced lung tumorigenesis.	Arsenic	34-41	CD274 molecule	Sus scrofa	69-74
34166680-11	2021	The results showed that prolonged arsenic exposure up-regulated PD-1/PD-L1, increased regulatory T cells (Tregs), decreased CD8/Treg ratio, inhibited T cell antitumor function in the lungs and enhanced lung tumor formation, while inhibition of PD-1/PD-L1 restored CD8/Treg ratio and T cell anti-tumor effector function, and mitigated arsenic-enhanced lung tumorigenesis.	Arsenic	34-41	CD274 molecule	Sus scrofa	249-254
34425169-7	2021	While the progression of gene changes was different for each subject, a common pattern was observed in arsenic treated cells over time, with early upregulation of oxidative stress responses (HMOX1, NQ01, TXN, TXNRD1) and down-regulation of immune/inflammatory responses (IKKalpha).	Arsenic	103-110	thioredoxin	Homo sapiens	204-207
34425169-7	2021	While the progression of gene changes was different for each subject, a common pattern was observed in arsenic treated cells over time, with early upregulation of oxidative stress responses (HMOX1, NQ01, TXN, TXNRD1) and down-regulation of immune/inflammatory responses (IKKalpha).	Arsenic	103-110	thioredoxin reductase 1	Homo sapiens	209-215
34425169-7	2021	While the progression of gene changes was different for each subject, a common pattern was observed in arsenic treated cells over time, with early upregulation of oxidative stress responses (HMOX1, NQ01, TXN, TXNRD1) and down-regulation of immune/inflammatory responses (IKKalpha).	Arsenic	103-110	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	271-279
34062077-0	2021	Riboflavin recovery of spermatogenic dysfunction via a dual inhibition of oxidative changes and regulation of the PINK1-mediated pathway in arsenic-injured rat model.	Arsenic	140-147	PTEN induced kinase 1	Rattus norvegicus	114-119
34539640-10	2021	Conclusion: Our findings showed that the overactive IL6 signal pathway led to autoimmune arthritis, especially in RA and AS.	Arsenic	121-123	interleukin 6	Homo sapiens	52-55
34091186-7	2021	Then, As or/and Sb induced ERS and triggered the ER apoptotic pathway by activating unfolded protein response (UPR)-associated genes ((PERK, ATF6, IRE1, XBP1, JNK, GRP78), and apoptosis-related genes (Caspase12, Caspase3, p53, CHOP).	Arsenic	6-8	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	135-139
34091186-7	2021	Then, As or/and Sb induced ERS and triggered the ER apoptotic pathway by activating unfolded protein response (UPR)-associated genes ((PERK, ATF6, IRE1, XBP1, JNK, GRP78), and apoptosis-related genes (Caspase12, Caspase3, p53, CHOP).	Arsenic	6-8	activating transcription factor 6	Mus musculus	141-145
34091186-7	2021	Then, As or/and Sb induced ERS and triggered the ER apoptotic pathway by activating unfolded protein response (UPR)-associated genes ((PERK, ATF6, IRE1, XBP1, JNK, GRP78), and apoptosis-related genes (Caspase12, Caspase3, p53, CHOP).	Arsenic	6-8	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	147-151
34091186-7	2021	Then, As or/and Sb induced ERS and triggered the ER apoptotic pathway by activating unfolded protein response (UPR)-associated genes ((PERK, ATF6, IRE1, XBP1, JNK, GRP78), and apoptosis-related genes (Caspase12, Caspase3, p53, CHOP).	Arsenic	6-8	X-box binding protein 1	Mus musculus	153-157
34091186-7	2021	Then, As or/and Sb induced ERS and triggered the ER apoptotic pathway by activating unfolded protein response (UPR)-associated genes ((PERK, ATF6, IRE1, XBP1, JNK, GRP78), and apoptosis-related genes (Caspase12, Caspase3, p53, CHOP).	Arsenic	6-8	mitogen-activated protein kinase 8	Mus musculus	159-162
34091186-7	2021	Then, As or/and Sb induced ERS and triggered the ER apoptotic pathway by activating unfolded protein response (UPR)-associated genes ((PERK, ATF6, IRE1, XBP1, JNK, GRP78), and apoptosis-related genes (Caspase12, Caspase3, p53, CHOP).	Arsenic	6-8	heat shock protein 5	Mus musculus	164-169
34091186-7	2021	Then, As or/and Sb induced ERS and triggered the ER apoptotic pathway by activating unfolded protein response (UPR)-associated genes ((PERK, ATF6, IRE1, XBP1, JNK, GRP78), and apoptosis-related genes (Caspase12, Caspase3, p53, CHOP).	Arsenic	6-8	caspase 12	Mus musculus	201-210
34091186-7	2021	Then, As or/and Sb induced ERS and triggered the ER apoptotic pathway by activating unfolded protein response (UPR)-associated genes ((PERK, ATF6, IRE1, XBP1, JNK, GRP78), and apoptosis-related genes (Caspase12, Caspase3, p53, CHOP).	Arsenic	6-8	caspase 3	Mus musculus	212-220
34091186-7	2021	Then, As or/and Sb induced ERS and triggered the ER apoptotic pathway by activating unfolded protein response (UPR)-associated genes ((PERK, ATF6, IRE1, XBP1, JNK, GRP78), and apoptosis-related genes (Caspase12, Caspase3, p53, CHOP).	Arsenic	6-8	transformation related protein 53, pseudogene	Mus musculus	222-225
34091186-7	2021	Then, As or/and Sb induced ERS and triggered the ER apoptotic pathway by activating unfolded protein response (UPR)-associated genes ((PERK, ATF6, IRE1, XBP1, JNK, GRP78), and apoptosis-related genes (Caspase12, Caspase3, p53, CHOP).	Arsenic	6-8	DNA-damage inducible transcript 3	Mus musculus	227-231
34118782-4	2021	Compared to other electron acceptors used in anaerobic respiration (e.g. N, S, Fe, Mn, and As), Se is one of the few elements whose end product is solid.	Arsenic	91-93	squalene epoxidase	Homo sapiens	96-98
34471155-0	2021	Arsenic leads to autophagy of keratinocytes by increasing aquaporin 3 expression.	Arsenic	0-7	aquaporin 3 (Gill blood group)	Homo sapiens	58-69
34471155-9	2021	Expression of aquaporin 3 is increased in arsenical cancers and in arsenic-treated keratinocytes.	Arsenic	67-74	aquaporin 3 (Gill blood group)	Homo sapiens	14-25
34471155-11	2021	Notably, the arsenic-induced autophagy was inhibited by pretreatment of keratinocytes with aquaporin inhibitors Auphen or AgNO3, or RNA interference against aquaporin 3.	Arsenic	13-20	aquaporin 3 (Gill blood group)	Homo sapiens	157-168
34471155-12	2021	The data indicates that the aquaporin 3 is an important cell membrane channel to mediate arsenic uptake and contributes to the arsenic-induced autophagy.	Arsenic	89-96	aquaporin 3 (Gill blood group)	Homo sapiens	28-39
34471155-12	2021	The data indicates that the aquaporin 3 is an important cell membrane channel to mediate arsenic uptake and contributes to the arsenic-induced autophagy.	Arsenic	127-134	aquaporin 3 (Gill blood group)	Homo sapiens	28-39
34166680-12	2021	In addition, inhibition of PD-1/PD-L1 could be a potential preventive strategy to mitigate the tumorigenic action of chronic arsenic exposure.	Arsenic	125-132	CD274 molecule	Sus scrofa	32-37
34425169-7	2021	While the progression of gene changes was different for each subject, a common pattern was observed in arsenic treated cells over time, with early upregulation of oxidative stress responses (HMOX1, NQ01, TXN, TXNRD1) and down-regulation of immune/inflammatory responses (IKKalpha).	Arsenic	103-110	heme oxygenase 1	Homo sapiens	191-196
34271453-4	2021	Although the oxidation of Fe2+ and As(III) during oxic storage was considerably faster, the As/Fe removal ratio was higher during anoxic storage (61-80+-5 microgAs/mgFe) compared to the oxic storage (45+-5 microgAs/mgFe).	Arsenic	92-94	general transcription factor IIE subunit 1	Homo sapiens	95-97
34229406-0	2021	Microglia-derived IL-1beta promoted neuronal apoptosis through ER stress-mediated signaling pathway PERK/eIF2alpha/ATF4/CHOP upon arsenic exposure.	Arsenic	130-137	epiregulin	Homo sapiens	63-65
34229406-0	2021	Microglia-derived IL-1beta promoted neuronal apoptosis through ER stress-mediated signaling pathway PERK/eIF2alpha/ATF4/CHOP upon arsenic exposure.	Arsenic	130-137	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	100-104
34229406-0	2021	Microglia-derived IL-1beta promoted neuronal apoptosis through ER stress-mediated signaling pathway PERK/eIF2alpha/ATF4/CHOP upon arsenic exposure.	Arsenic	130-137	eukaryotic translation initiation factor 2A	Homo sapiens	105-114
34229406-0	2021	Microglia-derived IL-1beta promoted neuronal apoptosis through ER stress-mediated signaling pathway PERK/eIF2alpha/ATF4/CHOP upon arsenic exposure.	Arsenic	130-137	activating transcription factor 4	Homo sapiens	115-119
34229406-0	2021	Microglia-derived IL-1beta promoted neuronal apoptosis through ER stress-mediated signaling pathway PERK/eIF2alpha/ATF4/CHOP upon arsenic exposure.	Arsenic	130-137	DNA damage inducible transcript 3	Homo sapiens	120-124
34229406-5	2021	Our findings demonstrated that arsenic-induced cognitive dysfunction, microglia activation, up-regulation and release of IL-1beta and ER stress-mediated apoptosis could be attenuated by minocycline, a recognized inhibitor of microglia activation.	Arsenic	31-38	interleukin 1 alpha	Homo sapiens	121-129
34229406-6	2021	In addition, the IL-1 receptor antagonist IL-1ra diminished arsenic-induced activation of ER stress-mediated apoptotic pathway PERK/eIF2alpha/ATF4/CHOP and neuronal apoptosis.	Arsenic	60-67	interleukin 1 receptor antagonist	Homo sapiens	42-48
34229406-6	2021	In addition, the IL-1 receptor antagonist IL-1ra diminished arsenic-induced activation of ER stress-mediated apoptotic pathway PERK/eIF2alpha/ATF4/CHOP and neuronal apoptosis.	Arsenic	60-67	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	127-131
34229406-6	2021	In addition, the IL-1 receptor antagonist IL-1ra diminished arsenic-induced activation of ER stress-mediated apoptotic pathway PERK/eIF2alpha/ATF4/CHOP and neuronal apoptosis.	Arsenic	60-67	eukaryotic translation initiation factor 2A	Homo sapiens	132-141
34229406-6	2021	In addition, the IL-1 receptor antagonist IL-1ra diminished arsenic-induced activation of ER stress-mediated apoptotic pathway PERK/eIF2alpha/ATF4/CHOP and neuronal apoptosis.	Arsenic	60-67	activating transcription factor 4	Homo sapiens	142-146
34229406-6	2021	In addition, the IL-1 receptor antagonist IL-1ra diminished arsenic-induced activation of ER stress-mediated apoptotic pathway PERK/eIF2alpha/ATF4/CHOP and neuronal apoptosis.	Arsenic	60-67	DNA damage inducible transcript 3	Homo sapiens	147-151
34444090-6	2021	In the total cohort, the toxic elements lead (Pb) and arsenic (As) showed a negative correlation with Se levels, while mercury (Hg), aluminum (Al) and cadmium (Cd) showed a positive correlation.	Arsenic	54-61	squalene epoxidase	Homo sapiens	102-104
34445052-2	2021	Arsenic is believed to exert its diabetogenic effects via multiple mechanisms, including alterations to insulin secretion and insulin sensitivity.	Arsenic	0-7	insulin	Homo sapiens	104-111
34445052-2	2021	Arsenic is believed to exert its diabetogenic effects via multiple mechanisms, including alterations to insulin secretion and insulin sensitivity.	Arsenic	0-7	insulin	Homo sapiens	126-133
34445052-7	2021	Dietary selenium deficiency resulted in similar effects on glucose tolerance and insulin secretion, with significant interactions between arsenic and dietary conditions in select insulin-related parameters.	Arsenic	138-145	insulin	Homo sapiens	179-186
34778748-0	2021	The transcription factor MYB40 is a central regulator in arsenic resistance in Arabidopsis.	Arsenic	57-64	myb domain protein 40	Arabidopsis thaliana	25-30
34778748-6	2021	Upon exposure to As(V), MYB40 directly repressed the expression of PHT1;1, which encodes a main Pi transporter.	Arsenic	17-20	myb domain protein 40	Arabidopsis thaliana	24-29
34778748-6	2021	Upon exposure to As(V), MYB40 directly repressed the expression of PHT1;1, which encodes a main Pi transporter.	Arsenic	17-20	phosphate transporter 1;1	Arabidopsis thaliana	67-73
34778748-10	2021	Together, our data demonstrate that AtMYB40 acts as a central regulator of As(V) responses, providing a genetic strategy for enhancing plant As(V) tolerance and reducing As(V) uptake to improve food safety.	Arsenic	75-77	myb domain protein 40	Arabidopsis thaliana	36-43
34392550-0	2022	Phytochelatin and coumarin enrichment in root exudates of arsenic-treated white lupin.	Arsenic	58-65	5'-nucleotidase, cytosolic IIIA	Homo sapiens	80-85
34392550-3	2022	Here, white lupin plants were exposed to arsenic in a semi-hydroponic system and their exudates were profiled using untargeted liquid chromatography tandem mass spectrometry.	Arsenic	41-48	5'-nucleotidase, cytosolic IIIA	Homo sapiens	12-17
34380335-11	2021	Betaine treatment significantly attenuated arsenic-induced decrease in renal eNOS expression.	Arsenic	43-50	nitric oxide synthase 3	Rattus norvegicus	77-81
34413646-9	2021	Conclusion: EA pretreatment improved AS-induced POCD in aged rats, and the underlying mechanism may be associated with inhibition of HMGB1-NF-kappaB via an alpha7-nAChR signal in the microglia.	Arsenic	37-39	high mobility group box 1	Rattus norvegicus	133-138
34444090-6	2021	In the total cohort, the toxic elements lead (Pb) and arsenic (As) showed a negative correlation with Se levels, while mercury (Hg), aluminum (Al) and cadmium (Cd) showed a positive correlation.	Arsenic	63-65	squalene epoxidase	Homo sapiens	102-104
34384184-8	2021	Relative mRNA level of bax increased for PSL combined with arsenic and for PSC combined with arsenic at 10 and 100 mug L-1 respectively.	Arsenic	59-66	BCL2 associated X, apoptosis regulator	Homo sapiens	23-26
34242508-0	2021	Insertion of CS2 into a Phosphorus-Arsenic Single Bond and Investigations on Phosphane Arsanyldithiocarboxylates.	Arsenic	35-42	chorionic somatomammotropin hormone 2	Homo sapiens	13-16
34384184-8	2021	Relative mRNA level of bax increased for PSL combined with arsenic and for PSC combined with arsenic at 10 and 100 mug L-1 respectively.	Arsenic	93-100	BCL2 associated X, apoptosis regulator	Homo sapiens	23-26
34080067-0	2021	High nuclear expression of HIF1alpha, synergizing with inactivation of LIMD1 and VHL, portray worst prognosis among the bladder cancer patients: association with arsenic prevalence.	Arsenic	162-169	hypoxia inducible factor 1 subunit alpha	Homo sapiens	27-36
34101025-2	2021	TNF polymorphisms have been reported to be associated with AS susceptibility, but the results of these previous studies have been inconsistent.	Arsenic	59-61	tumor necrosis factor	Homo sapiens	0-3
34488179-2	2021	Little has known about the impact of rice consumption on arsenic metabolism, which is related to insulin resistance.	Arsenic	57-64	insulin	Homo sapiens	97-104
34080067-1	2021	PURPOSE: Our study was aimed to understand the importance of LIMD1-VHL-HIF1alpha pathway in development of bladder carcinoma (BlCa) in association with arsenic prevalence.	Arsenic	152-159	LIM domain containing 1	Homo sapiens	61-66
34488179-3	2021	In this study, we examined the associations between rice consumption and arsenic metabolism, and between arsenic metabolism and insulin resistance in non-diabetic U.S adults who participated in the National Health and Nutrition Examination Survey (NHANES) 2003-2016.	Arsenic	105-112	insulin	Homo sapiens	128-135
34080067-1	2021	PURPOSE: Our study was aimed to understand the importance of LIMD1-VHL-HIF1alpha pathway in development of bladder carcinoma (BlCa) in association with arsenic prevalence.	Arsenic	152-159	von Hippel-Lindau tumor suppressor	Homo sapiens	67-70
34080067-1	2021	PURPOSE: Our study was aimed to understand the importance of LIMD1-VHL-HIF1alpha pathway in development of bladder carcinoma (BlCa) in association with arsenic prevalence.	Arsenic	152-159	hypoxia inducible factor 1 subunit alpha	Homo sapiens	71-80
34080067-10	2021	Additionally, patients with high arsenic content (> 112 ng/g, AsH) seemed to have recurrent promoter methylation in LIMD1, as well as co-methylation/alteration of LIMD1 and VHL gene.	Arsenic	33-40	LIM domain containing 1	Homo sapiens	116-121
34080067-10	2021	Additionally, patients with high arsenic content (> 112 ng/g, AsH) seemed to have recurrent promoter methylation in LIMD1, as well as co-methylation/alteration of LIMD1 and VHL gene.	Arsenic	33-40	von Hippel-Lindau tumor suppressor	Homo sapiens	173-176
34846426-0	2021	PSMA-targeted arsenic nanosheets: a platform for prostate cancer therapy via ferroptosis and ATM deficiency-triggered chemosensitization.	Arsenic	14-21	folate hydrolase 1	Homo sapiens	0-4
34846426-0	2021	PSMA-targeted arsenic nanosheets: a platform for prostate cancer therapy via ferroptosis and ATM deficiency-triggered chemosensitization.	Arsenic	14-21	ATM serine/threonine kinase	Homo sapiens	93-96
34846426-3	2021	Herein, we designed an inorganic metal-free nanoplatform, PSMA-targeted arsenic nanosheets (PMANs), which simultaneously increased glutathione (GSH) consumption, suppressed solute carrier family 7 member 11 (SLC7A11) and glutathione-dependent peroxidase 4 (GPX4) expression, and promoted the generation of reactive oxygen species (ROS) and lipid peroxides (LPO).	Arsenic	72-79	folate hydrolase 1	Homo sapiens	58-62
34846426-3	2021	Herein, we designed an inorganic metal-free nanoplatform, PSMA-targeted arsenic nanosheets (PMANs), which simultaneously increased glutathione (GSH) consumption, suppressed solute carrier family 7 member 11 (SLC7A11) and glutathione-dependent peroxidase 4 (GPX4) expression, and promoted the generation of reactive oxygen species (ROS) and lipid peroxides (LPO).	Arsenic	72-79	solute carrier family 7 member 11	Homo sapiens	173-206
