PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
19124283-2	2009	Recent studies have demonstrated that FALDH is involved in the last step of the conversion of 22-hydroxy-C22:0 into the dicarboxylic acid of C22:0 (C22:0-DCA).	Dichloroacetic Acid	154-157	aldehyde dehydrogenase 3 family member A2	Homo sapiens	38-43
19433108-11	2009	The increased levels of IL-13 in the sensitive individuals to mite antigen (rDER P I) and IFN-gamma in NiSO4 sensitized individuals confirm the role of the type TH2 response in the atopies and TH1 type in DCA.	Dichloroacetic Acid	205-208	interleukin 13	Homo sapiens	24-29
19426674-7	2009	Since DCA can inactivate GSTZ1-1 there is a possibility that long-term treatment of patients with DCA could cause GSTZ1-1 deficiency and susceptibility to oxidative stress and phenylalanine/tyrosine-induced WBC loss.	Dichloroacetic Acid	6-9	glutathione S-transferase zeta 1	Homo sapiens	25-32
19426674-7	2009	Since DCA can inactivate GSTZ1-1 there is a possibility that long-term treatment of patients with DCA could cause GSTZ1-1 deficiency and susceptibility to oxidative stress and phenylalanine/tyrosine-induced WBC loss.	Dichloroacetic Acid	98-101	glutathione S-transferase zeta 1	Homo sapiens	25-32
19426674-8	2009	However, although we found that DCA at 200mg/(kg day) causes a severe loss of hepatic GSTZ1-1 activity in BALB/c mice, it did not induce WBC cytotoxicity when combined with high dietary phenylalanine.	Dichloroacetic Acid	32-35	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	86-93
19147752-8	2009	Inhibition of PDK2 with dichloroacetate decreased HIF1alpha accumulation and reduced cell growth.	Dichloroacetic Acid	24-39	pyruvate dehydrogenase kinase 2	Homo sapiens	14-18
19147752-8	2009	Inhibition of PDK2 with dichloroacetate decreased HIF1alpha accumulation and reduced cell growth.	Dichloroacetic Acid	24-39	hypoxia inducible factor 1 subunit alpha	Homo sapiens	50-59
18658136-9	2008	Fluorescence quenching and enzyme activity data suggest that compounds AZD7545 and dichloroacetate lock PDK4 in the open and the closed conformational states, respectively.	Dichloroacetic Acid	83-98	pyruvate dehydrogenase kinase 4	Homo sapiens	104-108
18974089-11	2009	For DCA under these study conditions, the p53 and Tg.AC mice appear less sensitive to hepatocarcinogenesis than standard rodent models.	Dichloroacetic Acid	4-7	transformation related protein 53, pseudogene	Mus musculus	42-45
18647626-3	2008	DCA is metabolized by and inhibits the bifunctional zeta-1 family isoform of glutathione transferase/maleylacetoacetate isomerase.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	101-129
18493934-2	2008	The DCA effects on superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) activities and glutathione (GSH) level were assessed and correlated with each other and also with cellular viabilities in J774A.1 macrophage cells.	Dichloroacetic Acid	4-7	catalase	Mus musculus	47-55
18493934-2	2008	The DCA effects on superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) activities and glutathione (GSH) level were assessed and correlated with each other and also with cellular viabilities in J774A.1 macrophage cells.	Dichloroacetic Acid	4-7	catalase	Mus musculus	57-60
18493934-3	2008	A concentration of 24 mm of DCA resulted in time-dependent decreases in cellular viability and glutathione level, and time-dependent increases in SOD activity when incubated with the cells for 24-48 h. DCA also resulted in significant increases in CAT and GSH-Px activities of the viable cells when incubated with the cells for 36 and 48 h. The changes in antioxidant enzyme activities and GSH levels were found to be strongly correlated with each other, and with cellular viabilities at different time points.	Dichloroacetic Acid	28-31	catalase	Mus musculus	248-251
18493934-3	2008	A concentration of 24 mm of DCA resulted in time-dependent decreases in cellular viability and glutathione level, and time-dependent increases in SOD activity when incubated with the cells for 24-48 h. DCA also resulted in significant increases in CAT and GSH-Px activities of the viable cells when incubated with the cells for 36 and 48 h. The changes in antioxidant enzyme activities and GSH levels were found to be strongly correlated with each other, and with cellular viabilities at different time points.	Dichloroacetic Acid	202-205	catalase	Mus musculus	248-251
18627174-6	2008	Here we show that mutations of three amino acid residues located in the vicinity of the active site of PDHK2 (R250, T302, and Y320) make the kinase resistant to the inhibitory effect of DCA, thereby uncoupling the active site from the allosteric site.	Dichloroacetic Acid	186-189	pyruvate dehydrogenase kinase 2	Homo sapiens	103-108
18519799-14	2008	The use of dichloroacetic acid or leelamine, two PDK inhibitors, or a specific PDK4 siRNA demonstrated that PDK4 participated in glyceroneogenesis, therefore altering nonesterified fatty acid release in both basal and rosiglitazone-activated conditions.	Dichloroacetic Acid	11-30	pyruvate dehydrogenase kinase 4	Rattus norvegicus	108-112
18465755-0	2008	Dichloroacetate (DCA) sensitizes both wild-type and over expressing Bcl-2 prostate cancer cells in vitro to radiation.	Dichloroacetic Acid	0-15	BCL2 apoptosis regulator	Homo sapiens	68-73
18465755-0	2008	Dichloroacetate (DCA) sensitizes both wild-type and over expressing Bcl-2 prostate cancer cells in vitro to radiation.	Dichloroacetic Acid	17-20	BCL2 apoptosis regulator	Homo sapiens	68-73
18465755-3	2008	Recently, dichloroacetate (DCA) was proven to potentiate the apoptotic machinery by interacting with Bcl-2.	Dichloroacetic Acid	10-25	BCL2 apoptosis regulator	Homo sapiens	101-106
18465755-3	2008	Recently, dichloroacetate (DCA) was proven to potentiate the apoptotic machinery by interacting with Bcl-2.	Dichloroacetic Acid	27-30	BCL2 apoptosis regulator	Homo sapiens	101-106
18465755-5	2008	METHODS: PC-3-Bcl-2 and PC-3-Neo human prostate cancer cells treated with DCA in addition to irradiation were analyzed in vitro for changes in proliferation, clonogenic survival, apoptosis, cell cycle phase distribution, mitochondrial membrane potential, and expression of Bcl-2, Bcl-xL, Bax, or Bak proteins.	Dichloroacetic Acid	74-77	chromobox 8	Homo sapiens	9-13
18465755-9	2008	Treatment of PC-3-Bcl-2 or PC-3-Neo with DCA and irradiation resulted in marked changes in various members of the Bcl-2 family.	Dichloroacetic Acid	41-44	chromobox 8	Homo sapiens	13-17
18465755-9	2008	Treatment of PC-3-Bcl-2 or PC-3-Neo with DCA and irradiation resulted in marked changes in various members of the Bcl-2 family.	Dichloroacetic Acid	41-44	BCL2 apoptosis regulator	Homo sapiens	18-23
18465755-9	2008	Treatment of PC-3-Bcl-2 or PC-3-Neo with DCA and irradiation resulted in marked changes in various members of the Bcl-2 family.	Dichloroacetic Acid	41-44	BCL2 apoptosis regulator	Homo sapiens	114-119
18465755-11	2008	CONCLUSIONS: This is the first study to demonstrate DCA can effectively sensitize wild-type and over expressing Bcl-2 human prostate cancer cells to radiation by modulating the expression of key members of the Bcl-2 family.	Dichloroacetic Acid	52-55	BCL2 apoptosis regulator	Homo sapiens	112-117
18465755-11	2008	CONCLUSIONS: This is the first study to demonstrate DCA can effectively sensitize wild-type and over expressing Bcl-2 human prostate cancer cells to radiation by modulating the expression of key members of the Bcl-2 family.	Dichloroacetic Acid	52-55	BCL2 apoptosis regulator	Homo sapiens	210-215
18381750-1	2008	3alpha,12alpha-dihydroxy-5beta-cholan-24-oic acid (deoxycholic acid DCA) is able to discriminate between the R- and S-enantiomers of camphorquinone and endo-(+)-3-bromocamphor and select only the S-enantiomers from a racemic mixture.	Dichloroacetic Acid	68-71	mannosidase endo-alpha	Homo sapiens	152-162
18381750-7	2008	Cocrystallizing DCA with (1R)-endo-(+)-3-bromocamphor gives the free guest and a glassy solid.	Dichloroacetic Acid	16-19	mannosidase endo-alpha	Homo sapiens	30-40
18455732-8	2008	The effect of dichloroacetate to normalize I(peak) after diamide was blocked by the thioredoxin system inhibitors auranofin or 13-cis-retinoic acid, but I(ss) was not affected by either compound.	Dichloroacetic Acid	14-29	thioredoxin 1	Rattus norvegicus	84-95
18581513-2	2008	Dichloroacetate (DCA) inhibits pyruvate dehydrogenase kinase-1, indirectly activating mitochondrial pyruvate dehydrogenase.	Dichloroacetic Acid	0-15	pyruvate dehydrogenase kinase 1	Homo sapiens	31-62
18581513-2	2008	Dichloroacetate (DCA) inhibits pyruvate dehydrogenase kinase-1, indirectly activating mitochondrial pyruvate dehydrogenase.	Dichloroacetic Acid	17-20	pyruvate dehydrogenase kinase 1	Homo sapiens	31-62
18603070-7	2008	The clinically used drug dichloroacetate, known to increase the mitochondria-based glucose oxidation, reversed both the phenylephrine-induced mitochondrial hyperpolarization and nuclear factor of activated T lymphocytes (NFAT) activation.	Dichloroacetic Acid	25-40	nuclear factor of activated T-cells 5	Rattus norvegicus	221-225
18455732-9	2008	A pan-specific inhibitor of glutaredoxin and thioredoxin systems, 1,3-bis-(2-chloroethyl)-1-nitrosourea, also blocked the dichloroacetate effect on I(peak) but only partially inhibited the recovery of I(ss).	Dichloroacetic Acid	122-137	glutaredoxin	Rattus norvegicus	28-40
18455732-9	2008	A pan-specific inhibitor of glutaredoxin and thioredoxin systems, 1,3-bis-(2-chloroethyl)-1-nitrosourea, also blocked the dichloroacetate effect on I(peak) but only partially inhibited the recovery of I(ss).	Dichloroacetic Acid	122-137	thioredoxin 1	Rattus norvegicus	45-56
17200418-2	2007	Bile acids (deoxycholic acid, DCA; taurocholic acid, TCA) activated AKT and glycogen synthase (GS) in primary rat hepatocytes.	Dichloroacetic Acid	30-33	AKT serine/threonine kinase 1	Rattus norvegicus	68-71
18096758-11	2008	Hepatic GSTz1/MAAI-specific activity was inhibited equally by DCA treatment among all age groups, whereas plasma and urinary levels of maleylacetone, a natural substrate for this enzyme, increased with age.	Dichloroacetic Acid	62-65	glutathione S-transferase zeta 1	Homo sapiens	8-13
18096758-11	2008	Hepatic GSTz1/MAAI-specific activity was inhibited equally by DCA treatment among all age groups, whereas plasma and urinary levels of maleylacetone, a natural substrate for this enzyme, increased with age.	Dichloroacetic Acid	62-65	glutathione S-transferase zeta 1	Homo sapiens	14-18
18821149-3	2008	TCE, TCA, and DCA are relatively weak peroxisome proliferators (PP), a group of rodent hepatocarcinogens that activate a nuclear receptor, PP-activated receptor alpha (PPARalpha.	Dichloroacetic Acid	14-17	peroxisome proliferator activated receptor alpha	Mus musculus	168-177
17544412-0	2007	Amino acid residues responsible for the recognition of dichloroacetate by pyruvate dehydrogenase kinase 2.	Dichloroacetic Acid	55-70	pyruvate dehydrogenase kinase 2	Homo sapiens	74-105
17544412-2	2007	This study was undertaken in order to map the DCA-binding site of PDHK2.	Dichloroacetic Acid	46-49	pyruvate dehydrogenase kinase 2	Homo sapiens	66-71
18206410-7	2008	We also used dichloroacetate (DCA) to maximally activate PDH through dephosphorylation of E1alpha.	Dichloroacetic Acid	13-28	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	57-60
18206410-7	2008	We also used dichloroacetate (DCA) to maximally activate PDH through dephosphorylation of E1alpha.	Dichloroacetic Acid	30-33	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	57-60
18206410-8	2008	Exposure for 24h to 5mM DCA increased PDH activity in non-transduced control (mean 37% increase) and PDH deficient (mean 44% increase) cells.	Dichloroacetic Acid	24-27	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	38-41
18206410-9	2008	Exposure of transduced patient fibroblasts to DCA increased PDH activity up to 90% of the activity measured in untreated control cells.	Dichloroacetic Acid	46-49	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	60-63
18222525-5	2008	The cumulative normalized EEM volumes at regions II and IV (Phi(II+IV,)(n)) showed linear relationships with the yields of dichloroacetic acid (DCAA) (R(2)=0.60), chloroform (R(2)=0.42), dichloroacetonitrile (DCAN) (R(2)=0.53), and TOX (R(2)=0.63).	Dichloroacetic Acid	144-148	thymocyte selection associated high mobility group box	Homo sapiens	232-235
18444159-9	2008	The secondary bile acids DCA and LCA significantly increased occludin expression (P < 0.05), whereas phenol had no significant effect on the protein expression as compared to the negative control.	Dichloroacetic Acid	25-28	occludin	Homo sapiens	61-69
17683942-2	2007	We have determined structures of human PDK1 or PDK3 bound to the inhibitors AZD7545, dichloroacetate (DCA), and radicicol.	Dichloroacetic Acid	85-100	pyruvate dehydrogenase kinase 1	Homo sapiens	39-43
17683942-2	2007	We have determined structures of human PDK1 or PDK3 bound to the inhibitors AZD7545, dichloroacetate (DCA), and radicicol.	Dichloroacetic Acid	85-100	pyruvate dehydrogenase kinase 3	Homo sapiens	47-51
17683942-2	2007	We have determined structures of human PDK1 or PDK3 bound to the inhibitors AZD7545, dichloroacetate (DCA), and radicicol.	Dichloroacetic Acid	102-105	pyruvate dehydrogenase kinase 1	Homo sapiens	39-43
17683942-2	2007	We have determined structures of human PDK1 or PDK3 bound to the inhibitors AZD7545, dichloroacetate (DCA), and radicicol.	Dichloroacetic Acid	102-105	pyruvate dehydrogenase kinase 3	Homo sapiens	47-51
17683942-6	2007	Good DCA density is present in the helix bundle in the N-terminal domain of PDK1.	Dichloroacetic Acid	5-8	pyruvate dehydrogenase kinase 1	Homo sapiens	76-80
17683942-7	2007	Bound DCA promotes local conformational changes that are communicated to both nucleotide-binding and lipoyl-binding pockets of PDK1, leading to the inactivation of kinase activity.	Dichloroacetic Acid	6-9	pyruvate dehydrogenase kinase 1	Homo sapiens	127-131
17544412-4	2007	We also show that Y80 and D117 are required for the communication between the DCA-binding site and active site of PDHK2.	Dichloroacetic Acid	78-81	pyruvate dehydrogenase kinase 2	Homo sapiens	114-119
17432838-6	2007	Magnetic-field-independent contributions to the rate constant kr of T+/- --> (T0,S) relaxation are about 4.5 x 10(5) s-1 for DCA-POZ and -PTZ (due to a vibrational mechanism) and 3.5 x 10(6) s-1 for DCA-PSZ (due to spin rotational mechanism).	Dichloroacetic Acid	128-131	spindlin 1	Homo sapiens	218-222
17200418-3	2007	Incubation with a phosphatidyl inositol-3 kinase inhibitor or expression of dominant-negative AKT in primary rat hepatocytes abolished activation of AKT and GS by DCA and TCA.	Dichloroacetic Acid	163-166	AKT serine/threonine kinase 1	Rattus norvegicus	94-97
17200418-3	2007	Incubation with a phosphatidyl inositol-3 kinase inhibitor or expression of dominant-negative AKT in primary rat hepatocytes abolished activation of AKT and GS by DCA and TCA.	Dichloroacetic Acid	163-166	AKT serine/threonine kinase 1	Rattus norvegicus	149-152
17156782-2	2007	Peroxisome proliferators-activated receptor alpha, PPARbeta, PPARgamma1, and PPARgamma2 mRNA are all present in normal peritoneal and adhesion fibroblasts, and selectively rose in response to hypoxia and either DCA or NS-398.	Dichloroacetic Acid	211-214	peroxisome proliferator activated receptor delta	Homo sapiens	51-59
18958719-12	2007	DCA treatment decreased IL-10 and KC chemokine concentrations in the livers of MRL(+/+) mice, whereas T-helper cell cytokines (IL-4, IL-5, IL-10, IFNgamma, and GM-CSF), pro-inflammatory cytokines (IL-6, IL-12, and G-CSF), and KC chemokine were increased in the livers of DCA-treated B(6)C(3)F(1) mice.	Dichloroacetic Acid	0-3	interleukin 10	Mus musculus	24-29
18958719-12	2007	DCA treatment decreased IL-10 and KC chemokine concentrations in the livers of MRL(+/+) mice, whereas T-helper cell cytokines (IL-4, IL-5, IL-10, IFNgamma, and GM-CSF), pro-inflammatory cytokines (IL-6, IL-12, and G-CSF), and KC chemokine were increased in the livers of DCA-treated B(6)C(3)F(1) mice.	Dichloroacetic Acid	0-3	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	160-166
18958719-12	2007	DCA treatment decreased IL-10 and KC chemokine concentrations in the livers of MRL(+/+) mice, whereas T-helper cell cytokines (IL-4, IL-5, IL-10, IFNgamma, and GM-CSF), pro-inflammatory cytokines (IL-6, IL-12, and G-CSF), and KC chemokine were increased in the livers of DCA-treated B(6)C(3)F(1) mice.	Dichloroacetic Acid	0-3	interleukin 6	Mus musculus	197-201
18958719-12	2007	DCA treatment decreased IL-10 and KC chemokine concentrations in the livers of MRL(+/+) mice, whereas T-helper cell cytokines (IL-4, IL-5, IL-10, IFNgamma, and GM-CSF), pro-inflammatory cytokines (IL-6, IL-12, and G-CSF), and KC chemokine were increased in the livers of DCA-treated B(6)C(3)F(1) mice.	Dichloroacetic Acid	0-3	colony stimulating factor 3 (granulocyte)	Mus musculus	214-219
17222789-3	2007	Dichloroacetate (DCA) inhibits mitochondrial pyruvate dehydrogenase kinase (PDK), shifts metabolism from glycolysis to glucose oxidation, decreases DeltaPsim, increases mitochondrial H2O2, and activates Kv channels in all cancer, but not normal, cells; DCA upregulates Kv1.5 by an NFAT1-dependent mechanism.	Dichloroacetic Acid	0-15	potassium voltage-gated channel subfamily A member 5	Homo sapiens	269-274
17241159-4	2007	In myelinating co-cultures, DCA caused a dose- and exposure-dependent decrease of myelination, as determined by immunolabeling and immunoblotting for myelin basic protein (MBP), protein zero (P0), myelin-associated glycoprotein (MAG) and peripheral myelin protein 22 (PMP22).	Dichloroacetic Acid	28-31	myelin basic protein	Rattus norvegicus	150-170
17241159-4	2007	In myelinating co-cultures, DCA caused a dose- and exposure-dependent decrease of myelination, as determined by immunolabeling and immunoblotting for myelin basic protein (MBP), protein zero (P0), myelin-associated glycoprotein (MAG) and peripheral myelin protein 22 (PMP22).	Dichloroacetic Acid	28-31	myelin basic protein	Rattus norvegicus	172-175
17241159-4	2007	In myelinating co-cultures, DCA caused a dose- and exposure-dependent decrease of myelination, as determined by immunolabeling and immunoblotting for myelin basic protein (MBP), protein zero (P0), myelin-associated glycoprotein (MAG) and peripheral myelin protein 22 (PMP22).	Dichloroacetic Acid	28-31	myelin-associated glycoprotein	Rattus norvegicus	197-227
17241159-4	2007	In myelinating co-cultures, DCA caused a dose- and exposure-dependent decrease of myelination, as determined by immunolabeling and immunoblotting for myelin basic protein (MBP), protein zero (P0), myelin-associated glycoprotein (MAG) and peripheral myelin protein 22 (PMP22).	Dichloroacetic Acid	28-31	myelin-associated glycoprotein	Rattus norvegicus	229-232
17241159-4	2007	In myelinating co-cultures, DCA caused a dose- and exposure-dependent decrease of myelination, as determined by immunolabeling and immunoblotting for myelin basic protein (MBP), protein zero (P0), myelin-associated glycoprotein (MAG) and peripheral myelin protein 22 (PMP22).	Dichloroacetic Acid	28-31	peripheral myelin protein 22	Rattus norvegicus	238-266
17241159-4	2007	In myelinating co-cultures, DCA caused a dose- and exposure-dependent decrease of myelination, as determined by immunolabeling and immunoblotting for myelin basic protein (MBP), protein zero (P0), myelin-associated glycoprotein (MAG) and peripheral myelin protein 22 (PMP22).	Dichloroacetic Acid	28-31	peripheral myelin protein 22	Rattus norvegicus	268-273
17241159-7	2007	In isolated SC cultures, DCA decreased the expression of P0 and PMP22, while it increased the levels of p75(NTR) (neurotrophin receptor), as compared with non-DCA-treated samples.	Dichloroacetic Acid	25-28	peripheral myelin protein 22	Rattus norvegicus	64-69
17241159-7	2007	In isolated SC cultures, DCA decreased the expression of P0 and PMP22, while it increased the levels of p75(NTR) (neurotrophin receptor), as compared with non-DCA-treated samples.	Dichloroacetic Acid	25-28	nerve growth factor receptor	Rattus norvegicus	104-112
17268597-5	2007	Mn(dca)(2)(pym)(H(2)O), , which crystallizes in the monoclinic space group P2(1)/c, has a unique interdigitated 2D network that consists of double-bridged [Mn(2)(dca)(2)(pym)(2)(H(2)O)(2)](2+)"dimers" that are connected via single-bridging dca ligands.	Dichloroacetic Acid	3-6	H3 histone pseudogene 16	Homo sapiens	75-82
17222789-3	2007	Dichloroacetate (DCA) inhibits mitochondrial pyruvate dehydrogenase kinase (PDK), shifts metabolism from glycolysis to glucose oxidation, decreases DeltaPsim, increases mitochondrial H2O2, and activates Kv channels in all cancer, but not normal, cells; DCA upregulates Kv1.5 by an NFAT1-dependent mechanism.	Dichloroacetic Acid	0-15	nuclear factor of activated T cells 2	Homo sapiens	281-286
17222789-3	2007	Dichloroacetate (DCA) inhibits mitochondrial pyruvate dehydrogenase kinase (PDK), shifts metabolism from glycolysis to glucose oxidation, decreases DeltaPsim, increases mitochondrial H2O2, and activates Kv channels in all cancer, but not normal, cells; DCA upregulates Kv1.5 by an NFAT1-dependent mechanism.	Dichloroacetic Acid	17-20	potassium voltage-gated channel subfamily A member 5	Homo sapiens	269-274
17222789-3	2007	Dichloroacetate (DCA) inhibits mitochondrial pyruvate dehydrogenase kinase (PDK), shifts metabolism from glycolysis to glucose oxidation, decreases DeltaPsim, increases mitochondrial H2O2, and activates Kv channels in all cancer, but not normal, cells; DCA upregulates Kv1.5 by an NFAT1-dependent mechanism.	Dichloroacetic Acid	17-20	nuclear factor of activated T cells 2	Homo sapiens	281-286
17222789-5	2007	Molecular inhibition of PDK2 by siRNA mimics DCA.	Dichloroacetic Acid	45-48	pyruvate dehydrogenase kinase 2	Homo sapiens	24-28
17290740-1	2006	OBJECTIVE: To study on the DNA damage of p53 induced by dichloroacetic acid(DCA) and trichloroacetic acid( TCA), approve their genotoxicity and discuss molecular mechanism of their carcinogenic action.	Dichloroacetic Acid	56-75	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	41-44
17290740-1	2006	OBJECTIVE: To study on the DNA damage of p53 induced by dichloroacetic acid(DCA) and trichloroacetic acid( TCA), approve their genotoxicity and discuss molecular mechanism of their carcinogenic action.	Dichloroacetic Acid	76-79	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	41-44
17290740-5	2006	It was indicated that DCA can result in DNA damage of exon 7 of p53 gene of rat"s liver tissue, and there were two broken sites.	Dichloroacetic Acid	22-25	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	64-67
16393857-3	2005	The second form, FSD2 (molecular weight 27 kDa), contained only 13% of the fluoroacetate defluorination activity, had a pI = 7.8, and exhibited a high glutathione S-transferase (GST)-like activity towards dichloroacetic acid.	Dichloroacetic Acid	205-224	fibronectin type III and SPRY domain containing 2	Rattus norvegicus	17-21
16765624-9	2006	Ignoring the patient with the splicing mutation, DCA decreased average glycolysis (29%) in patient cells, but had no significant effect on control cells, and did not change LPR or the nucleoside triphosphate to diphosphate ratio (NTP/NDP) in either cell type.	Dichloroacetic Acid	49-52	norrin cystine knot growth factor NDP	Homo sapiens	234-237
