PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
35530281-9	2022	JTB protein itself is involved in mitotic spindle pathway by its role in cell division/cytokinesis, and within estrogen response early and late pathways, contributing to discrimination between luminal and mesenchymal breast cancer.	Phenobarbital	193-200	jumping translocation breakpoint	Homo sapiens	0-3
2100217-1	1990	An automatic kinetic method for the determination of micro amounts of vitamin B12 in pharmaceutical samples based on the fast formation of a coloured complex between the cobalt contained by this vitamin and PAR [4-(2-pyridilazo)resorcinol] in a weakly alkaline medium and on the use of the continuous addition of reagent technique for the mixing of sample and reagent is reported.	Vitamin B 12	70-81	jumping translocation breakpoint	Homo sapiens	207-210
2100217-1	1990	An automatic kinetic method for the determination of micro amounts of vitamin B12 in pharmaceutical samples based on the fast formation of a coloured complex between the cobalt contained by this vitamin and PAR [4-(2-pyridilazo)resorcinol] in a weakly alkaline medium and on the use of the continuous addition of reagent technique for the mixing of sample and reagent is reported.	Cobalt	170-176	jumping translocation breakpoint	Homo sapiens	207-210
28827033-5	2017	PARP1 activity (poly (ADP-ribose), PAR) was found to be greatly increased in cisplatin-resistant GC cells.	Cisplatin	77-86	jumping translocation breakpoint	Homo sapiens	0-3
28827033-6	2017	PARP1 inhibitors significantly enhanced cisplatin-induced DNA damage and apoptosis in the resistant GC cells via the inhibition of PAR.	Cisplatin	40-49	jumping translocation breakpoint	Homo sapiens	0-3
35530281-11	2022	Other upregulated proteins for overexpressed JTB condition are involved in multiple cellular functions and pathways that become dysregulated, such as tumor microenvironment (TME) acidification, the transmembrane transport pathways, glycolytic flux, iron metabolism and oxidative stress, metabolic reprogramming, nucleocytosolic mRNA transport, transcriptional activation, chromatin remodeling, modulation of cell death pathways, stress responsive pathways, and cancer drug resistance.	Iron	249-253	jumping translocation breakpoint	Homo sapiens	45-48
33262140-10	2021	At the MTD olaparib reduced PAR levels by over 95% and abolished radiation-induced PARylation.	olaparib	11-19	jumping translocation breakpoint	Homo sapiens	28-31
18963641-1	1984	The ion-pair extraction equilibria of the iron(II) and iron(III) chelates of 4-(2-pyridylazo)resorcinol (PAR, H(2)L) are described.	Iron	42-46	jumping translocation breakpoint	Homo sapiens	105-108
18963641-1	1984	The ion-pair extraction equilibria of the iron(II) and iron(III) chelates of 4-(2-pyridylazo)resorcinol (PAR, H(2)L) are described.	Iron	55-59	jumping translocation breakpoint	Homo sapiens	105-108
18963641-1	1984	The ion-pair extraction equilibria of the iron(II) and iron(III) chelates of 4-(2-pyridylazo)resorcinol (PAR, H(2)L) are described.	4-(2-pyridylazo)resorcinol	77-103	jumping translocation breakpoint	Homo sapiens	105-108
18963641-6	1984	The relationship between the forms and extraction properties of the iron(II) and iron(III) PAR chelates are discussed in connection with those of the nickel(II) and cobalt(III) complexes.	Iron	68-72	jumping translocation breakpoint	Homo sapiens	91-94
18963641-6	1984	The relationship between the forms and extraction properties of the iron(II) and iron(III) PAR chelates are discussed in connection with those of the nickel(II) and cobalt(III) complexes.	Iron	81-85	jumping translocation breakpoint	Homo sapiens	91-94
18963641-6	1984	The relationship between the forms and extraction properties of the iron(II) and iron(III) PAR chelates are discussed in connection with those of the nickel(II) and cobalt(III) complexes.	Nickel	150-156	jumping translocation breakpoint	Homo sapiens	91-94
18963641-6	1984	The relationship between the forms and extraction properties of the iron(II) and iron(III) PAR chelates are discussed in connection with those of the nickel(II) and cobalt(III) complexes.	Cobalt	165-171	jumping translocation breakpoint	Homo sapiens	91-94
18961957-2	1976	The complex [Zn(PAR)(2)](CDBA)(2), where PAR is the 4-(2-pyridylazo)resorcinol anion and CDBA is cetyldimethylbenzylammonium ion, is extracted from a solution buffered at pH 9.7 with carbonate/bicarbonate.	beta-cyclodextrin-benzaldehyde	25-29	jumping translocation breakpoint	Homo sapiens	16-19
18961957-2	1976	The complex [Zn(PAR)(2)](CDBA)(2), where PAR is the 4-(2-pyridylazo)resorcinol anion and CDBA is cetyldimethylbenzylammonium ion, is extracted from a solution buffered at pH 9.7 with carbonate/bicarbonate.	beta-cyclodextrin-benzaldehyde	25-29	jumping translocation breakpoint	Homo sapiens	41-44
18961957-2	1976	The complex [Zn(PAR)(2)](CDBA)(2), where PAR is the 4-(2-pyridylazo)resorcinol anion and CDBA is cetyldimethylbenzylammonium ion, is extracted from a solution buffered at pH 9.7 with carbonate/bicarbonate.	4-(2-pyridylazo)resorcinol anion	52-84	jumping translocation breakpoint	Homo sapiens	16-19
18961957-2	1976	The complex [Zn(PAR)(2)](CDBA)(2), where PAR is the 4-(2-pyridylazo)resorcinol anion and CDBA is cetyldimethylbenzylammonium ion, is extracted from a solution buffered at pH 9.7 with carbonate/bicarbonate.	Cetalkonium	97-124	jumping translocation breakpoint	Homo sapiens	16-19
4645701-0	1972	PAR-Palladium as an analytical reagent for hydrogen cyanide: application to the detection of thiocyanate and to biological and toxicological analysis.	Hydrogen Cyanide	43-59	jumping translocation breakpoint	Homo sapiens	0-3
4645701-0	1972	PAR-Palladium as an analytical reagent for hydrogen cyanide: application to the detection of thiocyanate and to biological and toxicological analysis.	thiocyanate	93-104	jumping translocation breakpoint	Homo sapiens	0-3
6083090-0	1967	[On the question of complexometric determination of aluminum in aluminum phosphate in the presence of PAR indicator].	Aluminum	52-60	jumping translocation breakpoint	Homo sapiens	102-105
4967065-0	1967	[On the possibility of the stabilization of titration of disodium versenate solution by means of lead nitrate in the presence of PAR indicator].	Edetic Acid	57-75	jumping translocation breakpoint	Homo sapiens	129-132
572891-1	1979	A 31-year-old healthy woman received Ritodrine (Pre-Par) from the 26th week of gestation because of twin pregnancy.	Ritodrine	37-46	jumping translocation breakpoint	Homo sapiens	52-55
33443209-6	2020	RNF146 inhibited PARP1 not through its E3 ligase function but rather by binding to and sequestering PAR, which enhanced the survival of cultured cells exposed to the dopaminergic neuronal toxin 6-OHDA or alpha-synuclein aggregation.	Oxidopamine	194-200	jumping translocation breakpoint	Homo sapiens	17-20
33433835-4	2021	ANS testing assessed autonomic function by finger capillary pulse to positional changes (PAR), vasoconstriction to cold (VC), and EKG R-R interval change (RRI) with deep breathing; the ENS measures of cutaneous EGG assessed gastric myoelectrical activity.	1-anilino-8-naphthalenesulfonate	0-3	jumping translocation breakpoint	Homo sapiens	89-92
26239116-2	2015	Thrombin administration to platelets evokes the synthesis of diacylglycerol downstream of PAR receptor activation.	Diglycerides	61-75	jumping translocation breakpoint	Homo sapiens	90-93
32787089-1	2020	Two novel theranostic agents HJTA and HJTB have been designed and synthesized by covalently linking a beta-carboline derivative, with antitumor activities and pH-responsive fluorescence, with a 2-exomethylenecyclohexanone moiety, which can be activated by the tumor-targeting glutathione (GSH)/glutathione S-transferase pi (GSTpi).	norharman	102-116	jumping translocation breakpoint	Homo sapiens	38-42