34846426-3	2021	Herein, we designed an inorganic metal-free nanoplatform, PSMA-targeted arsenic nanosheets (PMANs), which simultaneously increased glutathione (GSH) consumption, suppressed solute carrier family 7 member 11 (SLC7A11) and glutathione-dependent peroxidase 4 (GPX4) expression, and promoted the generation of reactive oxygen species (ROS) and lipid peroxides (LPO).	Arsenic	72-79	solute carrier family 7 member 11	Homo sapiens	208-215
34846426-3	2021	Herein, we designed an inorganic metal-free nanoplatform, PSMA-targeted arsenic nanosheets (PMANs), which simultaneously increased glutathione (GSH) consumption, suppressed solute carrier family 7 member 11 (SLC7A11) and glutathione-dependent peroxidase 4 (GPX4) expression, and promoted the generation of reactive oxygen species (ROS) and lipid peroxides (LPO).	Arsenic	72-79	glutathione peroxidase 4	Homo sapiens	221-255
34846426-3	2021	Herein, we designed an inorganic metal-free nanoplatform, PSMA-targeted arsenic nanosheets (PMANs), which simultaneously increased glutathione (GSH) consumption, suppressed solute carrier family 7 member 11 (SLC7A11) and glutathione-dependent peroxidase 4 (GPX4) expression, and promoted the generation of reactive oxygen species (ROS) and lipid peroxides (LPO).	Arsenic	72-79	glutathione peroxidase 4	Homo sapiens	257-261
34364923-5	2021	Moreover, arsenic-transformed ATF3 knockout (ATF3 KO-AsT) cells exhibited more aggressive characteristics, including acceleration in proliferation, resistance to chemotherapy and increase in migratory capacity.	Arsenic	10-17	activating transcription factor 3	Homo sapiens	30-34
34109987-6	2021	Previously, miRNA-31 was identified as a negative regulator of SATB2 during arsenic-induced cell transformation, and in the present study it was identified as a downstream target of RUNX2 during carcinogenesis.	Arsenic	76-83	SATB homeobox 2	Homo sapiens	63-68
34109987-6	2021	Previously, miRNA-31 was identified as a negative regulator of SATB2 during arsenic-induced cell transformation, and in the present study it was identified as a downstream target of RUNX2 during carcinogenesis.	Arsenic	76-83	RUNX family transcription factor 2	Homo sapiens	182-187
34132035-0	2021	Quantitative Proteomics Reveals Arsenic Attenuates Stem-Loop Binding Protein Stability via a Chaperone Complex Containing Heat Shock Proteins and ERp44.	Arsenic	32-39	stem-loop binding protein	Homo sapiens	51-76
34132035-0	2021	Quantitative Proteomics Reveals Arsenic Attenuates Stem-Loop Binding Protein Stability via a Chaperone Complex Containing Heat Shock Proteins and ERp44.	Arsenic	32-39	endoplasmic reticulum protein 44	Homo sapiens	146-151
34132035-4	2021	Our previous work has shown arsenic induces ubiquitin-proteasome dependent degradation of SLBP and contributes to lung cancer.	Arsenic	28-35	stem-loop binding protein	Homo sapiens	90-94
34132035-5	2021	In this study, we established the first comprehensive SLBP interaction network by affinity purification-mass spectrometry (AP-MS) analysis, and further demonstrated arsenic enhanced the association between SLBP and a crucial chaperone complex containing heat shock proteins (HSPs) and ERp44.	Arsenic	165-172	stem-loop binding protein	Homo sapiens	54-58
34132035-5	2021	In this study, we established the first comprehensive SLBP interaction network by affinity purification-mass spectrometry (AP-MS) analysis, and further demonstrated arsenic enhanced the association between SLBP and a crucial chaperone complex containing heat shock proteins (HSPs) and ERp44.	Arsenic	165-172	stem-loop binding protein	Homo sapiens	206-210
34132035-5	2021	In this study, we established the first comprehensive SLBP interaction network by affinity purification-mass spectrometry (AP-MS) analysis, and further demonstrated arsenic enhanced the association between SLBP and a crucial chaperone complex containing heat shock proteins (HSPs) and ERp44.	Arsenic	165-172	endoplasmic reticulum protein 44	Homo sapiens	285-290
34132035-6	2021	Strikingly, knockdown of these proteins markedly rescued the protein level of SLBP under arsenic exposure conditions, and abolished the increasing migration capacity of BEAS-2B cells induced by arsenic.	Arsenic	89-96	stem-loop binding protein	Homo sapiens	78-82
34132035-6	2021	Strikingly, knockdown of these proteins markedly rescued the protein level of SLBP under arsenic exposure conditions, and abolished the increasing migration capacity of BEAS-2B cells induced by arsenic.	Arsenic	194-201	stem-loop binding protein	Homo sapiens	78-82
34132035-7	2021	Taken together, our study provides a potential new mechanism that a chaperone complex containing HSPs and ERp44 attenuates the stability of SLBP under both normal and arsenic exposure conditions, which could be essential for arsenic-induced high cell migration.	Arsenic	167-174	endoplasmic reticulum protein 44	Homo sapiens	106-111
34132035-7	2021	Taken together, our study provides a potential new mechanism that a chaperone complex containing HSPs and ERp44 attenuates the stability of SLBP under both normal and arsenic exposure conditions, which could be essential for arsenic-induced high cell migration.	Arsenic	167-174	stem-loop binding protein	Homo sapiens	140-144
34132035-7	2021	Taken together, our study provides a potential new mechanism that a chaperone complex containing HSPs and ERp44 attenuates the stability of SLBP under both normal and arsenic exposure conditions, which could be essential for arsenic-induced high cell migration.	Arsenic	225-232	endoplasmic reticulum protein 44	Homo sapiens	106-111
34132035-7	2021	Taken together, our study provides a potential new mechanism that a chaperone complex containing HSPs and ERp44 attenuates the stability of SLBP under both normal and arsenic exposure conditions, which could be essential for arsenic-induced high cell migration.	Arsenic	225-232	stem-loop binding protein	Homo sapiens	140-144
34352348-12	2021	Moreover, 26 proteins were identified by phosphoproteomic with different phosphorylation pattern in animals from both groups, but SPATA18 was phosphorylated only in arsenic-exposed animals.	Arsenic	165-172	spermatogenesis associated 18	Rattus norvegicus	130-137
34364923-0	2021	ATF3 inhibits arsenic-induced malignant transformation of human bronchial epithelial cells by attenuating inflammation.	Arsenic	14-21	activating transcription factor 3	Homo sapiens	0-4
34364923-5	2021	Moreover, arsenic-transformed ATF3 knockout (ATF3 KO-AsT) cells exhibited more aggressive characteristics, including acceleration in proliferation, resistance to chemotherapy and increase in migratory capacity.	Arsenic	10-17	activating transcription factor 3	Homo sapiens	45-49
34364923-6	2021	RNA-seq revealed that pathways involved in inflammation, cell cycle, EMT and oncogenesis were affected due to ATF3 deficiency during chronic arsenic exposure.	Arsenic	141-148	activating transcription factor 3	Homo sapiens	110-114
34584857-3	2021	Hence, there is a need to investigate the effect of AS on the overall survival (OS), progression-free survival (PFS) and adverse effect profile in patients treated with EGFR TKIs.	Arsenic	52-54	epidermal growth factor receptor	Homo sapiens	169-173
34364923-8	2021	Our results demonstrate that ATF3 upregulated by chronic low-dose arsenic exposure represses cell transformation and acquisition of malignant characteristics through inhibiting the production of proinflammatory cytokines and activation of downstream proteins AKT and STAT3, providing a new strategy for the prevention of carcinogen-induced lung cancer.	Arsenic	66-73	activating transcription factor 3	Homo sapiens	29-33
34584857-16	2021	The OS for EGFR mutation positive patients only was as similarly significant as the OS in all patients taking EGFR TKI, while the PFS in mutation positive patients was significantly worsened with AS.	Arsenic	196-198	epidermal growth factor receptor	Homo sapiens	11-15
34364923-4	2021	ATF3 was upregulated during chronic exposure to 0.25 muM arsenic, and loss of ATF3 promoted arsenic-induced transformation.	Arsenic	57-64	activating transcription factor 3	Homo sapiens	0-4
34364923-8	2021	Our results demonstrate that ATF3 upregulated by chronic low-dose arsenic exposure represses cell transformation and acquisition of malignant characteristics through inhibiting the production of proinflammatory cytokines and activation of downstream proteins AKT and STAT3, providing a new strategy for the prevention of carcinogen-induced lung cancer.	Arsenic	66-73	AKT serine/threonine kinase 1	Homo sapiens	259-262
34364923-4	2021	ATF3 was upregulated during chronic exposure to 0.25 muM arsenic, and loss of ATF3 promoted arsenic-induced transformation.	Arsenic	92-99	activating transcription factor 3	Homo sapiens	0-4
34364923-4	2021	ATF3 was upregulated during chronic exposure to 0.25 muM arsenic, and loss of ATF3 promoted arsenic-induced transformation.	Arsenic	92-99	activating transcription factor 3	Homo sapiens	78-82
34364923-8	2021	Our results demonstrate that ATF3 upregulated by chronic low-dose arsenic exposure represses cell transformation and acquisition of malignant characteristics through inhibiting the production of proinflammatory cytokines and activation of downstream proteins AKT and STAT3, providing a new strategy for the prevention of carcinogen-induced lung cancer.	Arsenic	66-73	signal transducer and activator of transcription 3	Homo sapiens	267-272
34332517-0	2021	JAK2/STAT3 in role of arsenic-induced cell proliferation: a systematic review and meta-analysis.	Arsenic	22-29	Janus kinase 2	Homo sapiens	0-4
34332517-0	2021	JAK2/STAT3 in role of arsenic-induced cell proliferation: a systematic review and meta-analysis.	Arsenic	22-29	signal transducer and activator of transcription 3	Homo sapiens	5-10
34332517-2	2021	A large number of studies have shown that STAT3 plays an important role in cell malignant proliferation, but there are still many contradictions in the effect of arsenic on JAK2/STAT3.	Arsenic	162-169	signal transducer and activator of transcription 3	Homo sapiens	42-47
34332517-7	2021	In addition, this study also found that arsenic exposure dose (<5 mumol m-3), time(<24 h) and cell type were important sources of heterogeneity in the process of exploring the effects of arsenic on p-STAT3, IL-6 and p-JAK2.	Arsenic	187-194	signal transducer and activator of transcription 3	Homo sapiens	200-205
34332517-8	2021	Dose-effect relationship meta-analysis results showed that arsenic exposure significantly increased the expression level of IL-6.	Arsenic	59-66	interleukin 6	Homo sapiens	124-128
34332517-2	2021	A large number of studies have shown that STAT3 plays an important role in cell malignant proliferation, but there are still many contradictions in the effect of arsenic on JAK2/STAT3.	Arsenic	162-169	Janus kinase 2	Homo sapiens	173-177
34332517-2	2021	A large number of studies have shown that STAT3 plays an important role in cell malignant proliferation, but there are still many contradictions in the effect of arsenic on JAK2/STAT3.	Arsenic	162-169	signal transducer and activator of transcription 3	Homo sapiens	178-183
34332517-9	2021	When the arsenic exposure concentration was less than 7 mumol m-3, the expression level of p-JAK2 upregulated significantly as the arsenic exposure concentration gradually increasing.	Arsenic	9-16	Janus kinase 2	Homo sapiens	93-97
34332517-3	2021	This study aims to explore the role of JAK2/STAT3 in arsenic-induced cell proliferation.	Arsenic	53-60	Janus kinase 2	Homo sapiens	39-43
34332517-9	2021	When the arsenic exposure concentration was less than 7 mumol m-3, the expression level of p-JAK2 upregulated significantly as the arsenic exposure concentration gradually increasing.	Arsenic	131-138	Janus kinase 2	Homo sapiens	93-97
34332517-10	2021	Moreover, the expression level of p-STAT3 elevated significantly with the gradual increase of the arsenic concentration under 5 mumol m-3 of arsenic exposure, but the expression level of p-STAT3 gradually decreases when the concentration is greater than 5 mumol m-3.	Arsenic	98-105	signal transducer and activator of transcription 3	Homo sapiens	36-41
34332517-10	2021	Moreover, the expression level of p-STAT3 elevated significantly with the gradual increase of the arsenic concentration under 5 mumol m-3 of arsenic exposure, but the expression level of p-STAT3 gradually decreases when the concentration is greater than 5 mumol m-3.	Arsenic	98-105	signal transducer and activator of transcription 3	Homo sapiens	189-194
34332517-3	2021	This study aims to explore the role of JAK2/STAT3 in arsenic-induced cell proliferation.	Arsenic	53-60	signal transducer and activator of transcription 3	Homo sapiens	44-49
34332517-4	2021	METHODS: By taking normal cells as the research object and using Standard Mean Difference (SMD) as the effect size, meta-analysis was used to explore the effect of arsenic on JAK2/STAT3.	Arsenic	164-171	Janus kinase 2	Homo sapiens	175-179
34332517-4	2021	METHODS: By taking normal cells as the research object and using Standard Mean Difference (SMD) as the effect size, meta-analysis was used to explore the effect of arsenic on JAK2/STAT3.	Arsenic	164-171	signal transducer and activator of transcription 3	Homo sapiens	180-185
34332517-10	2021	Moreover, the expression level of p-STAT3 elevated significantly with the gradual increase of the arsenic concentration under 5 mumol m-3 of arsenic exposure, but the expression level of p-STAT3 gradually decreases when the concentration is greater than 5 mumol m-3.	Arsenic	141-148	signal transducer and activator of transcription 3	Homo sapiens	36-41
34332517-5	2021	Then, the dose-effect Meta was used to further clarify the dose-effect relationship of arsenic on JAK2/STAT3.	Arsenic	87-94	Janus kinase 2	Homo sapiens	98-102
34332517-10	2021	Moreover, the expression level of p-STAT3 elevated significantly with the gradual increase of the arsenic concentration under 5 mumol m-3 of arsenic exposure, but the expression level of p-STAT3 gradually decreases when the concentration is greater than 5 mumol m-3.	Arsenic	141-148	signal transducer and activator of transcription 3	Homo sapiens	189-194
34332517-5	2021	Then, the dose-effect Meta was used to further clarify the dose-effect relationship of arsenic on JAK2/STAT3.	Arsenic	87-94	signal transducer and activator of transcription 3	Homo sapiens	103-108
34332517-11	2021	CONCLUSIONS: Exposure to low dose of arsenic could promote the expression of JAK2/STAT3 and induce the malignant proliferation of cells through upregulating IL-6, and there was dose-effect relationship among them.	Arsenic	37-44	Janus kinase 2	Homo sapiens	77-81
34332517-11	2021	CONCLUSIONS: Exposure to low dose of arsenic could promote the expression of JAK2/STAT3 and induce the malignant proliferation of cells through upregulating IL-6, and there was dose-effect relationship among them.	Arsenic	37-44	signal transducer and activator of transcription 3	Homo sapiens	82-87
34332517-6	2021	RESULTS: Through meta-analysis, this study found that arsenic could promote the phosphorylation of STAT3 (SMD=4.21, 95%CI (1.05, 7.37)), and increase IL-6 and p-JAK2, Vimentin, VEGF expression levels, thereby inducing malignant cell proliferation.	Arsenic	54-61	signal transducer and activator of transcription 3	Homo sapiens	99-104
34332517-11	2021	CONCLUSIONS: Exposure to low dose of arsenic could promote the expression of JAK2/STAT3 and induce the malignant proliferation of cells through upregulating IL-6, and there was dose-effect relationship among them.	Arsenic	37-44	interleukin 6	Homo sapiens	157-161
34332517-6	2021	RESULTS: Through meta-analysis, this study found that arsenic could promote the phosphorylation of STAT3 (SMD=4.21, 95%CI (1.05, 7.37)), and increase IL-6 and p-JAK2, Vimentin, VEGF expression levels, thereby inducing malignant cell proliferation.	Arsenic	54-61	interleukin 6	Homo sapiens	150-154
34332517-6	2021	RESULTS: Through meta-analysis, this study found that arsenic could promote the phosphorylation of STAT3 (SMD=4.21, 95%CI (1.05, 7.37)), and increase IL-6 and p-JAK2, Vimentin, VEGF expression levels, thereby inducing malignant cell proliferation.	Arsenic	54-61	Janus kinase 2	Homo sapiens	161-165
34332517-6	2021	RESULTS: Through meta-analysis, this study found that arsenic could promote the phosphorylation of STAT3 (SMD=4.21, 95%CI (1.05, 7.37)), and increase IL-6 and p-JAK2, Vimentin, VEGF expression levels, thereby inducing malignant cell proliferation.	Arsenic	54-61	vimentin	Homo sapiens	167-175
34332517-6	2021	RESULTS: Through meta-analysis, this study found that arsenic could promote the phosphorylation of STAT3 (SMD=4.21, 95%CI (1.05, 7.37)), and increase IL-6 and p-JAK2, Vimentin, VEGF expression levels, thereby inducing malignant cell proliferation.	Arsenic	54-61	vascular endothelial growth factor A	Homo sapiens	177-181
34332517-7	2021	In addition, this study also found that arsenic exposure dose (<5 mumol m-3), time(<24 h) and cell type were important sources of heterogeneity in the process of exploring the effects of arsenic on p-STAT3, IL-6 and p-JAK2.	Arsenic	40-47	interleukin 6	Homo sapiens	207-211