16581029-3	2006	The objective of the present study was to evaluate whether administration of dichloroacetate, an inhibitor of maleyl acetoacetate isomerase (MAAI) to FAH-knockout mice could prevent acute pathological injury caused by NTBC withdrawal.	Dichloroacetic Acid	77-92	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	110-139
16581029-3	2006	The objective of the present study was to evaluate whether administration of dichloroacetate, an inhibitor of maleyl acetoacetate isomerase (MAAI) to FAH-knockout mice could prevent acute pathological injury caused by NTBC withdrawal.	Dichloroacetic Acid	77-92	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	141-145
16581029-3	2006	The objective of the present study was to evaluate whether administration of dichloroacetate, an inhibitor of maleyl acetoacetate isomerase (MAAI) to FAH-knockout mice could prevent acute pathological injury caused by NTBC withdrawal.	Dichloroacetic Acid	77-92	fumarylacetoacetate hydrolase	Mus musculus	150-153
16581029-7	2006	DCA was shown to inhibit hepatic MAAI activity to 86% (0.5g/L) and 94% (5g/L) of untreated wild-type mice.	Dichloroacetic Acid	0-3	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	33-37
16609361-1	2006	OBJECTIVES: The zeta-class glutathione transferase GSTZ1-1 catalyses the glutathione-dependent isomerization of maleylacetoacetate to fumarylacetoacetate in the tyrosine catabolic pathway and the biotransformation of alpha-halo acids, including dichloroacetic acid (DCA).	Dichloroacetic Acid	245-264	glutathione S-transferase zeta 1	Homo sapiens	51-58
16609361-1	2006	OBJECTIVES: The zeta-class glutathione transferase GSTZ1-1 catalyses the glutathione-dependent isomerization of maleylacetoacetate to fumarylacetoacetate in the tyrosine catabolic pathway and the biotransformation of alpha-halo acids, including dichloroacetic acid (DCA).	Dichloroacetic Acid	266-269	glutathione S-transferase zeta 1	Homo sapiens	51-58
16609361-9	2006	CONCLUSION: These SNPs may alter GSTZ1 expression, which may alter the pharmacokinetics of DCA, which is used therapeutically for the treatment of lactic acidosis.	Dichloroacetic Acid	91-94	glutathione S-transferase zeta 1	Homo sapiens	33-38
16199472-2	2006	DCA is biotransformed to glyoxylate by glutathione S-transferase zeta (GSTz1-1), which is identical to maleylacetoacetate isomerase, an enzyme of tyrosine catabolism.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Rattus norvegicus	71-78
16199472-2	2006	DCA is biotransformed to glyoxylate by glutathione S-transferase zeta (GSTz1-1), which is identical to maleylacetoacetate isomerase, an enzyme of tyrosine catabolism.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Rattus norvegicus	103-131
16199472-3	2006	Clinically relevant doses of DCA (mg/kg/day) decrease the activity and expression of GSTz1-1, which alters tyrosine metabolism and may cause hepatic and neurological toxicity.	Dichloroacetic Acid	29-32	glutathione S-transferase zeta 1	Rattus norvegicus	85-92
16290150-7	2005	II+III, IV, II+III/CS and IV/CS activities reached their lowest levels in association with a stroke-like episode, then increased with DCA treatment.	Dichloroacetic Acid	134-137	citrate synthase	Homo sapiens	19-21
16290150-7	2005	II+III, IV, II+III/CS and IV/CS activities reached their lowest levels in association with a stroke-like episode, then increased with DCA treatment.	Dichloroacetic Acid	134-137	citrate synthase	Homo sapiens	29-31
15705382-8	2005	The DCA treatment resulted in a statistically significant decrease in VEGF mRNA levels in adhesion (20%) and normal peritoneal (18%) fibroblasts.	Dichloroacetic Acid	4-7	vascular endothelial growth factor A	Homo sapiens	70-74
15539426-10	2005	Moreover, inhibitors of TRXR, which controls the reducing activity of TRX, also blocked upregulation of I(to) by insulin and dichloroacetate.	Dichloroacetic Acid	125-140	thioredoxin 1	Rattus norvegicus	24-27
15342954-12	2004	Hence, DBA, like DCA and TCA, induced hypomethylation of DNA and of the c-myc and IGF-II genes, increased mRNA expression of both genes, and caused peroxisome proliferation.	Dichloroacetic Acid	17-20	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	72-77
16399379-7	2005	DCA was found to be a mechanism-based inactivator of GSTZ, and proteomic studies showed that Cys-16 of human GSTZ1-1 is covalently modified by a reactive intermediate that contains glutathione and the carbon skeleton of DCA.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	109-116
16399379-7	2005	DCA was found to be a mechanism-based inactivator of GSTZ, and proteomic studies showed that Cys-16 of human GSTZ1-1 is covalently modified by a reactive intermediate that contains glutathione and the carbon skeleton of DCA.	Dichloroacetic Acid	220-223	glutathione S-transferase zeta 1	Homo sapiens	109-116
15342954-12	2004	Hence, DBA, like DCA and TCA, induced hypomethylation of DNA and of the c-myc and IGF-II genes, increased mRNA expression of both genes, and caused peroxisome proliferation.	Dichloroacetic Acid	17-20	insulin-like growth factor 2	Mus musculus	82-88
15236515-0	2004	Spin canting in the 3D anionic dicyanamide structure (SPh(3))Mn(dca)(3) (Ph = phenyl, dca = dicyanamide).	Dichloroacetic Acid	64-67	spectrin alpha, erythrocytic 1	Homo sapiens	54-60
15375007-8	2004	DCA depolarizes MCT-PAH PASMC mitochondria and causes release of H2O2 and cytochrome c, inducing a 10-fold increase in apoptosis within the PA media (TUNEL and caspase 3 activity) and decreasing proliferation (proliferating-cell nuclear antigen and BrdU assays).	Dichloroacetic Acid	0-3	caspase 3	Rattus norvegicus	160-169
15375007-9	2004	Immunoblots, immunohistochemistry, laser-captured microdissection-quantitative reverse-transcription polymerase chain reaction and patch-clamping show that DCA reverses the Kv1.5 downregulation in resistance PAs.	Dichloroacetic Acid	156-159	potassium voltage-gated channel subfamily A member 5	Rattus norvegicus	173-178
15375007-10	2004	In summary, DCA reverses PA remodeling by increasing the mitochondria-dependent apoptosis/proliferation ratio and upregulating Kv1.5 in the media.	Dichloroacetic Acid	12-15	potassium voltage-gated channel subfamily A member 5	Rattus norvegicus	127-132
15363585-0	2004	Role of the peroxisome proliferator-activated receptor alpha (PPARalpha) in responses to trichloroethylene and metabolites, trichloroacetate and dichloroacetate in mouse liver.	Dichloroacetic Acid	145-160	peroxisome proliferator activated receptor alpha	Mus musculus	12-60
15363585-0	2004	Role of the peroxisome proliferator-activated receptor alpha (PPARalpha) in responses to trichloroethylene and metabolites, trichloroacetate and dichloroacetate in mouse liver.	Dichloroacetic Acid	145-160	peroxisome proliferator activated receptor alpha	Mus musculus	62-71
15363585-4	2004	The objectives of this study were to determine whether effects of TCE, TCA and DCA in the liver associated with carcinogenesis are mediated by PPARalpha.	Dichloroacetic Acid	79-82	peroxisome proliferator activated receptor alpha	Mus musculus	143-152
15363585-9	2004	Increases in enzymes that catalyze beta- and omega-oxidation of fatty acids were dependent on PPARalpha after exposure to TCE, TCA or DCA.	Dichloroacetic Acid	134-137	peroxisome proliferator activated receptor alpha	Mus musculus	94-103
15277241-1	2004	Glutathione transferase zeta (GSTZ1-1) is the major enzyme that catalyzes the metabolism of alpha-halo acids such as dichloroacetic acid, a carcinogenic contaminant of chlorinated water.	Dichloroacetic Acid	117-136	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	30-37
15236515-0	2004	Spin canting in the 3D anionic dicyanamide structure (SPh(3))Mn(dca)(3) (Ph = phenyl, dca = dicyanamide).	Dichloroacetic Acid	86-89	spectrin alpha, erythrocytic 1	Homo sapiens	54-60
15236515-1	2004	Through use of the SPh(3)(+) (Ph = phenyl, C(6)H(5)) cation as a molecular template, a new three-dimensional Mn(dca)(3)(-) [dca = dicyanamide, N(CN)(2)(-)] anionic structure has been crystallized.	Dichloroacetic Acid	112-115	spectrin alpha, erythrocytic 1	Homo sapiens	19-25
15236515-1	2004	Through use of the SPh(3)(+) (Ph = phenyl, C(6)H(5)) cation as a molecular template, a new three-dimensional Mn(dca)(3)(-) [dca = dicyanamide, N(CN)(2)(-)] anionic structure has been crystallized.	Dichloroacetic Acid	124-127	spectrin alpha, erythrocytic 1	Homo sapiens	19-25
15236515-2	2004	At room temperature, (SPh(3))Mn(dca)(3) (1) crystallizes in the monoclinic space group P2(1)/c, with a = 11.7079(5) A, b = 12.8554(5) A, c = 16.8605(6) A, beta = 100.666(2) degrees, and V = 2493.8(3) A(3).	Dichloroacetic Acid	32-35	spectrin alpha, erythrocytic 1	Homo sapiens	22-28
15236515-2	2004	At room temperature, (SPh(3))Mn(dca)(3) (1) crystallizes in the monoclinic space group P2(1)/c, with a = 11.7079(5) A, b = 12.8554(5) A, c = 16.8605(6) A, beta = 100.666(2) degrees, and V = 2493.8(3) A(3).	Dichloroacetic Acid	32-35	H3 histone pseudogene 16	Homo sapiens	87-92
15144222-11	2004	The results of the present study demonstrate that GSTZ1-1 catalyzes the bioactivation of DCA to the reactive metabolite glyoxylate.	Dichloroacetic Acid	89-92	glutathione S-transferase zeta 1	Rattus norvegicus	50-57
15450858-2	2004	In this study, the effects of superoxide dismutase (SOD) and polyclonal tumor necrosis factor-alpha (TNF-alpha) antibodies on DCA- and TCA-induced SA production and cellular death have been tested on the J774.A1 macrophage cultures.	Dichloroacetic Acid	126-129	tumor necrosis factor	Homo sapiens	72-99
15450858-2	2004	In this study, the effects of superoxide dismutase (SOD) and polyclonal tumor necrosis factor-alpha (TNF-alpha) antibodies on DCA- and TCA-induced SA production and cellular death have been tested on the J774.A1 macrophage cultures.	Dichloroacetic Acid	126-129	tumor necrosis factor	Homo sapiens	101-110
15450858-6	2004	On the other hand, addition of TNF-alpha antibodies to the DCA- and TCA-treated cultures resulted in significant reduction of DCA- but not TCA-induced cellular death and SA production by the cells.	Dichloroacetic Acid	59-62	tumor necrosis factor	Homo sapiens	31-40
15450858-6	2004	On the other hand, addition of TNF-alpha antibodies to the DCA- and TCA-treated cultures resulted in significant reduction of DCA- but not TCA-induced cellular death and SA production by the cells.	Dichloroacetic Acid	126-129	tumor necrosis factor	Homo sapiens	31-40
15118288-6	2004	Postprocedural lumen CSA was largest after DCA-stent (11.2+/-2.7 mm2) and DCA (10.8+/-2.5 mm2) than stenting alone (9.0+/-2.9 mm2) (p<0.0005).	Dichloroacetic Acid	43-46	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	21-24
15118288-6	2004	Postprocedural lumen CSA was largest after DCA-stent (11.2+/-2.7 mm2) and DCA (10.8+/-2.5 mm2) than stenting alone (9.0+/-2.9 mm2) (p<0.0005).	Dichloroacetic Acid	74-77	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	21-24
15118288-8	2004	As a result, follow-up lumen CSA was largest after DCA-stent (DCA-stent: 9.1+/-3.4 mm2, DCA: 7.8+/-4.2 mm2, stent: 6.3+/-2.6 mm2, p<0.0005).	Dichloroacetic Acid	51-54	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	29-32
14711564-0	2004	Regulation of matrix metalloproteinase-1 and tissue inhibitor of matrix metalloproteinase-1 by dichloroacetic acid in human fibroblasts from normal peritoneum and adhesions.	Dichloroacetic Acid	95-114	matrix metallopeptidase 1	Homo sapiens	14-91
15144222-4	2004	The purpose of this study was to examine the GSTZ1-1-catalyzed bioactivation of DCA, including the reaction of DCA-derived glyoxylate with amino acid nucleophiles and the characterization of the structures and kinetics of adduct formation by LC/MS.	Dichloroacetic Acid	80-83	glutathione S-transferase zeta 1	Rattus norvegicus	45-52
15118614-0	2004	Regulation of expression of tissue plasminogen activator and plasminogen activator inhibitor-1 by dichloroacetic acid in human fibroblasts from normal peritoneum and adhesions.	Dichloroacetic Acid	98-117	serpin family E member 1	Homo sapiens	61-94
15118614-8	2004	Plasminogen activator inhibitor-1 messenger RNA expression was unaltered by dichloroacetic acid in normoxic normal peritoneal fibroblasts; but during culture under hypoxic conditions, dichloroacetic acid reduced plasminogen activator inhibitor-1 messenger RNA expression.	Dichloroacetic Acid	184-203	serpin family E member 1	Homo sapiens	0-33
15118614-8	2004	Plasminogen activator inhibitor-1 messenger RNA expression was unaltered by dichloroacetic acid in normoxic normal peritoneal fibroblasts; but during culture under hypoxic conditions, dichloroacetic acid reduced plasminogen activator inhibitor-1 messenger RNA expression.	Dichloroacetic Acid	184-203	serpin family E member 1	Homo sapiens	212-245
15118614-10	2004	As a result, in normal peritoneal fibroblasts under hypoxic conditions and in adhesion fibroblasts under normoxic and hypoxic conditions, dichloroacetic acid greatly increased the tissue plasminogen activator/plasminogen activator inhibitor-1 ratios.	Dichloroacetic Acid	138-157	serpin family E member 1	Homo sapiens	209-242
15118614-13	2004	Dichloroacetic acid reduces plasminogen activator inhibitor-1 production by hypoxic normal peritoneal fibroblasts and adhesion fibroblasts under hypoxic conditions.	Dichloroacetic Acid	0-19	serpin family E member 1	Homo sapiens	28-61
15036762-3	2004	Hypomethylation of DNA and the insulin-like growth factor-II (IGF-II) gene was determined in DCA- and TCA-promoted liver tumors.	Dichloroacetic Acid	93-96	insulin-like growth factor 2	Mus musculus	31-68
15036762-9	2004	mRNA expression of the IGF-II gene was increased in DCA- and TCA-promoted liver tumors but not in non-involved liver from DCA- and TCA-exposed mice.	Dichloroacetic Acid	52-55	insulin-like growth factor 2	Mus musculus	23-29
15036762-9	2004	mRNA expression of the IGF-II gene was increased in DCA- and TCA-promoted liver tumors but not in non-involved liver from DCA- and TCA-exposed mice.	Dichloroacetic Acid	122-125	insulin-like growth factor 2	Mus musculus	23-29
14662656-7	2004	The lactic acidosis induced by the NDUFV1 mutations could be partially corrected with the vitamins riboflavin and thiamine or with sodium dichloroacetate, an activator of the pyruvate dehydrogenase complex, resulting in significant increases in animal fitness.	Dichloroacetic Acid	131-153	NADH:ubiquinone oxidoreductase core subunit V1	Homo sapiens	35-41
14711564-6	2004	RESULT(S): Dichloroacetic acid stimulated peritoneal fibroblast MMP-1 mRNA expression under normoxic conditions; this stimulation was lost during hypoxia.	Dichloroacetic Acid	11-30	matrix metallopeptidase 1	Homo sapiens	64-69
14711564-7	2004	In adhesion fibroblasts, DCA increased MMP-1 mRNA expression; this effect was reversed by hypoxia.	Dichloroacetic Acid	25-28	matrix metallopeptidase 1	Homo sapiens	39-44
14599561-2	2003	DCA is biotransformed to glyoxylate by maleylacetoacetate isomerase (MAAI).	Dichloroacetic Acid	0-3	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	39-67
14711564-8	2004	Expression of TIMP-1 mRNA was insignificantly increased by DCA in normal peritoneal and adhesion fibroblasts under normoxic conditions; however under hypoxic conditions, DCA reduced TIMP-1 mRNA expression from both.	Dichloroacetic Acid	59-62	TIMP metallopeptidase inhibitor 1	Homo sapiens	14-20
14711564-8	2004	Expression of TIMP-1 mRNA was insignificantly increased by DCA in normal peritoneal and adhesion fibroblasts under normoxic conditions; however under hypoxic conditions, DCA reduced TIMP-1 mRNA expression from both.	Dichloroacetic Acid	170-173	TIMP metallopeptidase inhibitor 1	Homo sapiens	14-20
14711564-8	2004	Expression of TIMP-1 mRNA was insignificantly increased by DCA in normal peritoneal and adhesion fibroblasts under normoxic conditions; however under hypoxic conditions, DCA reduced TIMP-1 mRNA expression from both.	Dichloroacetic Acid	170-173	TIMP metallopeptidase inhibitor 1	Homo sapiens	182-188
15231452-5	2004	However, the elevated concentration of NPY in the VMH of anorectic TB rats was also normalized by the DCA treatment.	Dichloroacetic Acid	102-105	neuropeptide Y	Rattus norvegicus	39-42
14599561-2	2003	DCA is biotransformed to glyoxylate by maleylacetoacetate isomerase (MAAI).	Dichloroacetic Acid	0-3	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	69-73
14599561-3	2003	Previous studies have shown that DCA decreases MAAI activity in rat liver in a time- and dose-dependent manner and may target the protein for degradation in vivo.	Dichloroacetic Acid	33-36	glutathione S-transferase zeta 1	Rattus norvegicus	47-51
14599561-4	2003	We now report that the MAAI protein is depleted in a time- and dose-dependent manner in the livers of Sprague-Dawley rats exposed to DCA.	Dichloroacetic Acid	133-136	glutathione S-transferase zeta 1	Rattus norvegicus	23-27
12738512-0	2003	Regulation of transforming growth factor-beta, type III collagen, and fibronectin by dichloroacetic acid in human fibroblasts from normal peritoneum and adhesions.	Dichloroacetic Acid	85-104	fibronectin 1	Homo sapiens	70-81
14512880-12	2003	In conclusion, glycine-conjugated and free bile acids suppress bile acid synthesis and mRNA levels of CYP7A1 in the order CDCA > DCA > CA > UDCA.	Dichloroacetic Acid	123-126	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	102-108
12943907-7	2003	Precipitation from solvents such as DCA or TFA resulted in the rippled beta-sheet structure (PG I), while 3(1)-helix (PG II) was formed by precipitation from aqueous solutions of LiBr.	Dichloroacetic Acid	36-39	biglycan	Homo sapiens	93-97
12730618-2	2003	GSTZ1-1 is inactivated by dichloroacetic acid (DCA), which is used for the clinical management of congenital lactic acidosis and is a drinking-water contaminant.	Dichloroacetic Acid	26-45	glutathione S-transferase zeta 1	Rattus norvegicus	0-7
12730618-2	2003	GSTZ1-1 is inactivated by dichloroacetic acid (DCA), which is used for the clinical management of congenital lactic acidosis and is a drinking-water contaminant.	Dichloroacetic Acid	47-50	glutathione S-transferase zeta 1	Rattus norvegicus	0-7
12730618-5	2003	Urine from DCA-treated rats inhibited delta-aminolevulinic acid dehydratase (delta-ALAD) activity, which is used for the diagnosis of hereditary tyrosinemia type I.	Dichloroacetic Acid	11-14	aminolevulinate dehydratase	Rattus norvegicus	38-75
12730618-5	2003	Urine from DCA-treated rats inhibited delta-aminolevulinic acid dehydratase (delta-ALAD) activity, which is used for the diagnosis of hereditary tyrosinemia type I.	Dichloroacetic Acid	11-14	aminolevulinate dehydratase	Rattus norvegicus	77-87
12730618-10	2003	These data indicate that DCA-induced inactivation of GSTZ1-1 leads to formation of an MAA-derived intermediate, MA, that may be a mediator and biomarker for DCA-associated toxicities.	Dichloroacetic Acid	25-28	glutathione S-transferase zeta 1	Rattus norvegicus	53-60
12730618-10	2003	These data indicate that DCA-induced inactivation of GSTZ1-1 leads to formation of an MAA-derived intermediate, MA, that may be a mediator and biomarker for DCA-associated toxicities.	Dichloroacetic Acid	157-160	glutathione S-transferase zeta 1	Rattus norvegicus	53-60
12796364-4	2003	DCA also showed up-regulation of Toll-like receptor 2 and 3, as well as several tumor necrosis factor family ligands.	Dichloroacetic Acid	0-3	toll like receptor 2	Homo sapiens	33-59
12738512-7	2003	RESULT(S): DCA inhibited human peritoneal fibroblast and adhesion fibroblast TGF-beta1 mRNA expression under normoxic and hypoxic conditions.	Dichloroacetic Acid	11-14	transforming growth factor beta 1	Homo sapiens	77-86
12738512-8	2003	DCA also markedly reduced fibronectin and type III collagen expression under hypoxic conditions in fibroblasts from normal peritoneum and adhesions.	Dichloroacetic Acid	0-3	fibronectin 1	Homo sapiens	26-37
14713130-16	2003	3) Oral Dichloroacetate (DCA), a metabolic modulator, increases expression/function of Kv2.1 channels and decreases remodeling and PVR in rats with chronic-hypoxic pulmonary hypertension, partially via a tyrosine-kinase-dependent mechanism.	Dichloroacetic Acid	8-23	potassium voltage-gated channel subfamily B member 1	Rattus norvegicus	87-92
14713130-16	2003	3) Oral Dichloroacetate (DCA), a metabolic modulator, increases expression/function of Kv2.1 channels and decreases remodeling and PVR in rats with chronic-hypoxic pulmonary hypertension, partially via a tyrosine-kinase-dependent mechanism.	Dichloroacetic Acid	25-28	potassium voltage-gated channel subfamily B member 1	Rattus norvegicus	87-92
12019185-1	2002	Glutathione transferase zeta (GSTZ1-1) catalyzes the biotransformation of a range of alpha-haloacids, including dichloroacetic acid (DCA), and the penultimate step in the tyrosine degradation pathway.	Dichloroacetic Acid	112-131	glutathione S-transferase zeta 1	Rattus norvegicus	30-37
12441371-3	2002	Glutathione transferase zeta (GSTZ1-1) catalyzes the biotransformation of DCA and CFA, and DCA is a mechanism-based inactivator of GSTZ1-1.	Dichloroacetic Acid	74-77	glutathione S-transferase zeta 1	Rattus norvegicus	30-37
12441371-3	2002	Glutathione transferase zeta (GSTZ1-1) catalyzes the biotransformation of DCA and CFA, and DCA is a mechanism-based inactivator of GSTZ1-1.	Dichloroacetic Acid	91-94	glutathione S-transferase zeta 1	Rattus norvegicus	131-138
12441371-10	2002	Treatment of rats with DCA for 5 days to inactivate GSTZ1-1 failed to prevent metabolism of CFA to fluoride and did not block CFA-induced renal damage.	Dichloroacetic Acid	23-26	glutathione S-transferase zeta 1	Rattus norvegicus	52-59
12437329-3	2002	GSTZ1-1-catalyzed biotransformation of fluorine-lacking alpha,alpha-dihaloalkanoic acids, including dichloroacetic acid (DCA), results in the mechanism-based inactivation and covalent modification of the enzyme.	Dichloroacetic Acid	100-119	glutathione S-transferase zeta 1	Homo sapiens	0-7
12437329-3	2002	GSTZ1-1-catalyzed biotransformation of fluorine-lacking alpha,alpha-dihaloalkanoic acids, including dichloroacetic acid (DCA), results in the mechanism-based inactivation and covalent modification of the enzyme.	Dichloroacetic Acid	121-124	glutathione S-transferase zeta 1	Homo sapiens	0-7
12437329-12	2002	These findings explain the DCA-induced inactivation of GSTZ1-1 observed in humans and rats.	Dichloroacetic Acid	27-30	glutathione S-transferase zeta 1	Homo sapiens	55-62
12067850-4	2002	DCA infusion increased pyruvate dehydrogenase (PDH) activation above CON and HYP (3.10 +/- 0.23, 0.56 +/- 0.08, 0.69 +/- 0.05 mmol x kg wet muscle(-1) x min(-1), respectively) and significantly increased both acetyl-CoA and acetylcarnitine (11.0 +/- 0.7, 2.0 +/- 0.5, 2.2 +/- 0.5 mmol/kg dry muscle, respectively) at rest.	Dichloroacetic Acid	0-3	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	23-45
12067850-4	2002	DCA infusion increased pyruvate dehydrogenase (PDH) activation above CON and HYP (3.10 +/- 0.23, 0.56 +/- 0.08, 0.69 +/- 0.05 mmol x kg wet muscle(-1) x min(-1), respectively) and significantly increased both acetyl-CoA and acetylcarnitine (11.0 +/- 0.7, 2.0 +/- 0.5, 2.2 +/- 0.5 mmol/kg dry muscle, respectively) at rest.	Dichloroacetic Acid	0-3	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	47-50