32787089-1	2020	Two novel theranostic agents HJTA and HJTB have been designed and synthesized by covalently linking a beta-carboline derivative, with antitumor activities and pH-responsive fluorescence, with a 2-exomethylenecyclohexanone moiety, which can be activated by the tumor-targeting glutathione (GSH)/glutathione S-transferase pi (GSTpi).	Glutathione	276-287	jumping translocation breakpoint	Homo sapiens	38-42
32787089-1	2020	Two novel theranostic agents HJTA and HJTB have been designed and synthesized by covalently linking a beta-carboline derivative, with antitumor activities and pH-responsive fluorescence, with a 2-exomethylenecyclohexanone moiety, which can be activated by the tumor-targeting glutathione (GSH)/glutathione S-transferase pi (GSTpi).	Glutathione	289-292	jumping translocation breakpoint	Homo sapiens	38-42
32787089-1	2020	Two novel theranostic agents HJTA and HJTB have been designed and synthesized by covalently linking a beta-carboline derivative, with antitumor activities and pH-responsive fluorescence, with a 2-exomethylenecyclohexanone moiety, which can be activated by the tumor-targeting glutathione (GSH)/glutathione S-transferase pi (GSTpi).	Glutathione	294-305	jumping translocation breakpoint	Homo sapiens	38-42
32439163-4	2020	Here, we demonstrate that PAR glycohydrolases (PARGs) from mammals to bacteria have a robust endo-glycohydrolase activity, releasing protein-free PAR chains longer than three ADP-ribose units as early reaction products.	Adenosine Diphosphate Ribose	175-185	jumping translocation breakpoint	Homo sapiens	26-29
32439163-4	2020	Here, we demonstrate that PAR glycohydrolases (PARGs) from mammals to bacteria have a robust endo-glycohydrolase activity, releasing protein-free PAR chains longer than three ADP-ribose units as early reaction products.	Adenosine Diphosphate Ribose	175-185	jumping translocation breakpoint	Homo sapiens	47-50
32439163-5	2020	Released PAR chains are transient and rapidly degraded to monomeric ADP-ribose, which is consistent with a short half-life of PAR during DNA damage responses.	Adenosine Diphosphate Ribose	68-78	jumping translocation breakpoint	Homo sapiens	9-12
32439163-5	2020	Released PAR chains are transient and rapidly degraded to monomeric ADP-ribose, which is consistent with a short half-life of PAR during DNA damage responses.	Adenosine Diphosphate Ribose	68-78	jumping translocation breakpoint	Homo sapiens	126-129
32439163-6	2020	Computational simulations using a tri-ADP-ribose further support that PARG can efficiently bind to internal sites of PAR for the endo-glycosidic cleavage.	tri-adp-ribose	34-48	jumping translocation breakpoint	Homo sapiens	70-73
32092891-3	2020	A novel anti-stripping composite, montmorillonoid/Polyamide (OMMT/PAR), which possesses excellent thermal stability performance and is effective in preventing moisture damage, especially for acidic aggregates, was prepared.	montmorillonoid	34-49	jumping translocation breakpoint	Homo sapiens	66-69
32092891-3	2020	A novel anti-stripping composite, montmorillonoid/Polyamide (OMMT/PAR), which possesses excellent thermal stability performance and is effective in preventing moisture damage, especially for acidic aggregates, was prepared.	Nylons	50-59	jumping translocation breakpoint	Homo sapiens	66-69
31108565-2	2019	The studied PAR impurities are the genotoxic and nephrotoxic p-amino phenol (PAP) and the hepatotoxic and nephrotoxic chloroacetanilide, while 5-(4-nitrophenyl)-2-furaldehyde is reported to be a mutagenic and carcinogenic degradation product of DNS.	Aminophenols	63-75	jumping translocation breakpoint	Homo sapiens	12-15
31108565-2	2019	The studied PAR impurities are the genotoxic and nephrotoxic p-amino phenol (PAP) and the hepatotoxic and nephrotoxic chloroacetanilide, while 5-(4-nitrophenyl)-2-furaldehyde is reported to be a mutagenic and carcinogenic degradation product of DNS.	4-aminophenol	77-80	jumping translocation breakpoint	Homo sapiens	12-15
31108565-2	2019	The studied PAR impurities are the genotoxic and nephrotoxic p-amino phenol (PAP) and the hepatotoxic and nephrotoxic chloroacetanilide, while 5-(4-nitrophenyl)-2-furaldehyde is reported to be a mutagenic and carcinogenic degradation product of DNS.	2-chloroacetanilide	118-135	jumping translocation breakpoint	Homo sapiens	12-15
31108565-2	2019	The studied PAR impurities are the genotoxic and nephrotoxic p-amino phenol (PAP) and the hepatotoxic and nephrotoxic chloroacetanilide, while 5-(4-nitrophenyl)-2-furaldehyde is reported to be a mutagenic and carcinogenic degradation product of DNS.	5-(4-Nitrophenyl)-2-furaldehyde	143-174	jumping translocation breakpoint	Homo sapiens	12-15
31108565-2	2019	The studied PAR impurities are the genotoxic and nephrotoxic p-amino phenol (PAP) and the hepatotoxic and nephrotoxic chloroacetanilide, while 5-(4-nitrophenyl)-2-furaldehyde is reported to be a mutagenic and carcinogenic degradation product of DNS.	Dantrolene	245-248	jumping translocation breakpoint	Homo sapiens	12-15
31171201-4	2019	The second sensor, 4-(2-pyridylazo)-resorcinol-modified-TiO2NPs-based solid sensor (PAR@TiO2NPs), relies on the formation of a ternary complex between Ti(IV), PAR and H2O2.	4-(2-pyridylazo)resorcinol	19-46	jumping translocation breakpoint	Homo sapiens	84-87
31171201-4	2019	The second sensor, 4-(2-pyridylazo)-resorcinol-modified-TiO2NPs-based solid sensor (PAR@TiO2NPs), relies on the formation of a ternary complex between Ti(IV), PAR and H2O2.	4-(2-pyridylazo)resorcinol	19-46	jumping translocation breakpoint	Homo sapiens	159-162
31171201-4	2019	The second sensor, 4-(2-pyridylazo)-resorcinol-modified-TiO2NPs-based solid sensor (PAR@TiO2NPs), relies on the formation of a ternary complex between Ti(IV), PAR and H2O2.	tio2nps	56-63	jumping translocation breakpoint	Homo sapiens	84-87
31171201-4	2019	The second sensor, 4-(2-pyridylazo)-resorcinol-modified-TiO2NPs-based solid sensor (PAR@TiO2NPs), relies on the formation of a ternary complex between Ti(IV), PAR and H2O2.	tio2nps	56-63	jumping translocation breakpoint	Homo sapiens	159-162
31171201-4	2019	The second sensor, 4-(2-pyridylazo)-resorcinol-modified-TiO2NPs-based solid sensor (PAR@TiO2NPs), relies on the formation of a ternary complex between Ti(IV), PAR and H2O2.	tio2nps	88-95	jumping translocation breakpoint	Homo sapiens	84-87
31171201-4	2019	The second sensor, 4-(2-pyridylazo)-resorcinol-modified-TiO2NPs-based solid sensor (PAR@TiO2NPs), relies on the formation of a ternary complex between Ti(IV), PAR and H2O2.	tio2nps	88-95	jumping translocation breakpoint	Homo sapiens	159-162
31171201-4	2019	The second sensor, 4-(2-pyridylazo)-resorcinol-modified-TiO2NPs-based solid sensor (PAR@TiO2NPs), relies on the formation of a ternary complex between Ti(IV), PAR and H2O2.	Hydrogen Peroxide	167-171	jumping translocation breakpoint	Homo sapiens	84-87
31171201-6	2019	The limits of detection (LODs) of APTES@TiO2NPs-based paper sensor were 3.14 x 10-4 and 5.13 x 10-4 mol L-1 for H2O2 and TATP, respectively, whereas the LODs of PAR@TiO2NPs solid sensor were 6.06 x 10-7 and 3.54 x 10-7 mol L-1 for H2O2 and TATP, respectively.	tio2nps	40-47	jumping translocation breakpoint	Homo sapiens	161-164
31171201-6	2019	The limits of detection (LODs) of APTES@TiO2NPs-based paper sensor were 3.14 x 10-4 and 5.13 x 10-4 mol L-1 for H2O2 and TATP, respectively, whereas the LODs of PAR@TiO2NPs solid sensor were 6.06 x 10-7 and 3.54 x 10-7 mol L-1 for H2O2 and TATP, respectively.	Hydrogen Peroxide	112-116	jumping translocation breakpoint	Homo sapiens	161-164
31171201-6	2019	The limits of detection (LODs) of APTES@TiO2NPs-based paper sensor were 3.14 x 10-4 and 5.13 x 10-4 mol L-1 for H2O2 and TATP, respectively, whereas the LODs of PAR@TiO2NPs solid sensor were 6.06 x 10-7 and 3.54 x 10-7 mol L-1 for H2O2 and TATP, respectively.	triacetone triperoxide	121-125	jumping translocation breakpoint	Homo sapiens	161-164