34243768-11	2021	Arsenic-associated KEGG pathways included lysosome, autophagy, and mTOR signaling, AMPK signaling, and one carbon pool by folate.	Arsenic	0-7	mechanistic target of rapamycin kinase	Homo sapiens	67-71
34068557-11	2021	Conclusively these findings suggest that AS-induced chronic pain and depression comorbidity elicits changes in the cerebellum lobules VI, VII, VIII, which are ameliorated through the use of EA at ST36 via its action on TRPV1 and related molecular pathways.	Arsenic	41-43	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	219-224
34234179-3	2021	In this research, deep learning is used to automatically delineate the corneal interfaces and measure corneal thickness with high accuracy in post-DMEK AS-OCT B-scans.	Arsenic	152-154	plexin A2	Homo sapiens	155-158
34230564-5	2021	Tap water had an average pH of 5.24 +- 1.63, ranging from 3.86 to 8.89, with the average concentrations of As and Pb of 0.77 microg/L and 0.004 microg/L, respectively.	Arsenic	107-109	nuclear RNA export factor 1	Homo sapiens	0-3
34283078-0	2021	Blood Arsenic Levels as a Marker of Breast Cancer Risk among BRCA1 Carriers.	Arsenic	6-13	BRCA1 DNA repair associated	Homo sapiens	61-66
34185686-3	2021	The results indicated that nZVI clusters were well disaggregated and the BET specific surface area increased from 19.61 m2 g-1 to 46.04 m2 g-1 of S-nZVI@ATP, resulting in an enhanced removal efficiency of arsenic from 51.4% to 65.1% at 20 min.	Arsenic	205-212	delta/notch like EGF repeat containing	Homo sapiens	73-76
34068211-4	2021	It has been shown that MET plays a protective role against the toxic effects induced by different metals (Pb, Cd, Cu, Zn, B, Al, V, Ni, La, As, and Cr) by regulating both the enzymatic and non-enzymatic antioxidant plant defense systems.	Arsenic	140-142	SAFB like transcription modulator	Homo sapiens	23-26
34661159-6	2021	Hyperthermia and arsenic therapy destabilize PML/RARalpha via distinct mechanisms and are synergistic in primary patient samples and in vivo, including three refractory APL cases.	Arsenic	17-24	PML nuclear body scaffold	Homo sapiens	45-48
34661159-6	2021	Hyperthermia and arsenic therapy destabilize PML/RARalpha via distinct mechanisms and are synergistic in primary patient samples and in vivo, including three refractory APL cases.	Arsenic	17-24	retinoic acid receptor alpha	Homo sapiens	49-57
34335974-6	2021	Meanwhile, we also validated that environmental factor arsenic is able to induce mdig, NRP1 and NRP2, and genetic disruption of mdig lowered expression of NRP1 and NRP2.	Arsenic	55-62	ribosomal oxygenase 2	Homo sapiens	81-85
34335974-6	2021	Meanwhile, we also validated that environmental factor arsenic is able to induce mdig, NRP1 and NRP2, and genetic disruption of mdig lowered expression of NRP1 and NRP2.	Arsenic	55-62	neuropilin 1	Homo sapiens	87-91
34335974-6	2021	Meanwhile, we also validated that environmental factor arsenic is able to induce mdig, NRP1 and NRP2, and genetic disruption of mdig lowered expression of NRP1 and NRP2.	Arsenic	55-62	neuropilin 2	Homo sapiens	96-100
34335974-6	2021	Meanwhile, we also validated that environmental factor arsenic is able to induce mdig, NRP1 and NRP2, and genetic disruption of mdig lowered expression of NRP1 and NRP2.	Arsenic	55-62	ribosomal oxygenase 2	Homo sapiens	128-132
34335974-6	2021	Meanwhile, we also validated that environmental factor arsenic is able to induce mdig, NRP1 and NRP2, and genetic disruption of mdig lowered expression of NRP1 and NRP2.	Arsenic	55-62	neuropilin 1	Homo sapiens	155-159
34335974-6	2021	Meanwhile, we also validated that environmental factor arsenic is able to induce mdig, NRP1 and NRP2, and genetic disruption of mdig lowered expression of NRP1 and NRP2.	Arsenic	55-62	neuropilin 2	Homo sapiens	164-168
34091413-2	2021	Arsenic also induced in murine brains alpha-synuclein aggregates, a pathognomic feature of PD.	Arsenic	0-7	synuclein, alpha	Mus musculus	38-53
34221922-0	2021	Roles of SET7/9 and LSD1 in the Pathogenesis of Arsenic-induced Hepatocyte Apoptosis.	Arsenic	48-55	SET domain containing 7, histone lysine methyltransferase	Homo sapiens	9-15
34221922-0	2021	Roles of SET7/9 and LSD1 in the Pathogenesis of Arsenic-induced Hepatocyte Apoptosis.	Arsenic	48-55	lysine demethylase 1A	Homo sapiens	20-24
34221922-2	2021	To investigate whether histone H3 lysine 4 (H3K4) methyltransferase (SET7/9) and histone H3K4 demethyltransferase (LSD1/KDM1A) can regulate endoplasmic reticulum stress (ERS)-related apoptosis by modulating the changes of H3K4 methylations in liver cells treated with arsenic.	Arsenic	268-275	SET domain containing 7, histone lysine methyltransferase	Homo sapiens	69-75
34221922-2	2021	To investigate whether histone H3 lysine 4 (H3K4) methyltransferase (SET7/9) and histone H3K4 demethyltransferase (LSD1/KDM1A) can regulate endoplasmic reticulum stress (ERS)-related apoptosis by modulating the changes of H3K4 methylations in liver cells treated with arsenic.	Arsenic	268-275	lysine demethylase 1A	Homo sapiens	115-119
34221922-2	2021	To investigate whether histone H3 lysine 4 (H3K4) methyltransferase (SET7/9) and histone H3K4 demethyltransferase (LSD1/KDM1A) can regulate endoplasmic reticulum stress (ERS)-related apoptosis by modulating the changes of H3K4 methylations in liver cells treated with arsenic.	Arsenic	268-275	lysine demethylase 1A	Homo sapiens	120-125
34075102-7	2021	We found that stressors (proteasome inhibition and arsenic) increased p62 expression and that this shifted the nuclear:cytoplasmic TDP-43 ratio.	Arsenic	51-58	nucleoporin 62	Homo sapiens	70-73
34075102-7	2021	We found that stressors (proteasome inhibition and arsenic) increased p62 expression and that this shifted the nuclear:cytoplasmic TDP-43 ratio.	Arsenic	51-58	TAR DNA binding protein	Homo sapiens	131-137
35523338-0	2022	Nrf2 activation contributes to hepatic tumor-augmenting effects of developmental arsenic exposure.	Arsenic	81-88	nuclear factor, erythroid derived 2, like 2	Mus musculus	0-4
35523338-3	2022	However, the role of Nrf2, a key regulator in antioxidative response, in tumor-augmenting effects by developmental arsenic exposure is unclear.	Arsenic	115-122	nuclear factor, erythroid derived 2, like 2	Mus musculus	21-25
35525345-0	2022	Arsenic exposure elevated ROS promotes energy metabolic reprogramming with enhanced AKT-dependent HK2 expression.	Arsenic	0-7	AKT serine/threonine kinase 1	Homo sapiens	84-87
35523338-4	2022	In the present study, wild-type C57BL/6J and Nrf2-konckout (Nrf2-KO) were developmentally exposed to inorganic arsenic via drinking water.	Arsenic	111-118	nuclear factor, erythroid derived 2, like 2	Mus musculus	45-49
35525345-0	2022	Arsenic exposure elevated ROS promotes energy metabolic reprogramming with enhanced AKT-dependent HK2 expression.	Arsenic	0-7	hexokinase 2	Homo sapiens	98-101
35525345-10	2022	Taken together, our results indicated that ROS induced by low-dose arsenic exposure determined energy metabolic reprogramming and acted a critical regulator for AKT-dependent HK2 expression and aerobic glycolysis.	Arsenic	67-74	AKT serine/threonine kinase 1	Homo sapiens	161-164
35525345-10	2022	Taken together, our results indicated that ROS induced by low-dose arsenic exposure determined energy metabolic reprogramming and acted a critical regulator for AKT-dependent HK2 expression and aerobic glycolysis.	Arsenic	67-74	hexokinase 2	Homo sapiens	175-178
35525345-5	2022	Here, mtDNA copy number is enhanced in arsenic-exposed populations and a positive correlation between serum HK2 and urinary total arsenic was observed in the individuals with high urine arsenic (>= 0.032 mg/L).	Arsenic	39-46	hexokinase 2	Homo sapiens	108-111
35523338-4	2022	In the present study, wild-type C57BL/6J and Nrf2-konckout (Nrf2-KO) were developmentally exposed to inorganic arsenic via drinking water.	Arsenic	111-118	nuclear factor, erythroid derived 2, like 2	Mus musculus	60-64
35525345-5	2022	Here, mtDNA copy number is enhanced in arsenic-exposed populations and a positive correlation between serum HK2 and urinary total arsenic was observed in the individuals with high urine arsenic (>= 0.032 mg/L).	Arsenic	130-137	hexokinase 2	Homo sapiens	108-111
35525345-5	2022	Here, mtDNA copy number is enhanced in arsenic-exposed populations and a positive correlation between serum HK2 and urinary total arsenic was observed in the individuals with high urine arsenic (>= 0.032 mg/L).	Arsenic	186-193	hexokinase 2	Homo sapiens	108-111
35523338-6	2022	Developmental arsenic exposure aggravated tumor multiplicity and burden, and expression of PCNA and AFP in hepatic tumors induced by DEN.	Arsenic	14-21	proliferating cell nuclear antigen	Mus musculus	91-95
35525345-6	2022	In a rat model of trivalent arsenic (iAs3+) exposure, the levels of HK2, NDUFA9 and NDUFB8 were increased in the rats treated with iAs3+ daily by gavage for 12 weeks than those in the control rats.	Arsenic	28-35	hexokinase 2	Rattus norvegicus	68-71
35523338-6	2022	Developmental arsenic exposure aggravated tumor multiplicity and burden, and expression of PCNA and AFP in hepatic tumors induced by DEN.	Arsenic	14-21	alpha fetoprotein	Mus musculus	100-103
35523338-7	2022	Nrf2 activation as indicated by over-expression of Nrf2 and its downstream genes, including Gss, Gsr, p62, Gclc and Gclm, was found in liver tumors, as well as in the livers in developmentally arsenic-exposed pups at weaning.	Arsenic	193-200	nuclear factor, erythroid derived 2, like 2	Mus musculus	0-4
35525345-6	2022	In a rat model of trivalent arsenic (iAs3+) exposure, the levels of HK2, NDUFA9 and NDUFB8 were increased in the rats treated with iAs3+ daily by gavage for 12 weeks than those in the control rats.	Arsenic	28-35	NADH:ubiquinone oxidoreductase subunit A9	Rattus norvegicus	73-79
35523338-7	2022	Nrf2 activation as indicated by over-expression of Nrf2 and its downstream genes, including Gss, Gsr, p62, Gclc and Gclm, was found in liver tumors, as well as in the livers in developmentally arsenic-exposed pups at weaning.	Arsenic	193-200	nuclear factor, erythroid derived 2, like 2	Mus musculus	51-55
35523338-8	2022	Notably, Nrf2 deficiency attenuated tumor-augmenting effects and over-expression of Nrf2 downstream genes due to developmental arsenic exposure.	Arsenic	127-134	nuclear factor, erythroid derived 2, like 2	Mus musculus	9-13
35525345-6	2022	In a rat model of trivalent arsenic (iAs3+) exposure, the levels of HK2, NDUFA9 and NDUFB8 were increased in the rats treated with iAs3+ daily by gavage for 12 weeks than those in the control rats.	Arsenic	28-35	NADH:ubiquinone oxidoreductase subunit B8	Rattus norvegicus	84-90
35525345-7	2022	Subsequently, in a low-dose arsenic exposure cell model we found that 0.2 mumol/L iAs3+ induced aerobic glycolysis to promote L-02 cells proliferation and inhibit apoptosis, in which HK2 played an important role.	Arsenic	28-35	hexokinase 2	Homo sapiens	183-186
35405246-5	2022	The spatial distribution of Mn > 400 mug/L and Fe > 0.3 mg/L was compared and contrasted with that of the critical geogenic contaminant arsenic (As), confirming that high Fe concentrations are often associated with high As concentrations, whereas areas of high concentrations of Mn and As are frequently found adjacent to each other.	Arsenic	145-147	homeostatic iron regulator	Homo sapiens	166-173
35523338-8	2022	Notably, Nrf2 deficiency attenuated tumor-augmenting effects and over-expression of Nrf2 downstream genes due to developmental arsenic exposure.	Arsenic	127-134	nuclear factor, erythroid derived 2, like 2	Mus musculus	84-88
35413363-6	2022	Meanwhile, co-treatment with As and PSNPs induced apoptosis in the liver, which was confirmed by ultrastructure observation and changes in the expression of apoptosis indicators (P53, Bax, Bcl-2, Caspase-3, Caspase-9, Cleaved-Caspase-3 and Cytc).	Arsenic	29-31	transformation related protein 53, pseudogene	Mus musculus	179-182
35405246-5	2022	The spatial distribution of Mn > 400 mug/L and Fe > 0.3 mg/L was compared and contrasted with that of the critical geogenic contaminant arsenic (As), confirming that high Fe concentrations are often associated with high As concentrations, whereas areas of high concentrations of Mn and As are frequently found adjacent to each other.	Arsenic	220-222	homeostatic iron regulator	Homo sapiens	166-173
35452640-0	2022	The fate of co-existent cadmium and arsenic during Fe(II)-induced transformation of As(V)/Cd(II)-bearing ferrihydrite.	Arsenic	36-43	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	84-89
35468398-0	2022	SOX2 modulated astrocytic process plasticity is involved in arsenic-induced metabolic disorders.	Arsenic	60-67	SRY (sex determining region Y)-box 2	Mus musculus	0-4
35468398-5	2022	Arsenic exposure also impaired glucose sensing and the activation of proopiomelanocortin (POMC) neurons in the hypothalamus.	Arsenic	0-7	pro-opiomelanocortin-alpha	Mus musculus	69-88
35468398-5	2022	Arsenic exposure also impaired glucose sensing and the activation of proopiomelanocortin (POMC) neurons in the hypothalamus.	Arsenic	0-7	pro-opiomelanocortin-alpha	Mus musculus	90-94
35468398-7	2022	Further research revealed that arsenic exposure inhibited the expression of sex-determining region Y-Box 2 (SOX2), which decreased the expression level of insulin receptors (INSRs) and the phosphorylation of AKT.	Arsenic	31-38	SRY (sex determining region Y)-box 2	Mus musculus	76-106
35468398-7	2022	Further research revealed that arsenic exposure inhibited the expression of sex-determining region Y-Box 2 (SOX2), which decreased the expression level of insulin receptors (INSRs) and the phosphorylation of AKT.	Arsenic	31-38	SRY (sex determining region Y)-box 2	Mus musculus	108-112
35468398-7	2022	Further research revealed that arsenic exposure inhibited the expression of sex-determining region Y-Box 2 (SOX2), which decreased the expression level of insulin receptors (INSRs) and the phosphorylation of AKT.	Arsenic	31-38	thymoma viral proto-oncogene 1	Mus musculus	208-211
35468398-8	2022	The conditional deletion of astrocytic SOX2 exacerbated arsenic-induced effects on metabolic disorders, the impairment of hypothalamic astrocytic processes, and the inhibition of INSR/AKT signaling.	Arsenic	56-63	SRY (sex determining region Y)-box 2	Mus musculus	39-43
35468398-8	2022	The conditional deletion of astrocytic SOX2 exacerbated arsenic-induced effects on metabolic disorders, the impairment of hypothalamic astrocytic processes, and the inhibition of INSR/AKT signaling.	Arsenic	56-63	insulin receptor	Mus musculus	179-183
35468398-8	2022	The conditional deletion of astrocytic SOX2 exacerbated arsenic-induced effects on metabolic disorders, the impairment of hypothalamic astrocytic processes, and the inhibition of INSR/AKT signaling.	Arsenic	56-63	thymoma viral proto-oncogene 1	Mus musculus	184-187
35468398-9	2022	Furthermore, the arsenic-induced impairment of astrocytic processes and inhibitory effects on INSR/AKT signaling were reversed by SOX2 overexpression in primary hypothalamic astrocytes.	Arsenic	17-24	insulin receptor	Mus musculus	94-98
35468398-9	2022	Furthermore, the arsenic-induced impairment of astrocytic processes and inhibitory effects on INSR/AKT signaling were reversed by SOX2 overexpression in primary hypothalamic astrocytes.	Arsenic	17-24	thymoma viral proto-oncogene 1	Mus musculus	99-102
35468398-9	2022	Furthermore, the arsenic-induced impairment of astrocytic processes and inhibitory effects on INSR/AKT signaling were reversed by SOX2 overexpression in primary hypothalamic astrocytes.	Arsenic	17-24	SRY (sex determining region Y)-box 2	Mus musculus	130-134
35468398-10	2022	Together, we demonstrated here that chronic arsenic exposure caused metabolic disorders by impairing SOX2-modulated hypothalamic astrocytic process plasticity in mice.	Arsenic	44-51	SRY (sex determining region Y)-box 2	Mus musculus	101-105
35413363-6	2022	Meanwhile, co-treatment with As and PSNPs induced apoptosis in the liver, which was confirmed by ultrastructure observation and changes in the expression of apoptosis indicators (P53, Bax, Bcl-2, Caspase-3, Caspase-9, Cleaved-Caspase-3 and Cytc).	Arsenic	29-31	BCL2-associated X protein	Mus musculus	184-187
35468398-11	2022	Our study provides evidence of novel central regulatory mechanisms underlying arsenic-induced metabolic disorders and emphasizes the crucial role of SOX2 in regulating the process plasticity of adult astrocytes.	Arsenic	78-85	SRY (sex determining region Y)-box 2	Mus musculus	149-153
35413363-6	2022	Meanwhile, co-treatment with As and PSNPs induced apoptosis in the liver, which was confirmed by ultrastructure observation and changes in the expression of apoptosis indicators (P53, Bax, Bcl-2, Caspase-3, Caspase-9, Cleaved-Caspase-3 and Cytc).	Arsenic	29-31	B cell leukemia/lymphoma 2	Mus musculus	189-194
35413363-6	2022	Meanwhile, co-treatment with As and PSNPs induced apoptosis in the liver, which was confirmed by ultrastructure observation and changes in the expression of apoptosis indicators (P53, Bax, Bcl-2, Caspase-3, Caspase-9, Cleaved-Caspase-3 and Cytc).	Arsenic	29-31	caspase 3	Mus musculus	196-205