12127263-9	2002	Previous work had shown that DCA produces tumors in mice that display a diffuse immunoreactivity to a c-Jun antibody (Santa Cruz Biotechnology, SC-45), whereas TCA-induced tumors do not stain with this antibody.	Dichloroacetic Acid	29-32	jun proto-oncogene	Mus musculus	102-107
12127263-10	2002	In the present study, we compared the c-Jun phenotype of tumors induced by DCA or TCA alone to those induced when they are given together in various combinations and to those induced by TRI given in an aqueous vehicle.	Dichloroacetic Acid	75-78	jun proto-oncogene	Mus musculus	38-43
12127263-11	2002	When given in various combinations, DCA and TCA produced a few tumors that were c-Jun+, many that were c-Jun-, but a number with a mixed phenotype that increased with the relative dose of DCA.	Dichloroacetic Acid	36-39	jun proto-oncogene	Mus musculus	80-85
12127263-11	2002	When given in various combinations, DCA and TCA produced a few tumors that were c-Jun+, many that were c-Jun-, but a number with a mixed phenotype that increased with the relative dose of DCA.	Dichloroacetic Acid	36-39	jun proto-oncogene	Mus musculus	103-108
12019185-1	2002	Glutathione transferase zeta (GSTZ1-1) catalyzes the biotransformation of a range of alpha-haloacids, including dichloroacetic acid (DCA), and the penultimate step in the tyrosine degradation pathway.	Dichloroacetic Acid	133-136	glutathione S-transferase zeta 1	Rattus norvegicus	30-37
12019185-9	2002	These findings indicate that the DCA-induced inactivation of GSTZ1-1 in different tissues may result in multiorgan disorders that may be associated with perturbed tyrosine metabolism.	Dichloroacetic Acid	33-36	glutathione S-transferase zeta 1	Rattus norvegicus	61-68
11960676-20	2002	Reduced MAAI activity alone is unlikely to be the carcinogenic mode of action for DCA and may in fact, only be important during the early stages of DCA exposure.	Dichloroacetic Acid	82-85	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	8-12
12018993-2	2002	GSTZ1-1 also catalyzes the glutathione-dependent biotransformation of a range of alpha-haloacids, including dichloroacetic acid.	Dichloroacetic Acid	108-127	glutathione S-transferase zeta 1	Homo sapiens	0-7
11960676-20	2002	Reduced MAAI activity alone is unlikely to be the carcinogenic mode of action for DCA and may in fact, only be important during the early stages of DCA exposure.	Dichloroacetic Acid	148-151	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	8-12
11134557-6	2001	In livers of mice treated with DCA for 2-, 10-, and 52-week periods, insulin receptor (IR) protein levels were significantly depressed.	Dichloroacetic Acid	31-34	insulin receptor	Mus musculus	69-85
11742848-2	2002	To remedy this, we used dichloroacetate (DCA) infusion to increase the active form of PDH (PDH(a)) and, subsequently, measured leg O2 uptake and markers of anaerobic ATP provision during conditions of intense dynamic exercise, when the rate of muscle O2 uptake would be very high.	Dichloroacetic Acid	24-39	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	86-89
11742848-2	2002	To remedy this, we used dichloroacetate (DCA) infusion to increase the active form of PDH (PDH(a)) and, subsequently, measured leg O2 uptake and markers of anaerobic ATP provision during conditions of intense dynamic exercise, when the rate of muscle O2 uptake would be very high.	Dichloroacetic Acid	24-39	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	91-97
11742848-2	2002	To remedy this, we used dichloroacetate (DCA) infusion to increase the active form of PDH (PDH(a)) and, subsequently, measured leg O2 uptake and markers of anaerobic ATP provision during conditions of intense dynamic exercise, when the rate of muscle O2 uptake would be very high.	Dichloroacetic Acid	41-44	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	86-89
11742848-2	2002	To remedy this, we used dichloroacetate (DCA) infusion to increase the active form of PDH (PDH(a)) and, subsequently, measured leg O2 uptake and markers of anaerobic ATP provision during conditions of intense dynamic exercise, when the rate of muscle O2 uptake would be very high.	Dichloroacetic Acid	41-44	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	91-97
11742848-6	2002	After DCA administration, PDH(a) was four- to eightfold higher (P < 0.05) than Con at rest, and PDH(a) remained approximately 130% and 100% higher (P < 0.05) after 5 and 15 s of exercise, respectively.	Dichloroacetic Acid	6-9	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	26-32
11742848-6	2002	After DCA administration, PDH(a) was four- to eightfold higher (P < 0.05) than Con at rest, and PDH(a) remained approximately 130% and 100% higher (P < 0.05) after 5 and 15 s of exercise, respectively.	Dichloroacetic Acid	6-9	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	99-105
11790708-11	2002	In a mammalian expression system, DCA activated Kv2.1 by a tyrosine kinase-dependent mechanism.	Dichloroacetic Acid	34-37	potassium voltage-gated channel subfamily B member 1	Homo sapiens	48-53
11790708-12	2002	When given long-term, DCA partially restored I(K) and Kv2.1 expression in PASMCs without altering right ventricular pyruvate dehydrogenase activity, suggesting that the beneficial effects of DCA occur by nonmetabolic mechanisms.	Dichloroacetic Acid	22-25	potassium voltage-gated channel subfamily B member 1	Rattus norvegicus	54-59
11692075-1	2001	The zeta class glutathione transferases (GSTs) are known to catalyse the isomerization of maleylacetoacetate (MAA) to fumarylacetoacetate (FAA), and the biotransformation of dichloroacetic acid to glyoxylate.	Dichloroacetic Acid	174-193	glutathione S-transferase zeta 1	Homo sapiens	41-45
11259315-4	2001	In intact cells the NADH ED-FRAP was sensitive to temperature (Q(10) of 2.5) and to dehydrogenase activation by dichloroacetate or cAMP (twofold increase for each).	Dichloroacetic Acid	112-127	mechanistic target of rapamycin kinase	Homo sapiens	28-32
11259348-5	2001	One GST Z1 variant (GST Z1A) has significantly higher activity with dichloroacetic acid as a substrate than other GST Z1 isoforms.	Dichloroacetic Acid	68-87	glutathione S-transferase kappa 1	Homo sapiens	4-7
11259348-5	2001	One GST Z1 variant (GST Z1A) has significantly higher activity with dichloroacetic acid as a substrate than other GST Z1 isoforms.	Dichloroacetic Acid	68-87	glutathione S-transferase kappa 1	Homo sapiens	20-23
11259348-5	2001	One GST Z1 variant (GST Z1A) has significantly higher activity with dichloroacetic acid as a substrate than other GST Z1 isoforms.	Dichloroacetic Acid	68-87	glutathione S-transferase kappa 1	Homo sapiens	20-23
11950153-13	2001	DCA restored Kv2.1 expression and PASMC Kv current density to near normoxic levels.	Dichloroacetic Acid	0-3	potassium voltage-gated channel subfamily B member 1	Homo sapiens	13-18
11394246-7	2001	DCA lowered the plasma lactate and increased plasma IL-6 concentrations at rest.	Dichloroacetic Acid	0-3	interleukin 6	Homo sapiens	52-56
11394246-8	2001	IL-6 increased in response to exercise only during DCA treatment.	Dichloroacetic Acid	51-54	interleukin 6	Homo sapiens	0-4
11134557-6	2001	In livers of mice treated with DCA for 2-, 10-, and 52-week periods, insulin receptor (IR) protein levels were significantly depressed.	Dichloroacetic Acid	31-34	insulin receptor	Mus musculus	87-89
11134557-7	2001	Additionally, protein kinase B (PKBalpha) expression decreased significantly with DCA treatment.	Dichloroacetic Acid	82-85	thymoma viral proto-oncogene 1	Mus musculus	32-40
11134557-9	2001	In contrast to normal liver, IR protein was elevated in DCA-induced liver tumors relative to that in liver tissue of untreated animals and to an even greater extent when compared to adjacent normal liver in the treated animal.	Dichloroacetic Acid	56-59	insulin receptor	Mus musculus	29-31
11368331-8	2000	In addition to the MAI activity, the AtGSTZ1-1 also catalyzed the glutathione-dependent dehalogenation of dichloroacetic acid to glyoxylic acid.	Dichloroacetic Acid	106-125	glutathione S-transferase zeta 1	Arabidopsis thaliana	37-46
10748134-6	2000	PDK3 was poorly inhibited by pyruvate or dichloroacetate (DCA).	Dichloroacetic Acid	41-56	pyruvate dehydrogenase kinase 3	Homo sapiens	0-4
11001755-0	2000	Effects of PDH activation by dichloroacetate in human skeletal muscle during exercise in hypoxia.	Dichloroacetic Acid	29-44	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	11-14
11001755-3	2000	The present study investigated whether activation of PDH with dichloroacetate (DCA) before exercise would reduce lactate accumulation during exercise in acute hypoxia by increasing oxidative phosphorylation.	Dichloroacetic Acid	79-82	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	53-56
11001755-6	2000	DCA increased PDH activity at rest and at 1 min of exercise, resulting in increased acetyl-CoA concentration and acetylcarnitine concentration at rest and at 1 min.	Dichloroacetic Acid	0-3	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	14-17
10960769-3	2000	Hypomethylated and over-expression of c-jun and c-myc genes were found in DCA- and TCA-promoted liver tumors.	Dichloroacetic Acid	74-77	jun proto-oncogene	Mus musculus	38-43
10960769-5	2000	Thus, DCA- and TCA-promoted carcinogenesis appears to include decreased methylation and increased expression of c-jun and c-myc genes in the presence of increased DNA MTase activity.	Dichloroacetic Acid	6-9	jun proto-oncogene	Mus musculus	112-117
10960769-5	2000	Thus, DCA- and TCA-promoted carcinogenesis appears to include decreased methylation and increased expression of c-jun and c-myc genes in the presence of increased DNA MTase activity.	Dichloroacetic Acid	6-9	DNA methyltransferase (cytosine-5) 1	Mus musculus	167-172
11758968-0	2000	Expression of PPAR(alpha) in human hepatocytes and activation by trichloroacetate and dichloroacetate.	Dichloroacetic Acid	86-101	peroxisome proliferator activated receptor alpha	Homo sapiens	14-25
11758968-7	2000	In contrast human hepatocytes transfected with mPPAR(alpha) and mRXR(alpha) display increased expression of PPAR(alpha), and increased PPRE-reporter activity when treated with WY-14,643, TCA, and DCA.	Dichloroacetic Acid	196-199	peroxisome proliferator activated receptor alpha	Homo sapiens	48-58
10748134-10	2000	E2-activated PDK2 activity was stimulated >/=3-fold by reductive acetylation of E2; stimulated PDK2 retained high sensitivity to inhibition by ADP and DCA.	Dichloroacetic Acid	154-157	pyruvate dehydrogenase kinase 2	Homo sapiens	13-17
10748134-10	2000	E2-activated PDK2 activity was stimulated >/=3-fold by reductive acetylation of E2; stimulated PDK2 retained high sensitivity to inhibition by ADP and DCA.	Dichloroacetic Acid	154-157	pyruvate dehydrogenase kinase 2	Homo sapiens	98-102
10748134-6	2000	PDK3 was poorly inhibited by pyruvate or dichloroacetate (DCA).	Dichloroacetic Acid	58-61	pyruvate dehydrogenase kinase 3	Homo sapiens	0-4
10748134-9	2000	E2 activation of PDK2 resulted in a greatly enhanced sensitivity to inhibition by pyruvate or DCA; pyruvate was effective at significantly lower levels than DCA.	Dichloroacetic Acid	94-97	pyruvate dehydrogenase kinase 2	Homo sapiens	17-21
10748134-9	2000	E2 activation of PDK2 resulted in a greatly enhanced sensitivity to inhibition by pyruvate or DCA; pyruvate was effective at significantly lower levels than DCA.	Dichloroacetic Acid	157-160	pyruvate dehydrogenase kinase 2	Homo sapiens	17-21
10754212-3	2000	Hence, DCA-induced apoptosis requires caspase activity and both bcl-2 and PKC can determine the type of cell death induced by deoxycholic acid.	Dichloroacetic Acid	7-10	BCL2 apoptosis regulator	Homo sapiens	64-69
10953059-7	2000	Furthermore, HIV-1 strains resistant to L-CA and D-CA were selected in the presence of L-CA and D-CA, respectively.	Dichloroacetic Acid	49-53	protein tyrosine phosphatase receptor type C	Homo sapiens	87-91
10953059-7	2000	Furthermore, HIV-1 strains resistant to L-CA and D-CA were selected in the presence of L-CA and D-CA, respectively.	Dichloroacetic Acid	96-100	protein tyrosine phosphatase receptor type C	Homo sapiens	40-44
10953059-8	2000	Mutations were found in the V2, V3, and V4 loop region of the envelope glycoprotein gp120 of the L-CA and D-CA-resistant NL4.3 strains that were not present in the wild-type NL4.3 strain.	Dichloroacetic Acid	106-110	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	84-89
15992085-4	1999	Dichloroacetate (DCA, Ceresine) is a small molecule that activates pyruvate dehydrogenase (PDH) and crosses the blood-brain barrier.	Dichloroacetic Acid	0-15	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	67-89
10774822-0	2000	Effect of trichloroethylene and its metabolites, dichloroacetic acid and trichloroacetic acid, on the methylation and expression of c-Jun and c-Myc protooncogenes in mouse liver: prevention by methionine.	Dichloroacetic Acid	49-68	jun proto-oncogene	Mus musculus	132-137
10774822-8	2000	Decreased methylation in the promoter regions of the c-jun and c-myc genes and increased levels of their mRNA and proteins were found in livers of mice exposed to TCE, DCA, and TCA.	Dichloroacetic Acid	168-171	jun proto-oncogene	Mus musculus	53-58
10449128-1	1999	OBJECTIVE: To determine whether dichloroacetate (DCA) treatment can increase pyruvate dehydrogenase (PDH) activity in PDH-deficient cell lines harboring pathogenic mutations in the PDH E1alpha gene.	Dichloroacetic Acid	32-47	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	77-99
10449128-1	1999	OBJECTIVE: To determine whether dichloroacetate (DCA) treatment can increase pyruvate dehydrogenase (PDH) activity in PDH-deficient cell lines harboring pathogenic mutations in the PDH E1alpha gene.	Dichloroacetic Acid	32-47	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	101-104
10449128-1	1999	OBJECTIVE: To determine whether dichloroacetate (DCA) treatment can increase pyruvate dehydrogenase (PDH) activity in PDH-deficient cell lines harboring pathogenic mutations in the PDH E1alpha gene.	Dichloroacetic Acid	32-47	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	118-121
10449128-1	1999	OBJECTIVE: To determine whether dichloroacetate (DCA) treatment can increase pyruvate dehydrogenase (PDH) activity in PDH-deficient cell lines harboring pathogenic mutations in the PDH E1alpha gene.	Dichloroacetic Acid	49-52	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	77-99
10449128-1	1999	OBJECTIVE: To determine whether dichloroacetate (DCA) treatment can increase pyruvate dehydrogenase (PDH) activity in PDH-deficient cell lines harboring pathogenic mutations in the PDH E1alpha gene.	Dichloroacetic Acid	49-52	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	101-104
10449128-1	1999	OBJECTIVE: To determine whether dichloroacetate (DCA) treatment can increase pyruvate dehydrogenase (PDH) activity in PDH-deficient cell lines harboring pathogenic mutations in the PDH E1alpha gene.	Dichloroacetic Acid	49-52	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	118-121
10449128-5	1999	The relative effects of DCA treatment on PDH-deficient cell lines with E1alpha mutations primarily affecting polypeptide stability or catalytic activity were determined and the mechanism of enhancement of residual PDH activity explored.	Dichloroacetic Acid	24-27	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	41-44
10449128-6	1999	METHODS: The effect of chronic 5-day DCA treatment on PDH activity was assessed in PDH-deficient cell lines containing the R378H, R141Q, K387(FS), and R302C E1alpha mutations.	Dichloroacetic Acid	37-40	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	54-57
10449128-8	1999	RESULTS: Chronic DCA treatment resulted in 25% (p = 0.0434), 31% (p = 0.0014) increases in PDH activity in the K387(FS) and R378H cell lines, both of which are associated with decreased mutant polypeptide stability.	Dichloroacetic Acid	17-20	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	91-94
10449128-11	1999	CONCLUSIONS: Chronic DCA treatment can increase PDH activity in PDH-deficient cell lines harboring mutations that affect E1alpha stability, suggesting a biochemical criterion by which DCA-responsive patients might be selected.	Dichloroacetic Acid	21-24	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	48-51
10449128-11	1999	CONCLUSIONS: Chronic DCA treatment can increase PDH activity in PDH-deficient cell lines harboring mutations that affect E1alpha stability, suggesting a biochemical criterion by which DCA-responsive patients might be selected.	Dichloroacetic Acid	184-187	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	48-51
10377737-2	1999	The use of DCA 2000 device (Bayer) resulted in immediate (< 6 min) HbA1c values.	Dichloroacetic Acid	11-14	hemoglobin subunit alpha 1	Homo sapiens	70-74
10775321-7	2000	The k(inact) values for the dichloroacetate-induced inactivation of four polymorphic variants of recombinant human glutathione transferase zeta (hGSTZ1-1) were in the following order: variant 1a-1a < 1b-1b approximately 1c-1c approximately 1d-1d.	Dichloroacetic Acid	28-43	glutathione S-transferase zeta 1	Homo sapiens	145-153
10775321-8	2000	The dichloroacetate-induced inactivation of hGSTZ1-1 was irreversible.	Dichloroacetic Acid	4-19	glutathione S-transferase zeta 1	Homo sapiens	44-52
10581215-6	1999	A decreased sensitivity of human PPARalpha compared to mouse PPARalpha to trans-activation was observed with some (Wy-14, 643, PFOA), but not other, peroxisome proliferators (TCE metabolites, trichloroacetate and dichloroacetate; and DEHP metabolites, mono[2-ethylhexyl]phthalate and 2-ethylhexanoic acid).	Dichloroacetic Acid	213-228	peroxisome proliferator activated receptor alpha	Homo sapiens	33-42
10535746-6	1999	Although treatment with TFEC did not inhibit intrinsic pyruvate dehydrogenase complex (PDHC) activity, it inhibited dichloroacetate/Mg2+-mediated activation/dephosphorylation of PDHC in the PC12 cells by 90%.	Dichloroacetic Acid	116-131	transcription factor EC	Rattus norvegicus	24-28
10562618-4	1999	Resting PDH-a with DCA was increased significantly over AC and Con trials (3.58 +/- 0.4 vs. 0.52 +/- 0.1 and 0.74 +/- 0.1 mmol.	Dichloroacetic Acid	19-22	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	8-11
10409123-3	1999	DCA infusion increased pyruvate dehydrogenase (PDH) activation at rest (4.0 +/- 0.3 vs. 0.9 +/- 0.1 mmol.	Dichloroacetic Acid	0-3	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	23-45
10409123-3	1999	DCA infusion increased pyruvate dehydrogenase (PDH) activation at rest (4.0 +/- 0.3 vs. 0.9 +/- 0.1 mmol.	Dichloroacetic Acid	0-3	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	47-50
10409125-0	1999	PDH activation by dichloroacetate reduces TCA cycle intermediates at rest but not during exercise in humans.	Dichloroacetic Acid	18-33	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	0-3
10409125-1	1999	We hypothesized that dichloroacetate (DCA), which stimulates the pyruvate dehydrogenase complex (PDH), would attenuate the increase in muscle tricarboxylic acid cycle intermediates (TCAI) during exercise by increasing the oxidative disposal of pyruvate and attenuating the flux through anaplerotic pathways.	Dichloroacetic Acid	21-36	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	97-100
10409125-1	1999	We hypothesized that dichloroacetate (DCA), which stimulates the pyruvate dehydrogenase complex (PDH), would attenuate the increase in muscle tricarboxylic acid cycle intermediates (TCAI) during exercise by increasing the oxidative disposal of pyruvate and attenuating the flux through anaplerotic pathways.	Dichloroacetic Acid	38-41	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	97-100
10409125-3	1999	Resting active fraction of PDH (PDH(a)) was markedly increased (P </= 0.05) after DCA vs. Con (2.65 +/- 0.27 vs. 0.64 +/- 0.07 mmol.	Dichloroacetic Acid	85-88	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	27-30
10409125-3	1999	Resting active fraction of PDH (PDH(a)) was markedly increased (P </= 0.05) after DCA vs. Con (2.65 +/- 0.27 vs. 0.64 +/- 0.07 mmol.	Dichloroacetic Acid	85-88	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	32-38
10409125-11	1999	We conclude that DCA reduced TCAI pool size at rest by increasing the flux through PDH and diverting pyruvate away from anaplerotic pathways.	Dichloroacetic Acid	17-20	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	83-86
15992085-4	1999	Dichloroacetate (DCA, Ceresine) is a small molecule that activates pyruvate dehydrogenase (PDH) and crosses the blood-brain barrier.	Dichloroacetic Acid	0-15	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	91-94
15992085-4	1999	Dichloroacetate (DCA, Ceresine) is a small molecule that activates pyruvate dehydrogenase (PDH) and crosses the blood-brain barrier.	Dichloroacetic Acid	17-20	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	67-89
15992085-4	1999	Dichloroacetate (DCA, Ceresine) is a small molecule that activates pyruvate dehydrogenase (PDH) and crosses the blood-brain barrier.	Dichloroacetic Acid	17-20	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	91-94
9405293-8	1998	Apparent Ki values of the isoenzymes for the synthetic analogue of pyruvate, dichloroacetate, varied 40-fold, from 0.2 mM for PDK2 to 8 mM for PDK3.	Dichloroacetic Acid	77-92	pyruvate dehydrogenase kinase 2	Homo sapiens	126-130
9653059-6	1998	This corresponds to the differences in c-Jun immunoreactivity reported in tumors induced by DCA and TCA.	Dichloroacetic Acid	92-95	jun proto-oncogene	Mus musculus	39-44
9710955-8	1998	In animals exposed to either DCA or TCA for 11 days but not 44 weeks, the level of 5MeC in DNA was decreased in the liver.	Dichloroacetic Acid	29-32	chemokine (C-C motif) ligand 28	Mus musculus	84-87
9710955-11	1998	Termination of exposure to DCA, but not to TCA, resulted in an increase in the level of 5MeC in adenomas to the level found in noninvolved liver.	Dichloroacetic Acid	27-30	chemokine (C-C motif) ligand 28	Mus musculus	89-92
9530159-0	1998	Hepatic pyruvate dehydrogenase activity in humans: effect of cirrhosis, transplantation, and dichloroacetate.	Dichloroacetic Acid	93-108	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	8-30
9530159-8	1998	DCA increased PDHa in cirrhotic liver to 22.3 +/- 4.1 nmol.g wet wt-1.min-1 (P < 0.05 vs. no DCA) without altering PDHt.	Dichloroacetic Acid	0-3	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	14-18
9530159-10	1998	We conclude that decreased hepatic PDH activity secondary to decreased content may underlie lactic acidosis during OLT, which can be partially compensated by DCA administration.	Dichloroacetic Acid	158-161	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	35-38
9514176-1	1998	The effects of dichloroacetate (DCA) on fatty acid oxidation and flux through pyruvate dehydrogenase (PDH) were studied in ischemic, reperfused myocardium supplied with glucose, long-chain fatty acids, lactate, pyruvate, and acetoacetate.	Dichloroacetic Acid	15-30	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	78-100
9514176-1	1998	The effects of dichloroacetate (DCA) on fatty acid oxidation and flux through pyruvate dehydrogenase (PDH) were studied in ischemic, reperfused myocardium supplied with glucose, long-chain fatty acids, lactate, pyruvate, and acetoacetate.	Dichloroacetic Acid	32-35	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	78-100