30698666-1	2019	BACKGROUND: Increased vitamin B6 catabolism related to inflammation, as measured by the PAr index (the ratio of 4-pyridoxic acid over the sum of pyridoxal and pyridoxal-5"-phosphate), has been positively associated with lung cancer risk in two prospective European studies.	Vitamin B 6	22-32	jumping translocation breakpoint	Homo sapiens	88-91
30698666-1	2019	BACKGROUND: Increased vitamin B6 catabolism related to inflammation, as measured by the PAr index (the ratio of 4-pyridoxic acid over the sum of pyridoxal and pyridoxal-5"-phosphate), has been positively associated with lung cancer risk in two prospective European studies.	Pyridoxic Acid	112-128	jumping translocation breakpoint	Homo sapiens	88-91
30698666-1	2019	BACKGROUND: Increased vitamin B6 catabolism related to inflammation, as measured by the PAr index (the ratio of 4-pyridoxic acid over the sum of pyridoxal and pyridoxal-5"-phosphate), has been positively associated with lung cancer risk in two prospective European studies.	Pyridoxal	145-154	jumping translocation breakpoint	Homo sapiens	88-91
30698666-1	2019	BACKGROUND: Increased vitamin B6 catabolism related to inflammation, as measured by the PAr index (the ratio of 4-pyridoxic acid over the sum of pyridoxal and pyridoxal-5"-phosphate), has been positively associated with lung cancer risk in two prospective European studies.	Pyridoxal Phosphate	159-181	jumping translocation breakpoint	Homo sapiens	88-91
30384244-1	2019	To advocate environment friendly detection idea, we adopted the green chemical method to synthesis the 1-(2 amino ethyl) piperidine functionalized polyacrylonitrile fiber (APF) and the chromogenic fiber 4-(2-pyridylazo) resorcinol (APF-PAR).	polyacrylonitrile fiber	147-170	jumping translocation breakpoint	Homo sapiens	236-239
30384244-1	2019	To advocate environment friendly detection idea, we adopted the green chemical method to synthesis the 1-(2 amino ethyl) piperidine functionalized polyacrylonitrile fiber (APF) and the chromogenic fiber 4-(2-pyridylazo) resorcinol (APF-PAR).	4-(2-pyridylazo)resorcinol	203-230	jumping translocation breakpoint	Homo sapiens	236-239
30384244-4	2019	The chromogenic fiber APF-PAR can recognize the Hg2+ and Cu2+ in 2 s, which benefits from the rapid mass transfer and small fluid resistance of the chelating PAN fiber.	cupric ion	57-61	jumping translocation breakpoint	Homo sapiens	26-29
27149849-2	2016	Here, we report that nuclear PKM2 binds directly to poly-ADP ribose, and this PAR-binding capability is critical for its nuclear localization.	poly-adp	52-60	jumping translocation breakpoint	Homo sapiens	78-81
32046374-0	2020	Observation of Parthanatos Involvement in Diminished Ovarian Reserve Patients and Melatonin"s Protective Function Through Inhibiting ADP-Ribose (PAR) Expression and Preventing AIF Translocation into the Nucleus.	Melatonin	82-91	jumping translocation breakpoint	Homo sapiens	145-148
30130101-4	2018	The TbIII derivative, Tb-TEMPO-CN, also shows strong Tb-radical AF coupling, which has been rationalized using the ab initio CASSCF approach ( JTb-rad = -23.02 K, -16.7 cm-1) and confirmed by luminescence measurements.	tbiii	4-9	jumping translocation breakpoint	Homo sapiens	143-146
30130101-4	2018	The TbIII derivative, Tb-TEMPO-CN, also shows strong Tb-radical AF coupling, which has been rationalized using the ab initio CASSCF approach ( JTb-rad = -23.02 K, -16.7 cm-1) and confirmed by luminescence measurements.	Terbium	4-6	jumping translocation breakpoint	Homo sapiens	143-146
30130101-4	2018	The TbIII derivative, Tb-TEMPO-CN, also shows strong Tb-radical AF coupling, which has been rationalized using the ab initio CASSCF approach ( JTb-rad = -23.02 K, -16.7 cm-1) and confirmed by luminescence measurements.	Terbium	22-24	jumping translocation breakpoint	Homo sapiens	143-146
29930865-0	2018	Promoting Alcohol Reduction in Non-Treatment Seeking parents (PAReNTS): a protocol for a pilot feasibility cluster randomised controlled trial of alcohol screening and brief interventions to reduce parental alcohol use disorders in vulnerable families.	Alcohols	10-17	jumping translocation breakpoint	Homo sapiens	53-60
29930865-0	2018	Promoting Alcohol Reduction in Non-Treatment Seeking parents (PAReNTS): a protocol for a pilot feasibility cluster randomised controlled trial of alcohol screening and brief interventions to reduce parental alcohol use disorders in vulnerable families.	Alcohols	10-17	jumping translocation breakpoint	Homo sapiens	62-69
29930865-0	2018	Promoting Alcohol Reduction in Non-Treatment Seeking parents (PAReNTS): a protocol for a pilot feasibility cluster randomised controlled trial of alcohol screening and brief interventions to reduce parental alcohol use disorders in vulnerable families.	Alcohols	146-153	jumping translocation breakpoint	Homo sapiens	62-69
29930865-0	2018	Promoting Alcohol Reduction in Non-Treatment Seeking parents (PAReNTS): a protocol for a pilot feasibility cluster randomised controlled trial of alcohol screening and brief interventions to reduce parental alcohol use disorders in vulnerable families.	Alcohols	207-214	jumping translocation breakpoint	Homo sapiens	53-60
29930865-0	2018	Promoting Alcohol Reduction in Non-Treatment Seeking parents (PAReNTS): a protocol for a pilot feasibility cluster randomised controlled trial of alcohol screening and brief interventions to reduce parental alcohol use disorders in vulnerable families.	Alcohols	207-214	jumping translocation breakpoint	Homo sapiens	62-69
29930865-3	2018	The PAReNTS (Promoting Alcohol Reduction in Non-Treatment Seeking parents) trial aims to examine the feasibility and acceptability of a randomised controlled trial of brief alcohol interventions to reduce parental alcohol misuse.	Alcohols	23-30	jumping translocation breakpoint	Homo sapiens	4-11
29930865-3	2018	The PAReNTS (Promoting Alcohol Reduction in Non-Treatment Seeking parents) trial aims to examine the feasibility and acceptability of a randomised controlled trial of brief alcohol interventions to reduce parental alcohol misuse.	Alcohols	23-30	jumping translocation breakpoint	Homo sapiens	66-73
29930865-3	2018	The PAReNTS (Promoting Alcohol Reduction in Non-Treatment Seeking parents) trial aims to examine the feasibility and acceptability of a randomised controlled trial of brief alcohol interventions to reduce parental alcohol misuse.	Alcohols	173-180	jumping translocation breakpoint	Homo sapiens	4-11
29930865-3	2018	The PAReNTS (Promoting Alcohol Reduction in Non-Treatment Seeking parents) trial aims to examine the feasibility and acceptability of a randomised controlled trial of brief alcohol interventions to reduce parental alcohol misuse.	Alcohols	173-180	jumping translocation breakpoint	Homo sapiens	66-73
29930865-3	2018	The PAReNTS (Promoting Alcohol Reduction in Non-Treatment Seeking parents) trial aims to examine the feasibility and acceptability of a randomised controlled trial of brief alcohol interventions to reduce parental alcohol misuse.	Alcohols	214-221	jumping translocation breakpoint	Homo sapiens	4-11
29627626-1	2018	Poly (ADP-ribose) polymerase 1 (PARP1) is a DNA damage sensor that catalyzes the poly (ADP-ribose) (PAR) onto a variety of target proteins, such as histones, DSB repair factors and PARP1 itself under consumption of NAD+.	NAD	215-219	jumping translocation breakpoint	Homo sapiens	32-35
27686740-0	2016	Efficacy of poly (ADP-ribose) polymerase inhibitor olaparib against head and neck cancer cells: Predictions of drug sensitivity based on PAR-p53-NF-kappaB interactions.	olaparib	51-59	jumping translocation breakpoint	Homo sapiens	137-140
27686740-7	2016	We found that basal poly (ADP-ribose) (PAR) levels, but not PARP-1 levels, correlated with olaparib sensitivity.	olaparib	91-99	jumping translocation breakpoint	Homo sapiens	39-42
27686740-10	2016	As interference with p53 expression led to NF-kappaB reactivation, we concluded that elevated basal PAR and NF-kappaB levels are predictive of olaparib responsiveness in HNC cells; in addition, olaparib inhibits HNC cells via PAR-p53-NF-kappaB interactions.	olaparib	143-151	jumping translocation breakpoint	Homo sapiens	100-103