35413363-6	2022	Meanwhile, co-treatment with As and PSNPs induced apoptosis in the liver, which was confirmed by ultrastructure observation and changes in the expression of apoptosis indicators (P53, Bax, Bcl-2, Caspase-3, Caspase-9, Cleaved-Caspase-3 and Cytc).	Arsenic	29-31	caspase 9	Mus musculus	207-216
35490756-8	2022	Moreover, our analyses revealed associations between AS3MT variants and the fraction of mono-methylated arsenic in urine and showed that the Bolivian study groups had the highest frequency of alleles associated with more efficient arsenic metabolism reported so far.	Arsenic	104-111	arsenite methyltransferase	Homo sapiens	53-58
35413363-7	2022	Additionally, co-exposure of As and PSNPs induced pyroptosis in the liver through NLRP3/Caspase-1 pathway via targeting NLRP3, ASC, Pro-Caspase-1, GSDMD and Cleaved-Caspase-1 expressions.	Arsenic	29-31	NLR family, pyrin domain containing 3	Mus musculus	82-87
35413363-7	2022	Additionally, co-exposure of As and PSNPs induced pyroptosis in the liver through NLRP3/Caspase-1 pathway via targeting NLRP3, ASC, Pro-Caspase-1, GSDMD and Cleaved-Caspase-1 expressions.	Arsenic	29-31	caspase 1	Mus musculus	88-97
35413363-7	2022	Additionally, co-exposure of As and PSNPs induced pyroptosis in the liver through NLRP3/Caspase-1 pathway via targeting NLRP3, ASC, Pro-Caspase-1, GSDMD and Cleaved-Caspase-1 expressions.	Arsenic	29-31	NLR family, pyrin domain containing 3	Mus musculus	120-125
35413363-7	2022	Additionally, co-exposure of As and PSNPs induced pyroptosis in the liver through NLRP3/Caspase-1 pathway via targeting NLRP3, ASC, Pro-Caspase-1, GSDMD and Cleaved-Caspase-1 expressions.	Arsenic	29-31	steroid sulfatase	Mus musculus	127-130
35413363-7	2022	Additionally, co-exposure of As and PSNPs induced pyroptosis in the liver through NLRP3/Caspase-1 pathway via targeting NLRP3, ASC, Pro-Caspase-1, GSDMD and Cleaved-Caspase-1 expressions.	Arsenic	29-31	gasdermin D	Mus musculus	147-152
35395352-6	2022	Arsenic concentrations were greatest in the fine <63 mum fraction across all the different river environments (7.3-189 mg kg-1, or 1-26% of total sample As), attributed to fine-grained primary arsenopyrite and/or sorption of As(V) to fine solid-phases.	Arsenic	0-7	plexin A3	Homo sapiens	49-52
35381244-0	2022	Low dose of arsenic exacerbates toxicity to mice and IPEC-J2 cells exposed with deoxynivalenol: Aryl hydrocarbon receptor and autophagy might be novel therapeutic targets.	Arsenic	12-19	aryl hydrocarbon receptor	Sus scrofa	96-121
35390615-10	2022	In addition, negatively charged arsenate and other anions in the liquid phase could compete with As ions for adsorption sites to promote the release of As(V) and/or reductive desorption of As(III).	Arsenic	97-99	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	152-157
35598369-0	2022	Melatonin improves arsenic-induced hypertension through the inactivation of the Sirt1/autophagy pathway in rat.	Arsenic	19-26	sirtuin 1	Rattus norvegicus	80-85
35598369-9	2022	The exposure to As caused substantial histological damage in aorta tissue and changed vasoconstriction and vasorelaxation responses to KCl, PE, and Ach in isolated rat aorta.	Arsenic	16-18	acyl-CoA thioesterase 12	Rattus norvegicus	148-151
35598369-13	2022	In conclusion, our findings showed that Mel could have a protective effect against As-induced vascular toxicity by inhibiting apoptosis and the Sirt1/autophagy pathway.	Arsenic	83-85	sirtuin 1	Rattus norvegicus	144-149
35278445-0	2022	Elevated serum periostin levels among arsenic-exposed individuals and their associations with the features of asthma.	Arsenic	38-45	periostin	Homo sapiens	15-24
35490796-2	2022	Our previous study revealed that increased transcript levels of inflammatory genes (i.e. COX2, EGR1, and SOCS3) coupled with hypomethylation of the promoter regions of these genes was associated with increased DNA damage in arsenic-exposed newborns through their early childhood.	Arsenic	224-231	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	89-93
35278445-6	2022	Therefore, this study was designed to explore the associations of serum periostin levels with arsenic exposure and the features of asthma in 442 individuals in Bangladesh who participated in our previous study.	Arsenic	94-101	periostin	Homo sapiens	72-81
35278445-9	2022	In this study, we found that serum periostin levels of the participants were increased with increasing exposure to arsenic.	Arsenic	115-122	periostin	Homo sapiens	35-44
35278445-10	2022	Notably, even the participants with 10.1-50 mug/L arsenic in drinking water had significantly higher levels of periostin than participants with <10 mug/L of water arsenic.	Arsenic	50-57	periostin	Homo sapiens	111-120
35278445-13	2022	Additionally, causal mediation analyses revealed that arsenic exposure metrics had both direct and indirect (periostin-mediated) effects on the risk of RAO and asthma symptoms.	Arsenic	54-61	periostin	Homo sapiens	109-118
35278445-14	2022	Thus, the results suggested that periostin may be involved in the arsenic-related pathogenesis of Th2-mediated asthma.	Arsenic	66-73	periostin	Homo sapiens	33-42
35278445-15	2022	The elevated serum periostin levels may predict the greater risk of asthma among the people living in arsenic-endemic areas.	Arsenic	102-109	periostin	Homo sapiens	19-28
35490796-2	2022	Our previous study revealed that increased transcript levels of inflammatory genes (i.e. COX2, EGR1, and SOCS3) coupled with hypomethylation of the promoter regions of these genes was associated with increased DNA damage in arsenic-exposed newborns through their early childhood.	Arsenic	224-231	early growth response 1	Homo sapiens	95-99
35490796-2	2022	Our previous study revealed that increased transcript levels of inflammatory genes (i.e. COX2, EGR1, and SOCS3) coupled with hypomethylation of the promoter regions of these genes was associated with increased DNA damage in arsenic-exposed newborns through their early childhood.	Arsenic	224-231	suppressor of cytokine signaling 3	Homo sapiens	105-110
35373418-0	2022	Developmental arsenic exposure impairs cognition, directly targets DNMT3A, and reduces DNA methylation.	Arsenic	14-21	DNA methyltransferase 3A	Mus musculus	67-73
35580760-0	2022	Trivalent arsenic impairs the effector response of human CD4+ and CD8+ T cells to influenza A virus ex vivo.	Arsenic	10-17	CD4 molecule	Homo sapiens	57-60
35580760-0	2022	Trivalent arsenic impairs the effector response of human CD4+ and CD8+ T cells to influenza A virus ex vivo.	Arsenic	10-17	CD8a molecule	Homo sapiens	66-69
35513056-0	2022	Chronic arsenic exposure suppresses ATM pathway activation in human keratinocytes.	Arsenic	8-15	ATM serine/threonine kinase	Homo sapiens	36-39
35217035-5	2022	It was concluded that two selected Pseudomonas strains have NAFO functionality by addition of iron as iron reduction-oxidation pair in the arid soil, further potentially fixing NH4+ while As(III) can be effectively remediated through the FeOB participation in forms of adsorption and co-precipitation of Fe(OH)3 through an oxidation of Fe(II) process.	Arsenic	188-190	general transcription factor IIE subunit 1	Homo sapiens	304-311
35487149-4	2022	ArsI is a non-heme ferrous iron (Fe(II))-dependent dioxygenase that catalyzes oxygen-dependent cleavage of the carbon-arsenic (C-As) bond in trivalent organoarsenicals, degrading them to inorganic As(III).	Arsenic	118-125	arylsulfatase family member I	Homo sapiens	0-4
35621115-0	2022	Strain-induced spin-gapless semiconductors and pure thermal spin-current in magnetic black arsenic-phosphorus monolayers.	Arsenic	91-98	spindlin 1	Homo sapiens	15-19
35621115-0	2022	Strain-induced spin-gapless semiconductors and pure thermal spin-current in magnetic black arsenic-phosphorus monolayers.	Arsenic	91-98	spindlin 1	Homo sapiens	60-64
35373418-4	2022	Arsenic atoms directly bind to the cysteine-rich ADD domain of DNA methyltransferase 3A (DNMT3A), triggering ubiquitin- and proteasome-mediated degradation of DNMT3A in different cellular contexts.	Arsenic	0-7	DNA methyltransferase 3A	Mus musculus	63-87
35373418-4	2022	Arsenic atoms directly bind to the cysteine-rich ADD domain of DNA methyltransferase 3A (DNMT3A), triggering ubiquitin- and proteasome-mediated degradation of DNMT3A in different cellular contexts.	Arsenic	0-7	DNA methyltransferase 3A	Mus musculus	89-95
35373418-4	2022	Arsenic atoms directly bind to the cysteine-rich ADD domain of DNA methyltransferase 3A (DNMT3A), triggering ubiquitin- and proteasome-mediated degradation of DNMT3A in different cellular contexts.	Arsenic	0-7	DNA methyltransferase 3A	Mus musculus	159-165
35142421-9	2022	These results indicate that inorganic arsenic promotes the apoptosis of human immortal keratinocytes through the TGF-beta1/ERK signaling pathway.	Arsenic	38-45	transforming growth factor beta 1	Homo sapiens	113-122
35142421-3	2022	Previous studies have demonstrated that extracellular signal-regulated kinase (ERK) is related to arsenic-induced apoptosis.	Arsenic	98-105	mitogen-activated protein kinase 1	Homo sapiens	40-77
35142421-3	2022	Previous studies have demonstrated that extracellular signal-regulated kinase (ERK) is related to arsenic-induced apoptosis.	Arsenic	98-105	mitogen-activated protein kinase 1	Homo sapiens	79-82
35142421-5	2022	In this study, the associations between the TGF-beta1/ERK signaling pathway and arsenic-induced cell apoptosis were confirmed using the HaCaT cell model.	Arsenic	80-87	transforming growth factor beta 1	Homo sapiens	44-53
35089513-10	2022	From the PCA diagram, we can observe that those sampling points in the positive direction of PC1 were expected to have a high concentration of Cu, Zn, As, Ni while having extremely little sand content.	Arsenic	151-153	proprotein convertase subtilisin/kexin type 1	Homo sapiens	93-96
35142421-9	2022	These results indicate that inorganic arsenic promotes the apoptosis of human immortal keratinocytes through the TGF-beta1/ERK signaling pathway.	Arsenic	38-45	mitogen-activated protein kinase 1	Homo sapiens	123-126
35258777-11	2022	In addition, EA pretreatment notably reduced the AS-induced increased level of cleaved caspase-9, cleaved caspase-3 and expression of Cyt c, Bax/Bcl-2 ratio, as well as neuronal apoptosis rate in aged rats.	Arsenic	49-51	caspase 9	Rattus norvegicus	87-96
35142421-5	2022	In this study, the associations between the TGF-beta1/ERK signaling pathway and arsenic-induced cell apoptosis were confirmed using the HaCaT cell model.	Arsenic	80-87	mitogen-activated protein kinase 1	Homo sapiens	54-57
35258777-11	2022	In addition, EA pretreatment notably reduced the AS-induced increased level of cleaved caspase-9, cleaved caspase-3 and expression of Cyt c, Bax/Bcl-2 ratio, as well as neuronal apoptosis rate in aged rats.	Arsenic	49-51	caspase 3	Rattus norvegicus	106-115
35258777-11	2022	In addition, EA pretreatment notably reduced the AS-induced increased level of cleaved caspase-9, cleaved caspase-3 and expression of Cyt c, Bax/Bcl-2 ratio, as well as neuronal apoptosis rate in aged rats.	Arsenic	49-51	BCL2 associated X, apoptosis regulator	Rattus norvegicus	141-144
35258777-11	2022	In addition, EA pretreatment notably reduced the AS-induced increased level of cleaved caspase-9, cleaved caspase-3 and expression of Cyt c, Bax/Bcl-2 ratio, as well as neuronal apoptosis rate in aged rats.	Arsenic	49-51	BCL2, apoptosis regulator	Rattus norvegicus	145-150
35460952-6	2022	RESULTS: In our study, the association with metabolic principal component (mPC) 1 (reflecting non-essential and essential amino acids, including branched chain, and bacterial co-metabolism versus fatty acids and VLDL subclasses) was positive for Se and Zn, but inverse for Cu, arsenobetaine-corrected arsenic (As) and Sb.	Arsenic	301-308	mitochondrial pyruvate carrier 1	Homo sapiens	44-81
35460952-6	2022	RESULTS: In our study, the association with metabolic principal component (mPC) 1 (reflecting non-essential and essential amino acids, including branched chain, and bacterial co-metabolism versus fatty acids and VLDL subclasses) was positive for Se and Zn, but inverse for Cu, arsenobetaine-corrected arsenic (As) and Sb.	Arsenic	310-312	mitochondrial pyruvate carrier 1	Homo sapiens	44-81
35579678-0	2022	Histone demethylase JHDM2A participates in the repair of arsenic-induced DNA damage in L-02 cells by regulating DDB2.	Arsenic	57-64	lysine demethylase 3A	Homo sapiens	20-26
35579678-0	2022	Histone demethylase JHDM2A participates in the repair of arsenic-induced DNA damage in L-02 cells by regulating DDB2.	Arsenic	57-64	damage specific DNA binding protein 2	Homo sapiens	112-116
35579678-4	2022	In this study, an in vitro model was established using human normal hepatocytes L-02 to investigate the mechanism of the specific demethylase JHDM2A of H3K9me2 in the repair of arsenic-induced DNA damage in L-02 cells.	Arsenic	177-184	lysine demethylase 3A	Homo sapiens	142-148
35579678-7	2022	Thereafter, we overexpressed and repressed JHDM2A and found a close association between JHDM2A and arsenic-induced DNA damage.	Arsenic	99-106	lysine demethylase 3A	Homo sapiens	43-49
35579678-7	2022	Thereafter, we overexpressed and repressed JHDM2A and found a close association between JHDM2A and arsenic-induced DNA damage.	Arsenic	99-106	lysine demethylase 3A	Homo sapiens	88-94
35579678-9	2022	These results suggest a potential mechanism by which JHDM2A may regulate DDB2 gene expression, participate in the NBR process, and play a role in arsenic-induced DNA damage in L-02 cells, which is not the result of JHDM2A exerting demethylation on H3K9me2 in the DDB2 promoter region.	Arsenic	146-153	lysine demethylase 3A	Homo sapiens	53-59
35579678-9	2022	These results suggest a potential mechanism by which JHDM2A may regulate DDB2 gene expression, participate in the NBR process, and play a role in arsenic-induced DNA damage in L-02 cells, which is not the result of JHDM2A exerting demethylation on H3K9me2 in the DDB2 promoter region.	Arsenic	146-153	damage specific DNA binding protein 2	Homo sapiens	263-267
35510797-5	2022	Genetic analysis showed that the sec24c mutants are hypersensitive to cadmium (Cd) and arsenic (As) treatments due to mislocalization of ABCC1 and ABCC2, which results in defects in the vacuole compartmentalization of the toxic metals.	Arsenic	87-94	multidrug resistance-associated protein 1	Arabidopsis thaliana	137-142
35623570-3	2022	The subsoil profiles exhibited relatively high concentrations of As at 26.1-982 mg/kg (median of 112 mg/kg), and the As was dominated by As(V) (85-96%) and primarily associated with the residual fraction (50.7-94.7%).	Arsenic	117-119	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	137-142
35594310-0	2022	Effects of arsenic on the topology and solubility of promyelocytic leukemia (PML)-nuclear bodies.	Arsenic	11-18	PML nuclear body scaffold	Homo sapiens	77-80
35594310-2	2022	Trivalent arsenic (As3+) is known to cure APL by binding to cysteine residues of PML and enhance the degradation of PML-retinoic acid receptor alpha (RARalpha), a t(15;17) gene translocation product in APL cells, and restore PML-nuclear bodies (NBs).	Arsenic	10-17	PML nuclear body scaffold	Homo sapiens	81-84
35594310-2	2022	Trivalent arsenic (As3+) is known to cure APL by binding to cysteine residues of PML and enhance the degradation of PML-retinoic acid receptor alpha (RARalpha), a t(15;17) gene translocation product in APL cells, and restore PML-nuclear bodies (NBs).	Arsenic	10-17	retinoic acid receptor alpha	Homo sapiens	150-158
35594310-2	2022	Trivalent arsenic (As3+) is known to cure APL by binding to cysteine residues of PML and enhance the degradation of PML-retinoic acid receptor alpha (RARalpha), a t(15;17) gene translocation product in APL cells, and restore PML-nuclear bodies (NBs).	Arsenic	10-17	PML nuclear body scaffold	Homo sapiens	225-228
35627541-9	2022	Overall, the high prevalence of arsenic above the MPL in Guatemala City tap water represents a potential health risk that current water treatment processes are not optimized to remove.	Arsenic	32-39	nuclear RNA export factor 1	Homo sapiens	72-75
35569872-10	2022	The proposed sensing platform not only exhibits the trace level detection of As3+ ions in cost-effective manner but also opens a pathway for the development of state-of-art device fabrication for on-site detection of arsenic.	Arsenic	217-224	PDS5 cohesin associated factor B	Homo sapiens	77-80
35537205-0	2022	De Novo Design of the ArsR Regulated Pars Promoter Enables a Highly Sensitive Whole-Cell Biosensor for Arsenic Contamination.	Arsenic	103-110	DNA-binding transcriptional repressor ArsR	Escherichia coli str. K-12 substr. MG1655	22-26
35537205-3	2022	Here, we use the arsenic-responsive ArsR-Pars regulation system from Escherichia coli MG1655 as the sensing element and coupled gfp or lacZ as the reporter gene to construct the genetic circuit for characterizing the refactored promoters.	Arsenic	17-24	DNA-binding transcriptional repressor ArsR	Escherichia coli str. K-12 substr. MG1655	36-40
35364107-0	2022	Prenatal exposure to arsenic promotes sterile inflammation through the Polycomb repressive element EZH2 and accelerates skin tumorigenesis in mouse.	Arsenic	21-28	chromobox 2	Mus musculus	71-79