9514176-3	1998	In nonischemic control hearts, DCA increased PDH flux more than eightfold (from 0.68 +/- 0.28 to 5.81 +/- 1.16 micromol/min/g dry weight; n = 8 each group; p < 0.05) and significantly inhibited the oxidation of acetoacetate and fatty acids.	Dichloroacetic Acid	31-34	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	45-48
9818855-0	1998	Stabilization of the pyruvate dehydrogenase E1alpha subunit by dichloroacetate.	Dichloroacetic Acid	63-78	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	21-43
9818855-1	1998	OBJECTIVE: To test the effects of dichloroacetate (DCA) treatment on the rate of turnover of pyruvate dehydrogenase (PDH) subunits.	Dichloroacetic Acid	34-49	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	117-120
9818855-1	1998	OBJECTIVE: To test the effects of dichloroacetate (DCA) treatment on the rate of turnover of pyruvate dehydrogenase (PDH) subunits.	Dichloroacetic Acid	51-54	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	117-120
9818855-6	1998	METHODS: PDH subunit turnover rates were measured using pulse-chase methods in a normal fibroblastic cell line before and after chronic (5-day) treatment with 5 mM DCA.	Dichloroacetic Acid	164-167	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	9-12
9818855-7	1998	RESULTS: Chronic DCA treatment causes a more than twofold decrease in the apparent first-order rate constant for degradation of the PDH E1alpha subunit (kE1alpha(pre-DCA) = 0.025 +/- 0.006 hr(-1), n = 6; kE1alpha(post-DCA) = 0.011 /- 0.002 hr(-1), n = 3; p < 0.01) and a selective, progressive increase in the total cell PDH activity by 150 +/- 5% (p < 0.0005).	Dichloroacetic Acid	17-20	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	132-135
9818855-7	1998	RESULTS: Chronic DCA treatment causes a more than twofold decrease in the apparent first-order rate constant for degradation of the PDH E1alpha subunit (kE1alpha(pre-DCA) = 0.025 +/- 0.006 hr(-1), n = 6; kE1alpha(post-DCA) = 0.011 /- 0.002 hr(-1), n = 3; p < 0.01) and a selective, progressive increase in the total cell PDH activity by 150 +/- 5% (p < 0.0005).	Dichloroacetic Acid	17-20	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	324-327
9818855-7	1998	RESULTS: Chronic DCA treatment causes a more than twofold decrease in the apparent first-order rate constant for degradation of the PDH E1alpha subunit (kE1alpha(pre-DCA) = 0.025 +/- 0.006 hr(-1), n = 6; kE1alpha(post-DCA) = 0.011 /- 0.002 hr(-1), n = 3; p < 0.01) and a selective, progressive increase in the total cell PDH activity by 150 +/- 5% (p < 0.0005).	Dichloroacetic Acid	166-169	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	132-135
9818855-7	1998	RESULTS: Chronic DCA treatment causes a more than twofold decrease in the apparent first-order rate constant for degradation of the PDH E1alpha subunit (kE1alpha(pre-DCA) = 0.025 +/- 0.006 hr(-1), n = 6; kE1alpha(post-DCA) = 0.011 /- 0.002 hr(-1), n = 3; p < 0.01) and a selective, progressive increase in the total cell PDH activity by 150 +/- 5% (p < 0.0005).	Dichloroacetic Acid	166-169	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	132-135
9818855-8	1998	CONCLUSION: These results suggest an additional novel mechanism of action for the chronic DCA treatment of lactic acidemia; namely, inhibition of mitochondrial E1alpha subunit degradation leading to an increase in maximal PDH complex activity.	Dichloroacetic Acid	90-93	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	222-225
9703482-5	1998	Transient transfection studies have demonstrated that the TCE metabolites trichloroacetate and dichloroacetate both activate PPAR alpha, a major liver-expressed receptor isoform.	Dichloroacetic Acid	95-110	peroxisome proliferator activated receptor alpha	Mus musculus	125-135
9405293-8	1998	Apparent Ki values of the isoenzymes for the synthetic analogue of pyruvate, dichloroacetate, varied 40-fold, from 0.2 mM for PDK2 to 8 mM for PDK3.	Dichloroacetic Acid	77-92	pyruvate dehydrogenase kinase 3	Homo sapiens	143-147
9736484-10	1998	Peroxisomal bifunctional enzyme protein levels also increased in a concentration-dependent manner in both rat and mouse hepatocytes in response to dichloroacetate exposure.	Dichloroacetic Acid	147-162	enoyl-CoA hydratase and 3-hydroxyacyl CoA dehydrogenase	Rattus norvegicus	0-31
9395208-0	1997	Assessment of the mutagenicity of dichloroacetic acid in lacI transgenic B6C3F1 mouse liver.	Dichloroacetic Acid	34-53	tissue factor pathway inhibitor	Mus musculus	57-61
9395208-4	1997	DCA was administered continuously at either 1.0 or 3.5 g/l in drinking water to male transgenic B6C3F1 mice harboring the bacterial lacI gene.	Dichloroacetic Acid	0-3	tissue factor pathway inhibitor	Mus musculus	132-136
9395208-12	1997	This is consistent with the previous observation that the proportion of mutations at T:A sites in codon 61 of the H-ras gene was increased in DCA-induced liver tumors in B6C3F1 mice.	Dichloroacetic Acid	142-145	Harvey rat sarcoma virus oncogene	Mus musculus	114-119
9322450-1	1997	UNLABELLED: Dichloroacetate (DCA) stimulates pyruvate dehydrogenase (PDH), accelerating recovery of the postischemic heart.	Dichloroacetic Acid	12-27	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	45-67
9450646-6	1997	Addition of the PDH activator dichloracetate (0.01 M) resulted in complete restoration of PDH activity but not of mitochondrial function.	Dichloroacetic Acid	30-44	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	16-19
9450646-6	1997	Addition of the PDH activator dichloracetate (0.01 M) resulted in complete restoration of PDH activity but not of mitochondrial function.	Dichloroacetic Acid	30-44	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	90-93
9276648-0	1997	Dichloroacetic acid reduces Ha-ras codon 61 mutations in liver tumors from female B6C3F1 mice.	Dichloroacetic Acid	0-19	Harvey rat sarcoma virus oncogene	Mus musculus	28-34
9322450-1	1997	UNLABELLED: Dichloroacetate (DCA) stimulates pyruvate dehydrogenase (PDH), accelerating recovery of the postischemic heart.	Dichloroacetic Acid	12-27	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	69-72
9322450-1	1997	UNLABELLED: Dichloroacetate (DCA) stimulates pyruvate dehydrogenase (PDH), accelerating recovery of the postischemic heart.	Dichloroacetic Acid	29-32	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	45-67
9322450-1	1997	UNLABELLED: Dichloroacetate (DCA) stimulates pyruvate dehydrogenase (PDH), accelerating recovery of the postischemic heart.	Dichloroacetic Acid	29-32	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	69-72
9322450-2	1997	Because DCA also stimulates hepatic PDH, it may facilitate graft recovery during liver transplantation (OLT).	Dichloroacetic Acid	8-11	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	36-39
9322450-15	1997	IMPLICATIONS: We evaluated whether dichloroacetate, which stimulates pyruvate dehydrogenase, can accelerate recovery of graft liver hepatic function during liver transplantation, as indexed by oxygen consumption.	Dichloroacetic Acid	35-50	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	69-91
9154923-0	1997	Effect of nuclear protein HMG1 on in vitro slippage synthesis of the tandem repeat dTG x dCA.	Dichloroacetic Acid	89-92	high mobility group box 1	Rattus norvegicus	26-30
9194407-9	1997	DCA-induced lesions were found to display immunoreactivity to anti-c-Jun and anti-c-Fos antibodies, were predominantly basophilic, and contained very little glycogen relative to surrounding hepatocytes.	Dichloroacetic Acid	0-3	jun proto-oncogene	Mus musculus	67-72
9194407-9	1997	DCA-induced lesions were found to display immunoreactivity to anti-c-Jun and anti-c-Fos antibodies, were predominantly basophilic, and contained very little glycogen relative to surrounding hepatocytes.	Dichloroacetic Acid	0-3	FBJ osteosarcoma oncogene	Mus musculus	82-87
9154923-3	1997	We show here that HMG1 (modeled by the second HMG box motif from HMG1 of the rat, HMGb) binds to complexes formed from annealing unequal lengths of dTG x dCA and inhibits the in vitro elongation of these complexes by the Klenow fragment of DNA polymerase I at 37 degrees C. At 46 degrees C, HMGb enhances the elongation.	Dichloroacetic Acid	154-157	high mobility group box 1	Rattus norvegicus	18-22
9154923-3	1997	We show here that HMG1 (modeled by the second HMG box motif from HMG1 of the rat, HMGb) binds to complexes formed from annealing unequal lengths of dTG x dCA and inhibits the in vitro elongation of these complexes by the Klenow fragment of DNA polymerase I at 37 degrees C. At 46 degrees C, HMGb enhances the elongation.	Dichloroacetic Acid	154-157	high mobility group box 1	Rattus norvegicus	65-69
8638839-9	1996	DCA clearance was 0.997, 0.0, and 1.69 ml x kg(-1) x min(-1) during the paleohepatic, anhepatic, and neohepatic periods, respectively (P < 0.05).	Dichloroacetic Acid	0-3	CD59 molecule (CD59 blood group)	Homo sapiens	53-59
9070354-2	1997	Cytochrome P450 (CYP)-dependent metabolism of TRI produces chloral hydrate (CH) and is rate limiting in the ultimate production of trichloro- and/or dichloroacetic acid from TRI.	Dichloroacetic Acid	149-168	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
9070354-2	1997	Cytochrome P450 (CYP)-dependent metabolism of TRI produces chloral hydrate (CH) and is rate limiting in the ultimate production of trichloro- and/or dichloroacetic acid from TRI.	Dichloroacetic Acid	149-168	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	17-20
8975762-0	1996	Dichloroacetic acid treatment increases hepatic CYP2E1 in male and female rats.	Dichloroacetic Acid	0-19	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	48-54
8975762-9	1996	The results support the hypothesis that DCA increases CHCl3 metabolism, and therefore hepatotoxicity, by inducing CYP2E1.	Dichloroacetic Acid	40-43	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	114-120
8612405-14	1996	Dichloroacetate reversed the impairment of insulin-stimulated myocardial glucose uptake in septic rats, but did not influence skeletal muscle glucose uptake either under basal conditions or during insulin stimulation.	Dichloroacetic Acid	0-15	insulin	Homo sapiens	43-50
18623591-1	1996	We have studied the effect of the pyruvate dehydrogenase (PDH) activator, dichloroacetate (DCA), on the growth, metabolism, and productivity of the PQXB (1/2) hybridoma cell line.	Dichloroacetic Acid	74-89	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	34-56
18623591-1	1996	We have studied the effect of the pyruvate dehydrogenase (PDH) activator, dichloroacetate (DCA), on the growth, metabolism, and productivity of the PQXB (1/2) hybridoma cell line.	Dichloroacetic Acid	74-89	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	58-61
18623591-1	1996	We have studied the effect of the pyruvate dehydrogenase (PDH) activator, dichloroacetate (DCA), on the growth, metabolism, and productivity of the PQXB (1/2) hybridoma cell line.	Dichloroacetic Acid	91-94	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	34-56
18623591-1	1996	We have studied the effect of the pyruvate dehydrogenase (PDH) activator, dichloroacetate (DCA), on the growth, metabolism, and productivity of the PQXB (1/2) hybridoma cell line.	Dichloroacetic Acid	91-94	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	58-61
8616822-7	1996	Primary cultures of hepatocytes isolated from control and DCA treated mice exhibited similarly enhanced DNA synthesis in response to eGF, HGF, or aFGF alone or in combination with TGF-beta 1.	Dichloroacetic Acid	58-61	epidermal growth factor	Mus musculus	133-136
8616822-7	1996	Primary cultures of hepatocytes isolated from control and DCA treated mice exhibited similarly enhanced DNA synthesis in response to eGF, HGF, or aFGF alone or in combination with TGF-beta 1.	Dichloroacetic Acid	58-61	hepatocyte growth factor	Mus musculus	138-141
8616822-7	1996	Primary cultures of hepatocytes isolated from control and DCA treated mice exhibited similarly enhanced DNA synthesis in response to eGF, HGF, or aFGF alone or in combination with TGF-beta 1.	Dichloroacetic Acid	58-61	fibroblast growth factor 1	Mus musculus	146-150
8616822-7	1996	Primary cultures of hepatocytes isolated from control and DCA treated mice exhibited similarly enhanced DNA synthesis in response to eGF, HGF, or aFGF alone or in combination with TGF-beta 1.	Dichloroacetic Acid	58-61	transforming growth factor, beta 1	Mus musculus	180-190
8557697-11	1996	In contrast, the hepatocyte carrier had lower Km values than MCT1 for glycolate, chloroacetate, dichloroacetate, and 2-hydroxy-2-methylpropionate.	Dichloroacetic Acid	96-111	solute carrier family 16 member 1	Rattus norvegicus	61-65
8652022-0	1996	Leigh disease with deficiency of lipoamide dehydrogenase: treatment failure with dichloroacetate.	Dichloroacetic Acid	81-96	dihydrolipoamide dehydrogenase	Homo sapiens	33-56
7955063-3	1994	The mutation spectra of H-ras codon 61 mutations showed a significant decrease in AAA and increase in CTA mutations for dichloroacetic acid- and trichloroethylene-induced tumors when compared to combined controls.	Dichloroacetic Acid	120-139	Harvey rat sarcoma virus oncogene	Mus musculus	24-29
8685026-3	1996	The HbA1c normal range, determined by DCA 2000 and by laboratory method, were 4-5.2% and 4.5-6% respectively.	Dichloroacetic Acid	38-41	hemoglobin subunit alpha 1	Homo sapiens	4-8
7955063-8	1994	These findings suggest that exposure to dichloroacetic acid, trichloroethylene and tetrachloroethylene provides a selective growth advantage to spontaneously occurring mutations in codon 61 of H-ras and, at the same time, is responsible for a small number of unique molecular lesions suggestive of either a random genotoxic mode of action or a non-specific result of secondary DNA damage.	Dichloroacetic Acid	40-59	Harvey rat sarcoma virus oncogene	Mus musculus	193-198
1356994-4	1992	Postischemic DCA treatment also reduced brain lactate and increased pHi during reperfusion compared with controls (p < 0.05), but had little effect on PCr, ATP, or Pi during reperfusion.	Dichloroacetic Acid	13-16	glucose-6-phosphate isomerase	Rattus norvegicus	68-71
1356994-3	1992	Preischemic treatment with DCA did not affect brain lactate or pHi during ischemia, but reduced lactate and increased pHi after 30 min of reperfusion (p < 0.05 vs. controls) and facilitated the recovery of PCr and ATP during reperfusion.	Dichloroacetic Acid	27-30	glucose-6-phosphate isomerase	Rattus norvegicus	118-121
10155068-2	1994	Further investigation is suggested and warranted and use of DCA may aid in management of cardiogenic shock patients.	Dichloroacetic Acid	60-63	activation induced cytidine deaminase	Homo sapiens	68-71
8142598-3	1993	Furthermore, maximal stimulation of pyruvate dehydrogenase (PDH) by dichloroacetate (DCA) treatment in conjunction with cachectin/TNF abolished lactate production, but increased glucose uptake persisted.	Dichloroacetic Acid	68-83	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	36-58
8142598-3	1993	Furthermore, maximal stimulation of pyruvate dehydrogenase (PDH) by dichloroacetate (DCA) treatment in conjunction with cachectin/TNF abolished lactate production, but increased glucose uptake persisted.	Dichloroacetic Acid	68-83	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	60-63
8142598-3	1993	Furthermore, maximal stimulation of pyruvate dehydrogenase (PDH) by dichloroacetate (DCA) treatment in conjunction with cachectin/TNF abolished lactate production, but increased glucose uptake persisted.	Dichloroacetic Acid	85-88	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	36-58
8142598-3	1993	Furthermore, maximal stimulation of pyruvate dehydrogenase (PDH) by dichloroacetate (DCA) treatment in conjunction with cachectin/TNF abolished lactate production, but increased glucose uptake persisted.	Dichloroacetic Acid	85-88	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	60-63
1600837-4	1992	Stimulation of PDH by DCA increases peripheral oxidation of alanine and lactate, thereby interrupting the Cori and alanine cycles and reducing the availability of three-carbon precursors for gluconeogenesis.	Dichloroacetic Acid	22-25	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	15-18
1600837-8	1992	In genetic models of insulin-dependent diabetes, oral administration of DCA significantly reduces insulin requirements and blood levels of glucose and triglycerides.	Dichloroacetic Acid	72-75	insulin	Homo sapiens	21-28
2219132-0	1990	Increased expression of c-myc and c-Ha-ras in dichloroacetate and trichloroacetate-induced liver tumors in B6C3F1 mice.	Dichloroacetic Acid	46-61	myelocytomatosis oncogene	Mus musculus	26-29
1590531-4	1992	We measured native and dichloroacetate (DCA)-activated pyruvate dehydrogenase (PDH) complex activities in two patients (#1 and 2) using cultured lymphoblastoid cell lines which were transformed by EB virus and the results were normal.	Dichloroacetic Acid	23-38	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	55-77
1590531-4	1992	We measured native and dichloroacetate (DCA)-activated pyruvate dehydrogenase (PDH) complex activities in two patients (#1 and 2) using cultured lymphoblastoid cell lines which were transformed by EB virus and the results were normal.	Dichloroacetic Acid	23-38	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	79-82
1590531-4	1992	We measured native and dichloroacetate (DCA)-activated pyruvate dehydrogenase (PDH) complex activities in two patients (#1 and 2) using cultured lymphoblastoid cell lines which were transformed by EB virus and the results were normal.	Dichloroacetic Acid	40-43	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	55-77
1590531-4	1992	We measured native and dichloroacetate (DCA)-activated pyruvate dehydrogenase (PDH) complex activities in two patients (#1 and 2) using cultured lymphoblastoid cell lines which were transformed by EB virus and the results were normal.	Dichloroacetic Acid	40-43	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	79-82
1878534-6	1991	The mean renal clearance of DCA was 42.9 ml h-1.	Dichloroacetic Acid	28-31	H1.5 linker histone, cluster member	Homo sapiens	44-47
2219132-0	1990	Increased expression of c-myc and c-Ha-ras in dichloroacetate and trichloroacetate-induced liver tumors in B6C3F1 mice.	Dichloroacetic Acid	46-61	Harvey rat sarcoma virus oncogene	Mus musculus	34-42
2219132-3	1990	Myc expression was similar in hyperplastic nodules and carcinomas induced by DCA, but was significantly higher in TCA-induced carcinomas than in hyperplastic nodules and carcinomas produced by DCA.	Dichloroacetic Acid	77-80	myelocytomatosis oncogene	Mus musculus	0-3
2219132-3	1990	Myc expression was similar in hyperplastic nodules and carcinomas induced by DCA, but was significantly higher in TCA-induced carcinomas than in hyperplastic nodules and carcinomas produced by DCA.	Dichloroacetic Acid	193-196	myelocytomatosis oncogene	Mus musculus	0-3
2318357-10	1990	At the 1.1 g/kg dose, however, DCA markedly increased the frequency and severity of toxicity and decreased transketolase activity 25%, compared to controls.	Dichloroacetic Acid	31-34	transketolase	Rattus norvegicus	107-120
2318357-12	1990	Inhibition of transketolase by DCA in vivo was not due to a direct action on the enzyme, however, since DCA, glyoxylate, or oxalate had no appreciable effects on transketolase activity in vitro.	Dichloroacetic Acid	31-34	transketolase	Rattus norvegicus	14-27
2318357-15	1990	We conclude that stimulation by DCA of thiamine-requiring enzymes may lead to depletion of total body thiamine stores and to both a fall in transketolase activity and an increase in oxalate accumulation in vivo.	Dichloroacetic Acid	32-35	transketolase	Rattus norvegicus	140-153
33811107-5	2020	Sustained administration of DCA to the mother over 72h decreased the hepatic expression of the DCA-metabolizing enzyme GSTZ1 in the fetuses exposed to the drug, leading to higher fetal plasma DCA concentrations during continued dosing, and reduced plasma lactate levels.	Dichloroacetic Acid	28-31	maleylacetoacetate isomerase	Ovis aries	119-124
33973079-10	2021	DCA demonstrated that the nomogram was higher than the TNM staging system and the TNM staging system combined with PG-SGA.	Dichloroacetic Acid	0-3	teneurin transmembrane protein 1	Homo sapiens	55-58
33812409-4	2021	The cells in DCA high dose group were treated by TRAIL 0.5 mug/ml for 24 h, and were divided into DCA high dose + TRAIL group.	Dichloroacetic Acid	13-16	TNF superfamily member 10	Homo sapiens	49-54
33812409-10	2021	The relative expression of DR4 mRNA and protein in the control group, DCA low, medium and high dose groups was increased sequentially (r=0.624, 0.704).	Dichloroacetic Acid	70-73	TNF receptor superfamily member 10a	Homo sapiens	27-30
33812409-11	2021	The inhibition rate of cell proliferation of the cells in the control group, DCA high dose group, TRAIL group, DCA high dose + TRAIL group was increased sequentially (r=0.653, 0.754, 0.709, 0.725) at 24, 48 and 72 h. CONCLUSION: DCA can reverse the methylation level of DR4 gene promoter in ML K562 cells and up-regulate the expression of DR4, which may enhance the proliferation inhibition and apoptosis promotion effects of TRAIL on K562 cells.	Dichloroacetic Acid	111-114	TNF receptor superfamily member 10a	Homo sapiens	270-273
33812409-11	2021	The inhibition rate of cell proliferation of the cells in the control group, DCA high dose group, TRAIL group, DCA high dose + TRAIL group was increased sequentially (r=0.653, 0.754, 0.709, 0.725) at 24, 48 and 72 h. CONCLUSION: DCA can reverse the methylation level of DR4 gene promoter in ML K562 cells and up-regulate the expression of DR4, which may enhance the proliferation inhibition and apoptosis promotion effects of TRAIL on K562 cells.	Dichloroacetic Acid	111-114	TNF receptor superfamily member 10a	Homo sapiens	339-342
33812409-11	2021	The inhibition rate of cell proliferation of the cells in the control group, DCA high dose group, TRAIL group, DCA high dose + TRAIL group was increased sequentially (r=0.653, 0.754, 0.709, 0.725) at 24, 48 and 72 h. CONCLUSION: DCA can reverse the methylation level of DR4 gene promoter in ML K562 cells and up-regulate the expression of DR4, which may enhance the proliferation inhibition and apoptosis promotion effects of TRAIL on K562 cells.	Dichloroacetic Acid	111-114	TNF receptor superfamily member 10a	Homo sapiens	270-273
33812409-11	2021	The inhibition rate of cell proliferation of the cells in the control group, DCA high dose group, TRAIL group, DCA high dose + TRAIL group was increased sequentially (r=0.653, 0.754, 0.709, 0.725) at 24, 48 and 72 h. CONCLUSION: DCA can reverse the methylation level of DR4 gene promoter in ML K562 cells and up-regulate the expression of DR4, which may enhance the proliferation inhibition and apoptosis promotion effects of TRAIL on K562 cells.	Dichloroacetic Acid	111-114	TNF receptor superfamily member 10a	Homo sapiens	339-342
33811107-10	2020	Like other reported species, DCA mediated inhibition of GSTZ1 was also observed in ewes which resulted in the reduced metabolism of DCA after a prolonged administration.	Dichloroacetic Acid	29-32	maleylacetoacetate isomerase	Ovis aries	56-61