27686740-10	2016	As interference with p53 expression led to NF-kappaB reactivation, we concluded that elevated basal PAR and NF-kappaB levels are predictive of olaparib responsiveness in HNC cells; in addition, olaparib inhibits HNC cells via PAR-p53-NF-kappaB interactions.	olaparib	194-202	jumping translocation breakpoint	Homo sapiens	226-229
26778300-13	2016	CONCLUSION: A high percentage of nuclear staining of ERCC1, RAD51, and PAR, assessed by immunohistochemistry, correlated with worse OS for patients with mUC treated with first-line platinum combination chemotherapy, supporting the evidence of the DNA repair pathways" role in the prognosis of mUC.	Platinum	181-189	jumping translocation breakpoint	Homo sapiens	71-74
26778300-14	2016	We also report new evidence that RAD51 and PAR might play a role in the platinum response.	Platinum	72-80	jumping translocation breakpoint	Homo sapiens	43-46
25981132-6	2015	Olaparib concentrations that resulted in radiosensitization prevented PAR induction by irradiation.	olaparib	0-8	jumping translocation breakpoint	Homo sapiens	70-73
24038812-8	2014	RESULTS: Olaparib induced growth inhibition, median (range) IC50 = 3.6 (1-33.8) microM, and inhibited PAR activity in pediatric solid tumor cell lines.	olaparib	9-17	jumping translocation breakpoint	Homo sapiens	102-105
25663523-6	2015	The proteolytic and peptidic PAR activators also stimulated the release of IL-6 and IL-8, as well as PGE2, with a rank order of potency of PAR-1 > PAR-2.	Dinoprostone	101-105	jumping translocation breakpoint	Homo sapiens	29-32
24920161-1	2014	Poly(ADP-ribose), or PAR, is a cellular polymer implicated in DNA/RNA metabolism, cell death, and cellular stress response via its role as a post-translational modification, signaling molecule, and scaffolding element.	Poly Adenosine Diphosphate Ribose	0-15	jumping translocation breakpoint	Homo sapiens	21-24
24038812-10	2014	In RD-ES and NGP xenografts, olaparib inhibited PAR activity by 88-100% as a single agent and 100% when administered with cyclophosphamide/topotecan.	olaparib	29-37	jumping translocation breakpoint	Homo sapiens	48-51
24191052-1	2013	Poly (ADP ribose) (PAR) formation catalyzed by PAR polymerase 1 in response to genotoxic stress mediates cell death due to necrosis and apoptosis.	Poly Adenosine Diphosphate Ribose	0-17	jumping translocation breakpoint	Homo sapiens	19-22
24191052-1	2013	Poly (ADP ribose) (PAR) formation catalyzed by PAR polymerase 1 in response to genotoxic stress mediates cell death due to necrosis and apoptosis.	Poly Adenosine Diphosphate Ribose	0-17	jumping translocation breakpoint	Homo sapiens	47-50
24191052-4	2013	PARG and ARH3, acting in tandem, regulate nuclear and cytoplasmic PAR degradation following hydrogen peroxide (H2O2) exposure.	Hydrogen Peroxide	92-109	jumping translocation breakpoint	Homo sapiens	0-3
24191052-4	2013	PARG and ARH3, acting in tandem, regulate nuclear and cytoplasmic PAR degradation following hydrogen peroxide (H2O2) exposure.	Hydrogen Peroxide	111-115	jumping translocation breakpoint	Homo sapiens	0-3
22490786-7	2012	Treatment with FK866 (10 mg/kg), the best known and characterized NAMPT inhibitor, at 1 h and 6 h after SCI rescued motor function, preserved perilesional gray and white matter, restored anti-apoptotic and neurotrophic factors, prevented the activation of neutrophils, microglia and astrocytes and inhibited the elevation of NAMPT, PAR, TNF-alpha, IL-1beta, Bax expression and NF-kappaB activity.We show for the first time that FK866, a specific inhibitor of NAMPT, administered after SCI, is capable of reducing the secondary inflammatory injury and partly reduce permanent damage.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	15-20	jumping translocation breakpoint	Homo sapiens	332-335
24004243-1	2013	The four-coordinate scandium phosphinidene complex, [LSc(mu-PAr)]2 (L = (MeC(NDIPP)CHC(Me)(NCH2CH2N((i)Pr)2)), DIPP = 2,6-((i)Pr)2C6H3; Ar = 2,6-Me2C6H3) (1), has been synthesized in good yield, and its reactivity has been investigated.	Phosphinidene	29-42	jumping translocation breakpoint	Homo sapiens	60-63
24004243-3	2013	First, two-electron reduction occurs when substrates as 2,2"-bipyridine, elemental selenium, elemental tellurium, Me3P S, or Ph3P E (E = S, Se) is used, resulting in the oxidative coupling of two phosphinidene ligands 2[PAr](2-) into a diphosphene ligand [ArP-PAr](2-).	2,2'-Dipyridyl	56-71	jumping translocation breakpoint	Homo sapiens	220-223
24004243-3	2013	First, two-electron reduction occurs when substrates as 2,2"-bipyridine, elemental selenium, elemental tellurium, Me3P S, or Ph3P E (E = S, Se) is used, resulting in the oxidative coupling of two phosphinidene ligands 2[PAr](2-) into a diphosphene ligand [ArP-PAr](2-).	2,2'-Dipyridyl	56-71	jumping translocation breakpoint	Homo sapiens	260-263
24004243-3	2013	First, two-electron reduction occurs when substrates as 2,2"-bipyridine, elemental selenium, elemental tellurium, Me3P S, or Ph3P E (E = S, Se) is used, resulting in the oxidative coupling of two phosphinidene ligands 2[PAr](2-) into a diphosphene ligand [ArP-PAr](2-).	Selenium	83-91	jumping translocation breakpoint	Homo sapiens	220-223
24004243-3	2013	First, two-electron reduction occurs when substrates as 2,2"-bipyridine, elemental selenium, elemental tellurium, Me3P S, or Ph3P E (E = S, Se) is used, resulting in the oxidative coupling of two phosphinidene ligands 2[PAr](2-) into a diphosphene ligand [ArP-PAr](2-).	Selenium	83-91	jumping translocation breakpoint	Homo sapiens	260-263
24004243-3	2013	First, two-electron reduction occurs when substrates as 2,2"-bipyridine, elemental selenium, elemental tellurium, Me3P S, or Ph3P E (E = S, Se) is used, resulting in the oxidative coupling of two phosphinidene ligands 2[PAr](2-) into a diphosphene ligand [ArP-PAr](2-).	Tellurium	103-112	jumping translocation breakpoint	Homo sapiens	220-223
24004243-3	2013	First, two-electron reduction occurs when substrates as 2,2"-bipyridine, elemental selenium, elemental tellurium, Me3P S, or Ph3P E (E = S, Se) is used, resulting in the oxidative coupling of two phosphinidene ligands 2[PAr](2-) into a diphosphene ligand [ArP-PAr](2-).	Tellurium	103-112	jumping translocation breakpoint	Homo sapiens	260-263
24004243-3	2013	First, two-electron reduction occurs when substrates as 2,2"-bipyridine, elemental selenium, elemental tellurium, Me3P S, or Ph3P E (E = S, Se) is used, resulting in the oxidative coupling of two phosphinidene ligands 2[PAr](2-) into a diphosphene ligand [ArP-PAr](2-).	trimethyl phosphine	114-120	jumping translocation breakpoint	Homo sapiens	220-223
24004243-3	2013	First, two-electron reduction occurs when substrates as 2,2"-bipyridine, elemental selenium, elemental tellurium, Me3P S, or Ph3P E (E = S, Se) is used, resulting in the oxidative coupling of two phosphinidene ligands 2[PAr](2-) into a diphosphene ligand [ArP-PAr](2-).	trimethyl phosphine	114-120	jumping translocation breakpoint	Homo sapiens	260-263
24004243-3	2013	First, two-electron reduction occurs when substrates as 2,2"-bipyridine, elemental selenium, elemental tellurium, Me3P S, or Ph3P E (E = S, Se) is used, resulting in the oxidative coupling of two phosphinidene ligands 2[PAr](2-) into a diphosphene ligand [ArP-PAr](2-).	triphenylphosphine	125-129	jumping translocation breakpoint	Homo sapiens	220-223
24004243-3	2013	First, two-electron reduction occurs when substrates as 2,2"-bipyridine, elemental selenium, elemental tellurium, Me3P S, or Ph3P E (E = S, Se) is used, resulting in the oxidative coupling of two phosphinidene ligands 2[PAr](2-) into a diphosphene ligand [ArP-PAr](2-).	triphenylphosphine	125-129	jumping translocation breakpoint	Homo sapiens	260-263
24004243-3	2013	First, two-electron reduction occurs when substrates as 2,2"-bipyridine, elemental selenium, elemental tellurium, Me3P S, or Ph3P E (E = S, Se) is used, resulting in the oxidative coupling of two phosphinidene ligands 2[PAr](2-) into a diphosphene ligand [ArP-PAr](2-).	Phosphinidene	196-209	jumping translocation breakpoint	Homo sapiens	220-223