35364107-0	2022	Prenatal exposure to arsenic promotes sterile inflammation through the Polycomb repressive element EZH2 and accelerates skin tumorigenesis in mouse.	Arsenic	21-28	enhancer of zeste 2 polycomb repressive complex 2 subunit	Mus musculus	99-103
35378173-7	2022	Arsenic reduced the width of the pericryptal lamina propria by 1.6-fold, and reduced Pdgfra mRNA expression, which is expressed in intestinal telocytes and trophocytes, by 4.2-fold.	Arsenic	0-7	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	85-91
35378173-11	2022	Our results suggest arsenic impairs intestinal trophocytes and telocytes, leading to alterations in the Bmp signaling pathway.	Arsenic	20-27	bone morphogenetic protein 4	Mus musculus	104-107
35074374-0	2022	Cortex metabolome and proteome analysis reveals chronic arsenic exposure via drinking water induces developmental neurotoxicity through hnRNP L mediated mitochondrial dysfunction in male rats.	Arsenic	56-63	heterogeneous nuclear ribonucleoprotein L	Rattus norvegicus	136-143
35074374-7	2022	Chronic arsenic exposure affected the cognitive function by inducing the overproduction of amyloid-beta (Abeta) peptides and the redox imbalance in the mitochondria.	Arsenic	8-15	amyloid beta precursor protein	Rattus norvegicus	105-110
35074374-11	2022	These findings suggest hnRNP L could be a potential target for the treatment of arsenic-induced neurotoxicity.	Arsenic	80-87	heterogeneous nuclear ribonucleoprotein L	Rattus norvegicus	23-30
35510797-5	2022	Genetic analysis showed that the sec24c mutants are hypersensitive to cadmium (Cd) and arsenic (As) treatments due to mislocalization of ABCC1 and ABCC2, which results in defects in the vacuole compartmentalization of the toxic metals.	Arsenic	87-94	multidrug resistance-associated protein 2	Arabidopsis thaliana	147-152
35510797-5	2022	Genetic analysis showed that the sec24c mutants are hypersensitive to cadmium (Cd) and arsenic (As) treatments due to mislocalization of ABCC1 and ABCC2, which results in defects in the vacuole compartmentalization of the toxic metals.	Arsenic	96-98	multidrug resistance-associated protein 1	Arabidopsis thaliana	137-142
35510797-5	2022	Genetic analysis showed that the sec24c mutants are hypersensitive to cadmium (Cd) and arsenic (As) treatments due to mislocalization of ABCC1 and ABCC2, which results in defects in the vacuole compartmentalization of the toxic metals.	Arsenic	96-98	multidrug resistance-associated protein 2	Arabidopsis thaliana	147-152
35378400-9	2022	Our findings suggested that necroptosis induced by microglia-derived TNF-alpha upon arsenite exposure partially played a role in arsenic-induced cell death which underlie the fundamental event of arsenic-related neurotoxicity.	Arsenic	196-203	tumor necrosis factor	Homo sapiens	69-78
35244730-2	2022	In human and mouse, inorganic arsenic (iAs) is metabolized in a series of methylation steps catalyzed by arsenic (3) methyltransferase (AS3MT), forming methylated arsenite (MAsIII), dimethylarsenite (DMAIII) and the volatile trimethylarsine (TMA).	Arsenic	30-37	arsenite methyltransferase	Mus musculus	136-141
35244730-2	2022	In human and mouse, inorganic arsenic (iAs) is metabolized in a series of methylation steps catalyzed by arsenic (3) methyltransferase (AS3MT), forming methylated arsenite (MAsIII), dimethylarsenite (DMAIII) and the volatile trimethylarsine (TMA).	Arsenic	105-112	arsenite methyltransferase	Mus musculus	136-141
35244730-3	2022	The methylation of arsenic is coordinated by four conserved cysteines proposed to participate in catalysis, namely C33, C62, C157, and C207 in mouse AS3MT.	Arsenic	19-26	CD82 antigen	Mus musculus	115-118
35244730-3	2022	The methylation of arsenic is coordinated by four conserved cysteines proposed to participate in catalysis, namely C33, C62, C157, and C207 in mouse AS3MT.	Arsenic	19-26	inositol polyphosphate 5-phosphatase K	Mus musculus	120-123
35244730-3	2022	The methylation of arsenic is coordinated by four conserved cysteines proposed to participate in catalysis, namely C33, C62, C157, and C207 in mouse AS3MT.	Arsenic	19-26	arsenite methyltransferase	Mus musculus	149-154
35378400-5	2022	Although there were evidences suggested that arsenic could induce both microglia activation and TNF-alpha production in the nervous system, the mechanism of arsenic-induced neurotoxicity due to microglia activation is rarely studied.	Arsenic	45-52	tumor necrosis factor	Homo sapiens	96-105
35351628-9	2022	The study reveals that minocycline administration reversed arsenic-induced increased expression of CD68, ROS, NO, cytokine production, phagocytosis and TREM2 expression.	Arsenic	59-66	CD68 antigen	Mus musculus	99-103
35378400-5	2022	Although there were evidences suggested that arsenic could induce both microglia activation and TNF-alpha production in the nervous system, the mechanism of arsenic-induced neurotoxicity due to microglia activation is rarely studied.	Arsenic	157-164	tumor necrosis factor	Homo sapiens	96-105
35378400-6	2022	In addition, the role of microglia-derived TNF-alpha in response to arsenic exposure in necroptosis has not been documented before.	Arsenic	68-75	tumor necrosis factor	Homo sapiens	43-52
35351628-9	2022	The study reveals that minocycline administration reversed arsenic-induced increased expression of CD68, ROS, NO, cytokine production, phagocytosis and TREM2 expression.	Arsenic	59-66	triggering receptor expressed on myeloid cells 2	Mus musculus	152-157
35351628-10	2022	Arsenic-induced reduced expression of PSD95 protein was reversed by minocycline, although the mRNA of PSD95 was unaltered among different groups.	Arsenic	0-7	discs large MAGUK scaffold protein 4	Mus musculus	38-43
35351628-10	2022	Arsenic-induced reduced expression of PSD95 protein was reversed by minocycline, although the mRNA of PSD95 was unaltered among different groups.	Arsenic	0-7	discs large MAGUK scaffold protein 4	Mus musculus	102-107
35063782-3	2022	The maximum adsorption capacities normalized to SSA (qm,nor) of S-siderite and l-siderite were 0.161 and 0.174 mg/m2 for As(III), and 1.460 and 0.360 mg/m2 for As(V), respectively, indicating that the sorption affinity of S-siderite depends more on the arsenic species (III and V).	Arsenic	253-260	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	160-165
35478061-5	2022	Arsenic and mercury showed significant associations with the incidence of ER-positive, ER-negative, PR-positive, and PR-negative breast cancers.	Arsenic	0-7	epiregulin	Homo sapiens	74-76
35175559-6	2022	Supporting this, arsenic-treated male rats demonstrated larger reduction in the hippocampal NeuN and %-surviving neurons, together with increased apoptosis and altered BMP2/Smad and BDNF/TrkB pathways compared to their female counterparts.	Arsenic	17-24	RNA binding fox-1 homolog 3	Rattus norvegicus	92-96
35175559-6	2022	Supporting this, arsenic-treated male rats demonstrated larger reduction in the hippocampal NeuN and %-surviving neurons, together with increased apoptosis and altered BMP2/Smad and BDNF/TrkB pathways compared to their female counterparts.	Arsenic	17-24	bone morphogenetic protein 2	Rattus norvegicus	168-172
35175559-6	2022	Supporting this, arsenic-treated male rats demonstrated larger reduction in the hippocampal NeuN and %-surviving neurons, together with increased apoptosis and altered BMP2/Smad and BDNF/TrkB pathways compared to their female counterparts.	Arsenic	17-24	brain-derived neurotrophic factor	Rattus norvegicus	182-186
35175559-6	2022	Supporting this, arsenic-treated male rats demonstrated larger reduction in the hippocampal NeuN and %-surviving neurons, together with increased apoptosis and altered BMP2/Smad and BDNF/TrkB pathways compared to their female counterparts.	Arsenic	17-24	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	187-191
35566158-1	2022	Arsenic (As) is common in the human living environment and a certain amount of exposure to As can lead to liver damage; this toxic effect has been proved to be closely related to intracellular PINK1/Parkin pathway-mediated mitophagy.	Arsenic	0-7	PTEN induced kinase 1	Homo sapiens	193-198
35566158-1	2022	Arsenic (As) is common in the human living environment and a certain amount of exposure to As can lead to liver damage; this toxic effect has been proved to be closely related to intracellular PINK1/Parkin pathway-mediated mitophagy.	Arsenic	9-11	PTEN induced kinase 1	Homo sapiens	193-198
35566158-1	2022	Arsenic (As) is common in the human living environment and a certain amount of exposure to As can lead to liver damage; this toxic effect has been proved to be closely related to intracellular PINK1/Parkin pathway-mediated mitophagy.	Arsenic	91-93	PTEN induced kinase 1	Homo sapiens	193-198
35478061-5	2022	Arsenic and mercury showed significant associations with the incidence of ER-positive, ER-negative, PR-positive, and PR-negative breast cancers.	Arsenic	0-7	epiregulin	Homo sapiens	87-89
35566158-5	2022	In conclusion, our results indicate that DIP can reduce As-induced PINK1/Parkin pathway-mediated hepatic mitophagy through scavenging ROS and exert hepatoprotective effects, providing experimental data and theoretical basis for the development of medicinal value of Dictyophora as a dual-use food and medicinal fungus.	Arsenic	56-58	PTEN induced kinase 1	Homo sapiens	67-72
35478061-5	2022	Arsenic and mercury showed significant associations with the incidence of ER-positive, ER-negative, PR-positive, and PR-negative breast cancers.	Arsenic	0-7	transmembrane protein 37	Homo sapiens	100-102
35478061-5	2022	Arsenic and mercury showed significant associations with the incidence of ER-positive, ER-negative, PR-positive, and PR-negative breast cancers.	Arsenic	0-7	transmembrane protein 37	Homo sapiens	117-119
35323907-2	2022	Yap8 plays a crucial role during arsenic stress since it regulates expression of the resistance genes ACR2 and ACR3.	Arsenic	33-40	Arr1p	Saccharomyces cerevisiae S288C	0-4
35323907-2	2022	Yap8 plays a crucial role during arsenic stress since it regulates expression of the resistance genes ACR2 and ACR3.	Arsenic	33-40	Arr2p	Saccharomyces cerevisiae S288C	102-106
35323907-2	2022	Yap8 plays a crucial role during arsenic stress since it regulates expression of the resistance genes ACR2 and ACR3.	Arsenic	33-40	Arr3p	Saccharomyces cerevisiae S288C	111-115
35323907-8	2022	Thus, Etp1 impacts gene expression under arsenic and other stress conditions but the mechanistic details remain to be elucidated.	Arsenic	41-48	Etp1p	Saccharomyces cerevisiae S288C	6-10
35410083-0	2022	Interaction between Single Nucleotide Polymorphisms (SNP) of Tumor Necrosis Factor-Alpha (TNF-alpha) Gene and Plasma Arsenic and the Effect on Estimated Glomerular Filtration Rate (eGFR).	Arsenic	117-124	tumor necrosis factor	Homo sapiens	61-88
35625704-0	2022	Arsenic Activates the ER Stress-Associated Unfolded Protein Response via the Activating Transcription Factor 6 in Human Bronchial Epithelial Cells.	Arsenic	0-7	transcription factor A, mitochondrial	Homo sapiens	88-110
35357260-5	2022	The result showed that the maximum biomethane yield and P release were respectively 502.743 mLCH4/gVS and 168.674 mg/L at the optimum conditions of Ppy/Fe3O4 (20.0014 mg/L), HA (5.0018 mg/L), As (1.448 mg/L) and co-digestion (25.0001%).	Arsenic	192-194	pancreatic polypeptide	Sus scrofa	148-151
35436022-0	2022	Quercetin attenuates the proliferation of arsenic-related lung cancer cells via a caspase-dependent DNA damage signaling.	Arsenic	42-49	caspase 2	Homo sapiens	82-89
35517780-9	2022	Results: Montelukast was effective at reducing arsenic-induced cell migration and mesenchymal protein (fibronectin, MMP-2, N-cadherin, beta-catenin, and SMAD2/3) expression.	Arsenic	47-54	fibronectin 1	Homo sapiens	103-114
35517780-9	2022	Results: Montelukast was effective at reducing arsenic-induced cell migration and mesenchymal protein (fibronectin, MMP-2, N-cadherin, beta-catenin, and SMAD2/3) expression.	Arsenic	47-54	matrix metallopeptidase 2	Homo sapiens	116-121
35517780-9	2022	Results: Montelukast was effective at reducing arsenic-induced cell migration and mesenchymal protein (fibronectin, MMP-2, N-cadherin, beta-catenin, and SMAD2/3) expression.	Arsenic	47-54	cadherin 2	Homo sapiens	123-133
35517780-9	2022	Results: Montelukast was effective at reducing arsenic-induced cell migration and mesenchymal protein (fibronectin, MMP-2, N-cadherin, beta-catenin, and SMAD2/3) expression.	Arsenic	47-54	catenin beta 1	Homo sapiens	135-147
35517780-9	2022	Results: Montelukast was effective at reducing arsenic-induced cell migration and mesenchymal protein (fibronectin, MMP-2, N-cadherin, beta-catenin, and SMAD2/3) expression.	Arsenic	47-54	SMAD family member 2	Homo sapiens	153-160
35517780-13	2022	The expression of fibronectin, MMP-2 induced by arsenic was further enhanced by the combination treatment compared with montelukast treatment only.	Arsenic	48-55	fibronectin 1	Homo sapiens	18-29
35517780-13	2022	The expression of fibronectin, MMP-2 induced by arsenic was further enhanced by the combination treatment compared with montelukast treatment only.	Arsenic	48-55	matrix metallopeptidase 2	Homo sapiens	31-36
35357829-0	2022	Caging-Pnictogen-Induced Superconductivity in Skutterudites IrX3 (X = As, P).	Arsenic	70-72	iroquois homeobox 3	Homo sapiens	60-64
35404942-0	2022	Exposure to arsenic and level of Vitamin D influence the number of Th17 cells and production of IL-17A in human peripheral blood mononuclear cells in adults.	Arsenic	12-19	interleukin 17A	Homo sapiens	96-102
35404942-9	2022	Collectively, we find that exposure to As via drinking water is associated with alterations in Th17 numbers and IL-17A production, and that these associations may be modified by Vitamin D status.	Arsenic	39-41	interleukin 17A	Homo sapiens	112-118
35410083-0	2022	Interaction between Single Nucleotide Polymorphisms (SNP) of Tumor Necrosis Factor-Alpha (TNF-alpha) Gene and Plasma Arsenic and the Effect on Estimated Glomerular Filtration Rate (eGFR).	Arsenic	117-124	tumor necrosis factor	Homo sapiens	90-99
35410083-12	2022	This study found that certain SNPs of the TNF-alpha gene would be robust to the decline of eGFR caused by As exposure.	Arsenic	106-108	tumor necrosis factor	Homo sapiens	42-51
35132447-5	2022	Arsenic exposure was assessed based on urinary concentrations of arsenic species, such as inorganic arsenic, As(III) and As(V), monomethylarsonic acid (MMA), dimethylarsinic acid (DMA), and arsenobetaine (AsB), using high-performance liquid chromatography with inductively coupled plasma mass spectrometry, followed by determination of biomarkers, malondialdehyde and c-peptide.	Arsenic	0-7	insulin	Homo sapiens	368-377
35132447-9	2022	Additionally, malondialdehyde and c-peptide levels were significantly associated with urinary concentrations of various arsenic species.	Arsenic	120-127	insulin	Homo sapiens	34-43
35313999-0	2022	Lentinan alleviates arsenic-induced hepatotoxicity in mice via downregulation of OX40/IL-17A and activation of Nrf2 signaling.	Arsenic	20-27	tumor necrosis factor receptor superfamily, member 4	Mus musculus	81-85
35363433-4	2022	The indicators reflecting arsenic-induced skin lesions (Krt1 and Krt10) were also significantly elevated, which contributed to the occurrence of skin lesions.	Arsenic	26-33	keratin 1	Homo sapiens	56-60
35363433-4	2022	The indicators reflecting arsenic-induced skin lesions (Krt1 and Krt10) were also significantly elevated, which contributed to the occurrence of skin lesions.	Arsenic	26-33	keratin 10	Homo sapiens	65-70
35363433-5	2022	Our results also confirmed the association between METTL3 with inflammatory homeostasis and arsenic-induced skin lesions using arsenic-exposed human skin samples.	Arsenic	127-134	methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit	Homo sapiens	51-57
35363433-6	2022	In the arsenic-exposed group, the upregulation of METTL3 exacerbated the increase in cytokine levels (IL-6, IL-17, and IL-10), which was associated with the upregulation of keratins (Krt1 and Krt10).	Arsenic	7-14	methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit	Homo sapiens	50-56
35363433-6	2022	In the arsenic-exposed group, the upregulation of METTL3 exacerbated the increase in cytokine levels (IL-6, IL-17, and IL-10), which was associated with the upregulation of keratins (Krt1 and Krt10).	Arsenic	7-14	interleukin 6	Homo sapiens	102-106
35363433-6	2022	In the arsenic-exposed group, the upregulation of METTL3 exacerbated the increase in cytokine levels (IL-6, IL-17, and IL-10), which was associated with the upregulation of keratins (Krt1 and Krt10).	Arsenic	7-14	interleukin 17A	Homo sapiens	108-113
35363433-6	2022	In the arsenic-exposed group, the upregulation of METTL3 exacerbated the increase in cytokine levels (IL-6, IL-17, and IL-10), which was associated with the upregulation of keratins (Krt1 and Krt10).	Arsenic	7-14	interleukin 10	Homo sapiens	119-124
35363433-6	2022	In the arsenic-exposed group, the upregulation of METTL3 exacerbated the increase in cytokine levels (IL-6, IL-17, and IL-10), which was associated with the upregulation of keratins (Krt1 and Krt10).	Arsenic	7-14	keratin 1	Homo sapiens	183-187
35363433-6	2022	In the arsenic-exposed group, the upregulation of METTL3 exacerbated the increase in cytokine levels (IL-6, IL-17, and IL-10), which was associated with the upregulation of keratins (Krt1 and Krt10).	Arsenic	7-14	keratin 10	Homo sapiens	192-197