33811107-10	2020	Like other reported species, DCA mediated inhibition of GSTZ1 was also observed in ewes which resulted in the reduced metabolism of DCA after a prolonged administration.	Dichloroacetic Acid	132-135	maleylacetoacetate isomerase	Ovis aries	56-61
33811107-5	2020	Sustained administration of DCA to the mother over 72h decreased the hepatic expression of the DCA-metabolizing enzyme GSTZ1 in the fetuses exposed to the drug, leading to higher fetal plasma DCA concentrations during continued dosing, and reduced plasma lactate levels.	Dichloroacetic Acid	95-98	maleylacetoacetate isomerase	Ovis aries	119-124
34950023-6	2021	In addition, AngII-treated SD rats had an increased Warburg effect and ERS levels and enhanced atrial fibrosis progression to AF compared to wild-type SD rats, and these conditions were reversed by sodium hydrosulfide (NaHS), dichloroacetic acid (DCA) or 4-phenylbutyric acid (4-PBA) supplementation.	Dichloroacetic Acid	226-245	angiotensinogen	Rattus norvegicus	13-18
25016301-7	2014	The relative significance of lignin phenols as chlorination DBP precursors generally follows the order of TCAA > DCAA&chloroform.	Dichloroacetic Acid	116-120	D-box binding PAR bZIP transcription factor	Homo sapiens	60-63
25016301-8	2014	The relative significance of lignin phenols to DBP formation by chloramination follows the order: TCAA > DCAA&DCAN > chloroform.	Dichloroacetic Acid	108-112	D-box binding PAR bZIP transcription factor	Homo sapiens	47-50
34678088-8	2022	PI3K pathway inhibitor LY294002 or MEK pathway inhibitor U0126, or Warburg effect inhibitor DCA was used to carry out western blot and glucose metabolism experiments, and the results showed that PDGFBB/PDGFRbeta mainly activated the PI3K/AKT/mTOR/ c-Myc pathway to promote aerobic glycolysis in osteosarcoma HOS cells.	Dichloroacetic Acid	92-95	platelet derived growth factor receptor beta	Homo sapiens	202-211
34678088-8	2022	PI3K pathway inhibitor LY294002 or MEK pathway inhibitor U0126, or Warburg effect inhibitor DCA was used to carry out western blot and glucose metabolism experiments, and the results showed that PDGFBB/PDGFRbeta mainly activated the PI3K/AKT/mTOR/ c-Myc pathway to promote aerobic glycolysis in osteosarcoma HOS cells.	Dichloroacetic Acid	92-95	AKT serine/threonine kinase 1	Homo sapiens	238-241
34678088-8	2022	PI3K pathway inhibitor LY294002 or MEK pathway inhibitor U0126, or Warburg effect inhibitor DCA was used to carry out western blot and glucose metabolism experiments, and the results showed that PDGFBB/PDGFRbeta mainly activated the PI3K/AKT/mTOR/ c-Myc pathway to promote aerobic glycolysis in osteosarcoma HOS cells.	Dichloroacetic Acid	92-95	mechanistic target of rapamycin kinase	Homo sapiens	242-246
34678088-8	2022	PI3K pathway inhibitor LY294002 or MEK pathway inhibitor U0126, or Warburg effect inhibitor DCA was used to carry out western blot and glucose metabolism experiments, and the results showed that PDGFBB/PDGFRbeta mainly activated the PI3K/AKT/mTOR/ c-Myc pathway to promote aerobic glycolysis in osteosarcoma HOS cells.	Dichloroacetic Acid	92-95	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	248-253
34851727-7	2022	DCA increased mitochondrial activity, increasing oxidative phosphorylation (PCI, PCI+II)) per tissue weight or per unit of citrate synthase.	Dichloroacetic Acid	0-3	citrate synthase	Homo sapiens	123-139
34950023-6	2021	In addition, AngII-treated SD rats had an increased Warburg effect and ERS levels and enhanced atrial fibrosis progression to AF compared to wild-type SD rats, and these conditions were reversed by sodium hydrosulfide (NaHS), dichloroacetic acid (DCA) or 4-phenylbutyric acid (4-PBA) supplementation.	Dichloroacetic Acid	247-250	angiotensinogen	Rattus norvegicus	13-18
34950023-7	2021	Finally, low CSE levels in AngII-induced HL-1 cells were concentration- and time-dependent and associated with mitochondrial dysfunction, apoptosis, the Warburg effect and ERS, and these effects were reversed by NaHS, DCA or 4-PBA supplementation.	Dichloroacetic Acid	218-221	cystathionine gamma-lyase	Rattus norvegicus	13-16
34950023-7	2021	Finally, low CSE levels in AngII-induced HL-1 cells were concentration- and time-dependent and associated with mitochondrial dysfunction, apoptosis, the Warburg effect and ERS, and these effects were reversed by NaHS, DCA or 4-PBA supplementation.	Dichloroacetic Acid	218-221	angiotensinogen	Rattus norvegicus	27-32
34488935-7	2021	Leelamine, huzhangoside A and otobaphenol induced PDH activity-dependent apoptosis, whereas AZD7545, VER-246608 and DCA effectively enhanced PDHA1 activity but little toxic to cancer cells.	Dichloroacetic Acid	116-119	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	141-146
34595798-10	2021	There was a concominant decrease of TGF-beta and lactic acid levels with DCA treatment (p < 0.05).	Dichloroacetic Acid	73-76	transforming growth factor alpha	Rattus norvegicus	36-44
34595798-11	2021	DCA also improved ovarian reserve with higher AMH levels (p < 0.05).	Dichloroacetic Acid	0-3	anti-Mullerian hormone	Rattus norvegicus	46-49
34746589-4	2021	The results showed that compound 1b is the most active as PDK1 and LDHA inhibitor with IC50 values (mug/mL) of 57.10 and 64.10 compared to 25.75 and 15.60, which were produced by the standard inhibitors sodium dichloroacetate and sodium oxamate, respectively.	Dichloroacetic Acid	203-225	pyruvate dehydrogenase kinase 1	Homo sapiens	58-62
34787860-0	2021	Mitigation of doxorubicin-induced cardiotoxicity by dichloroacetate: potential roles of restoration of PGC-1alpha/SIRT3 signaling and suppression of oxidative stress and apoptosis.	Dichloroacetic Acid	52-67	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	103-113
34787860-0	2021	Mitigation of doxorubicin-induced cardiotoxicity by dichloroacetate: potential roles of restoration of PGC-1alpha/SIRT3 signaling and suppression of oxidative stress and apoptosis.	Dichloroacetic Acid	52-67	sirtuin 3	Mus musculus	114-119
34787860-8	2021	Additionally, histopathology and transmission electron microscopy revealed structural damage alleviation by DOX/DCA combination, which was confirmed biochemically via significant suppression of elevated CK-MB and AST levels.	Dichloroacetic Acid	112-115	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	213-216
34712383-0	2021	DCA Protects against Oxidation Injury Attributed to Cerebral Ischemia-Reperfusion by Regulating Glycolysis through PDK2-PDH-Nrf2 Axis.	Dichloroacetic Acid	0-3	pyruvate dehydrogenase kinase, isoenzyme 2	Mus musculus	115-119
34712383-0	2021	DCA Protects against Oxidation Injury Attributed to Cerebral Ischemia-Reperfusion by Regulating Glycolysis through PDK2-PDH-Nrf2 Axis.	Dichloroacetic Acid	0-3	nuclear factor, erythroid derived 2, like 2	Mus musculus	124-128
34787860-10	2021	Of note, co-treatment with DCA effectively restored PGC-1alpha/SIRT-3 signaling and normalized the mitochondrial DNA index.	Dichloroacetic Acid	27-30	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	52-62
34787860-10	2021	Of note, co-treatment with DCA effectively restored PGC-1alpha/SIRT-3 signaling and normalized the mitochondrial DNA index.	Dichloroacetic Acid	27-30	sirtuin 3	Mus musculus	63-69
34787860-11	2021	Moreover, events downstream of DOX-triggered mitochondrial dysfunction such as oxidative stress and p53-dependent apoptosis were all abrogated by combination with DCA.	Dichloroacetic Acid	163-166	transformation related protein 53, pseudogene	Mus musculus	100-103
34746589-4	2021	The results showed that compound 1b is the most active as PDK1 and LDHA inhibitor with IC50 values (mug/mL) of 57.10 and 64.10 compared to 25.75 and 15.60, which were produced by the standard inhibitors sodium dichloroacetate and sodium oxamate, respectively.	Dichloroacetic Acid	203-225	lactate dehydrogenase A	Homo sapiens	67-71
35462304-5	2022	Moreover, this design significantly downregulates CD39 and CD73 expression than DCA or MnFe2O4 alone, which consequently decreases the extracellular ATP catabolism.	Dichloroacetic Acid	80-83	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	50-54
34252986-6	2021	Furthermore, loss of PDK4 expression or treatment with the PDK4 inhibitor dichloroacetate was able to significantly increase rituximab-induced cell apoptosis in DLBCL cells.	Dichloroacetic Acid	74-89	pyruvate dehydrogenase kinase 4	Homo sapiens	21-25
34252986-6	2021	Furthermore, loss of PDK4 expression or treatment with the PDK4 inhibitor dichloroacetate was able to significantly increase rituximab-induced cell apoptosis in DLBCL cells.	Dichloroacetic Acid	74-89	pyruvate dehydrogenase kinase 4	Homo sapiens	59-63
34332981-0	2021	Dichloroacetate enhances the anti-tumor effect of sorafenib via modulating the ROS-JNK-Mcl-1 pathway in liver cancer cells.	Dichloroacetic Acid	0-15	mitogen-activated protein kinase 8	Homo sapiens	83-86
34332981-9	2021	Furthermore, we found that the ROS-JNK pathway was obviously activated in the DCA combined sorafenib group.	Dichloroacetic Acid	78-81	mitogen-activated protein kinase 8	Homo sapiens	35-38
34332981-11	2021	Antioxidant NAC could alleviate the synergetic effects of DCA and sorafenib on ROS generation, JNK activation, Mcl-1 degradation, and cell apoptosis.	Dichloroacetic Acid	58-61	synuclein alpha	Homo sapiens	12-15
34332981-11	2021	Antioxidant NAC could alleviate the synergetic effects of DCA and sorafenib on ROS generation, JNK activation, Mcl-1 degradation, and cell apoptosis.	Dichloroacetic Acid	58-61	mitogen-activated protein kinase 8	Homo sapiens	95-98
34332981-14	2021	These findings indicate that DCA enhances the anti-tumor effect of sorafenib via the ROS-JNK-Mcl-1 pathway in liver cancer cells.	Dichloroacetic Acid	29-32	mitogen-activated protein kinase 8	Homo sapiens	89-92
34124936-0	2021	The CDK8 inhibitor DCA promotes a tolerogenic chemical immunophenotype in CD4+ T cells via a novel CDK8-GATA3-FOXP3 pathway.	Dichloroacetic Acid	19-22	cyclin dependent kinase 8	Homo sapiens	4-8
34124936-0	2021	The CDK8 inhibitor DCA promotes a tolerogenic chemical immunophenotype in CD4+ T cells via a novel CDK8-GATA3-FOXP3 pathway.	Dichloroacetic Acid	19-22	CD4 molecule	Homo sapiens	74-77
34124936-0	2021	The CDK8 inhibitor DCA promotes a tolerogenic chemical immunophenotype in CD4+ T cells via a novel CDK8-GATA3-FOXP3 pathway.	Dichloroacetic Acid	19-22	cyclin dependent kinase 8	Homo sapiens	99-103
34124936-0	2021	The CDK8 inhibitor DCA promotes a tolerogenic chemical immunophenotype in CD4+ T cells via a novel CDK8-GATA3-FOXP3 pathway.	Dichloroacetic Acid	19-22	GATA binding protein 3	Homo sapiens	104-109
34124936-0	2021	The CDK8 inhibitor DCA promotes a tolerogenic chemical immunophenotype in CD4+ T cells via a novel CDK8-GATA3-FOXP3 pathway.	Dichloroacetic Acid	19-22	forkhead box P3	Homo sapiens	110-115
34124936-3	2021	The high-specificity, low-toxicity cyclin dependent kinase 8 (CDK8) inhibitor DCA exerts a distinct tolerogenic profile in both innate and adaptive immune cells.	Dichloroacetic Acid	78-81	cyclin dependent kinase 8	Homo sapiens	35-60
34124936-3	2021	The high-specificity, low-toxicity cyclin dependent kinase 8 (CDK8) inhibitor DCA exerts a distinct tolerogenic profile in both innate and adaptive immune cells.	Dichloroacetic Acid	78-81	cyclin dependent kinase 8	Homo sapiens	62-66
34124936-5	2021	This unique chemical immunophenotype led to mechanistic studies showing that DCA promotes Treg differentiation in part by regulating a previously undescribed CDK8-GATA3-FOXP3 pathway that regulates early pathways of Foxp3 expression.	Dichloroacetic Acid	77-80	cyclin dependent kinase 8	Homo sapiens	158-162
34124936-5	2021	This unique chemical immunophenotype led to mechanistic studies showing that DCA promotes Treg differentiation in part by regulating a previously undescribed CDK8-GATA3-FOXP3 pathway that regulates early pathways of Foxp3 expression.	Dichloroacetic Acid	77-80	GATA binding protein 3	Homo sapiens	163-168
34124936-5	2021	This unique chemical immunophenotype led to mechanistic studies showing that DCA promotes Treg differentiation in part by regulating a previously undescribed CDK8-GATA3-FOXP3 pathway that regulates early pathways of Foxp3 expression.	Dichloroacetic Acid	77-80	forkhead box P3	Homo sapiens	169-174
34124936-5	2021	This unique chemical immunophenotype led to mechanistic studies showing that DCA promotes Treg differentiation in part by regulating a previously undescribed CDK8-GATA3-FOXP3 pathway that regulates early pathways of Foxp3 expression.	Dichloroacetic Acid	77-80	forkhead box P3	Homo sapiens	216-221
35123968-10	2022	Based on NCS models, we observed U-shaped associations of urinary DCAA with serum PRGE and PRL; each ln-unit increment in urinary DCAA concentrations above 3.61 mug/L and 6.30 mug/L was associated with 18.9% (95% CI: 4.8%, 34.7%) and 23.3% (95% CI: -0.92%, 53.5%) increase in serum PRGE and PRL, respectively.	Dichloroacetic Acid	66-70	prolactin	Homo sapiens	91-94
35123968-10	2022	Based on NCS models, we observed U-shaped associations of urinary DCAA with serum PRGE and PRL; each ln-unit increment in urinary DCAA concentrations above 3.61 mug/L and 6.30 mug/L was associated with 18.9% (95% CI: 4.8%, 34.7%) and 23.3% (95% CI: -0.92%, 53.5%) increase in serum PRGE and PRL, respectively.	Dichloroacetic Acid	66-70	prolactin	Homo sapiens	291-294
35123968-10	2022	Based on NCS models, we observed U-shaped associations of urinary DCAA with serum PRGE and PRL; each ln-unit increment in urinary DCAA concentrations above 3.61 mug/L and 6.30 mug/L was associated with 18.9% (95% CI: 4.8%, 34.7%) and 23.3% (95% CI: -0.92%, 53.5%) increase in serum PRGE and PRL, respectively.	Dichloroacetic Acid	130-134	prolactin	Homo sapiens	91-94
35123968-10	2022	Based on NCS models, we observed U-shaped associations of urinary DCAA with serum PRGE and PRL; each ln-unit increment in urinary DCAA concentrations above 3.61 mug/L and 6.30 mug/L was associated with 18.9% (95% CI: 4.8%, 34.7%) and 23.3% (95% CI: -0.92%, 53.5%) increase in serum PRGE and PRL, respectively.	Dichloroacetic Acid	130-134	prolactin	Homo sapiens	291-294
34712383-7	2021	We investigated the mechanism by which DCA regulates glycolysis and protects the oxidative damage induced by I/R injury through the PDK2-PDH-Nrf2 axis.	Dichloroacetic Acid	39-42	pyruvate dehydrogenase kinase, isoenzyme 2	Mus musculus	132-136
34712383-7	2021	We investigated the mechanism by which DCA regulates glycolysis and protects the oxidative damage induced by I/R injury through the PDK2-PDH-Nrf2 axis.	Dichloroacetic Acid	39-42	nuclear factor, erythroid derived 2, like 2	Mus musculus	141-145
34712383-8	2021	As indicated from the results of this study, DCA may improve glycolysis, reduce oxidative stress and neuronal death, damage the blood-brain barrier, and promote the recovery of oxidative metabolism through inhibiting PDK2 and activating PDH.	Dichloroacetic Acid	45-48	pyruvate dehydrogenase kinase, isoenzyme 2	Mus musculus	217-221
34712383-10	2021	Moreover, as suggested from the results, DCA elevated the content of Nrf2 as well as HO-1, i.e., the downstream antioxidant proteins pertaining to Nrf2, while decreasing the damage of BBB and the degradation of tight junction proteins.	Dichloroacetic Acid	41-44	nuclear factor, erythroid derived 2, like 2	Mus musculus	69-73
34712383-10	2021	Moreover, as suggested from the results, DCA elevated the content of Nrf2 as well as HO-1, i.e., the downstream antioxidant proteins pertaining to Nrf2, while decreasing the damage of BBB and the degradation of tight junction proteins.	Dichloroacetic Acid	41-44	heme oxygenase 1	Mus musculus	85-89
34712383-10	2021	Moreover, as suggested from the results, DCA elevated the content of Nrf2 as well as HO-1, i.e., the downstream antioxidant proteins pertaining to Nrf2, while decreasing the damage of BBB and the degradation of tight junction proteins.	Dichloroacetic Acid	41-44	nuclear factor, erythroid derived 2, like 2	Mus musculus	147-151
34712383-15	2021	To sum up, as revealed from the mentioned results, DCA could exert the neuroprotective effect on oxidative stress and blood-brain barrier after brain I/R injury via PDK2-PDH-Nrf2 pathway activation.	Dichloroacetic Acid	51-54	pyruvate dehydrogenase kinase, isoenzyme 2	Mus musculus	165-169
34712383-15	2021	To sum up, as revealed from the mentioned results, DCA could exert the neuroprotective effect on oxidative stress and blood-brain barrier after brain I/R injury via PDK2-PDH-Nrf2 pathway activation.	Dichloroacetic Acid	51-54	nuclear factor, erythroid derived 2, like 2	Mus musculus	174-178
34712383-16	2021	Accordingly, the PDK2-PDH-Nrf2 pathway may play a key role and provide a new pharmacology target in cerebral IS and I/R protection by DCA.	Dichloroacetic Acid	134-137	pyruvate dehydrogenase kinase, isoenzyme 2	Mus musculus	17-21
34712383-16	2021	Accordingly, the PDK2-PDH-Nrf2 pathway may play a key role and provide a new pharmacology target in cerebral IS and I/R protection by DCA.	Dichloroacetic Acid	134-137	nuclear factor, erythroid derived 2, like 2	Mus musculus	26-30
34685598-9	2021	Primary HSC upregulated the NLRP3 inflammasome and early fibrotic markers when stimulated with DCA, but not LCA.	Dichloroacetic Acid	95-98	NLR family, pyrin domain containing 3	Mus musculus	28-33
34576192-11	2021	Metformin and DCA inhibited mTOR complex I signaling through upregulated AMPK-independent REDD1.	Dichloroacetic Acid	14-17	mechanistic target of rapamycin kinase	Homo sapiens	28-32
34576192-11	2021	Metformin and DCA inhibited mTOR complex I signaling through upregulated AMPK-independent REDD1.	Dichloroacetic Acid	14-17	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	73-77
34576192-11	2021	Metformin and DCA inhibited mTOR complex I signaling through upregulated AMPK-independent REDD1.	Dichloroacetic Acid	14-17	DNA damage inducible transcript 4	Homo sapiens	90-95
34445316-5	2021	The DCA-induced PDK1 suppression was partially dependent on hypoxia-inducible factor-1alpha (HIF-1alpha), a transcriptional regulator of PDK1, in cancer cells but not in L6 myotubes.	Dichloroacetic Acid	4-7	pyruvate dehydrogenase kinase 1	Homo sapiens	16-20
34445316-5	2021	The DCA-induced PDK1 suppression was partially dependent on hypoxia-inducible factor-1alpha (HIF-1alpha), a transcriptional regulator of PDK1, in cancer cells but not in L6 myotubes.	Dichloroacetic Acid	4-7	hypoxia inducible factor 1 subunit alpha	Homo sapiens	60-91
34445316-5	2021	The DCA-induced PDK1 suppression was partially dependent on hypoxia-inducible factor-1alpha (HIF-1alpha), a transcriptional regulator of PDK1, in cancer cells but not in L6 myotubes.	Dichloroacetic Acid	4-7	hypoxia inducible factor 1 subunit alpha	Homo sapiens	93-103
34445316-5	2021	The DCA-induced PDK1 suppression was partially dependent on hypoxia-inducible factor-1alpha (HIF-1alpha), a transcriptional regulator of PDK1, in cancer cells but not in L6 myotubes.	Dichloroacetic Acid	4-7	pyruvate dehydrogenase kinase 1	Homo sapiens	137-141
34445316-6	2021	However, the DCA-induced alterations in the mRNA and the protein levels of PDK1 and/or PDK2 did not always occur in parallel, implicating a role for post-transcriptional mechanisms.	Dichloroacetic Acid	13-16	pyruvate dehydrogenase kinase 1	Homo sapiens	75-79
34445316-6	2021	However, the DCA-induced alterations in the mRNA and the protein levels of PDK1 and/or PDK2 did not always occur in parallel, implicating a role for post-transcriptional mechanisms.	Dichloroacetic Acid	13-16	pyruvate dehydrogenase kinase 2	Homo sapiens	87-91
34364387-8	2021	Moreover, 3Br-P + DCA significantly induced apoptosis and necrosis, activation of caspase 3 activity, depolarize the mitochondrial membrane potential, and ROS production.	Dichloroacetic Acid	18-21	caspase 3	Homo sapiens	82-91
34364387-9	2021	At a molecular level, 3Br-P + DCA treatment remarkably down-regulated the expression of Bcl-2, while up-regulated the expression of Bax.	Dichloroacetic Acid	30-33	BCL2 apoptosis regulator	Homo sapiens	88-93
34364387-9	2021	At a molecular level, 3Br-P + DCA treatment remarkably down-regulated the expression of Bcl-2, while up-regulated the expression of Bax.	Dichloroacetic Acid	30-33	BCL2 associated X, apoptosis regulator	Homo sapiens	132-135
35462304-5	2022	Moreover, this design significantly downregulates CD39 and CD73 expression than DCA or MnFe2O4 alone, which consequently decreases the extracellular ATP catabolism.	Dichloroacetic Acid	80-83	5'-nucleotidase ecto	Homo sapiens	59-63
35488732-8	2022	Therefore, dichloroacetate (DCA), a PDK1 inhibitor, was used in vivo to shift intrasynovial tendon ATP production from glycolysis to OXPHOS.	Dichloroacetic Acid	11-26	pyruvate dehydrogenase kinase 1	Canis lupus familiaris	36-40
35488732-8	2022	Therefore, dichloroacetate (DCA), a PDK1 inhibitor, was used in vivo to shift intrasynovial tendon ATP production from glycolysis to OXPHOS.	Dichloroacetic Acid	28-31	pyruvate dehydrogenase kinase 1	Canis lupus familiaris	36-40
35488732-9	2022	Oral DCA administration reduced serum lactate concentration and increased acetyl-CoA content in repaired intrasynovial tendons and led to reduced TLR4 and IL1B and increased IGF1, SCX, and TGFB3 expressions in treated intrasynovial tendons compared to controls.	Dichloroacetic Acid	5-8	toll like receptor 4	Canis lupus familiaris	146-150
35488732-9	2022	Oral DCA administration reduced serum lactate concentration and increased acetyl-CoA content in repaired intrasynovial tendons and led to reduced TLR4 and IL1B and increased IGF1, SCX, and TGFB3 expressions in treated intrasynovial tendons compared to controls.	Dichloroacetic Acid	5-8	interleukin 1 beta	Canis lupus familiaris	155-159
35488732-9	2022	Oral DCA administration reduced serum lactate concentration and increased acetyl-CoA content in repaired intrasynovial tendons and led to reduced TLR4 and IL1B and increased IGF1, SCX, and TGFB3 expressions in treated intrasynovial tendons compared to controls.	Dichloroacetic Acid	5-8	insulin like growth factor 1	Canis lupus familiaris	174-178
35488732-9	2022	Oral DCA administration reduced serum lactate concentration and increased acetyl-CoA content in repaired intrasynovial tendons and led to reduced TLR4 and IL1B and increased IGF1, SCX, and TGFB3 expressions in treated intrasynovial tendons compared to controls.	Dichloroacetic Acid	5-8	LOW QUALITY PROTEIN: basic helix-loop-helix transcription factor scleraxis	Canis lupus familiaris	180-183
35488732-9	2022	Oral DCA administration reduced serum lactate concentration and increased acetyl-CoA content in repaired intrasynovial tendons and led to reduced TLR4 and IL1B and increased IGF1, SCX, and TGFB3 expressions in treated intrasynovial tendons compared to controls.	Dichloroacetic Acid	5-8	transforming growth factor beta 3	Canis lupus familiaris	189-194
35455448-2	2022	Similarly, Dichloroacetate (DCA), an pyruvate dehydrogenase kinase 1 (PKD1) inhibitor, has gained huge attention as a potential anticancer drug.	Dichloroacetic Acid	11-26	polycystin 1, transient receptor potential channel interacting	Mus musculus	70-74
35436282-2	2022	The effect of dichloroacetate (DCA) is to switch glucose metabolism (cellular respiration) to a more efficient process involving oxygen, reduce the production of lactic acid, activate the respiratory chain, change the potential of the mitochondrial membrane, and release pro-apoptotic mediators (cytochrome c and AIF) into the cytosol.	Dichloroacetic Acid	14-29	cytochrome c, somatic	Homo sapiens	296-308