24004243-3	2013	First, two-electron reduction occurs when substrates as 2,2"-bipyridine, elemental selenium, elemental tellurium, Me3P S, or Ph3P E (E = S, Se) is used, resulting in the oxidative coupling of two phosphinidene ligands 2[PAr](2-) into a diphosphene ligand [ArP-PAr](2-).	Phosphinidene	196-209	jumping translocation breakpoint	Homo sapiens	260-263
24004243-3	2013	First, two-electron reduction occurs when substrates as 2,2"-bipyridine, elemental selenium, elemental tellurium, Me3P S, or Ph3P E (E = S, Se) is used, resulting in the oxidative coupling of two phosphinidene ligands 2[PAr](2-) into a diphosphene ligand [ArP-PAr](2-).	Diphosphene	236-247	jumping translocation breakpoint	Homo sapiens	220-223
24004243-3	2013	First, two-electron reduction occurs when substrates as 2,2"-bipyridine, elemental selenium, elemental tellurium, Me3P S, or Ph3P E (E = S, Se) is used, resulting in the oxidative coupling of two phosphinidene ligands 2[PAr](2-) into a diphosphene ligand [ArP-PAr](2-).	Diphosphene	236-247	jumping translocation breakpoint	Homo sapiens	260-263
23947964-4	2013	The "original" signature performed on fresh frozen tissue (70G-FFT) could be further developed to a paraffin-based signature (70G-PAR) to reduce test failures.	Paraffin	100-108	jumping translocation breakpoint	Homo sapiens	130-133
23626849-9	2013	The observed variations of pCO2 were explained through a statistical model considering wind direction and speed together with PAR irradiance.	pco2	27-31	jumping translocation breakpoint	Homo sapiens	126-129
23659110-0	2013	[Interannual changes in PAR and soil moisture during the warm season may be more important for directing of annual carbon balance in tundra than temperature fluctuations].	Carbon	115-121	jumping translocation breakpoint	Homo sapiens	24-27
22079049-5	2012	The JTB structure has a distant relationship to the midkine/pleiotrophin fold, particularly in the conservation of distinctive disulfide bridge patterns.	Disulfides	127-136	jumping translocation breakpoint	Homo sapiens	4-7
22276544-3	2012	Understanding the conditions under which SA polymorphism can exist at such pseudo-autosomal (or PAR) loci should increase understanding of the evolution of recombination between sex chromosome pairs, and can help predict when we may expect potentially empirically detectable allele frequency differences between the sexes.	2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine	41-43	jumping translocation breakpoint	Homo sapiens	96-99
22276544-6	2012	We confirm the previous major conclusion that SA polymorphisms are generally maintained in a larger region of parameter space if the locus is in the PAR than if it is autosomal.	2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine	46-48	jumping translocation breakpoint	Homo sapiens	149-152
22079049-6	2012	The structure of this newly characterized small cysteine-rich domain suggests potential involvement of JTB in interactions with proteins or extracellular matrix and may help to uncover the elusive biological functions of this protein.	Cysteine	48-56	jumping translocation breakpoint	Homo sapiens	103-106
19814731-5	2009	KEY RESULTS: Quercetin, apigenin and genistein impaired platelet aggregation, as well as 5-HT release and calcium mobilization, induced by thrombin and PAR-APs.	Quercetin	13-22	jumping translocation breakpoint	Homo sapiens	152-155
20096995-0	2010	PAR immobilized colorimetric fiber for heavy metal ion detection and adsorption.	Metals	45-50	jumping translocation breakpoint	Homo sapiens	0-3
20096995-1	2010	A new wearable colorimetric fiber for heavy metal ion detection and adsorption has been synthesized by first aminating a commercially available polyacrylonitrile fiber with ethylenediamine and then covalently immobilizing 4-(2-pyridylazo)-1,3-benzenediol (PAR) on the modified fiber through a Mannich reaction.	4-(2-pyridylazo)resorcinol	222-254	jumping translocation breakpoint	Homo sapiens	256-259
20096995-3	2010	In neutral aqueous solutions, the PAR immobilized fiber responds selectively to heavy metal ions, such as Hg(2+), Pb(2+), Cd(2+), Zn(2+), Ni(2+) and Cu(2+) with a color change from red-orange to dark-brown.	Metals	86-91	jumping translocation breakpoint	Homo sapiens	34-37
20096995-3	2010	In neutral aqueous solutions, the PAR immobilized fiber responds selectively to heavy metal ions, such as Hg(2+), Pb(2+), Cd(2+), Zn(2+), Ni(2+) and Cu(2+) with a color change from red-orange to dark-brown.	Lead	114-116	jumping translocation breakpoint	Homo sapiens	34-37
20096995-3	2010	In neutral aqueous solutions, the PAR immobilized fiber responds selectively to heavy metal ions, such as Hg(2+), Pb(2+), Cd(2+), Zn(2+), Ni(2+) and Cu(2+) with a color change from red-orange to dark-brown.	Cadmium	122-124	jumping translocation breakpoint	Homo sapiens	34-37
20096995-3	2010	In neutral aqueous solutions, the PAR immobilized fiber responds selectively to heavy metal ions, such as Hg(2+), Pb(2+), Cd(2+), Zn(2+), Ni(2+) and Cu(2+) with a color change from red-orange to dark-brown.	Zinc	130-132	jumping translocation breakpoint	Homo sapiens	34-37
20096995-3	2010	In neutral aqueous solutions, the PAR immobilized fiber responds selectively to heavy metal ions, such as Hg(2+), Pb(2+), Cd(2+), Zn(2+), Ni(2+) and Cu(2+) with a color change from red-orange to dark-brown.	Copper	149-151	jumping translocation breakpoint	Homo sapiens	34-37
21870251-2	2011	Since PARP-1 gene is expressed constitutively, its activation cannot be surmised from increased expression of its mRNA or protein, but by demonstrating the consequences of its catalytic -reaction which results in consumption of the substrate nicotinamide adenine dinucleotide (NAD(+)) and formation of three products, namely, polymer of ADP-ribose (pADPr or PAR), nicotinamide, and protons.	NAD	242-275	jumping translocation breakpoint	Homo sapiens	6-9
21870251-2	2011	Since PARP-1 gene is expressed constitutively, its activation cannot be surmised from increased expression of its mRNA or protein, but by demonstrating the consequences of its catalytic -reaction which results in consumption of the substrate nicotinamide adenine dinucleotide (NAD(+)) and formation of three products, namely, polymer of ADP-ribose (pADPr or PAR), nicotinamide, and protons.	NAD	277-283	jumping translocation breakpoint	Homo sapiens	6-9
21870251-2	2011	Since PARP-1 gene is expressed constitutively, its activation cannot be surmised from increased expression of its mRNA or protein, but by demonstrating the consequences of its catalytic -reaction which results in consumption of the substrate nicotinamide adenine dinucleotide (NAD(+)) and formation of three products, namely, polymer of ADP-ribose (pADPr or PAR), nicotinamide, and protons.	Adenosine Diphosphate Ribose	337-347	jumping translocation breakpoint	Homo sapiens	6-9
21870251-2	2011	Since PARP-1 gene is expressed constitutively, its activation cannot be surmised from increased expression of its mRNA or protein, but by demonstrating the consequences of its catalytic -reaction which results in consumption of the substrate nicotinamide adenine dinucleotide (NAD(+)) and formation of three products, namely, polymer of ADP-ribose (pADPr or PAR), nicotinamide, and protons.	Niacinamide	242-254	jumping translocation breakpoint	Homo sapiens	6-9
19814731-5	2009	KEY RESULTS: Quercetin, apigenin and genistein impaired platelet aggregation, as well as 5-HT release and calcium mobilization, induced by thrombin and PAR-APs.	Calcium	106-113	jumping translocation breakpoint	Homo sapiens	152-155
17902181-4	2007	METHODS: PAR expression was depleted by small interfering RNA (siRNA) and its subsequent effects on proliferation of PC3 cells were determined by the trypan blue exclusion assay.	Trypan Blue	150-161	jumping translocation breakpoint	Homo sapiens	9-12