35358544-3	2022	Maximal As(III) removal was obtained at adsorbent dose 1 gL-1, pH 7, ultrasonication time 30 min, temperature 298 K, and initial arsenic concentration 50 mgL-1.	Arsenic	129-136	LLGL scribble cell polarity complex component 1	Homo sapiens	154-159
35313999-0	2022	Lentinan alleviates arsenic-induced hepatotoxicity in mice via downregulation of OX40/IL-17A and activation of Nrf2 signaling.	Arsenic	20-27	nuclear factor, erythroid derived 2, like 2	Mus musculus	111-115
35313999-5	2022	Further, immunoblotting experiments showed that Lentinan intervention downregulated the levels of OX40, IL-17A, and NLRP3 signals, while elevated the levels of anti-oxidative Nrf2, NQO1 signals compared to arsenic treatment group.	Arsenic	206-213	NAD(P)H dehydrogenase, quinone 1	Mus musculus	181-185
35402611-8	2022	The results demonstrated that through reduced pathological changes of hepatic and increased serum AST, ALT, TP, ALB, and A/G levels, DIP ameliorated liver fibrosis induced by As as reflected.	Arsenic	175-177	thymidine phosphorylase	Rattus norvegicus	108-110
35402611-8	2022	The results demonstrated that through reduced pathological changes of hepatic and increased serum AST, ALT, TP, ALB, and A/G levels, DIP ameliorated liver fibrosis induced by As as reflected.	Arsenic	175-177	albumin	Rattus norvegicus	112-115
35272572-0	2022	The effect of GSK-3beta in arsenic-induced apoptosis of malignant tumor cells: a systematic review and meta-analysis.	Arsenic	27-34	glycogen synthase kinase 3 alpha	Homo sapiens	14-23
35272572-4	2022	Nonetheless, the regulation of GSK-3beta by arsenic remains controversial.	Arsenic	44-51	glycogen synthase kinase 3 alpha	Homo sapiens	31-40
35272572-5	2022	The study aimed to clarify the mechanism of GSK-3beta in arsenic-induced apoptosis of tumor cells.	Arsenic	57-64	glycogen synthase kinase 3 alpha	Homo sapiens	44-53
35272572-6	2022	MATERIALS AND METHODS: We included 19 articles, which conducts the role of GSK-3beta in the process of arsenic-induced tumor cell apoptosis by the meta-analysis.	Arsenic	103-110	glycogen synthase kinase 3 alpha	Homo sapiens	75-84
35272572-7	2022	RESULTS: Compared with that of control group, the expression of GSK-3beta (SMD= -0.92, 95% CI (-1.78, -0.06)), p-Akt (SMD= -5.46,95% CI (-8.67, -2.24)) were increased in the arsenic intervention group.	Arsenic	174-181	glycogen synthase kinase 3 alpha	Homo sapiens	64-73
35272572-7	2022	RESULTS: Compared with that of control group, the expression of GSK-3beta (SMD= -0.92, 95% CI (-1.78, -0.06)), p-Akt (SMD= -5.46,95% CI (-8.67, -2.24)) were increased in the arsenic intervention group.	Arsenic	174-181	AKT serine/threonine kinase 1	Homo sapiens	113-116
35272572-8	2022	Meanwhile, the combined treatment of arsenic and Akt agonists can inhibit p-GSK-3beta.	Arsenic	37-44	glycogen synthase kinase 3 alpha	Homo sapiens	76-85
35272572-9	2022	Using the dose and time subgroup analysis, it was shown that the low-dose (<5 mumol/L) and sub-chronic (>24 h) arsenic exposure could inhibit the expression of p-Akt (P < 0.05).	Arsenic	111-118	AKT serine/threonine kinase 1	Homo sapiens	162-165
35272572-10	2022	In the subgroup analysis of GSK-3beta sites, arsenic could inhibit p-Akt and GSK-3beta (Ser9) (SMD = -0.95, 95% CI (-1.56, -0.33)).	Arsenic	45-52	glycogen synthase kinase 3 alpha	Homo sapiens	28-37
35272572-10	2022	In the subgroup analysis of GSK-3beta sites, arsenic could inhibit p-Akt and GSK-3beta (Ser9) (SMD = -0.95, 95% CI (-1.56, -0.33)).	Arsenic	45-52	AKT serine/threonine kinase 1	Homo sapiens	69-72
35272572-10	2022	In the subgroup analysis of GSK-3beta sites, arsenic could inhibit p-Akt and GSK-3beta (Ser9) (SMD = -0.95, 95% CI (-1.56, -0.33)).	Arsenic	45-52	glycogen synthase kinase 3 alpha	Homo sapiens	77-86
35272572-11	2022	There was a positive dose-response relationship between arsenic and p-GSK-3beta when the dose of arsenic was less than 8 mumol/L.	Arsenic	56-63	glycogen synthase kinase 3 alpha	Homo sapiens	70-79
35272572-11	2022	There was a positive dose-response relationship between arsenic and p-GSK-3beta when the dose of arsenic was less than 8 mumol/L.	Arsenic	97-104	glycogen synthase kinase 3 alpha	Homo sapiens	70-79
35272572-12	2022	The expression of Mcl-1 and pro-caspase-3 were decreased, while the loss of mitochondrial membrane potential and cleaved-caspase-3 increased significantly when arsenic stimulated GSK-3beta (Ser9) (P < 0.05).	Arsenic	160-167	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	18-23
35272572-12	2022	The expression of Mcl-1 and pro-caspase-3 were decreased, while the loss of mitochondrial membrane potential and cleaved-caspase-3 increased significantly when arsenic stimulated GSK-3beta (Ser9) (P < 0.05).	Arsenic	160-167	caspase 3	Homo sapiens	28-41
35272572-12	2022	The expression of Mcl-1 and pro-caspase-3 were decreased, while the loss of mitochondrial membrane potential and cleaved-caspase-3 increased significantly when arsenic stimulated GSK-3beta (Ser9) (P < 0.05).	Arsenic	160-167	caspase 3	Homo sapiens	121-130
35272572-12	2022	The expression of Mcl-1 and pro-caspase-3 were decreased, while the loss of mitochondrial membrane potential and cleaved-caspase-3 increased significantly when arsenic stimulated GSK-3beta (Ser9) (P < 0.05).	Arsenic	160-167	glycogen synthase kinase 3 alpha	Homo sapiens	179-188
35272572-13	2022	CONCLUSION: The study revealed that arsenic could induce tumor cell apoptosis, by inhibiting p-Akt/GSK-3beta, and triggering the Mcl-1-dependent mitochondrial apoptosis pathway.	Arsenic	36-43	AKT serine/threonine kinase 1	Homo sapiens	95-98
35272572-13	2022	CONCLUSION: The study revealed that arsenic could induce tumor cell apoptosis, by inhibiting p-Akt/GSK-3beta, and triggering the Mcl-1-dependent mitochondrial apoptosis pathway.	Arsenic	36-43	glycogen synthase kinase 3 alpha	Homo sapiens	99-108
35272572-13	2022	CONCLUSION: The study revealed that arsenic could induce tumor cell apoptosis, by inhibiting p-Akt/GSK-3beta, and triggering the Mcl-1-dependent mitochondrial apoptosis pathway.	Arsenic	36-43	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	129-134
35189519-6	2022	Two inflammatory signalling pathways, i.e., TLR2/MyD88/NF-kappaB and IL-6/STAT-3, were activated, along with inflammatory cell infiltration and the elevated mRNA expression of pro-inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma) and myeloperoxidase (MPO) in the gastric tissue of mice exposed to arsenic.	Arsenic	306-313	toll-like receptor 2	Mus musculus	44-48
35189519-6	2022	Two inflammatory signalling pathways, i.e., TLR2/MyD88/NF-kappaB and IL-6/STAT-3, were activated, along with inflammatory cell infiltration and the elevated mRNA expression of pro-inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma) and myeloperoxidase (MPO) in the gastric tissue of mice exposed to arsenic.	Arsenic	306-313	myeloid differentiation primary response gene 88	Mus musculus	49-54
35288486-15	2022	CONCLUSION: MiR-29a elevation induces the increase of autophagy by down-regulating the PI3K/AKT/mTOR pathway in the progression of AS, indicating that miR-29a is a novel therapeutic strategy for AS.	Arsenic	195-197	mechanistic target of rapamycin kinase	Mus musculus	96-100
35189519-6	2022	Two inflammatory signalling pathways, i.e., TLR2/MyD88/NF-kappaB and IL-6/STAT-3, were activated, along with inflammatory cell infiltration and the elevated mRNA expression of pro-inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma) and myeloperoxidase (MPO) in the gastric tissue of mice exposed to arsenic.	Arsenic	306-313	interleukin 6	Mus musculus	69-73
35189519-6	2022	Two inflammatory signalling pathways, i.e., TLR2/MyD88/NF-kappaB and IL-6/STAT-3, were activated, along with inflammatory cell infiltration and the elevated mRNA expression of pro-inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma) and myeloperoxidase (MPO) in the gastric tissue of mice exposed to arsenic.	Arsenic	306-313	tumor necrosis factor	Mus musculus	204-213
35189519-9	2022	The arsenic-mediated gene expression of pro-inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma), MPO and IL-6/STAT3 and TLR2/MyD88/NF-kappaB pathways was found down-regulated.	Arsenic	4-11	tumor necrosis factor	Mus musculus	68-77
35189519-9	2022	The arsenic-mediated gene expression of pro-inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma), MPO and IL-6/STAT3 and TLR2/MyD88/NF-kappaB pathways was found down-regulated.	Arsenic	4-11	interleukin 1 alpha	Mus musculus	79-87
35189519-9	2022	The arsenic-mediated gene expression of pro-inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma), MPO and IL-6/STAT3 and TLR2/MyD88/NF-kappaB pathways was found down-regulated.	Arsenic	4-11	interferon gamma	Mus musculus	92-101
35189519-9	2022	The arsenic-mediated gene expression of pro-inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma), MPO and IL-6/STAT3 and TLR2/MyD88/NF-kappaB pathways was found down-regulated.	Arsenic	4-11	myeloperoxidase	Mus musculus	104-107
35189519-9	2022	The arsenic-mediated gene expression of pro-inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma), MPO and IL-6/STAT3 and TLR2/MyD88/NF-kappaB pathways was found down-regulated.	Arsenic	4-11	interleukin 6	Mus musculus	112-116
35189519-9	2022	The arsenic-mediated gene expression of pro-inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma), MPO and IL-6/STAT3 and TLR2/MyD88/NF-kappaB pathways was found down-regulated.	Arsenic	4-11	signal transducer and activator of transcription 3	Mus musculus	117-122
35189519-9	2022	The arsenic-mediated gene expression of pro-inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma), MPO and IL-6/STAT3 and TLR2/MyD88/NF-kappaB pathways was found down-regulated.	Arsenic	4-11	toll-like receptor 2	Mus musculus	127-131
35189519-9	2022	The arsenic-mediated gene expression of pro-inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma), MPO and IL-6/STAT3 and TLR2/MyD88/NF-kappaB pathways was found down-regulated.	Arsenic	4-11	myeloid differentiation primary response gene 88	Mus musculus	132-137
35189519-9	2022	The arsenic-mediated gene expression of pro-inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma), MPO and IL-6/STAT3 and TLR2/MyD88/NF-kappaB pathways was found down-regulated.	Arsenic	4-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	138-147
35288486-15	2022	CONCLUSION: MiR-29a elevation induces the increase of autophagy by down-regulating the PI3K/AKT/mTOR pathway in the progression of AS, indicating that miR-29a is a novel therapeutic strategy for AS.	Arsenic	131-133	microRNA 29a	Mus musculus	12-19
35288486-15	2022	CONCLUSION: MiR-29a elevation induces the increase of autophagy by down-regulating the PI3K/AKT/mTOR pathway in the progression of AS, indicating that miR-29a is a novel therapeutic strategy for AS.	Arsenic	131-133	thymoma viral proto-oncogene 1	Mus musculus	92-95
35288486-15	2022	CONCLUSION: MiR-29a elevation induces the increase of autophagy by down-regulating the PI3K/AKT/mTOR pathway in the progression of AS, indicating that miR-29a is a novel therapeutic strategy for AS.	Arsenic	131-133	mechanistic target of rapamycin kinase	Mus musculus	96-100
35288486-15	2022	CONCLUSION: MiR-29a elevation induces the increase of autophagy by down-regulating the PI3K/AKT/mTOR pathway in the progression of AS, indicating that miR-29a is a novel therapeutic strategy for AS.	Arsenic	131-133	microRNA 29a	Mus musculus	151-158
35288486-15	2022	CONCLUSION: MiR-29a elevation induces the increase of autophagy by down-regulating the PI3K/AKT/mTOR pathway in the progression of AS, indicating that miR-29a is a novel therapeutic strategy for AS.	Arsenic	195-197	microRNA 29a	Mus musculus	151-158
35288486-15	2022	CONCLUSION: MiR-29a elevation induces the increase of autophagy by down-regulating the PI3K/AKT/mTOR pathway in the progression of AS, indicating that miR-29a is a novel therapeutic strategy for AS.	Arsenic	195-197	microRNA 29a	Mus musculus	12-19
35288486-15	2022	CONCLUSION: MiR-29a elevation induces the increase of autophagy by down-regulating the PI3K/AKT/mTOR pathway in the progression of AS, indicating that miR-29a is a novel therapeutic strategy for AS.	Arsenic	195-197	thymoma viral proto-oncogene 1	Mus musculus	92-95
35298964-2	2022	As the rate-limiting enzyme subunit of GSH synthesis, GCLC may be an important target for arsenic to induce apoptosis through mitochondrial apoptosis pathway to exert anti-tumor effect.	Arsenic	90-97	glutamate-cysteine ligase catalytic subunit	Homo sapiens	54-58
35320977-1	2022	Chronic arsenic exposure is a risk factor for human fatty liver disease, and the ERK signaling pathway plays an important role in the regulation of liver lipid metabolism.	Arsenic	8-15	mitogen-activated protein kinase 1	Homo sapiens	81-84
35298964-6	2022	Therefore, the purpose of this study was to investigate whether NaAsO2 might induce mitochondrial damage and apoptosis of cervical cancer cells through NF-kappaB/ miR-21 /GCLC induced oxidative stress, and play the anti-tumor role of arsenic as a potential drug for the treatment of cervical cancer.	Arsenic	234-241	nuclear factor kappa B subunit 1	Homo sapiens	152-161
35298964-6	2022	Therefore, the purpose of this study was to investigate whether NaAsO2 might induce mitochondrial damage and apoptosis of cervical cancer cells through NF-kappaB/ miR-21 /GCLC induced oxidative stress, and play the anti-tumor role of arsenic as a potential drug for the treatment of cervical cancer.	Arsenic	234-241	microRNA 21	Homo sapiens	163-169
35298964-6	2022	Therefore, the purpose of this study was to investigate whether NaAsO2 might induce mitochondrial damage and apoptosis of cervical cancer cells through NF-kappaB/ miR-21 /GCLC induced oxidative stress, and play the anti-tumor role of arsenic as a potential drug for the treatment of cervical cancer.	Arsenic	234-241	glutamate-cysteine ligase catalytic subunit	Homo sapiens	171-175
35320977-3	2022	Here, by constructing a rat model of liver lipid metabolism disorder induced by chronic arsenic exposure, we demonstrated that ERK might regulate arsenic-induced liver lipid metabolism disorders through the PPAR signaling pathway.	Arsenic	88-95	Eph receptor B1	Rattus norvegicus	127-130
35320977-3	2022	Here, by constructing a rat model of liver lipid metabolism disorder induced by chronic arsenic exposure, we demonstrated that ERK might regulate arsenic-induced liver lipid metabolism disorders through the PPAR signaling pathway.	Arsenic	146-153	Eph receptor B1	Rattus norvegicus	127-130
35320977-3	2022	Here, by constructing a rat model of liver lipid metabolism disorder induced by chronic arsenic exposure, we demonstrated that ERK might regulate arsenic-induced liver lipid metabolism disorders through the PPAR signaling pathway.	Arsenic	146-153	peroxisome proliferator activated receptor alpha	Rattus norvegicus	207-211
35320977-4	2022	Arsenic could upregulate the expression of PPARgamma and CD36 in the rat liver, decrease the expression of PPARalpha and CPT-1 in the rat liver, increase the organ coefficient of the rat liver, decrease the content of TG in rat serum, and promote fat deposition in the rat liver.	Arsenic	0-7	peroxisome proliferator activated receptor gamma	Homo sapiens	43-52
35320977-4	2022	Arsenic could upregulate the expression of PPARgamma and CD36 in the rat liver, decrease the expression of PPARalpha and CPT-1 in the rat liver, increase the organ coefficient of the rat liver, decrease the content of TG in rat serum, and promote fat deposition in the rat liver.	Arsenic	0-7	peroxisome proliferator activated receptor alpha	Rattus norvegicus	107-116
35320977-4	2022	Arsenic could upregulate the expression of PPARgamma and CD36 in the rat liver, decrease the expression of PPARalpha and CPT-1 in the rat liver, increase the organ coefficient of the rat liver, decrease the content of TG in rat serum, and promote fat deposition in the rat liver.	Arsenic	0-7	carnitine palmitoyltransferase 1A	Homo sapiens	121-126
35320977-2	2022	However, whether ERK plays a role in the progression of arsenic-induced liver lipid metabolism disorder and the specific mechanism remain unclear.	Arsenic	56-63	mitogen-activated protein kinase 1	Homo sapiens	17-20
35320977-5	2022	In the arsenic-induced rat model of hepatic lipid metabolism disorder, we found that the expression of p-ERK was increased.	Arsenic	7-14	Eph receptor B1	Rattus norvegicus	105-108
35323780-6	2022	Post-treated HFs from 11.35 mL/min of DER showed 93.8% of MWCO value with up to 90% and 70% rejection of the arsenic and chromium metallic ions, respectively, in comparison with all other formulated HFs.	Arsenic	109-116	solute carrier family 35 member G1	Homo sapiens	0-4
35320977-6	2022	In order to further explore whether the ERK signaling pathway was involved in arsenic-induced liver lipid metabolism disorder, we exposed L-02 cells to different arsenic concentrations, and the results showed that arsenic significantly increased the expression of P-ERK in L-02 cells in a dose-dependent manner.	Arsenic	78-85	mitogen-activated protein kinase 1	Homo sapiens	40-43