35436282-2	2022	The effect of dichloroacetate (DCA) is to switch glucose metabolism (cellular respiration) to a more efficient process involving oxygen, reduce the production of lactic acid, activate the respiratory chain, change the potential of the mitochondrial membrane, and release pro-apoptotic mediators (cytochrome c and AIF) into the cytosol.	Dichloroacetic Acid	14-29	apoptosis inducing factor mitochondria associated 1	Homo sapiens	313-316
35436282-2	2022	The effect of dichloroacetate (DCA) is to switch glucose metabolism (cellular respiration) to a more efficient process involving oxygen, reduce the production of lactic acid, activate the respiratory chain, change the potential of the mitochondrial membrane, and release pro-apoptotic mediators (cytochrome c and AIF) into the cytosol.	Dichloroacetic Acid	31-34	cytochrome c, somatic	Homo sapiens	296-308
35436282-2	2022	The effect of dichloroacetate (DCA) is to switch glucose metabolism (cellular respiration) to a more efficient process involving oxygen, reduce the production of lactic acid, activate the respiratory chain, change the potential of the mitochondrial membrane, and release pro-apoptotic mediators (cytochrome c and AIF) into the cytosol.	Dichloroacetic Acid	31-34	apoptosis inducing factor mitochondria associated 1	Homo sapiens	313-316
35455448-2	2022	Similarly, Dichloroacetate (DCA), an pyruvate dehydrogenase kinase 1 (PKD1) inhibitor, has gained huge attention as a potential anticancer drug.	Dichloroacetic Acid	28-31	polycystin 1, transient receptor potential channel interacting	Mus musculus	70-74
35409102-4	2022	DCA strongly reduced PDH phosphorylation and increased the oxygen consumption rate:extracellular acidification rate (OCR:ECAR) ratio up to 6-fold.	Dichloroacetic Acid	0-3	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	21-24
35360068-8	2022	Conclusions: The CDKAL1 rs7747752 C carrier status and low GUDCA/DCA had significant additive interactions on the risk of GDM with the effect from interaction with DCA being partially mediated via increasing LPC18:0.	Dichloroacetic Acid	164-167	CDK5 regulatory subunit associated protein 1 like 1	Homo sapiens	17-23
34498942-9	2022	DCA inhibited the activity of PDK4 but increased the expression of PDK4 due to a feedback mechanism.	Dichloroacetic Acid	0-3	pyruvate dehydrogenase kinase 4	Homo sapiens	30-34
34498942-9	2022	DCA inhibited the activity of PDK4 but increased the expression of PDK4 due to a feedback mechanism.	Dichloroacetic Acid	0-3	pyruvate dehydrogenase kinase 4	Homo sapiens	67-71
35217717-5	2022	We show here that dichloroacetate (DCA), which induces oxidative phosphorylation (OXPHOS) in tumor cells, induces the expression of such ligands, e.g. MICA/B, ULBP1 and ICAM-I, by a wtp53-dependent mechanism.	Dichloroacetic Acid	18-33	UL16 binding protein 1	Homo sapiens	159-164
35134532-6	2022	Dichloroacetate reversed the increased phosphorylation of pyruvate dehydrogenase in rd10 retina and increased histone acetylation and levels of TP53-induced glycolysis and apoptosis regulator (TIGAR), which redirected glucose metabolism toward the pentose phosphate pathway.	Dichloroacetic Acid	0-15	phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide	Mus musculus	84-88
35134532-6	2022	Dichloroacetate reversed the increased phosphorylation of pyruvate dehydrogenase in rd10 retina and increased histone acetylation and levels of TP53-induced glycolysis and apoptosis regulator (TIGAR), which redirected glucose metabolism toward the pentose phosphate pathway.	Dichloroacetic Acid	0-15	Trp53 induced glycolysis regulatory phosphatase	Mus musculus	144-191
35134532-6	2022	Dichloroacetate reversed the increased phosphorylation of pyruvate dehydrogenase in rd10 retina and increased histone acetylation and levels of TP53-induced glycolysis and apoptosis regulator (TIGAR), which redirected glucose metabolism toward the pentose phosphate pathway.	Dichloroacetic Acid	0-15	Trp53 induced glycolysis regulatory phosphatase	Mus musculus	193-198
34498942-6	2022	An siRNA targeting PDK4, a lentiviral PDK4 overexpression vector and dichloroacetic acid (DCA) were used to regulate the expression and activity of PDK4.	Dichloroacetic Acid	69-88	pyruvate dehydrogenase kinase 4	Homo sapiens	148-152
34498942-6	2022	An siRNA targeting PDK4, a lentiviral PDK4 overexpression vector and dichloroacetic acid (DCA) were used to regulate the expression and activity of PDK4.	Dichloroacetic Acid	90-93	pyruvate dehydrogenase kinase 4	Homo sapiens	148-152
35217717-5	2022	We show here that dichloroacetate (DCA), which induces oxidative phosphorylation (OXPHOS) in tumor cells, induces the expression of such ligands, e.g. MICA/B, ULBP1 and ICAM-I, by a wtp53-dependent mechanism.	Dichloroacetic Acid	35-38	UL16 binding protein 1	Homo sapiens	159-164
35035660-14	2022	More importantly, the BACH1-based model indicated positive clinical applicability by DCA curves.	Dichloroacetic Acid	85-88	BTB domain and CNC homolog 1	Homo sapiens	22-27
35104792-5	2022	Given its capacity for sustained epigenetic reprogramming, the authors hypothesized that DCA would be an effective immunotherapeutic agent in treating IDHmut gliomas in an NK cell-dependent manner by upregulating epigenetically repressed activating NKG2D ligands in IDHmut tumors.	Dichloroacetic Acid	89-92	killer cell lectin-like receptor subfamily K, member 1	Mus musculus	249-254
3132456-8	1988	The suppression of VIP effects by dichloroacetate (5 mM) and pyruvate (10 mM) and the significant decrease (18%) of the activity of the pyruvate dehydrogenase complex after incubation of the cells with the neuropeptide, support the hypothesis that the effects of VIP on glucose oxidation may occur through an inhibition of the pyruvate dehydrogenase complex.	Dichloroacetic Acid	34-49	vasoactive intestinal peptide	Rattus norvegicus	19-22
2723637-1	1989	The objective of this study was to determine whether administration of dichloroacetate (DCA), an activator of pyruvate dehydrogenase (PDH), improves recovery of energy metabolites following transient cerebral ischemia.	Dichloroacetic Acid	71-86	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	110-132
2723637-1	1989	The objective of this study was to determine whether administration of dichloroacetate (DCA), an activator of pyruvate dehydrogenase (PDH), improves recovery of energy metabolites following transient cerebral ischemia.	Dichloroacetic Acid	71-86	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	134-137
2723637-1	1989	The objective of this study was to determine whether administration of dichloroacetate (DCA), an activator of pyruvate dehydrogenase (PDH), improves recovery of energy metabolites following transient cerebral ischemia.	Dichloroacetic Acid	88-91	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	110-132
2723637-1	1989	The objective of this study was to determine whether administration of dichloroacetate (DCA), an activator of pyruvate dehydrogenase (PDH), improves recovery of energy metabolites following transient cerebral ischemia.	Dichloroacetic Acid	88-91	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	134-137
2723637-4	1989	PDH was markedly inhibited at 20 min reperfusion in both groups, but was reactivated to a greater extent in DCA-treated animals at 60 min and 4 h reperfusion.	Dichloroacetic Acid	108-111	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	0-3
2723637-6	1989	However, later in reperfusion, DCA enhanced the postischemic reactivation of PDH and prevented the secondary failure of energy metabolism in caudate nucleus.	Dichloroacetic Acid	31-34	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	77-80
2751069-3	1989	These results suggest that oral administration of DCA causes significant increases in the activities of the PDH complex and TCA cycle not only in the platelets but also in various tissues of humans, which is important as a pathway for production of energy, resulting in decreases in the lactate and pyruvate levels in the blood and cerebrospinal fluid.	Dichloroacetic Acid	50-53	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	108-111
3426575-1	1987	The oxidation of 1,1,2,2-tetrachloroethane to dichloroacetic acid was investigated with rat liver microsomes and purified cytochrome P-450.	Dichloroacetic Acid	46-65	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	122-138
3925292-10	1985	In contrast, insulin levels fell markedly with DCA infusion and remained depressed throughout the infusion and recovery periods.	Dichloroacetic Acid	47-50	insulin	Canis lupus familiaris	13-20
3440441-3	1987	We also found that DCA activated the PDH complex and the tricarboxylic acid cycle, which is an important pathway of energy metabolism, in the brain and other tissues, and lowered the lactate level in the blood and cerebrospinal fluid.	Dichloroacetic Acid	19-22	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	37-40
6128194-6	1982	The results are consistent with a scheme whereby 1,1,2,2-tetrachloroethane is metabolized by cytochrome P-450 to dichloroacetyl chloride, which can bind covalently to various nucleophiles or hydrolyze to dichloroacetic acid.	Dichloroacetic Acid	204-223	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	93-109
6630519-3	1983	To investigate the mechanism of its cholesterol-lowering action, we studied the effects of DCA and its hepatic metabolites, glyoxylate and oxalate, on the activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG CoA reductase) obtained from livers of healthy, reverse light-cycled rats.	Dichloroacetic Acid	91-94	3-hydroxy-3-methylglutaryl-CoA reductase	Rattus norvegicus	167-233
6882465-3	1983	The effects of dichloroacetate depend on experimental conditions and the intensity of its catabolization into oxalate: the resultant action of dichloroacetate on tested parameters combines the effects of pyruvate dehydrogenase activation on the one hand, and pyruvate carboxylase inhibition by oxalate on the other.	Dichloroacetic Acid	15-30	pyruvate carboxylase	Rattus norvegicus	259-279
6882465-3	1983	The effects of dichloroacetate depend on experimental conditions and the intensity of its catabolization into oxalate: the resultant action of dichloroacetate on tested parameters combines the effects of pyruvate dehydrogenase activation on the one hand, and pyruvate carboxylase inhibition by oxalate on the other.	Dichloroacetic Acid	143-158	pyruvate carboxylase	Rattus norvegicus	259-279
6300332-7	1983	PDHb phosphatase had similar kinetic properties in purified mitochondria and in homogenate: dependence on Mg and Ca, independence of dichloroacetate, and inhibition by NaF and K-phosphate.	Dichloroacetic Acid	133-148	pyruvate dehydrogenase E1 subunit beta	Rattus norvegicus	0-4
7271831-0	1981	Cytochrome P-450-dependent metabolism of 1,1,2,2-tetrachloroethane to dichloroacetic acid in vitro.	Dichloroacetic Acid	70-89	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-16
834145-2	1977	Dichloroacetate significantly inhibited glucose formation from endogenous substrates and from added precursors (e.g., lactate, pyruvate, or glycerate) which enter the gluconeogenic pathway prior to the level of glyceraldehyde-3-phosphate dehydrogenase (GPDH).	Dichloroacetic Acid	0-15	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	211-251
834145-2	1977	Dichloroacetate significantly inhibited glucose formation from endogenous substrates and from added precursors (e.g., lactate, pyruvate, or glycerate) which enter the gluconeogenic pathway prior to the level of glyceraldehyde-3-phosphate dehydrogenase (GPDH).	Dichloroacetic Acid	0-15	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	253-257
32347035-0	2021	Changes in Serum Levels and Gene Expression of PGC-1alpha in The Cardiac Muscle of Diabetic Rats: The Effect of Dichloroacetate and Endurance Training.	Dichloroacetic Acid	112-127	PPARG coactivator 1 alpha	Rattus norvegicus	47-57
124874-4	1975	The hepatic activity of glucokinase and pyruvate kinase were significantly lower in both DCA-treated nondiabetic and DCA-treated diabetic animals than values observed for untreated animals.	Dichloroacetic Acid	89-92	glucokinase	Rattus norvegicus	24-35
124874-4	1975	The hepatic activity of glucokinase and pyruvate kinase were significantly lower in both DCA-treated nondiabetic and DCA-treated diabetic animals than values observed for untreated animals.	Dichloroacetic Acid	117-120	glucokinase	Rattus norvegicus	24-35
124874-5	1975	However, DCA therapy was accompanied by remarkable increases in the activities of glucose-6-phosphate dehydrogenase and malic enzyme in both nondiabetic and diabetic animals.	Dichloroacetic Acid	9-12	glucose-6-phosphate dehydrogenase	Rattus norvegicus	82-115
124874-6	1975	Glucose-6-phosphate dehydrogenase was 3-fold higher in DCA-treated nondiabetic animals whereas malic enzyme activity was 10-fold higher in the treated animals than observed in the untreated animals.	Dichloroacetic Acid	55-58	glucose-6-phosphate dehydrogenase	Rattus norvegicus	0-33
33931028-5	2021	Recently, we found evidence for synergism between dichloroacetate (DCA), a pyruvate dehydrogenase kinase inhibitor, and the HIF-1alpha inhibitor PX-478.	Dichloroacetic Acid	50-65	hypoxia inducible factor 1 subunit alpha	Homo sapiens	124-134
33931028-5	2021	Recently, we found evidence for synergism between dichloroacetate (DCA), a pyruvate dehydrogenase kinase inhibitor, and the HIF-1alpha inhibitor PX-478.	Dichloroacetic Acid	67-70	hypoxia inducible factor 1 subunit alpha	Homo sapiens	124-134
33529321-6	2021	Finally, we demonstrate that artesunate, CoA, and dichloroacetate improve TfR1 palmitoylation and decrease iron overload, paving the road for evidence-based therapeutic strategies at the actionable level of TfR1 palmitoylation in FRDA.	Dichloroacetic Acid	50-65	transferrin receptor	Homo sapiens	74-78
33529321-6	2021	Finally, we demonstrate that artesunate, CoA, and dichloroacetate improve TfR1 palmitoylation and decrease iron overload, paving the road for evidence-based therapeutic strategies at the actionable level of TfR1 palmitoylation in FRDA.	Dichloroacetic Acid	50-65	transferrin receptor	Homo sapiens	207-211
33405312-0	2021	Dichloroacetate attenuates the stemness of hepatocellular carcinoma cells via promoting nucleus-cytoplasm translocation of YAP.	Dichloroacetic Acid	0-15	Yes1 associated transcriptional regulator	Homo sapiens	123-126
33405312-4	2021	Furthermore, we indicated that DCA promoted the nucleus-cytoplasm translocation of YAP, but not TAZ, another critical executor of Hippo pathway.	Dichloroacetic Acid	31-34	Yes1 associated transcriptional regulator	Homo sapiens	83-86
33285186-5	2021	Similar to mammalian GPBAR1, zebrafish gpbar1 contains similar domain composition, shows a dose-dependent activation by bile acids including INT777, LCA, DCA, CDCA and CA, and can be induced by viral infection.	Dichloroacetic Acid	154-157	G protein-coupled bile acid receptor 1	Danio rerio	39-45
32347035-3	2021	The purpose of this study was to investigate changes in serum levels and cardiac muscle expression of PGC-1alpha in diabetic rats in response to the administration of dichloroacetate (DCA) and endurance training.	Dichloroacetic Acid	167-182	PPARG coactivator 1 alpha	Rattus norvegicus	102-112
32347035-3	2021	The purpose of this study was to investigate changes in serum levels and cardiac muscle expression of PGC-1alpha in diabetic rats in response to the administration of dichloroacetate (DCA) and endurance training.	Dichloroacetic Acid	184-187	PPARG coactivator 1 alpha	Rattus norvegicus	102-112
32347035-6	2021	Intraperitoneal injection of DCA of 50 mg/ kg body weight was used for the inhibition of Pyruvate Dehydrogenase Kinase 4 (PDK4) in the myocardium.	Dichloroacetic Acid	29-32	pyruvate dehydrogenase kinase 4	Rattus norvegicus	89-120
32347035-6	2021	Intraperitoneal injection of DCA of 50 mg/ kg body weight was used for the inhibition of Pyruvate Dehydrogenase Kinase 4 (PDK4) in the myocardium.	Dichloroacetic Acid	29-32	pyruvate dehydrogenase kinase 4	Rattus norvegicus	122-126
32347035-9	2021	Results: The results of the study showed that PDK4 gene expression in the endurance training group, diabetes+endurance training group, diabetes+endurance training+DCA group and endurance training+DCA group was higher compared to the control group.	Dichloroacetic Acid	163-166	pyruvate dehydrogenase kinase 4	Rattus norvegicus	46-50
32347035-9	2021	Results: The results of the study showed that PDK4 gene expression in the endurance training group, diabetes+endurance training group, diabetes+endurance training+DCA group and endurance training+DCA group was higher compared to the control group.	Dichloroacetic Acid	196-199	pyruvate dehydrogenase kinase 4	Rattus norvegicus	46-50
32347035-10	2021	Expression of PGC-1alpha was higher in the endurance training group compared to the control group but was lower compared to the control group in diabetes+endurance training+DCA group and diabetes+DCA group (P<0.05).	Dichloroacetic Acid	173-176	PPARG coactivator 1 alpha	Rattus norvegicus	14-24
32658145-4	2020	Oral administration of dichloroacetate (DCA) significantly increased mitochondrial respiratory function by inhibiting pyruvate dehydrogenase kinase (PDK) and decreased GFAP and Iba-1 immunoreactivity in spinal cord.	Dichloroacetic Acid	23-38	glial fibrillary acidic protein	Rattus norvegicus	168-172
33316932-6	2020	As expected, DCA treatment decreased phosphorylated pyruvate dehydrogenase (PDH) and lowered both extracellular acidification rate (ECAR) and lactate production.	Dichloroacetic Acid	13-16	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	52-74
33316932-6	2020	As expected, DCA treatment decreased phosphorylated pyruvate dehydrogenase (PDH) and lowered both extracellular acidification rate (ECAR) and lactate production.	Dichloroacetic Acid	13-16	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	76-79
32658145-4	2020	Oral administration of dichloroacetate (DCA) significantly increased mitochondrial respiratory function by inhibiting pyruvate dehydrogenase kinase (PDK) and decreased GFAP and Iba-1 immunoreactivity in spinal cord.	Dichloroacetic Acid	23-38	allograft inflammatory factor 1	Rattus norvegicus	177-182
32658145-4	2020	Oral administration of dichloroacetate (DCA) significantly increased mitochondrial respiratory function by inhibiting pyruvate dehydrogenase kinase (PDK) and decreased GFAP and Iba-1 immunoreactivity in spinal cord.	Dichloroacetic Acid	40-43	glial fibrillary acidic protein	Rattus norvegicus	168-172
32658145-4	2020	Oral administration of dichloroacetate (DCA) significantly increased mitochondrial respiratory function by inhibiting pyruvate dehydrogenase kinase (PDK) and decreased GFAP and Iba-1 immunoreactivity in spinal cord.	Dichloroacetic Acid	40-43	allograft inflammatory factor 1	Rattus norvegicus	177-182
33135418-8	2020	Further immunofluorescence and ELISA assays confirmed that signal transduction pathways related to cholesterol metabolism (LCAT-CE, PON1-HDL, and SRB1-HDL metabolic pathways) and bile acid metabolism (CYP7A1-CA/CDCA/DCA metabolic pathways) were disturbed.	Dichloroacetic Acid	212-215	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	201-207
32873592-0	2020	Exposure of Rats to Multiple Oral Doses of Dichloroacetate Results in Upregulation of Hepatic GSTs and NQO1.	Dichloroacetic Acid	43-58	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	103-107
32873593-6	2020	Here, we examined the expression and activity of GSTZ1 in cytosol and mitochondria of liver, kidney, heart, and brain 24 hours after completion of 8-days oral dosing of 100 mg/kg/day sodium DCA to juvenile and adult Sprague Dawley rats.	Dichloroacetic Acid	183-193	glutathione S-transferase zeta 1	Rattus norvegicus	49-54
33151963-5	2020	Chemical manipulation of PDH using dichloroacetic acid (DCA) will promote oxidative phosphorylation over glycolysis and decrease inflammation.	Dichloroacetic Acid	35-54	Pyruvate dehydrogenase E1 alpha subunit	Drosophila melanogaster	25-28
33151963-5	2020	Chemical manipulation of PDH using dichloroacetic acid (DCA) will promote oxidative phosphorylation over glycolysis and decrease inflammation.	Dichloroacetic Acid	56-59	Pyruvate dehydrogenase E1 alpha subunit	Drosophila melanogaster	25-28
33151963-10	2020	While Drosomycin and cecropin A expression increased in sepsis survivors, DCA treatment decreased both and selectively increased defensin.	Dichloroacetic Acid	74-77	Defensin	Drosophila melanogaster	129-137
32873593-8	2020	In DCA-treated rats, liver retained higher expression and activity of GSTZ1 with DCA than other tissues, irrespective of rodent age.	Dichloroacetic Acid	3-6	glutathione S-transferase zeta 1	Rattus norvegicus	70-75
32873592-3	2020	Repetitive DCA dosing causes downregulation of its metabolizing enzyme, GSTZ1, which is also critical in the detoxification of maleylacetoacetate and maleylacetone.	Dichloroacetic Acid	11-14	glutathione S-transferase zeta 1	Homo sapiens	72-77
32873593-8	2020	In DCA-treated rats, liver retained higher expression and activity of GSTZ1 with DCA than other tissues, irrespective of rodent age.	Dichloroacetic Acid	81-84	glutathione S-transferase zeta 1	Rattus norvegicus	70-75
32873593-9	2020	DCA-treated juvenile rats retained more GSTZ1 activity with DCA than adults.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Rattus norvegicus	40-45
32873593-9	2020	DCA-treated juvenile rats retained more GSTZ1 activity with DCA than adults.	Dichloroacetic Acid	60-63	glutathione S-transferase zeta 1	Rattus norvegicus	40-45
32873592-5	2020	We hypothesized that DCA-mediated depletion of GSTZ1 causes oxidative stress and used the rat to examine induction of GSTs and antioxidant enzymes after repeated DCA exposure.	Dichloroacetic Acid	21-24	glutathione S-transferase zeta 1	Rattus norvegicus	47-52
32873593-11	2020	DCA-treated rats retained activity with EPNPP, despite losing over 98% of GSTZ1 protein.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Rattus norvegicus	74-79
32873592-5	2020	We hypothesized that DCA-mediated depletion of GSTZ1 causes oxidative stress and used the rat to examine induction of GSTs and antioxidant enzymes after repeated DCA exposure.	Dichloroacetic Acid	21-24	glutathione S-transferase cluster	Mus musculus	118-122
32873592-9	2020	In comparison to acetate-treated controls, DCA dosing increased the relative expression of GSTA1/A2 irrespective of rodent age, whereas only adults displayed higher levels of GSTM1 and GSTO1.	Dichloroacetic Acid	43-46	glutathione S-transferase alpha 1	Rattus norvegicus	91-96
32873592-10	2020	NQO1 expression and activity were higher in juveniles after DCA dosing.	Dichloroacetic Acid	60-63	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	0-4
32873592-12	2020	Levels of GCLC and GSS were higher and lower, respectively, in adults treated with DCA.	Dichloroacetic Acid	83-86	glutathione synthetase	Rattus norvegicus	19-22
32873592-13	2020	We conclude that DCA-mediated depletion of GSTZ1 causes oxidative stress and promotes the induction of antioxidant enzymes that may vary between age groups.	Dichloroacetic Acid	17-20	glutathione S-transferase zeta 1	Rattus norvegicus	43-48