18980982-8	2008	A single ABT-888 dose (3 or 12.5 mg/kg) reduced intratumor PAR levels by >95%.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	9-12	jumping translocation breakpoint	Homo sapiens	59-62
19823047-7	2009	CONCLUSIONS: ABT-888 hits its therapeutic target by significantly reducing PAR levels and the ratio of PAR to PARP-1 in human tumor cells detected by immunohistochemistry.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	13-16	jumping translocation breakpoint	Homo sapiens	75-78
19823047-7	2009	CONCLUSIONS: ABT-888 hits its therapeutic target by significantly reducing PAR levels and the ratio of PAR to PARP-1 in human tumor cells detected by immunohistochemistry.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	13-16	jumping translocation breakpoint	Homo sapiens	103-106
19634909-5	2009	ZinCleav-1 has a K(d) of 0.23 pM for Zn(2+) as measured by competitive titration with [Zn(PAR)(2)] (PAR = 4-(2-pyridyl-2-azo) resorcinol).	Zinc	37-43	jumping translocation breakpoint	Homo sapiens	90-93
19634909-5	2009	ZinCleav-1 has a K(d) of 0.23 pM for Zn(2+) as measured by competitive titration with [Zn(PAR)(2)] (PAR = 4-(2-pyridyl-2-azo) resorcinol).	Zinc	37-39	jumping translocation breakpoint	Homo sapiens	90-93
19617970-1	2009	The phosphanylidene-sigma(4)-phosphorane reagents Me(3)P[double bond, length as m-dash]PAr (Ar = 2,4,6-(t)Bu(3)C(6)H(2) and 2,6-Mes(2)C(6)H(3)) are good delivery vehicles of the terminal phosphinidene moiety, PAr, to early-transition metals composed of zirconium and vanadium.	phosphanylidene	4-19	jumping translocation breakpoint	Homo sapiens	87-90
19617970-1	2009	The phosphanylidene-sigma(4)-phosphorane reagents Me(3)P[double bond, length as m-dash]PAr (Ar = 2,4,6-(t)Bu(3)C(6)H(2) and 2,6-Mes(2)C(6)H(3)) are good delivery vehicles of the terminal phosphinidene moiety, PAr, to early-transition metals composed of zirconium and vanadium.	phosphanylidene	4-19	jumping translocation breakpoint	Homo sapiens	209-212
19617970-1	2009	The phosphanylidene-sigma(4)-phosphorane reagents Me(3)P[double bond, length as m-dash]PAr (Ar = 2,4,6-(t)Bu(3)C(6)H(2) and 2,6-Mes(2)C(6)H(3)) are good delivery vehicles of the terminal phosphinidene moiety, PAr, to early-transition metals composed of zirconium and vanadium.	(4)-phosphorane	25-40	jumping translocation breakpoint	Homo sapiens	87-90
19617970-1	2009	The phosphanylidene-sigma(4)-phosphorane reagents Me(3)P[double bond, length as m-dash]PAr (Ar = 2,4,6-(t)Bu(3)C(6)H(2) and 2,6-Mes(2)C(6)H(3)) are good delivery vehicles of the terminal phosphinidene moiety, PAr, to early-transition metals composed of zirconium and vanadium.	trimethyl phosphine	50-56	jumping translocation breakpoint	Homo sapiens	87-90
18980982-9	2008	ABT-888 (1.56-25 mg/kg) significantly decreased PAR levels at 2 h post-dosing.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	0-3	jumping translocation breakpoint	Homo sapiens	48-51
17596111-0	2007	Megestrol acetate NCD oral suspension -- Par Pharmaceutical: megestrol acetate nanocrystal dispersion oral suspension, PAR 100.2, PAR-100.2.	Megestrol Acetate	0-17	jumping translocation breakpoint	Homo sapiens	41-44
17963432-0	2007	Megestrol acetate NCD oral suspension--Par Pharmaceutical: megestrol acetate nanocrystal dispersion oral suspension, PAR 100.2, PAR-100.2.	Megestrol Acetate	0-17	jumping translocation breakpoint	Homo sapiens	39-42
17596111-1	2007	Par Pharmaceutical has developed megestrol acetate (Megace ES) oral suspension for the treatment of anorexia, cachexia and a significant weight loss associated with AIDS.	Megestrol Acetate	33-50	jumping translocation breakpoint	Homo sapiens	0-3
17963432-1	2007	Par Pharmaceutical has developed megestrol acetate (Megace ES) oral suspension for the treatment of anorexia, cachexia and a significant weight loss associated with AIDS.	Megestrol Acetate	33-50	jumping translocation breakpoint	Homo sapiens	0-3
17963432-1	2007	Par Pharmaceutical has developed megestrol acetate (Megace ES) oral suspension for the treatment of anorexia, cachexia and a significant weight loss associated with AIDS.	Megestrol Acetate	52-61	jumping translocation breakpoint	Homo sapiens	0-3
17963432-2	2007	Par Pharmaceutical used Elan Corporation"s NanoCrystal Dispersion (NCD) technology to develop an advanced, concentrated formulation of megestrol acetate with improved bioavailability, more rapid onset of action, more convenient dosing and a lower dosing regimen compared with the original marketed formulation of megestrol acetate oral suspension.	Megestrol Acetate	135-152	jumping translocation breakpoint	Homo sapiens	0-3
17963432-2	2007	Par Pharmaceutical used Elan Corporation"s NanoCrystal Dispersion (NCD) technology to develop an advanced, concentrated formulation of megestrol acetate with improved bioavailability, more rapid onset of action, more convenient dosing and a lower dosing regimen compared with the original marketed formulation of megestrol acetate oral suspension.	Megestrol Acetate	313-330	jumping translocation breakpoint	Homo sapiens	0-3
17963432-4	2007	The new megestrol acetate NCD formulation represents a line-extension of Par"s megestrol acetate oral suspension (800mg/20mL, Megace O/S) that has been marketed for anorexia, cachexia and AIDS-related weight loss since July 2001.	Megestrol Acetate	8-25	jumping translocation breakpoint	Homo sapiens	73-76
17596111-1	2007	Par Pharmaceutical has developed megestrol acetate (Megace ES) oral suspension for the treatment of anorexia, cachexia and a significant weight loss associated with AIDS.	Megestrol Acetate	52-61	jumping translocation breakpoint	Homo sapiens	0-3
17596111-2	2007	Par Pharmaceutical used Elan Corporation"s NanoCrystal Dispersion (NCD) technology to develop an advanced, concentrated formulation of megestrol acetate with improved bioavailability, more rapid onset of action, more convenient dosing and a lower dosing regimen compared with the original marketed formulation of megestrol acetate oral suspension.	Megestrol Acetate	135-152	jumping translocation breakpoint	Homo sapiens	0-3
17596111-2	2007	Par Pharmaceutical used Elan Corporation"s NanoCrystal Dispersion (NCD) technology to develop an advanced, concentrated formulation of megestrol acetate with improved bioavailability, more rapid onset of action, more convenient dosing and a lower dosing regimen compared with the original marketed formulation of megestrol acetate oral suspension.	Megestrol Acetate	313-330	jumping translocation breakpoint	Homo sapiens	0-3
17596111-4	2007	The new megestrol acetate NCD formulation represents a line-extension of Par"s megestrol acetate oral suspension (800mg/20mL, Megace O/S) that has been marketed for anorexia, cachexia and AIDS-related weight loss since July 2001.	Megestrol Acetate	8-25	jumping translocation breakpoint	Homo sapiens	73-76
17596111-5	2007	Par"s megestrol acetate is the generic version of Bristol-Myers Squibb"s Megace Oral Suspension.	Acetates	16-23	jumping translocation breakpoint	Homo sapiens	0-3
17963432-5	2007	Par"s megestrol acetate is the generic version of Bristol-Myers Squibb"s Megace Oral Suspension.	Acetates	16-23	jumping translocation breakpoint	Homo sapiens	0-3
17596111-7	2007	Par Pharmaceutical will market megestol acetate NCD oral suspension under the Megace brand name.	megestol acetate	31-47	jumping translocation breakpoint	Homo sapiens	0-3
17963432-7	2007	Par Pharmaceutical will market megestol acetate NCD oral suspension under the Megace brand name.	megestol acetate	31-47	jumping translocation breakpoint	Homo sapiens	0-3
17963432-10	2007	The NDA for the product was accepted for review by the agency in September 2004, following its submission in June of that year.Par Pharmaceutical commenced the first of two phase III clinical trials of megestrol acetate oral suspension (PAR 100.2) in cancer-induced anorexia in the first quarter of 2006.	Megestrol Acetate	202-219	jumping translocation breakpoint	Homo sapiens	127-130