35320977-6	2022	In order to further explore whether the ERK signaling pathway was involved in arsenic-induced liver lipid metabolism disorder, we exposed L-02 cells to different arsenic concentrations, and the results showed that arsenic significantly increased the expression of P-ERK in L-02 cells in a dose-dependent manner.	Arsenic	78-85	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	264-269
35320977-6	2022	In order to further explore whether the ERK signaling pathway was involved in arsenic-induced liver lipid metabolism disorder, we exposed L-02 cells to different arsenic concentrations, and the results showed that arsenic significantly increased the expression of P-ERK in L-02 cells in a dose-dependent manner.	Arsenic	162-169	mitogen-activated protein kinase 1	Homo sapiens	40-43
35320977-6	2022	In order to further explore whether the ERK signaling pathway was involved in arsenic-induced liver lipid metabolism disorder, we exposed L-02 cells to different arsenic concentrations, and the results showed that arsenic significantly increased the expression of P-ERK in L-02 cells in a dose-dependent manner.	Arsenic	162-169	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	264-269
35320977-6	2022	In order to further explore whether the ERK signaling pathway was involved in arsenic-induced liver lipid metabolism disorder, we exposed L-02 cells to different arsenic concentrations, and the results showed that arsenic significantly increased the expression of P-ERK in L-02 cells in a dose-dependent manner.	Arsenic	214-221	mitogen-activated protein kinase 1	Homo sapiens	40-43
35320977-6	2022	In order to further explore whether the ERK signaling pathway was involved in arsenic-induced liver lipid metabolism disorder, we exposed L-02 cells to different arsenic concentrations, and the results showed that arsenic significantly increased the expression of P-ERK in L-02 cells in a dose-dependent manner.	Arsenic	214-221	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	264-269
35320977-8	2022	In conclusion, ERK may be involved in arsenic-induced liver lipid metabolism disorder by regulating the PPAR signaling pathway.	Arsenic	38-45	mitogen-activated protein kinase 1	Homo sapiens	15-18
35320977-8	2022	In conclusion, ERK may be involved in arsenic-induced liver lipid metabolism disorder by regulating the PPAR signaling pathway.	Arsenic	38-45	peroxisome proliferator activated receptor alpha	Rattus norvegicus	104-108
35299870-10	2022	Increased hippocampal amyloid plaques levels of APP/PS mice and cognitive decline provided evidence that arsenic exposure aggravated an existing Alzheimer"s disease-like phenotype.	Arsenic	105-112	amyloid beta precursor protein	Homo sapiens	48-54
35258182-2	2022	A total of 16 heavy metal elements (Al, Si, K, Ca, V, Cr, Mn, Fe, Ni, Cu, Zn, As, Se, Ba, Pb, and Cd) in PM1 were continuously determined by an online heavy metal observation instrument in Zhengzhou city from January 7 to 25, 2021.	Arsenic	78-80	transmembrane protein 11	Homo sapiens	105-108
35299870-12	2022	We also show that human relevant, chronic arsenic exposure has deleterious effects on adult APP/PS mice and exacerbates existing Alzheimer"s disease-like symptoms.	Arsenic	42-49	amyloid beta precursor protein	Homo sapiens	92-98
35104878-0	2022	Cytoplasmic switch of ARS2 isoforms promotes nonsense-mediated mRNA decay and arsenic sensitivity.	Arsenic	78-85	serrate, RNA effector molecule	Homo sapiens	22-26
35241635-0	2022	Human endothelial cells promote arsenic-transformed lung epithelial cells to induce tumor growth and angiogenesis through interleukin-8 induction.	Arsenic	32-39	C-X-C motif chemokine ligand 8	Homo sapiens	122-135
35015217-7	2022	Melatonin showed to have binding energy with ATF6 as - 4.8 kJ, with PERK as - 3.2 kJ, with XBP1 as - 4.8 kJ, with Nrf2 as - 4.5 kJ, and with that of NFkappaB as - 4.2 kJ, which implies it interacts well with them.	Arsenic	50-52	activating transcription factor 6	Homo sapiens	45-49
35229267-6	2022	In arsenic solution, the total arsenic adsorption capacity of Pe-FeLs was much higher than that of ferric lignin and PE, which showed Pe-FeLs had the ability to adsorb arsenic.	Arsenic	3-10	plasmalemma vesicle associated protein	Homo sapiens	65-69
35229267-6	2022	In arsenic solution, the total arsenic adsorption capacity of Pe-FeLs was much higher than that of ferric lignin and PE, which showed Pe-FeLs had the ability to adsorb arsenic.	Arsenic	3-10	plasmalemma vesicle associated protein	Homo sapiens	137-141
35229267-6	2022	In arsenic solution, the total arsenic adsorption capacity of Pe-FeLs was much higher than that of ferric lignin and PE, which showed Pe-FeLs had the ability to adsorb arsenic.	Arsenic	31-38	plasmalemma vesicle associated protein	Homo sapiens	65-69
35229267-6	2022	In arsenic solution, the total arsenic adsorption capacity of Pe-FeLs was much higher than that of ferric lignin and PE, which showed Pe-FeLs had the ability to adsorb arsenic.	Arsenic	31-38	plasmalemma vesicle associated protein	Homo sapiens	137-141
35229267-6	2022	In arsenic solution, the total arsenic adsorption capacity of Pe-FeLs was much higher than that of ferric lignin and PE, which showed Pe-FeLs had the ability to adsorb arsenic.	Arsenic	168-175	plasmalemma vesicle associated protein	Homo sapiens	65-69
35229267-6	2022	In arsenic solution, the total arsenic adsorption capacity of Pe-FeLs was much higher than that of ferric lignin and PE, which showed Pe-FeLs had the ability to adsorb arsenic.	Arsenic	168-175	plasmalemma vesicle associated protein	Homo sapiens	137-141
35229267-8	2022	With applying Pe-FeLs system under the soil, arsenic was significantly reduced by 25.5 ~ 53.4% in heavily, moderately, and lower arsenic-polluted soils, the biomass of the romaine lettuce increased and arsenic accumulation in the romaine lettuce decreased.	Arsenic	45-52	plasmalemma vesicle associated protein	Homo sapiens	17-21
35229267-8	2022	With applying Pe-FeLs system under the soil, arsenic was significantly reduced by 25.5 ~ 53.4% in heavily, moderately, and lower arsenic-polluted soils, the biomass of the romaine lettuce increased and arsenic accumulation in the romaine lettuce decreased.	Arsenic	202-209	plasmalemma vesicle associated protein	Homo sapiens	17-21
35226250-3	2022	Here, we showed that arsenic treatment facilitated methyltransferase-like 14 (METTL14)-mediated m6A methylation, and that METTL14 interference reversed arsenic-impaired hepatic insulin sensitivity.	Arsenic	21-28	methyltransferase 14, N6-adenosine-methyltransferase subunit	Homo sapiens	51-76
35226250-3	2022	Here, we showed that arsenic treatment facilitated methyltransferase-like 14 (METTL14)-mediated m6A methylation, and that METTL14 interference reversed arsenic-impaired hepatic insulin sensitivity.	Arsenic	21-28	methyltransferase 14, N6-adenosine-methyltransferase subunit	Homo sapiens	78-85
35226250-3	2022	Here, we showed that arsenic treatment facilitated methyltransferase-like 14 (METTL14)-mediated m6A methylation, and that METTL14 interference reversed arsenic-impaired hepatic insulin sensitivity.	Arsenic	21-28	methyltransferase 14, N6-adenosine-methyltransferase subunit	Homo sapiens	122-129
35226250-4	2022	We previously showed that arsenic-induced NOD-like receptor protein 3 (NLRP3) inflammasome activation contributed to hepatic IR.	Arsenic	26-33	NLR family pyrin domain containing 3	Homo sapiens	42-69
35226250-4	2022	We previously showed that arsenic-induced NOD-like receptor protein 3 (NLRP3) inflammasome activation contributed to hepatic IR.	Arsenic	26-33	NLR family pyrin domain containing 3	Homo sapiens	71-76
35226250-5	2022	However, the regulatory mechanisms underlying the role of arsenic toward the post-transcriptional modification of NLRP3 remain unclear.	Arsenic	58-65	NLR family pyrin domain containing 3	Homo sapiens	114-119
35226250-6	2022	Here, we showed that NLRP3 mRNA stability was enhanced by METTL14-mediated m6A methylation during arsenic-induced hepatic IR.	Arsenic	98-105	NLR family pyrin domain containing 3	Homo sapiens	21-26
35226250-7	2022	Furthermore, we demonstrated that arsenite methyltransferase (AS3MT), an essential enzyme in arsenic metabolic processes, interacted with NLRP3 to activate the inflammasome, thereby contributing to arsenic-induced hepatic IR.	Arsenic	93-100	arsenite methyltransferase	Homo sapiens	62-67
35226250-7	2022	Furthermore, we demonstrated that arsenite methyltransferase (AS3MT), an essential enzyme in arsenic metabolic processes, interacted with NLRP3 to activate the inflammasome, thereby contributing to arsenic-induced hepatic IR.	Arsenic	93-100	NLR family pyrin domain containing 3	Homo sapiens	138-143
35226250-7	2022	Furthermore, we demonstrated that arsenite methyltransferase (AS3MT), an essential enzyme in arsenic metabolic processes, interacted with NLRP3 to activate the inflammasome, thereby contributing to arsenic-induced hepatic IR.	Arsenic	198-205	arsenite methyltransferase	Homo sapiens	62-67
35226250-7	2022	Furthermore, we demonstrated that arsenite methyltransferase (AS3MT), an essential enzyme in arsenic metabolic processes, interacted with NLRP3 to activate the inflammasome, thereby contributing to arsenic-induced hepatic IR.	Arsenic	198-205	NLR family pyrin domain containing 3	Homo sapiens	138-143
35226250-9	2022	In summary, we showed that AS3MT-induced m6A modification critically regulated NLRP3 inflammasome activation during arsenic-induced hepatic IR, and we identified a novel post-transcriptional function of AS3MT in promoting arsenicosis.	Arsenic	116-123	arsenite methyltransferase	Homo sapiens	203-208
35232368-9	2022	Moreover, arsenic administration caused mitochondrial complexes impairment and reduction of acetylcholinesterase level.	Arsenic	10-17	acetylcholinesterase	Rattus norvegicus	92-112
35104878-5	2022	ARS2 isoform exchange is also relevant during arsenic stress, where cytoplasmic ARS2 promotes a global response to arsenic in a CBC-independent manner.	Arsenic	115-122	serrate, RNA effector molecule	Homo sapiens	0-4
35188613-0	2022	Arsenic concentration in topsoil of central Chile is associated with aberrant methylation of P53 gene in human blood cells: a cross-sectional study.	Arsenic	0-7	tumor protein p53	Homo sapiens	93-96
35104878-5	2022	ARS2 isoform exchange is also relevant during arsenic stress, where cytoplasmic ARS2 promotes a global response to arsenic in a CBC-independent manner.	Arsenic	115-122	serrate, RNA effector molecule	Homo sapiens	80-84
35137586-5	2022	Remarkably, in two cases, i.e., Mb and GAPDH, the formation of a bound metallic fragment that lacked the arsenic center was highlighted.	Arsenic	105-112	myoglobin	Homo sapiens	32-34
35137586-5	2022	Remarkably, in two cases, i.e., Mb and GAPDH, the formation of a bound metallic fragment that lacked the arsenic center was highlighted.	Arsenic	105-112	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	39-44
35167029-6	2022	Arsenic has been shown to inactivate endothelial nitric oxide synthase leading to a reduction of the generation and bioavailability of nitric oxide.	Arsenic	0-7	nitric oxide synthase 3	Homo sapiens	37-70
35202923-7	2022	The common covariant DEGs between arsenic induction and CA intervention was screened by comparative transcriptomic analysis methods.	Arsenic	34-41	delta(4)-desaturase, sphingolipid 1	Mus musculus	21-25
35202923-9	2022	RESULTS: Transcriptome results showed that 220 DEGs were identified after arsenic induction.	Arsenic	74-81	delta(4)-desaturase, sphingolipid 1	Mus musculus	47-51
35202923-13	2022	The mRNA expressions of Fgf21 and Plin2 were significantly increased (P < 0.05) and the mRNA expressions of Cyp2b10, Cyp7a1, Per2 and Mylip were significantly decreased (P < 0.05) after arsenic induction.	Arsenic	186-193	fibroblast growth factor 21	Mus musculus	24-29
35202923-13	2022	The mRNA expressions of Fgf21 and Plin2 were significantly increased (P < 0.05) and the mRNA expressions of Cyp2b10, Cyp7a1, Per2 and Mylip were significantly decreased (P < 0.05) after arsenic induction.	Arsenic	186-193	predicted gene 12551	Mus musculus	34-39
35202923-13	2022	The mRNA expressions of Fgf21 and Plin2 were significantly increased (P < 0.05) and the mRNA expressions of Cyp2b10, Cyp7a1, Per2 and Mylip were significantly decreased (P < 0.05) after arsenic induction.	Arsenic	186-193	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	108-115
35063159-1	2022	In this study, a novel flexible and disposable electrochemical sensor was fabricated through the straightforward laser-induced synthesis of catalytic Au nanoparticles (AuNPs)@LIG composite for the square wave stripping voltammetry (SWASV) determination of arsenic in soil.	Arsenic	256-263	ubiquitin conjugating enzyme E2 K	Homo sapiens	175-178
35063159-5	2022	Additionally, the mechanism of AuNPs@LIG synthesis by laser induction was also investigated, and the deposition potential and the deposition time for the SWASV determination of arsenic were also optimized.	Arsenic	177-184	ubiquitin conjugating enzyme E2 K	Homo sapiens	37-40
35202923-13	2022	The mRNA expressions of Fgf21 and Plin2 were significantly increased (P < 0.05) and the mRNA expressions of Cyp2b10, Cyp7a1, Per2 and Mylip were significantly decreased (P < 0.05) after arsenic induction.	Arsenic	186-193	cytochrome P450, family 7, subfamily a, polypeptide 1	Mus musculus	117-123
35202923-13	2022	The mRNA expressions of Fgf21 and Plin2 were significantly increased (P < 0.05) and the mRNA expressions of Cyp2b10, Cyp7a1, Per2 and Mylip were significantly decreased (P < 0.05) after arsenic induction.	Arsenic	186-193	period circadian clock 2	Mus musculus	125-129
35202923-13	2022	The mRNA expressions of Fgf21 and Plin2 were significantly increased (P < 0.05) and the mRNA expressions of Cyp2b10, Cyp7a1, Per2 and Mylip were significantly decreased (P < 0.05) after arsenic induction.	Arsenic	186-193	myosin regulatory light chain interacting protein	Mus musculus	134-139
35215628-6	2022	At pH 10, the maximum arsenic removal in the presence of B1, B2, and B3 was 96%, 94%, and 93%, respectively.	Arsenic	22-29	immunoglobulin kappa variable 7-3 (pseudogene)	Homo sapiens	57-71
35210942-5	2022	The arsenic markedly increased the activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST).	Arsenic	4-11	glutamic pyruvic transaminase, soluble	Mus musculus	53-77
35210942-5	2022	The arsenic markedly increased the activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST).	Arsenic	4-11	glutamic pyruvic transaminase, soluble	Mus musculus	79-82
35210942-6	2022	The myeloperoxidase (MPO) activities increased in the liver at 25 and 50 mg/L arsenic for 3 months as well as in the kidney at both 1 and 3 months.	Arsenic	78-85	myeloperoxidase	Mus musculus	4-19
35210942-6	2022	The myeloperoxidase (MPO) activities increased in the liver at 25 and 50 mg/L arsenic for 3 months as well as in the kidney at both 1 and 3 months.	Arsenic	78-85	myeloperoxidase	Mus musculus	21-24
35210942-7	2022	An increased expression of inflammatory indicators (IL-1beta, IL-12, and TNF-alpha) at 25 and 50 mg/L arsenic for 1 and 3 months in the liver and kidney, as well as IL-1beta in the liver for 3 months and in the kidney at 50 mg/L for 1 and 3 months were demonstrated in our experiments.	Arsenic	102-109	interleukin 1 alpha	Mus musculus	52-60
35210942-7	2022	An increased expression of inflammatory indicators (IL-1beta, IL-12, and TNF-alpha) at 25 and 50 mg/L arsenic for 1 and 3 months in the liver and kidney, as well as IL-1beta in the liver for 3 months and in the kidney at 50 mg/L for 1 and 3 months were demonstrated in our experiments.	Arsenic	102-109	tumor necrosis factor	Mus musculus	73-82
35210942-9	2022	Moreover, arsenic enhanced the expression of MAPK/Nrf2/NF-kappaB signaling molecules.	Arsenic	10-17	nuclear factor, erythroid derived 2, like 2	Mus musculus	50-54
35210942-9	2022	Moreover, arsenic enhanced the expression of MAPK/Nrf2/NF-kappaB signaling molecules.	Arsenic	10-17	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	55-64
35042327-12	2022	By a logical selection of singlet carbenes, stable 2-phosha-1,3-butadiene and 2-arsa-1,3-butadiene compounds, as well as related radical cations and dications, can be prepared as crystalline solids.The relevance of NHV ligands as potent pi-donors has been demonstrated for the stabilization of elusive electrophilic phosphinidene and arsinidene complexes {(NHV)E}Fe(CO)4 (E = P or As).	Arsenic	381-383	guided entry of tail-anchored proteins factor 3, ATPase	Homo sapiens	80-86
35180596-15	2022	Our study also demonstrated that the PSTs could be a "cleaner" alternative to SSTs for analytes such as Cr, As, Cd, Hg, Tl, Pb and U.	Arsenic	108-110	kallikrein related peptidase 4	Homo sapiens	37-41
35164302-8	2022	Administration of arsenic in mice showed a reduction of acetylcholinesterase activity in the brain which was counteracted by Acacia nilotica polyphenolics.	Arsenic	18-25	acetylcholinesterase	Mus musculus	56-76
35120684-10	2022	PC2 (Mn and As) primarily comes from fossil fuel burning and pesticides and fertilizers containing Mn and As compounds.	Arsenic	12-14	polycystin 2, transient receptor potential cation channel	Homo sapiens	0-3