32873592-14	2020	Significance Statement Treatment with the investigational drug, DCA, results in loss of GSTZ1 and subsequent increases in body burden of the electrophilic tyrosine metabolites, maleylacetoacetate and maleylacetone.	Dichloroacetic Acid	64-67	glutathione S-transferase zeta 1	Rattus norvegicus	88-93
32873592-16	2020	Therefore, we determined whether pharmacological depletion of GSTZ1 through repeat administration of DCA produced similar changes in the liver, which could affect responses to other drugs and toxicants.	Dichloroacetic Acid	101-104	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	62-67
32873593-0	2020	Effects of Multiple Doses of Dichloroacetate on GSTZ1 Expression and Activity in Liver and Extrahepatic Tissues of Young and Adult Rats.	Dichloroacetic Acid	29-44	glutathione S-transferase zeta 1	Rattus norvegicus	48-53
32873593-1	2020	GSTZ1, expressed in liver and several extrahepatic tissues, catalyzes dechlorination of dichloroacetate (DCA) to glyoxylate.	Dichloroacetic Acid	88-103	glutathione S-transferase zeta 1	Rattus norvegicus	0-5
32873593-1	2020	GSTZ1, expressed in liver and several extrahepatic tissues, catalyzes dechlorination of dichloroacetate (DCA) to glyoxylate.	Dichloroacetic Acid	105-108	glutathione S-transferase zeta 1	Rattus norvegicus	0-5
32873593-5	2020	One dose of DCA to Sprague-Dawley rats reduced GSTZ1 expression and activity more in liver than extrahepatic tissues, however the effects of multiple doses of DCA that mimic its therapeutic use have not been studied.	Dichloroacetic Acid	12-15	glutathione S-transferase zeta 1	Rattus norvegicus	47-52
33002152-15	2020	:: For 16 years the DCA system has proven to be reliable and robust and operators at Aboriginal medical services have demonstrated they are able to conduct point-of-care testing for urine albumin to creatinine ratio that consistently meets analytic performance standards.	Dichloroacetic Acid	20-23	albumin	Homo sapiens	188-195
33087819-7	2020	The effect of TGF-beta1 on PDC activity, acetyl-CoA, alphaSMA and pro-collagen I was also ameliorated by sodium dichloroacetate, a small molecule inhibitor of PDK.	Dichloroacetic Acid	105-127	transforming growth factor beta 1	Homo sapiens	14-23
33087819-7	2020	The effect of TGF-beta1 on PDC activity, acetyl-CoA, alphaSMA and pro-collagen I was also ameliorated by sodium dichloroacetate, a small molecule inhibitor of PDK.	Dichloroacetic Acid	105-127	actin alpha 1, skeletal muscle	Homo sapiens	53-61
32357971-1	2020	Previous work has shown that hepatic levels of human glutathione transferase zeta 1 (GSTZ1) protein, involved in tyrosine catabolism and responsible for metabolism of the investigational drug dichloroacetate, increase in cytosol after birth before reaching a plateau around age seven.	Dichloroacetic Acid	192-207	glutathione S-transferase zeta 1	Homo sapiens	53-83
32841551-12	2020	Moreover, the results showed that the neuroinflammation factors (TNF-alpha, IL-6, IL-1beta) in DCA treatment groups increased significantly compared with the control pups.	Dichloroacetic Acid	95-98	tumor necrosis factor	Homo sapiens	65-74
32841551-12	2020	Moreover, the results showed that the neuroinflammation factors (TNF-alpha, IL-6, IL-1beta) in DCA treatment groups increased significantly compared with the control pups.	Dichloroacetic Acid	95-98	interleukin 6	Homo sapiens	76-80
32841551-12	2020	Moreover, the results showed that the neuroinflammation factors (TNF-alpha, IL-6, IL-1beta) in DCA treatment groups increased significantly compared with the control pups.	Dichloroacetic Acid	95-98	interleukin 1 alpha	Homo sapiens	82-90
32841551-13	2020	And we also found that DCA treatment caused a differential modulation of proteins (BDNF, cAMP-response element-binding protein1 (CREB1), p-CREB1, postsynaptic density-95 (PSD-95), synapsin I, p-synapsin I), and mRNA (BDNF, PSD-95).	Dichloroacetic Acid	23-26	brain derived neurotrophic factor	Homo sapiens	83-87
32841551-13	2020	And we also found that DCA treatment caused a differential modulation of proteins (BDNF, cAMP-response element-binding protein1 (CREB1), p-CREB1, postsynaptic density-95 (PSD-95), synapsin I, p-synapsin I), and mRNA (BDNF, PSD-95).	Dichloroacetic Acid	23-26	cAMP responsive element binding protein 1	Homo sapiens	89-127
32841551-13	2020	And we also found that DCA treatment caused a differential modulation of proteins (BDNF, cAMP-response element-binding protein1 (CREB1), p-CREB1, postsynaptic density-95 (PSD-95), synapsin I, p-synapsin I), and mRNA (BDNF, PSD-95).	Dichloroacetic Acid	23-26	cAMP responsive element binding protein 1	Homo sapiens	129-134
32841551-13	2020	And we also found that DCA treatment caused a differential modulation of proteins (BDNF, cAMP-response element-binding protein1 (CREB1), p-CREB1, postsynaptic density-95 (PSD-95), synapsin I, p-synapsin I), and mRNA (BDNF, PSD-95).	Dichloroacetic Acid	23-26	cAMP responsive element binding protein 1	Homo sapiens	139-144
32841551-13	2020	And we also found that DCA treatment caused a differential modulation of proteins (BDNF, cAMP-response element-binding protein1 (CREB1), p-CREB1, postsynaptic density-95 (PSD-95), synapsin I, p-synapsin I), and mRNA (BDNF, PSD-95).	Dichloroacetic Acid	23-26	discs large MAGUK scaffold protein 4	Homo sapiens	146-169
32841551-13	2020	And we also found that DCA treatment caused a differential modulation of proteins (BDNF, cAMP-response element-binding protein1 (CREB1), p-CREB1, postsynaptic density-95 (PSD-95), synapsin I, p-synapsin I), and mRNA (BDNF, PSD-95).	Dichloroacetic Acid	23-26	discs large MAGUK scaffold protein 4	Homo sapiens	171-177
32841551-13	2020	And we also found that DCA treatment caused a differential modulation of proteins (BDNF, cAMP-response element-binding protein1 (CREB1), p-CREB1, postsynaptic density-95 (PSD-95), synapsin I, p-synapsin I), and mRNA (BDNF, PSD-95).	Dichloroacetic Acid	23-26	synapsin I	Homo sapiens	180-190
32841551-13	2020	And we also found that DCA treatment caused a differential modulation of proteins (BDNF, cAMP-response element-binding protein1 (CREB1), p-CREB1, postsynaptic density-95 (PSD-95), synapsin I, p-synapsin I), and mRNA (BDNF, PSD-95).	Dichloroacetic Acid	23-26	synapsin I	Homo sapiens	194-204
32841551-13	2020	And we also found that DCA treatment caused a differential modulation of proteins (BDNF, cAMP-response element-binding protein1 (CREB1), p-CREB1, postsynaptic density-95 (PSD-95), synapsin I, p-synapsin I), and mRNA (BDNF, PSD-95).	Dichloroacetic Acid	23-26	brain derived neurotrophic factor	Homo sapiens	217-221
32841551-13	2020	And we also found that DCA treatment caused a differential modulation of proteins (BDNF, cAMP-response element-binding protein1 (CREB1), p-CREB1, postsynaptic density-95 (PSD-95), synapsin I, p-synapsin I), and mRNA (BDNF, PSD-95).	Dichloroacetic Acid	23-26	discs large MAGUK scaffold protein 4	Homo sapiens	223-229
32436178-0	2020	Correction to: Mitochondrial Modulation by Dichloroacetate Reduces Toxicity of Aberrant Glial Cells and Gliosis in the SOD1G93A Rat Model of Amyotrophic Lateral Sclerosis.	Dichloroacetic Acid	43-58	superoxide dismutase 1	Rattus norvegicus	119-123
32615946-13	2020	The same accounts for the combination of Dichloroacetate (PDH activation) and NHI-2 (LDH-A inhibition).	Dichloroacetic Acid	41-56	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	58-61
32473093-6	2020	Dichloroacetic acid treatment elevated acetyl-CoA levels, restored mTORC1 activation, inhibited autophagy, and increased hepatic triglycerides in Acox1-LKO mice.	Dichloroacetic Acid	0-19	CREB regulated transcription coactivator 1	Mus musculus	67-73
32473093-6	2020	Dichloroacetic acid treatment elevated acetyl-CoA levels, restored mTORC1 activation, inhibited autophagy, and increased hepatic triglycerides in Acox1-LKO mice.	Dichloroacetic Acid	0-19	acyl-Coenzyme A oxidase 1, palmitoyl	Mus musculus	146-151
32996739-13	2020	Instead, in tumors treated with MTF alone and in combination with DCA the total CD68+ TAMs count was almost 27% (p < 0.05) and 43% lower (p < 0.05) correspondingly than that in control, but this decrease was not accompanied by redistribution of CD68+/CD206+ and CD68+/D206- subsets.	Dichloroacetic Acid	66-69	CD68 antigen	Mus musculus	80-84
32996739-13	2020	Instead, in tumors treated with MTF alone and in combination with DCA the total CD68+ TAMs count was almost 27% (p < 0.05) and 43% lower (p < 0.05) correspondingly than that in control, but this decrease was not accompanied by redistribution of CD68+/CD206+ and CD68+/D206- subsets.	Dichloroacetic Acid	66-69	CD68 antigen	Mus musculus	245-249
32996739-13	2020	Instead, in tumors treated with MTF alone and in combination with DCA the total CD68+ TAMs count was almost 27% (p < 0.05) and 43% lower (p < 0.05) correspondingly than that in control, but this decrease was not accompanied by redistribution of CD68+/CD206+ and CD68+/D206- subsets.	Dichloroacetic Acid	66-69	mannose receptor, C type 1	Mus musculus	251-256
32996739-13	2020	Instead, in tumors treated with MTF alone and in combination with DCA the total CD68+ TAMs count was almost 27% (p < 0.05) and 43% lower (p < 0.05) correspondingly than that in control, but this decrease was not accompanied by redistribution of CD68+/CD206+ and CD68+/D206- subsets.	Dichloroacetic Acid	66-69	CD68 antigen	Mus musculus	245-249
32473169-0	2020	Dichloroacetate prevents TGFbeta-induced epithelial-mesenchymal transition of retinal pigment epithelial cells.	Dichloroacetic Acid	0-15	transforming growth factor alpha	Homo sapiens	25-32
32473169-8	2020	In the present study, we have investigated the role of DCA in preventing TGFbeta2 induced EMT of RPE cell line, ARPE-19.	Dichloroacetic Acid	55-58	transforming growth factor beta 2	Homo sapiens	73-81
32357971-1	2020	Previous work has shown that hepatic levels of human glutathione transferase zeta 1 (GSTZ1) protein, involved in tyrosine catabolism and responsible for metabolism of the investigational drug dichloroacetate, increase in cytosol after birth before reaching a plateau around age seven.	Dichloroacetic Acid	192-207	glutathione S-transferase zeta 1	Homo sapiens	85-90
32357971-11	2020	SIGNIFICANCE STATEMENT: Hepatic GSTZ1 is responsible for metabolism of the tyrosine catabolite maleylacetoacetate as well as the investigational drug dichloroacetate.	Dichloroacetic Acid	150-165	glutathione S-transferase zeta 1	Homo sapiens	32-37
32298384-8	2020	Urine measures of DCAs have an 82% ability to predict cognitively healthy participants with normal CSF amyloid/Tau.	Dichloroacetic Acid	18-22	microtubule associated protein tau	Homo sapiens	111-114
32577402-0	2020	Improved lactate control with dichloroacetate in a case with severe neonatal lactic acidosis due to MTFMT mitochondrial translation disorder.	Dichloroacetic Acid	30-45	mitochondrial methionyl-tRNA formyltransferase	Homo sapiens	100-105
32577402-7	2020	This is the first report using dichloroacetate in a patient with MTFMT deficiency, which may be a potential therapeutic option that warrants further study.	Dichloroacetic Acid	31-46	mitochondrial methionyl-tRNA formyltransferase	Homo sapiens	65-70
32617141-0	2020	Combination of Dichloroacetate and Atorvastatin Regulates Excessive Proliferation and Oxidative Stress in Pulmonary Arterial Hypertension Development via p38 Signaling.	Dichloroacetic Acid	15-30	mitogen-activated protein kinase 14	Homo sapiens	154-157
32617141-10	2020	Furthermore, suppression of the p38 pathway through the specific inhibitor SB203580 attenuated cell death and oxidative stress at a level consistent with that of DCA/ATO combination treatment.	Dichloroacetic Acid	162-165	mitogen-activated protein kinase 14	Homo sapiens	32-35
32617141-11	2020	These observations suggested a complementary effect of DCA and ATO on rescuing PASMCs from a PAH phenotype through p38 activation via the regulation of mitochondrial-related cell death and oxidative stress.	Dichloroacetic Acid	55-58	mitogen-activated protein kinase 14	Homo sapiens	115-118
31930988-13	2020	Knockdown of pyruvate dehydrogenase kinase 4 (PDK4) or inhibition with dichloroacetate reduced the upregulation of Atoh1 mRNA following LKB1 knockdown in Ls174t cells.	Dichloroacetic Acid	71-86	atonal bHLH transcription factor 1	Homo sapiens	115-120
32087318-12	2020	Furthermore, dichloroacetate sodium (DCA), an agonist of pyruvate dehydrogenase, could stimulate PAI-1 expression, which was suppressed by HKSWF.	Dichloroacetic Acid	13-35	serpin family E member 1	Rattus norvegicus	97-102
32087318-12	2020	Furthermore, dichloroacetate sodium (DCA), an agonist of pyruvate dehydrogenase, could stimulate PAI-1 expression, which was suppressed by HKSWF.	Dichloroacetic Acid	37-40	serpin family E member 1	Rattus norvegicus	97-102
31759926-11	2020	Acetate, a precursor of acetyl-CoA (a product of fatty acid beta-oxidation [FAO]), or dichloroacetate, a compound that promotes pyruvate oxidation and generation of mitochondrial acetyl-CoA, were used for metabolic intervention RESULTS: Crypt cells rapidly absorbed labeled fatty acid, and mRNA levels of Lgr5+ stem cell markers (Lgr5, Olfm4, Smoc2, Msi1, and Ascl2) were downregulated in organoids incubated with etomoxir, an inhibitor of FAO, indicating that FAO was required for renewal of ISCs.	Dichloroacetic Acid	86-101	leucine rich repeat containing G protein coupled receptor 5	Mus musculus	305-309
31759926-11	2020	Acetate, a precursor of acetyl-CoA (a product of fatty acid beta-oxidation [FAO]), or dichloroacetate, a compound that promotes pyruvate oxidation and generation of mitochondrial acetyl-CoA, were used for metabolic intervention RESULTS: Crypt cells rapidly absorbed labeled fatty acid, and mRNA levels of Lgr5+ stem cell markers (Lgr5, Olfm4, Smoc2, Msi1, and Ascl2) were downregulated in organoids incubated with etomoxir, an inhibitor of FAO, indicating that FAO was required for renewal of ISCs.	Dichloroacetic Acid	86-101	leucine rich repeat containing G protein coupled receptor 5	Mus musculus	330-334
31759926-11	2020	Acetate, a precursor of acetyl-CoA (a product of fatty acid beta-oxidation [FAO]), or dichloroacetate, a compound that promotes pyruvate oxidation and generation of mitochondrial acetyl-CoA, were used for metabolic intervention RESULTS: Crypt cells rapidly absorbed labeled fatty acid, and mRNA levels of Lgr5+ stem cell markers (Lgr5, Olfm4, Smoc2, Msi1, and Ascl2) were downregulated in organoids incubated with etomoxir, an inhibitor of FAO, indicating that FAO was required for renewal of ISCs.	Dichloroacetic Acid	86-101	olfactomedin 4	Mus musculus	336-341
31759926-11	2020	Acetate, a precursor of acetyl-CoA (a product of fatty acid beta-oxidation [FAO]), or dichloroacetate, a compound that promotes pyruvate oxidation and generation of mitochondrial acetyl-CoA, were used for metabolic intervention RESULTS: Crypt cells rapidly absorbed labeled fatty acid, and mRNA levels of Lgr5+ stem cell markers (Lgr5, Olfm4, Smoc2, Msi1, and Ascl2) were downregulated in organoids incubated with etomoxir, an inhibitor of FAO, indicating that FAO was required for renewal of ISCs.	Dichloroacetic Acid	86-101	SPARC related modular calcium binding 2	Mus musculus	343-348
31759926-11	2020	Acetate, a precursor of acetyl-CoA (a product of fatty acid beta-oxidation [FAO]), or dichloroacetate, a compound that promotes pyruvate oxidation and generation of mitochondrial acetyl-CoA, were used for metabolic intervention RESULTS: Crypt cells rapidly absorbed labeled fatty acid, and mRNA levels of Lgr5+ stem cell markers (Lgr5, Olfm4, Smoc2, Msi1, and Ascl2) were downregulated in organoids incubated with etomoxir, an inhibitor of FAO, indicating that FAO was required for renewal of ISCs.	Dichloroacetic Acid	86-101	musashi RNA-binding protein 1	Mus musculus	350-354
31759926-11	2020	Acetate, a precursor of acetyl-CoA (a product of fatty acid beta-oxidation [FAO]), or dichloroacetate, a compound that promotes pyruvate oxidation and generation of mitochondrial acetyl-CoA, were used for metabolic intervention RESULTS: Crypt cells rapidly absorbed labeled fatty acid, and mRNA levels of Lgr5+ stem cell markers (Lgr5, Olfm4, Smoc2, Msi1, and Ascl2) were downregulated in organoids incubated with etomoxir, an inhibitor of FAO, indicating that FAO was required for renewal of ISCs.	Dichloroacetic Acid	86-101	achaete-scute family bHLH transcription factor 2	Mus musculus	360-365
31919406-4	2020	The DCA-responsive proteins in AMPK pathway were enriched using proteomic profiling technology.	Dichloroacetic Acid	4-7	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	31-35
31919406-5	2020	The effect of DCA on CAB39-AMPK signal pathway was analysed.	Dichloroacetic Acid	14-17	calcium binding protein 39	Homo sapiens	21-26
31919406-5	2020	The effect of DCA on CAB39-AMPK signal pathway was analysed.	Dichloroacetic Acid	14-17	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	27-31
31919406-7	2020	The DCA-responsive miRNAs that target CAB39 were assayed.	Dichloroacetic Acid	4-7	calcium binding protein 39	Homo sapiens	38-43
31919406-10	2020	DCA could upregulate CAB39 expression, which activates the AMPK/mTOR signalling pathway.	Dichloroacetic Acid	0-3	calcium binding protein 39	Homo sapiens	21-26
31919406-10	2020	DCA could upregulate CAB39 expression, which activates the AMPK/mTOR signalling pathway.	Dichloroacetic Acid	0-3	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	59-63
31919406-10	2020	DCA could upregulate CAB39 expression, which activates the AMPK/mTOR signalling pathway.	Dichloroacetic Acid	0-3	mechanistic target of rapamycin kinase	Homo sapiens	64-68
31919406-11	2020	CAB39 was confirmed to be a direct target of miR-107 regulated by DCA.	Dichloroacetic Acid	66-69	calcium binding protein 39	Homo sapiens	0-5
31919406-11	2020	CAB39 was confirmed to be a direct target of miR-107 regulated by DCA.	Dichloroacetic Acid	66-69	microRNA 107	Homo sapiens	45-52
31759926-17	2020	Incubation of organoids derived from double-knockout mice with acetate or dichloroacetate restored stem cells CONCLUSIONS: In mice, the transcription factors HNF4A and HNF4G regulate expression of genes required for fatty acid oxidation and are required for renewal of intestinal stem cells.	Dichloroacetic Acid	74-89	hepatic nuclear factor 4, alpha	Mus musculus	158-163
31759926-17	2020	Incubation of organoids derived from double-knockout mice with acetate or dichloroacetate restored stem cells CONCLUSIONS: In mice, the transcription factors HNF4A and HNF4G regulate expression of genes required for fatty acid oxidation and are required for renewal of intestinal stem cells.	Dichloroacetic Acid	74-89	hepatocyte nuclear factor 4, gamma	Mus musculus	168-173
31930988-13	2020	Knockdown of pyruvate dehydrogenase kinase 4 (PDK4) or inhibition with dichloroacetate reduced the upregulation of Atoh1 mRNA following LKB1 knockdown in Ls174t cells.	Dichloroacetic Acid	71-86	serine/threonine kinase 11	Homo sapiens	136-140
31930988-14	2020	Cells with LKB1 knockdown had a reduced rate of oxygen consumption, which was partially restored by PDK4 inhibition with dichloroacetate.	Dichloroacetic Acid	121-136	serine/threonine kinase 11	Mus musculus	11-15
31930988-14	2020	Cells with LKB1 knockdown had a reduced rate of oxygen consumption, which was partially restored by PDK4 inhibition with dichloroacetate.	Dichloroacetic Acid	121-136	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	100-104
32029721-7	2020	Inhibition of PDKs using dichloroacetate (DCA) restored acetyl-CoA generation and histone acetylation under hypoxia.	Dichloroacetic Acid	25-40	pyruvate dehydrogenase kinase 1	Homo sapiens	14-18
32029721-7	2020	Inhibition of PDKs using dichloroacetate (DCA) restored acetyl-CoA generation and histone acetylation under hypoxia.	Dichloroacetic Acid	42-45	pyruvate dehydrogenase kinase 1	Homo sapiens	14-18
32047474-7	2019	Furthermore, the PDK1 antagonist dichloroacetate could repress the osteogenic ability of MC3T3-E1 cells, although HIF-1alpha was upregulated when transduced with adenovirus-HIF-1alpha construct.	Dichloroacetic Acid	33-48	pyruvate dehydrogenase kinase, isoenzyme 1	Mus musculus	17-21
31645370-6	2020	Cyp2a12 KO mice showed the accumulation of DCAs, whereas Cyp2c70 KO mice lacked MCAs and exhibited markedly increased hepatobiliary proportions of CDCA.	Dichloroacetic Acid	43-47	cytochrome P450, family 2, subfamily a, polypeptide 12	Mus musculus	0-7
31597953-0	2020	Dichloroacetate restores colorectal cancer chemosensitivity through the p53/miR-149-3p/PDK2-mediated glucose metabolic pathway.	Dichloroacetic Acid	0-15	tumor protein p53	Homo sapiens	72-75
31597953-0	2020	Dichloroacetate restores colorectal cancer chemosensitivity through the p53/miR-149-3p/PDK2-mediated glucose metabolic pathway.	Dichloroacetic Acid	0-15	microRNA 149	Homo sapiens	76-83
31597953-0	2020	Dichloroacetate restores colorectal cancer chemosensitivity through the p53/miR-149-3p/PDK2-mediated glucose metabolic pathway.	Dichloroacetic Acid	0-15	pyruvate dehydrogenase kinase 2	Homo sapiens	87-91
31597953-4	2020	Using the microarray assay, we noted that miR-149-3p was involved in the chemoresistance of CRC, which was modulated by wild-type p53 after DCA treatment.	Dichloroacetic Acid	140-143	tumor protein p53	Homo sapiens	130-133
31597953-9	2020	Taken together, we determined that the p53/miR-149-3p/PDK2 signaling pathway can potentially be targeted with DCA treatment to overcome chemoresistant CRC.	Dichloroacetic Acid	110-113	tumor protein p53	Homo sapiens	39-42
31597953-9	2020	Taken together, we determined that the p53/miR-149-3p/PDK2 signaling pathway can potentially be targeted with DCA treatment to overcome chemoresistant CRC.	Dichloroacetic Acid	110-113	microRNA 149	Homo sapiens	43-50
31597953-9	2020	Taken together, we determined that the p53/miR-149-3p/PDK2 signaling pathway can potentially be targeted with DCA treatment to overcome chemoresistant CRC.	Dichloroacetic Acid	110-113	pyruvate dehydrogenase kinase 2	Homo sapiens	54-58
31792175-7	2019	Treatment of endometriosis HPMCs with the pyruvate dehydrogenase kinase (PDK) inhibitor/PDH activator dichloroacetate (DCA) normalizes HPMC metabolism, reduces lactate secretion, and abrogates endometrial stromal cell proliferation in a coculture model.	Dichloroacetic Acid	102-117	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	88-91
31878280-7	2019	Furthermore, CRC cell lines exposed to hypoxia or dichloroacetate treatment showed the downregulation of TRAP1 upon GSNOR silencing and this resulted in increased TRAP1 mono/polyubiquitination.	Dichloroacetic Acid	50-65	TNF receptor associated protein 1	Homo sapiens	105-110
31878280-7	2019	Furthermore, CRC cell lines exposed to hypoxia or dichloroacetate treatment showed the downregulation of TRAP1 upon GSNOR silencing and this resulted in increased TRAP1 mono/polyubiquitination.	Dichloroacetic Acid	50-65	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	116-121
31878280-7	2019	Furthermore, CRC cell lines exposed to hypoxia or dichloroacetate treatment showed the downregulation of TRAP1 upon GSNOR silencing and this resulted in increased TRAP1 mono/polyubiquitination.	Dichloroacetic Acid	50-65	TNF receptor associated protein 1	Homo sapiens	163-168