17596111-10	2007	The NDA for the product was accepted for review by the agency in September 2004, following its submission in June of that year.Par Pharmaceutical commenced the first of two phase III clinical trials of megestrol acetate oral suspension (PAR 100.2) in cancer-induced anorexia in the first quarter of 2006.	Megestrol Acetate	202-219	jumping translocation breakpoint	Homo sapiens	127-130
17963432-12	2007	The company intends to discuss future development options in this indication with the FDA.New formulations or dosage forms of megestrol acetate concentrated suspension are also in development; Par Pharmaceutical believes these may be available sometime after 2008.	Megestrol Acetate	126-143	jumping translocation breakpoint	Homo sapiens	193-196
17596111-12	2007	The company intends to discuss future development options in this indication with the FDA.New formulations or dosage forms of megestrol acetate concentrated suspension are also in development; Par Pharmaceutical believes these may be available sometime after 2008.	Megestrol Acetate	126-143	jumping translocation breakpoint	Homo sapiens	193-196
17963432-15	2007	The patent covers more than 30 additional claims in connection with Par Pharmaceutical"s novel formulation of megestrol acetate, and includes claims relating to the advanced formulation of megestrol acetate, specifically to the reduction of the food effect seen with previous formulations of megestrol acetate.	Megestrol Acetate	110-127	jumping translocation breakpoint	Homo sapiens	68-71
17963432-21	2007	Both companies settled the lawsuit in July 2004 with Par granting a licence to Teva USA for a limited number of units and Par receiving royalties on Teva USA"s net sales of megestrol acetate oral suspension.	Megestrol Acetate	173-190	jumping translocation breakpoint	Homo sapiens	53-56
17596111-15	2007	The patent covers more than 30 additional claims in connection with Par Pharmaceutical"s novel formulation of megestrol acetate, and includes claims relating to the advanced formulation of megestrol acetate, specifically to the reduction of the food effect seen with previous formulations of megestrol acetate.	Megestrol Acetate	110-127	jumping translocation breakpoint	Homo sapiens	68-71
17596111-21	2007	Both companies settled the lawsuit in July 2004 with Par granting a licence to Teva USA for a limited number of units and Par receiving royalties on Teva USA"s net sales of megestrol acetate oral suspension.	Megestrol Acetate	173-190	jumping translocation breakpoint	Homo sapiens	53-56
16763722-7	2006	Dihydrotestosterone (DHT) regulated PAR mRNA expression in LNCaP cells and the effect was inhibited by the AR antagonist, flutamide.	Flutamide	122-131	jumping translocation breakpoint	Homo sapiens	36-39
16223779-6	2006	Inhibition of PAR-mediated Akt phosphorylation in the presence of the Gq-selective inhibitor YM-254890 was restored to the normal extent achieved by PAR agonists if supplemented with Gi signaling, indicating that Gq does not have any direct effect on Akt phosphorylation.	glycylglutamine	70-72	jumping translocation breakpoint	Homo sapiens	14-17
16770051-4	2006	The method is based on the preconcentration of the complexes of beryllium-acetylacetone plus morin, oxine, PAN and PAR on activated carbon at different pH values.	Carbon	132-138	jumping translocation breakpoint	Homo sapiens	115-118
16763722-7	2006	Dihydrotestosterone (DHT) regulated PAR mRNA expression in LNCaP cells and the effect was inhibited by the AR antagonist, flutamide.	Dihydrotestosterone	0-19	jumping translocation breakpoint	Homo sapiens	36-39
16763722-7	2006	Dihydrotestosterone (DHT) regulated PAR mRNA expression in LNCaP cells and the effect was inhibited by the AR antagonist, flutamide.	Dihydrotestosterone	21-24	jumping translocation breakpoint	Homo sapiens	36-39
16223779-6	2006	Inhibition of PAR-mediated Akt phosphorylation in the presence of the Gq-selective inhibitor YM-254890 was restored to the normal extent achieved by PAR agonists if supplemented with Gi signaling, indicating that Gq does not have any direct effect on Akt phosphorylation.	glycylglutamine	70-72	jumping translocation breakpoint	Homo sapiens	149-152
16223779-6	2006	Inhibition of PAR-mediated Akt phosphorylation in the presence of the Gq-selective inhibitor YM-254890 was restored to the normal extent achieved by PAR agonists if supplemented with Gi signaling, indicating that Gq does not have any direct effect on Akt phosphorylation.	YM-254890	93-102	jumping translocation breakpoint	Homo sapiens	14-17
16223779-6	2006	Inhibition of PAR-mediated Akt phosphorylation in the presence of the Gq-selective inhibitor YM-254890 was restored to the normal extent achieved by PAR agonists if supplemented with Gi signaling, indicating that Gq does not have any direct effect on Akt phosphorylation.	YM-254890	93-102	jumping translocation breakpoint	Homo sapiens	149-152
16223779-6	2006	Inhibition of PAR-mediated Akt phosphorylation in the presence of the Gq-selective inhibitor YM-254890 was restored to the normal extent achieved by PAR agonists if supplemented with Gi signaling, indicating that Gq does not have any direct effect on Akt phosphorylation.	glycylglutamine	213-215	jumping translocation breakpoint	Homo sapiens	14-17
18969978-2	2005	The method is based on the sorption of Ni(II) ions in a minicolumn containing the synthesized resin, posterior desorption using an acid solution and measurement of the nickel by spectrophotometry (PAR method).	Nickel	168-174	jumping translocation breakpoint	Homo sapiens	197-200
15316986-0	2004	Generating and dimerizing the transient 16-electron phosphinidene complex [Cp*Ir=PAr]: a theoretical and experimental study.	Phosphinidene	52-65	jumping translocation breakpoint	Homo sapiens	81-84
15900749-3	2005	The results also showed that the emissions of isoprene were affected by both temperature and PAR(Photosynthetic Active Radiation), while monoterpene emissions were mainly temperature-dependent.	isoprene	46-54	jumping translocation breakpoint	Homo sapiens	93-96
15316986-4	2004	Transient 16-electron phosphinidene complex [Cp*Ir=PAr] could not be detected experimentally.	Phosphinidene	22-35	jumping translocation breakpoint	Homo sapiens	51-54
15137505-6	2004	The protective effects of high PAR against elevated UV-B may also be indirect, by increasing leaf thickness and the concentration of flavonoids and other phenolic compounds known to be important in UV screening.	Flavonoids	133-143	jumping translocation breakpoint	Homo sapiens	31-34
12038489-5	2000	The penetration of UV and PAR into the water column can be measured.	Water	39-44	jumping translocation breakpoint	Homo sapiens	26-29
14741720-6	2004	Transfection of NIH3T3 cells with increased ectopic PAR expression with a 22 mer oligonucleotide in antisense orientation with PAR mRNA abrogated their ability to form colonies in soft agar.	Oligonucleotides	81-96	jumping translocation breakpoint	Homo sapiens	52-55
14741720-6	2004	Transfection of NIH3T3 cells with increased ectopic PAR expression with a 22 mer oligonucleotide in antisense orientation with PAR mRNA abrogated their ability to form colonies in soft agar.	Oligonucleotides	81-96	jumping translocation breakpoint	Homo sapiens	127-130
14741720-6	2004	Transfection of NIH3T3 cells with increased ectopic PAR expression with a 22 mer oligonucleotide in antisense orientation with PAR mRNA abrogated their ability to form colonies in soft agar.	Agar	185-189	jumping translocation breakpoint	Homo sapiens	52-55
14741720-6	2004	Transfection of NIH3T3 cells with increased ectopic PAR expression with a 22 mer oligonucleotide in antisense orientation with PAR mRNA abrogated their ability to form colonies in soft agar.	Agar	185-189	jumping translocation breakpoint	Homo sapiens	127-130
18969240-3	2003	Cobalt was complexed with pyridylazo compounds (PAN, PAR, 5-Br-PADAP) in an aqueous surfactant medium and it was concentrated in the surfactant rich phase after phase separation.	Cobalt	0-6	jumping translocation breakpoint	Homo sapiens	53-56