34998823-9	2022	These findings indicate a previously unrecognized role of APOBEC3B in arsenic-triggered somatic mutation, and might open new avenues to reduce DNA mutagenesis by targeting the FTO/m6A axis.	Arsenic	70-77	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	58-66
35001170-0	2022	SUMOylation regulates the number and size of promyelocytic leukemia-nuclear bodies (PML-NBs) and arsenic perturbs SUMO dynamics on PML by insolubilizing PML in THP-1 cells.	Arsenic	97-104	PML nuclear body scaffold	Homo sapiens	131-134
35001170-0	2022	SUMOylation regulates the number and size of promyelocytic leukemia-nuclear bodies (PML-NBs) and arsenic perturbs SUMO dynamics on PML by insolubilizing PML in THP-1 cells.	Arsenic	97-104	PML nuclear body scaffold	Homo sapiens	153-156
35051766-7	2022	Efficiency of arsenic metabolism was evaluated by a polymorphism (rs3740393) in the main arsenic methylating gene AS3MT measured by TaqMan allelic discrimination, and by the relative fractions of urinary inorganic arsenic metabolites.	Arsenic	14-21	arsenite methyltransferase	Homo sapiens	114-119
35065503-0	2022	Feed-additive Limosilactobacillus fermentum GR-3 reduces arsenic accumulation in Procambarus clarkii.	Arsenic	57-64	semaphorin 4D	Homo sapiens	44-48
35065504-0	2022	Association of urinary arsenic with insulin resistance: Cross-sectional analysis of the National Health and Nutrition Examination Survey, 2015-2016.	Arsenic	23-30	insulin	Homo sapiens	36-43
35065504-1	2022	BACKGROUND: Long-term arsenic exposure is associated with diabetes in adults, the mechanism of which involves insulin resistance.	Arsenic	22-29	insulin	Homo sapiens	110-117
35065504-2	2022	The relationship between arsenic and insulin resistance in adults is unclear.	Arsenic	25-32	insulin	Homo sapiens	37-44
35065504-3	2022	We analyzed the relationship between urinary arsenic and insulin resistance in US adults.	Arsenic	45-52	insulin	Homo sapiens	57-64
35065504-6	2022	The association between urinary arsenic and insulin resistance was evaluated by analyzing the urinary arsenic level and homeostasis model assessment-insulin resistance.	Arsenic	32-39	insulin	Homo sapiens	44-51
35065504-6	2022	The association between urinary arsenic and insulin resistance was evaluated by analyzing the urinary arsenic level and homeostasis model assessment-insulin resistance.	Arsenic	32-39	insulin	Homo sapiens	149-156
35065504-9	2022	CONCLUSIONS: In most subgroups, after similar adjustment, the relationship between urine total arsenic and insulin resistance remained.	Arsenic	95-102	insulin	Homo sapiens	107-114
35065504-10	2022	Total arsenic exposure in urine may be associated with insulin resistance.	Arsenic	6-13	insulin	Homo sapiens	55-62
34998823-0	2022	m6A demethylation of cytidine deaminase APOBEC3B mRNA orchestrates arsenic-induced mutagenesis.	Arsenic	67-74	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	40-48
34998823-4	2022	Herein we show that APOBEC3B is upregulated and required for arsenic-induced DNA damage and mutagenesis.	Arsenic	61-68	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	20-28
34998823-5	2022	We found that arsenic treatment causes a decrease of N6-methyladenosine (m6A) modification near the stop codon of APOBEC3B, consequently increasing the stability of APOBEC3B mRNA.	Arsenic	14-21	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	114-122
34998823-5	2022	We found that arsenic treatment causes a decrease of N6-methyladenosine (m6A) modification near the stop codon of APOBEC3B, consequently increasing the stability of APOBEC3B mRNA.	Arsenic	14-21	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	165-173
34998823-6	2022	We further reveal that the demethylase FTO is responsible for arsenic-reduced m6A modification of APOBEC3B, leading to increased APOBEC3B expression and DNA mutation rates in a manner dependent on the m6A reader YTHDF2.	Arsenic	62-69	methyl-CpG binding domain protein 2	Homo sapiens	27-38
34998823-6	2022	We further reveal that the demethylase FTO is responsible for arsenic-reduced m6A modification of APOBEC3B, leading to increased APOBEC3B expression and DNA mutation rates in a manner dependent on the m6A reader YTHDF2.	Arsenic	62-69	FTO alpha-ketoglutarate dependent dioxygenase	Homo sapiens	39-42
34998823-6	2022	We further reveal that the demethylase FTO is responsible for arsenic-reduced m6A modification of APOBEC3B, leading to increased APOBEC3B expression and DNA mutation rates in a manner dependent on the m6A reader YTHDF2.	Arsenic	62-69	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	98-106
34998823-6	2022	We further reveal that the demethylase FTO is responsible for arsenic-reduced m6A modification of APOBEC3B, leading to increased APOBEC3B expression and DNA mutation rates in a manner dependent on the m6A reader YTHDF2.	Arsenic	62-69	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	129-137
34998823-6	2022	We further reveal that the demethylase FTO is responsible for arsenic-reduced m6A modification of APOBEC3B, leading to increased APOBEC3B expression and DNA mutation rates in a manner dependent on the m6A reader YTHDF2.	Arsenic	62-69	YTH N6-methyladenosine RNA binding protein 2	Homo sapiens	212-218
34998823-7	2022	Our in vivo data also confirm that APOBEC3B is a downstream target of FTO in arsenic-exposed lung tissues.	Arsenic	77-84	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	35-43
34998823-7	2022	Our in vivo data also confirm that APOBEC3B is a downstream target of FTO in arsenic-exposed lung tissues.	Arsenic	77-84	FTO alpha-ketoglutarate dependent dioxygenase	Homo sapiens	70-73
34998823-9	2022	These findings indicate a previously unrecognized role of APOBEC3B in arsenic-triggered somatic mutation, and might open new avenues to reduce DNA mutagenesis by targeting the FTO/m6A axis.	Arsenic	70-77	FTO alpha-ketoglutarate dependent dioxygenase	Homo sapiens	176-179
35120684-10	2022	PC2 (Mn and As) primarily comes from fossil fuel burning and pesticides and fertilizers containing Mn and As compounds.	Arsenic	106-108	polycystin 2, transient receptor potential cation channel	Homo sapiens	0-3
35064870-3	2022	The results show that arsenic can induce the hypermethylation of 6 sites in the Foxp3 promoter by upregulating the expression of recombinant DNA Methyltransferase 1 (Dnmt1) mRNA, leading to the downregulation of Foxp3 mRNA, Tregs, and interleukin 10 (IL-10, anti-inflammatory cytokine) levels, and increased the levels of interleukin 17 (IL-17, pro-inflammatory cytokine) in the peripheral blood of patients with arsenic poisoning.	Arsenic	22-29	DNA methyltransferase 1	Homo sapiens	141-164
35098445-5	2022	The data show that the median serum As, Cd, and Hg levels were relatively higher in females (As = 1.78 ng mL-1, Cd = 1.00 ng mL-1, Hg = 0.96 ng mL-1) than those in males (As = 1.22 ng mL-1, Cd = 0.91 ng mL-1, Hg = 0.95 ng mL-1).	Arsenic	36-38	L1 cell adhesion molecule	Mus musculus	106-110
35098445-5	2022	The data show that the median serum As, Cd, and Hg levels were relatively higher in females (As = 1.78 ng mL-1, Cd = 1.00 ng mL-1, Hg = 0.96 ng mL-1) than those in males (As = 1.22 ng mL-1, Cd = 0.91 ng mL-1, Hg = 0.95 ng mL-1).	Arsenic	36-38	L1 cell adhesion molecule	Mus musculus	125-129
35098445-5	2022	The data show that the median serum As, Cd, and Hg levels were relatively higher in females (As = 1.78 ng mL-1, Cd = 1.00 ng mL-1, Hg = 0.96 ng mL-1) than those in males (As = 1.22 ng mL-1, Cd = 0.91 ng mL-1, Hg = 0.95 ng mL-1).	Arsenic	36-38	L1 cell adhesion molecule	Mus musculus	144-148
35098445-5	2022	The data show that the median serum As, Cd, and Hg levels were relatively higher in females (As = 1.78 ng mL-1, Cd = 1.00 ng mL-1, Hg = 0.96 ng mL-1) than those in males (As = 1.22 ng mL-1, Cd = 0.91 ng mL-1, Hg = 0.95 ng mL-1).	Arsenic	36-38	L1 cell adhesion molecule	Mus musculus	184-188
35098445-5	2022	The data show that the median serum As, Cd, and Hg levels were relatively higher in females (As = 1.78 ng mL-1, Cd = 1.00 ng mL-1, Hg = 0.96 ng mL-1) than those in males (As = 1.22 ng mL-1, Cd = 0.91 ng mL-1, Hg = 0.95 ng mL-1).	Arsenic	36-38	L1 cell adhesion molecule	Mus musculus	203-207
35098445-5	2022	The data show that the median serum As, Cd, and Hg levels were relatively higher in females (As = 1.78 ng mL-1, Cd = 1.00 ng mL-1, Hg = 0.96 ng mL-1) than those in males (As = 1.22 ng mL-1, Cd = 0.91 ng mL-1, Hg = 0.95 ng mL-1).	Arsenic	36-38	L1 cell adhesion molecule	Mus musculus	222-226
35064870-2	2022	The effect of methylation of the forkhead box P3 (Foxp3) promoter region on arsenic-induced disruption of pro- and anti-inflammatory T cell balance was first evaluated in this study, between the control and arsenism groups.	Arsenic	76-83	forkhead box P3	Homo sapiens	33-48
35064870-2	2022	The effect of methylation of the forkhead box P3 (Foxp3) promoter region on arsenic-induced disruption of pro- and anti-inflammatory T cell balance was first evaluated in this study, between the control and arsenism groups.	Arsenic	76-83	forkhead box P3	Homo sapiens	50-55
35064870-3	2022	The results show that arsenic can induce the hypermethylation of 6 sites in the Foxp3 promoter by upregulating the expression of recombinant DNA Methyltransferase 1 (Dnmt1) mRNA, leading to the downregulation of Foxp3 mRNA, Tregs, and interleukin 10 (IL-10, anti-inflammatory cytokine) levels, and increased the levels of interleukin 17 (IL-17, pro-inflammatory cytokine) in the peripheral blood of patients with arsenic poisoning.	Arsenic	22-29	DNA methyltransferase 1	Homo sapiens	166-171
35064870-3	2022	The results show that arsenic can induce the hypermethylation of 6 sites in the Foxp3 promoter by upregulating the expression of recombinant DNA Methyltransferase 1 (Dnmt1) mRNA, leading to the downregulation of Foxp3 mRNA, Tregs, and interleukin 10 (IL-10, anti-inflammatory cytokine) levels, and increased the levels of interleukin 17 (IL-17, pro-inflammatory cytokine) in the peripheral blood of patients with arsenic poisoning.	Arsenic	22-29	forkhead box P3	Homo sapiens	80-85
35064870-3	2022	The results show that arsenic can induce the hypermethylation of 6 sites in the Foxp3 promoter by upregulating the expression of recombinant DNA Methyltransferase 1 (Dnmt1) mRNA, leading to the downregulation of Foxp3 mRNA, Tregs, and interleukin 10 (IL-10, anti-inflammatory cytokine) levels, and increased the levels of interleukin 17 (IL-17, pro-inflammatory cytokine) in the peripheral blood of patients with arsenic poisoning.	Arsenic	22-29	forkhead box P3	Homo sapiens	212-217
35064870-3	2022	The results show that arsenic can induce the hypermethylation of 6 sites in the Foxp3 promoter by upregulating the expression of recombinant DNA Methyltransferase 1 (Dnmt1) mRNA, leading to the downregulation of Foxp3 mRNA, Tregs, and interleukin 10 (IL-10, anti-inflammatory cytokine) levels, and increased the levels of interleukin 17 (IL-17, pro-inflammatory cytokine) in the peripheral blood of patients with arsenic poisoning.	Arsenic	22-29	interleukin 10	Homo sapiens	235-249
35064870-3	2022	The results show that arsenic can induce the hypermethylation of 6 sites in the Foxp3 promoter by upregulating the expression of recombinant DNA Methyltransferase 1 (Dnmt1) mRNA, leading to the downregulation of Foxp3 mRNA, Tregs, and interleukin 10 (IL-10, anti-inflammatory cytokine) levels, and increased the levels of interleukin 17 (IL-17, pro-inflammatory cytokine) in the peripheral blood of patients with arsenic poisoning.	Arsenic	22-29	interleukin 10	Homo sapiens	251-256
35064870-3	2022	The results show that arsenic can induce the hypermethylation of 6 sites in the Foxp3 promoter by upregulating the expression of recombinant DNA Methyltransferase 1 (Dnmt1) mRNA, leading to the downregulation of Foxp3 mRNA, Tregs, and interleukin 10 (IL-10, anti-inflammatory cytokine) levels, and increased the levels of interleukin 17 (IL-17, pro-inflammatory cytokine) in the peripheral blood of patients with arsenic poisoning.	Arsenic	22-29	interleukin 17A	Homo sapiens	322-336
35064870-3	2022	The results show that arsenic can induce the hypermethylation of 6 sites in the Foxp3 promoter by upregulating the expression of recombinant DNA Methyltransferase 1 (Dnmt1) mRNA, leading to the downregulation of Foxp3 mRNA, Tregs, and interleukin 10 (IL-10, anti-inflammatory cytokine) levels, and increased the levels of interleukin 17 (IL-17, pro-inflammatory cytokine) in the peripheral blood of patients with arsenic poisoning.	Arsenic	22-29	interleukin 17A	Homo sapiens	338-343
34935849-0	2022	Cs3CuAs4Q8 (Q = S, Se): unique two-dimensional layered inorganic thioarsenates with the lowest Cu-to-As ratio and remarkable photocurrent responses.	Arsenic	101-103	squalene epoxidase	Homo sapiens	19-21
35038100-6	2022	PC1 comprises EC, TDS, As, Fe, TOC, and HCO3- with moderate loadings, which suggests microbially mediated degradation of organic matter (OM), helps in reductive dissolution of arsenic-bearing Fe-Mn oxyhydroxides.	Arsenic	23-25	proprotein convertase subtilisin/kexin type 1	Homo sapiens	0-3
35038100-6	2022	PC1 comprises EC, TDS, As, Fe, TOC, and HCO3- with moderate loadings, which suggests microbially mediated degradation of organic matter (OM), helps in reductive dissolution of arsenic-bearing Fe-Mn oxyhydroxides.	Arsenic	176-183	proprotein convertase subtilisin/kexin type 1	Homo sapiens	0-3
35039759-9	2022	In this study, integrin-linked kinase (ILK) was one of the most significant pathways identified between both arsenic exposed population which plays a key role in eliciting a protective response to oxidative damage in epidermal cells.	Arsenic	109-116	integrin linked kinase	Homo sapiens	15-37
35039759-9	2022	In this study, integrin-linked kinase (ILK) was one of the most significant pathways identified between both arsenic exposed population which plays a key role in eliciting a protective response to oxidative damage in epidermal cells.	Arsenic	109-116	integrin linked kinase	Homo sapiens	39-42
35072517-16	2022	Our preliminary proteomic analysis demonstrated that the expression of the canonical isoforms of the splice regulators DDX42, RMB25, and SRRM2 were induced upon chronic arsenic exposure, corroborating the splicing predictions.	Arsenic	169-176	DEAD-box helicase 42	Homo sapiens	119-124
34974760-5	2022	In summary, our results demonstrated that ROS contributes to the malignant phenotype of arsenic-transformed human hepatocyte L-02-As via the activation of Akt pathway.	Arsenic	88-95	AKT serine/threonine kinase 1	Homo sapiens	155-158
34974760-0	2022	Malignant growth of arsenic-transformed cells depends on activated Akt induced by reactive oxygen species.	Arsenic	20-27	AKT serine/threonine kinase 1	Homo sapiens	67-70
34974760-2	2022	Meanwhile, compared with normal L-02 cells, arsenic-transformed malignant cells, L-02-As displayed more ROS and significantly higher Cyclin D1 expression as well as aerobic glycolysis.	Arsenic	44-51	cyclin D1	Homo sapiens	133-142
35072517-16	2022	Our preliminary proteomic analysis demonstrated that the expression of the canonical isoforms of the splice regulators DDX42, RMB25, and SRRM2 were induced upon chronic arsenic exposure, corroborating the splicing predictions.	Arsenic	169-176	serine/arginine repetitive matrix 2	Homo sapiens	137-142
35010728-0	2022	Additive and Interactive Associations of Environmental and Sociodemographic Factors with the Genotypes of Three Glutathione S-Transferase Genes in Relation to the Blood Arsenic Concentrations of Children in Jamaica.	Arsenic	169-176	glutathione S-transferase kappa 1	Homo sapiens	112-137
35070938-3	2022	IgG1:IgG2a ratios in brain tissues from BTBR mice exposed to As (BTBR-As) were significantly higher than those of BTBR-control mice (BTBR-C), but this change did not occur in FVB mice exposed to As.	Arsenic	61-63	immunoglobulin heavy constant gamma 1 (G1m marker)	Mus musculus	0-4
35070938-3	2022	IgG1:IgG2a ratios in brain tissues from BTBR mice exposed to As (BTBR-As) were significantly higher than those of BTBR-control mice (BTBR-C), but this change did not occur in FVB mice exposed to As.	Arsenic	61-63	immunoglobulin heavy variable V1-9	Mus musculus	5-10
35070938-3	2022	IgG1:IgG2a ratios in brain tissues from BTBR mice exposed to As (BTBR-As) were significantly higher than those of BTBR-control mice (BTBR-C), but this change did not occur in FVB mice exposed to As.	Arsenic	70-72	immunoglobulin heavy constant gamma 1 (G1m marker)	Mus musculus	0-4
35070938-3	2022	IgG1:IgG2a ratios in brain tissues from BTBR mice exposed to As (BTBR-As) were significantly higher than those of BTBR-control mice (BTBR-C), but this change did not occur in FVB mice exposed to As.	Arsenic	70-72	immunoglobulin heavy variable V1-9	Mus musculus	5-10
35070938-3	2022	IgG1:IgG2a ratios in brain tissues from BTBR mice exposed to As (BTBR-As) were significantly higher than those of BTBR-control mice (BTBR-C), but this change did not occur in FVB mice exposed to As.	Arsenic	195-197	immunoglobulin heavy constant gamma 1 (G1m marker)	Mus musculus	0-4
35070938-3	2022	IgG1:IgG2a ratios in brain tissues from BTBR mice exposed to As (BTBR-As) were significantly higher than those of BTBR-control mice (BTBR-C), but this change did not occur in FVB mice exposed to As.	Arsenic	195-197	immunoglobulin heavy variable V1-9	Mus musculus	5-10