15049356-5	2003	In-water measurements are used to establish the relationship between the PAR and the spectral attenuation coefficient in the Baltic Sea via regression analysis.	Water	3-8	jumping translocation breakpoint	Homo sapiens	73-76
12400649-0	2002	Flow-injection analysis of copper(II) with PAR in the presence of EDTA.	cupric ion	27-37	jumping translocation breakpoint	Homo sapiens	43-46
12400649-0	2002	Flow-injection analysis of copper(II) with PAR in the presence of EDTA.	Edetic Acid	66-70	jumping translocation breakpoint	Homo sapiens	43-46
12033459-3	2002	Since DNA of epidermal cells represents a well-known chromophore for UVB irradiation, and UVB is known to generate H2O2 in keratinocytes, we hypothesized that PAR is a very sensitive marker of UVB- and H2O2-induced apoptosis in keratinocytes.	Hydrogen Peroxide	115-119	jumping translocation breakpoint	Homo sapiens	159-162
12033459-3	2002	Since DNA of epidermal cells represents a well-known chromophore for UVB irradiation, and UVB is known to generate H2O2 in keratinocytes, we hypothesized that PAR is a very sensitive marker of UVB- and H2O2-induced apoptosis in keratinocytes.	Hydrogen Peroxide	202-206	jumping translocation breakpoint	Homo sapiens	159-162
12033459-5	2002	Both, UVB and H2O2 treatment induced PAR formation in HaCaT cells in a dose-dependent manner, and its formation was detected as early as 4 h after irradiation, and at lower UVB doses (10 mJ/cm2) than observed by DNA laddering and the TUNEL assay.	Hydrogen Peroxide	14-18	jumping translocation breakpoint	Homo sapiens	37-40
9099997-9	1997	About 2.2 microg t-PAR protein was purified from cell lysate of 1.0 X 10(9) HUVEC as a single band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) by gel filtration with TSK-3000SW and reversed phase separation with high performance liquid chromatography (HPLC).	Sodium Dodecyl Sulfate	102-124	jumping translocation breakpoint	Homo sapiens	19-22
9532321-7	1998	Both doses of ipratropium bromide nasal spray significantly reduced the hypersecretion associated with PAR, compared with placebo.	Ipratropium	14-33	jumping translocation breakpoint	Homo sapiens	103-106
18967724-1	1999	A colorimetric flow injection-system for the determination of Cu(II) in waters based on complexation reaction with 4-(2-pyridylazo)-resorcinol, usually termed PAR, is described.	cu(ii)	62-68	jumping translocation breakpoint	Homo sapiens	159-162
18967724-1	1999	A colorimetric flow injection-system for the determination of Cu(II) in waters based on complexation reaction with 4-(2-pyridylazo)-resorcinol, usually termed PAR, is described.	4-(2-pyridylazo)resorcinol	115-142	jumping translocation breakpoint	Homo sapiens	159-162
10072807-2	1997	METHOD: Observe effects of 8-MOP on the isolated human pulmonary artery rings(PAR) obtained from 11 patients undergoing lobectomy for lung carcinoma.	Methoxsalen	27-32	jumping translocation breakpoint	Homo sapiens	78-81
10072807-3	1997	RESULTS: (1)8-MOP(2 x 10(-5) mol/L) caused significant relaxation of PAR precontracted with noradreline (NA) by 88% (P < 0.001) and this effect of 8-MOP was independent on the endothelium of the pulmonary arteries.	Methoxsalen	12-17	jumping translocation breakpoint	Homo sapiens	69-72
10072807-3	1997	RESULTS: (1)8-MOP(2 x 10(-5) mol/L) caused significant relaxation of PAR precontracted with noradreline (NA) by 88% (P < 0.001) and this effect of 8-MOP was independent on the endothelium of the pulmonary arteries.	noradreline	92-103	jumping translocation breakpoint	Homo sapiens	69-72
9099997-9	1997	About 2.2 microg t-PAR protein was purified from cell lysate of 1.0 X 10(9) HUVEC as a single band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) by gel filtration with TSK-3000SW and reversed phase separation with high performance liquid chromatography (HPLC).	polyacrylamide	125-139	jumping translocation breakpoint	Homo sapiens	19-22
8189642-2	1994	Pulmonary vascular response to oxygen was evaluated by the percent change in pulmonary arteriolar resistance after 100% oxygen inhalation (% delta PAR), and its relation to the pressure-flow relationship during incremental exercise was assessed.	Oxygen	31-37	jumping translocation breakpoint	Homo sapiens	147-150
8927481-5	1996	PAR can be triggered in various ways such as: interactions with the central or peripherical nervous system, non-specific release of mediators, enzyme inhibition due to hereditary or pharmacologically induced enzyme deficiencies and pharmacological properties of some natural food constituents such as biogenic amines.	Amines	310-316	jumping translocation breakpoint	Homo sapiens	0-3
8927481-7	1996	PAR to food additives occurs frequently in patients suffering from urticaria, asthma and may be accompanied by history of aspirin or NSAI pseudoallergic reactions.	Aspirin	122-129	jumping translocation breakpoint	Homo sapiens	0-3
8927481-8	1996	The same additives (azo dyes, sulphites, benzoates) are used in various drug formulations and may be responsible for eliciting PAR.	Azo Compounds	20-28	jumping translocation breakpoint	Homo sapiens	127-130
8927481-8	1996	The same additives (azo dyes, sulphites, benzoates) are used in various drug formulations and may be responsible for eliciting PAR.	Sulfites	30-39	jumping translocation breakpoint	Homo sapiens	127-130
8927481-8	1996	The same additives (azo dyes, sulphites, benzoates) are used in various drug formulations and may be responsible for eliciting PAR.	Benzoates	41-50	jumping translocation breakpoint	Homo sapiens	127-130
8219225-1	1993	The high-affinity receptor that binds human urokinase-type plasminogen activator (hu-PAR) is a glycosyl-phosphatidylinositol (GPI)-anchored cell-surface glycoprotein that belongs to the Ly-6 superfamily of T-cell-activating receptors.	Glycosylphosphatidylinositols	95-124	jumping translocation breakpoint	Homo sapiens	85-88
8219225-1	1993	The high-affinity receptor that binds human urokinase-type plasminogen activator (hu-PAR) is a glycosyl-phosphatidylinositol (GPI)-anchored cell-surface glycoprotein that belongs to the Ly-6 superfamily of T-cell-activating receptors.	Glycosylphosphatidylinositols	126-129	jumping translocation breakpoint	Homo sapiens	85-88
8219225-4	1993	Introduction of as few as 13 murine residues (six of 13 variables) into the N-terminal region of hu-PAR abrogated binding to recombinant human pro-u-PA, whereas the opposite chimera, a mu-PAR carrying six of 13 human residues, was positive for binding.	Proline	143-147	jumping translocation breakpoint	Homo sapiens	100-103
8219225-5	1993	Within this region, the mu-PAR domain 1 could be minimally humanized to bind human pro-u-PA by a substitution of as few as four of the six nonconserved residues, thereby identifying the residues arginine-2, lysine-7, threonine-8, and glycine-10 as important in determining binding specificity.	Arginine	195-203	jumping translocation breakpoint	Homo sapiens	27-30
8219225-5	1993	Within this region, the mu-PAR domain 1 could be minimally humanized to bind human pro-u-PA by a substitution of as few as four of the six nonconserved residues, thereby identifying the residues arginine-2, lysine-7, threonine-8, and glycine-10 as important in determining binding specificity.	Threonine	217-226	jumping translocation breakpoint	Homo sapiens	27-30
8219225-5	1993	Within this region, the mu-PAR domain 1 could be minimally humanized to bind human pro-u-PA by a substitution of as few as four of the six nonconserved residues, thereby identifying the residues arginine-2, lysine-7, threonine-8, and glycine-10 as important in determining binding specificity.	Glycine	234-241	jumping translocation breakpoint	Homo sapiens	27-30
8515600-5	1993	Nifedipine (NFP) reduced the maximum values of both TPR and PAR at the end of CPT.	Nifedipine	0-10	jumping translocation breakpoint	Homo sapiens	60-63