31792175-7	2019	Treatment of endometriosis HPMCs with the pyruvate dehydrogenase kinase (PDK) inhibitor/PDH activator dichloroacetate (DCA) normalizes HPMC metabolism, reduces lactate secretion, and abrogates endometrial stromal cell proliferation in a coculture model.	Dichloroacetic Acid	119-122	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	88-91
31768777-0	2019	Comparison of Antitumor Effects of Combined and Separate Treatment with NO Synthase Inhibitor T1023 and PDK1 Inhibitor Dichloroacetate.	Dichloroacetic Acid	119-134	pyruvate dehydrogenase kinase 1	Homo sapiens	104-108
31351004-7	2019	The efficacy of the combination of DCA with the HA synthesis inhibitor 4-methylumbelliferone was evaluated in 2D and 3D cell cultures and in a nude mouse tumor xenograft regression model by immunoblot, immunochemistry, and FACS analysis.	Dichloroacetic Acid	35-38	acyl-CoA synthetase long-chain family member 1	Mus musculus	223-227
31768777-3	2019	These results attest to synergetic antitumor effects NOS inhibitor T1023 and PDK1 inhibitor dichloroacetate producing antiangiogenic and hypoxia-targeted cytotoxic effects, during their combined administration, which allows overcoming the adaptive potential of the tumors.	Dichloroacetic Acid	92-107	pyruvate dehydrogenase kinase 1	Homo sapiens	77-81
31442532-7	2019	Although treating FBXL4 fibroblasts with DCA improved extracellular acidification, in line with reduced lactate levels in patients, DCA treatment did not improve any of the other mitochondrial functions.	Dichloroacetic Acid	41-44	F-box and leucine rich repeat protein 4	Homo sapiens	18-23
31442532-8	2019	Nonetheless, we highlight DCA as a potentially effective drug for the management of elevated lactate and cardiomyopathy in patients with pathogenic FBXL4 variants.	Dichloroacetic Acid	26-29	F-box and leucine rich repeat protein 4	Homo sapiens	148-153
31768777-1	2019	Combined chronic treatment of Ehrlich solid carcinoma (EC) with an NOS inhibitor 1-isobutanoyl-2-isopropylisothiourea hydrobromide (T1023) and a PDK1 inhibitor dichloroacetate was accompanied by statistically significant synergetic antitumor effects manifested in a significant and stable suppression of neoplasm growth (by 55-65%).	Dichloroacetic Acid	160-175	pyruvate dehydrogenase kinase 1	Homo sapiens	145-149
31509699-3	2019	In this way, we have developed a conjugate AlbA-DCA, which can induce a marked increase in intracellular ROS and alleviate the accumulation of lactic acid in TME.	Dichloroacetic Acid	48-51	T-associated maternal effect	Mus musculus	158-161
31524376-0	2019	Mitochondrial Glutathione Transferase Zeta 1 is Inactivated More Rapidly by Dichloroacetate than the Cytosolic Enzyme in Adult and Juvenile Rat Liver.	Dichloroacetic Acid	76-91	glutathione S-transferase zeta 1	Rattus norvegicus	14-44
31524376-2	2019	Repeated dosing of DCA results in reduced drug clearance due to inactivation of glutathione transferase zeta1 (GSTZ1), its metabolizing enzyme.	Dichloroacetic Acid	19-22	glutathione S-transferase zeta 1	Rattus norvegicus	80-109
31524376-2	2019	Repeated dosing of DCA results in reduced drug clearance due to inactivation of glutathione transferase zeta1 (GSTZ1), its metabolizing enzyme.	Dichloroacetic Acid	19-22	glutathione S-transferase zeta 1	Rattus norvegicus	111-116
31524376-3	2019	We investigated the time course of inactivation of GSTZ1 in hepatic cytosol and mitochondria after one oral dose of 100 mg/kg DCA to female Sprague-Dawley rats aged 4 wk (young) and 52 wk (adult) as models for children and adults, respectively.	Dichloroacetic Acid	126-129	glutathione S-transferase zeta 1	Rattus norvegicus	51-56
31524376-4	2019	GSTZ1 activity with both DCA and an endogenous substrate, maleylacetone (MA), as well as GSTZ1 protein expression were rapidly reduced in cytosol from both ages following DCA treatment.	Dichloroacetic Acid	25-28	glutathione S-transferase zeta 1	Rattus norvegicus	0-5
31524376-4	2019	GSTZ1 activity with both DCA and an endogenous substrate, maleylacetone (MA), as well as GSTZ1 protein expression were rapidly reduced in cytosol from both ages following DCA treatment.	Dichloroacetic Acid	171-174	glutathione S-transferase zeta 1	Rattus norvegicus	0-5
31524376-4	2019	GSTZ1 activity with both DCA and an endogenous substrate, maleylacetone (MA), as well as GSTZ1 protein expression were rapidly reduced in cytosol from both ages following DCA treatment.	Dichloroacetic Acid	171-174	glutathione S-transferase zeta 1	Rattus norvegicus	89-94
31524376-5	2019	In mitochondria, loss of GSTZ1 protein and activity with DCA were even more rapid.	Dichloroacetic Acid	57-60	glutathione S-transferase zeta 1	Rattus norvegicus	25-30
31524376-6	2019	The cytosolic in vivo half-lives of loss of GSTZ1 activity with DCA were 1.05 +- 0.03 and 0.82 +- 0.02 h (mean +- S.D., n=6) for young and adult rats, respectively, with inactivation significantly more rapid in adult rats, p&lt;0.001.	Dichloroacetic Acid	64-67	glutathione S-transferase zeta 1	Rattus norvegicus	44-49
31524376-9	2019	The in vitro GSTZ1 inactivation half-lives following incubation with 2 mM DCA in the presence of physiological chloride (Cl-) concentrations (cytosol 44 mM, mitochondria 1-2 mM) exhibited marked differences between subcellular fractions, being 3 times longer in the cytosol than mitochondria, regardless of age, suggesting that the lower Cl- concentration in mitochondria explained the faster degradation of GSTZ1.	Dichloroacetic Acid	74-77	glutathione S-transferase zeta 1	Rattus norvegicus	13-18
31524376-9	2019	The in vitro GSTZ1 inactivation half-lives following incubation with 2 mM DCA in the presence of physiological chloride (Cl-) concentrations (cytosol 44 mM, mitochondria 1-2 mM) exhibited marked differences between subcellular fractions, being 3 times longer in the cytosol than mitochondria, regardless of age, suggesting that the lower Cl- concentration in mitochondria explained the faster degradation of GSTZ1.	Dichloroacetic Acid	74-77	glutathione S-transferase zeta 1	Rattus norvegicus	408-413
31524376-10	2019	These results demonstrate for the first time that rat mitochondrial GSTZ1 is more readily inactivated by DCA than cytosolic GSTZ1, and cytosolic GSTZ1 is inactivated more rapidly in adult than young rats.	Dichloroacetic Acid	105-108	glutathione S-transferase zeta 1	Rattus norvegicus	68-73
31762813-0	2019	Dichloroacetate Overcomes Oxaliplatin Chemoresistance in Colorectal Cancer through the miR-543/PTEN/Akt/mTOR Pathway.	Dichloroacetic Acid	0-15	microRNA 543	Homo sapiens	87-94
31762813-0	2019	Dichloroacetate Overcomes Oxaliplatin Chemoresistance in Colorectal Cancer through the miR-543/PTEN/Akt/mTOR Pathway.	Dichloroacetic Acid	0-15	phosphatase and tensin homolog	Homo sapiens	95-99
31762813-0	2019	Dichloroacetate Overcomes Oxaliplatin Chemoresistance in Colorectal Cancer through the miR-543/PTEN/Akt/mTOR Pathway.	Dichloroacetic Acid	0-15	AKT serine/threonine kinase 1	Homo sapiens	100-103
31762813-0	2019	Dichloroacetate Overcomes Oxaliplatin Chemoresistance in Colorectal Cancer through the miR-543/PTEN/Akt/mTOR Pathway.	Dichloroacetic Acid	0-15	mechanistic target of rapamycin kinase	Homo sapiens	104-108
31762813-5	2019	A microRNA (miRNA) array was used for screen, and miR-543 was identified and shown to be downregulated after DCA treatment.	Dichloroacetic Acid	109-112	microRNA 543	Homo sapiens	50-57
31762813-8	2019	The validated target gene, PTEN, was negatively regulated by miR-543 both in vitro and in vivo, and PTEN was upregulated by DCA through miR-543.	Dichloroacetic Acid	124-127	phosphatase and tensin homolog	Homo sapiens	27-31
31762813-8	2019	The validated target gene, PTEN, was negatively regulated by miR-543 both in vitro and in vivo, and PTEN was upregulated by DCA through miR-543.	Dichloroacetic Acid	124-127	phosphatase and tensin homolog	Homo sapiens	100-104
31762813-8	2019	The validated target gene, PTEN, was negatively regulated by miR-543 both in vitro and in vivo, and PTEN was upregulated by DCA through miR-543.	Dichloroacetic Acid	124-127	microRNA 543	Homo sapiens	136-143
31762813-9	2019	In addition, overexpression of miR-543 reversed the inhibition of colony formation after DCA treatment.	Dichloroacetic Acid	89-92	microRNA 543	Homo sapiens	31-38
31762813-12	2019	In conclusion, DCA restored chemosensitivity through miR-543/PTEN/Akt/mTOR pathway, and miR-543 may be a potential marker or therapeutic target for chemoresistance in CRC.	Dichloroacetic Acid	15-18	microRNA 543	Homo sapiens	53-60
31762813-12	2019	In conclusion, DCA restored chemosensitivity through miR-543/PTEN/Akt/mTOR pathway, and miR-543 may be a potential marker or therapeutic target for chemoresistance in CRC.	Dichloroacetic Acid	15-18	phosphatase and tensin homolog	Homo sapiens	61-65
31762813-12	2019	In conclusion, DCA restored chemosensitivity through miR-543/PTEN/Akt/mTOR pathway, and miR-543 may be a potential marker or therapeutic target for chemoresistance in CRC.	Dichloroacetic Acid	15-18	AKT serine/threonine kinase 1	Homo sapiens	66-69
31762813-12	2019	In conclusion, DCA restored chemosensitivity through miR-543/PTEN/Akt/mTOR pathway, and miR-543 may be a potential marker or therapeutic target for chemoresistance in CRC.	Dichloroacetic Acid	15-18	mechanistic target of rapamycin kinase	Homo sapiens	70-74
31087038-6	2019	We found that the increase of miR-144 levels, shown to be downregulated in U87 and DBTRG human GB cell lines, as well as in GB tumor samples, promoted the downregulation of mRNA of enzymes involved in bioenergetic pathways, with consequent alterations in cell metabolism, impairment of migratory capacity, and sensitization of DBTRG cells to a chemotherapeutic drug, the dichloroacetate (DCA).	Dichloroacetic Acid	371-386	microRNA 144	Homo sapiens	30-37
31624634-0	2019	GSTZ1 genotypes correlate with dichloroacetate pharmacokinetics and chronic side effects in multiple myeloma patients in a pilot phase 2 clinical trial.	Dichloroacetic Acid	31-46	glutathione S-transferase zeta 1	Homo sapiens	0-5
31624634-1	2019	Dichloroacetate (DCA) is an investigational drug targeting the glycolytic hallmark of cancer by inhibiting pyruvate dehydrogenase kinases (PDK).	Dichloroacetic Acid	0-15	pyruvate dehydrogenase kinase 2	Homo sapiens	139-142
31624634-1	2019	Dichloroacetate (DCA) is an investigational drug targeting the glycolytic hallmark of cancer by inhibiting pyruvate dehydrogenase kinases (PDK).	Dichloroacetic Acid	17-20	pyruvate dehydrogenase kinase 2	Homo sapiens	139-142
31624634-3	2019	GSTZ1 is also irreversibly inactivated by DCA.	Dichloroacetic Acid	42-45	glutathione S-transferase zeta 1	Homo sapiens	0-5
31624634-11	2019	The initial half-life of DCA was shorter in two patients, correlating with heterozygosity for GSTZ1*A genotype, a high enzyme activity variant.	Dichloroacetic Acid	25-28	glutathione S-transferase zeta 1	Homo sapiens	94-99
31624634-12	2019	Over 3 months, one patient maintained DCA trough concentrations approximately threefold higher than other patients, which correlated with a low activity promoter genotype (-1002A, rs7160195) for GSTZ1.	Dichloroacetic Acid	38-41	glutathione S-transferase zeta 1	Homo sapiens	195-200
31624634-14	2019	Overall, serum concentrations of DCA were sufficient to inhibit the constitutive target PDK2, but unlikely to inhibit targets induced in cancer.	Dichloroacetic Acid	33-36	pyruvate dehydrogenase kinase 2	Homo sapiens	88-92
31624634-15	2019	Promoter GSTZ1 polymorphisms may be important determinants of DCA concentrations and neuropathy during chronic treatment.	Dichloroacetic Acid	62-65	glutathione S-transferase zeta 1	Homo sapiens	9-14
31570705-0	2019	Therapeutic effect of dichloroacetate against atherosclerosis via hepatic FGF21 induction mediated by acute AMPK activation.	Dichloroacetic Acid	22-37	fibroblast growth factor 21	Mus musculus	74-79
31570705-2	2019	The effect of dichloroacetate (DCA), a general pyruvate dehydrogenase kinase (PDK) inhibitor, on in vivo energy expenditure in ApoE-/- mice fed a western diet (WD) has not yet been investigated.	Dichloroacetic Acid	14-29	apolipoprotein E	Mus musculus	127-131
31570705-3	2019	WD-fed ApoE-/- mice developed atherosclerotic plaques and hyperlipidemia along with obesity, which were significantly ameliorated by DCA administration.	Dichloroacetic Acid	133-136	apolipoprotein E	Mus musculus	7-11
31570705-6	2019	In addition, we found that DCA stimulated hepatic fibroblast growth factor 21 (Fgf21) mRNA expression, which might be important for lowering lipid levels and insulin sensitization via BAT activation, in a dose- and time-dependent manner associated with serum FGF21 levels.	Dichloroacetic Acid	27-30	fibroblast growth factor 21	Mus musculus	50-77
31570705-6	2019	In addition, we found that DCA stimulated hepatic fibroblast growth factor 21 (Fgf21) mRNA expression, which might be important for lowering lipid levels and insulin sensitization via BAT activation, in a dose- and time-dependent manner associated with serum FGF21 levels.	Dichloroacetic Acid	27-30	fibroblast growth factor 21	Mus musculus	79-84
31570705-6	2019	In addition, we found that DCA stimulated hepatic fibroblast growth factor 21 (Fgf21) mRNA expression, which might be important for lowering lipid levels and insulin sensitization via BAT activation, in a dose- and time-dependent manner associated with serum FGF21 levels.	Dichloroacetic Acid	27-30	fibroblast growth factor 21	Mus musculus	259-264
31570705-7	2019	Interestingly, Fgf21 mRNA expression was mediated in an AMP-activated protein kinase (AMPK)-dependent manner within several minutes after DCA treatment independent of peroxisome proliferator-activated receptor alpha (PPARalpha).	Dichloroacetic Acid	138-141	fibroblast growth factor 21	Mus musculus	15-20
31570705-8	2019	Taken together, the results suggest that enhanced glucose oxidation by DCA protects against atherosclerosis by inducing hepatic FGF21 expression and BAT activation, resulting in augmented energy expenditure for heat generation.	Dichloroacetic Acid	71-74	fibroblast growth factor 21	Mus musculus	128-133
31527683-4	2019	Here, we show that Os(II) complex 2 [Os(eta6-pcym)(bphen)(dca)]PF6 (pcym = p-cymene, bphen = bathophenanthroline, and dca = dichloroacetate), is capable of efficient and selective killing CSCs in heterogeneous populations of human breast cancer cells MCF-7 and SKBR-3.	Dichloroacetic Acid	58-61	sperm associated antigen 17	Homo sapiens	63-66
31527683-4	2019	Here, we show that Os(II) complex 2 [Os(eta6-pcym)(bphen)(dca)]PF6 (pcym = p-cymene, bphen = bathophenanthroline, and dca = dichloroacetate), is capable of efficient and selective killing CSCs in heterogeneous populations of human breast cancer cells MCF-7 and SKBR-3.	Dichloroacetic Acid	124-139	sperm associated antigen 17	Homo sapiens	63-66
31646108-9	2019	In vivo experiments revealed synergistic improved overall survival and enhanced inhibition of tumor growth upon co-treatment with dichloroacetate (DCA), a PDK inhibitor, and PD-L1 antibody, accompanied by increased IFN-gamma secretion by monocytes infiltrating tumor islets.	Dichloroacetic Acid	130-145	interferon gamma	Homo sapiens	215-224
31646108-9	2019	In vivo experiments revealed synergistic improved overall survival and enhanced inhibition of tumor growth upon co-treatment with dichloroacetate (DCA), a PDK inhibitor, and PD-L1 antibody, accompanied by increased IFN-gamma secretion by monocytes infiltrating tumor islets.	Dichloroacetic Acid	147-150	interferon gamma	Homo sapiens	215-224
31578313-5	2019	We found that combination of PDK1 knockdown or inhibition by dichloroacetic acid (DCA) with ASCT2 knockdown or with cetuximab treatment induced ROS overproduction and apoptosis in HNSCC cells, and this effect was independent of effective inhibition of EGFR downstream pathways but could be lessened by N-acetyl cysteine, an anti-oxidative agent.	Dichloroacetic Acid	61-80	solute carrier family 1 member 5	Homo sapiens	92-97
31578313-5	2019	We found that combination of PDK1 knockdown or inhibition by dichloroacetic acid (DCA) with ASCT2 knockdown or with cetuximab treatment induced ROS overproduction and apoptosis in HNSCC cells, and this effect was independent of effective inhibition of EGFR downstream pathways but could be lessened by N-acetyl cysteine, an anti-oxidative agent.	Dichloroacetic Acid	61-80	epidermal growth factor receptor	Homo sapiens	252-256
31578313-5	2019	We found that combination of PDK1 knockdown or inhibition by dichloroacetic acid (DCA) with ASCT2 knockdown or with cetuximab treatment induced ROS overproduction and apoptosis in HNSCC cells, and this effect was independent of effective inhibition of EGFR downstream pathways but could be lessened by N-acetyl cysteine, an anti-oxidative agent.	Dichloroacetic Acid	82-85	epidermal growth factor receptor	Homo sapiens	252-256
31578313-7	2019	Our findings call for potentially novel clinical trials of combining cetuximab and DCA in patients with cetuximab-sensitive EGFR-overexpressing tumors and patients with cetuximab-resistant EGFR-overexpressing tumors.	Dichloroacetic Acid	83-86	epidermal growth factor receptor	Homo sapiens	124-128
31400415-8	2019	TAK1 deletion significantly attenuated these effects induced by TCE, TCA or DCA on CD4+ T cells.	Dichloroacetic Acid	76-79	mitogen-activated protein kinase kinase kinase 7	Tribolium castaneum	0-4
31330915-9	2019	In spite of their higher tumorigenic potential, L929dt or mitochondrial L929dt cybrid cells are sensitive both in vitro and in vivo to the PDK1 inhibitor dichloroacetate, which favors OXPHOS, suggesting benefits for the use of metabolic inhibitors in the treatment of especially aggressive tumors.	Dichloroacetic Acid	154-169	pyruvate dehydrogenase kinase, isoenzyme 1	Mus musculus	139-143
31087038-6	2019	We found that the increase of miR-144 levels, shown to be downregulated in U87 and DBTRG human GB cell lines, as well as in GB tumor samples, promoted the downregulation of mRNA of enzymes involved in bioenergetic pathways, with consequent alterations in cell metabolism, impairment of migratory capacity, and sensitization of DBTRG cells to a chemotherapeutic drug, the dichloroacetate (DCA).	Dichloroacetic Acid	388-391	microRNA 144	Homo sapiens	30-37
30969803-3	2019	Both inhibitors evidently suppressed the induction of fibronectin and collagen type I in obstructed kidneys, with DCA also showing inhibitory effects on collagen type IV and alpha-smooth muscle actin (alpha-SMA).	Dichloroacetic Acid	114-117	actin gamma 2, smooth muscle	Rattus norvegicus	174-199
31109089-7	2019	Notably, DCA downregulated the expression of the cancer stem cells markers CD24/CD44/EPCAM only in PANC-1 but inhibited spheroid formation/viability in both cell lines.	Dichloroacetic Acid	9-12	pancreas protein 1	Mus musculus	99-105
30969803-3	2019	Both inhibitors evidently suppressed the induction of fibronectin and collagen type I in obstructed kidneys, with DCA also showing inhibitory effects on collagen type IV and alpha-smooth muscle actin (alpha-SMA).	Dichloroacetic Acid	114-117	actin alpha 2, smooth muscle, aorta	Mus musculus	201-210
30092712-8	2019	Furthermore, our data showed that inhibition of PDK1 activity by treatment with dichloroacetate inhibits the lactate production and oxygen consumption rate of ectopic stromal cells.	Dichloroacetic Acid	80-95	pyruvate dehydrogenase kinase 1	Homo sapiens	48-52
31109089-4	2019	PANC-1 and BXPC-3 treated with DCA showed a marked decrease in cell proliferation and migration which did not correlate with enhanced apoptosis indicating a cytostatic rather than a cytotoxic effect.	Dichloroacetic Acid	31-34	pancreas protein 1	Mus musculus	0-6
31109089-7	2019	Notably, DCA downregulated the expression of the cancer stem cells markers CD24/CD44/EPCAM only in PANC-1 but inhibited spheroid formation/viability in both cell lines.	Dichloroacetic Acid	9-12	CD24a antigen	Mus musculus	75-79
31109089-7	2019	Notably, DCA downregulated the expression of the cancer stem cells markers CD24/CD44/EPCAM only in PANC-1 but inhibited spheroid formation/viability in both cell lines.	Dichloroacetic Acid	9-12	CD44 antigen	Mus musculus	80-84
31109089-7	2019	Notably, DCA downregulated the expression of the cancer stem cells markers CD24/CD44/EPCAM only in PANC-1 but inhibited spheroid formation/viability in both cell lines.	Dichloroacetic Acid	9-12	epithelial cell adhesion molecule	Mus musculus	85-90
31156438-0	2019	Sodium Dichloroacetate Stimulates Angiogenesis by Improving Endothelial Precursor Cell Function in an AKT/GSK-3beta/Nrf2 Dependent Pathway in Vascular Dementia Rats.	Dichloroacetic Acid	0-22	AKT serine/threonine kinase 1	Rattus norvegicus	102-105
31156438-0	2019	Sodium Dichloroacetate Stimulates Angiogenesis by Improving Endothelial Precursor Cell Function in an AKT/GSK-3beta/Nrf2 Dependent Pathway in Vascular Dementia Rats.	Dichloroacetic Acid	0-22	glycogen synthase kinase 3 beta	Rattus norvegicus	106-115
31156438-0	2019	Sodium Dichloroacetate Stimulates Angiogenesis by Improving Endothelial Precursor Cell Function in an AKT/GSK-3beta/Nrf2 Dependent Pathway in Vascular Dementia Rats.	Dichloroacetic Acid	0-22	NFE2 like bZIP transcription factor 2	Rattus norvegicus	116-120
31156438-5	2019	We found that long-term DCA administration improved cognitive function in VD rats, reduced brain infarct size and brain atrophy, increased VEGF and bFGF levels in vivo, promoted angiogenesis in damaged areas, and significantly improved EPC function in VD rats.	Dichloroacetic Acid	24-27	vascular endothelial growth factor A	Rattus norvegicus	139-143
31156438-5	2019	We found that long-term DCA administration improved cognitive function in VD rats, reduced brain infarct size and brain atrophy, increased VEGF and bFGF levels in vivo, promoted angiogenesis in damaged areas, and significantly improved EPC function in VD rats.	Dichloroacetic Acid	24-27	fibroblast growth factor 2	Rattus norvegicus	148-152
31156438-6	2019	Compared with the VD group, AKT, Nrf2, eNOS expression, and intracellular NO levels were elevated in EPCs of DCA-treated VD rats.	Dichloroacetic Acid	109-112	AKT serine/threonine kinase 1	Rattus norvegicus	28-31
31156438-6	2019	Compared with the VD group, AKT, Nrf2, eNOS expression, and intracellular NO levels were elevated in EPCs of DCA-treated VD rats.	Dichloroacetic Acid	109-112	NFE2 like bZIP transcription factor 2	Rattus norvegicus	33-37
31156438-6	2019	Compared with the VD group, AKT, Nrf2, eNOS expression, and intracellular NO levels were elevated in EPCs of DCA-treated VD rats.	Dichloroacetic Acid	109-112	nitric oxide synthase 3	Rattus norvegicus	39-43
30837223-11	2019	Moreover, the PDK4 inhibitor dichloroacetate reversed chemoresistance to sorafenib or cisplatin in HCC stem cells derived from four HCC cell lines.	Dichloroacetic Acid	29-44	pyruvate dehydrogenase kinase 4	Homo sapiens	14-18
31179315-8	2019	The Slc12a2 gene RNA expression level was found to be significantly decreased only in gonad-intact and in castrated DCA-treated males.	Dichloroacetic Acid	116-119	solute carrier family 12 member 2	Rattus norvegicus	4-11
30657576-0	2019	DCA can improve the ACI-induced neurological impairment through negative regulation of Nrf2 signaling pathway.	Dichloroacetic Acid	0-3	NFE2 like bZIP transcription factor 2	Rattus norvegicus	87-91
30948782-4	2019	Metabolic stress induced by the pyruvate dehydrogenase kinase-1 (PDK1) inhibitor dichloroacetate (DCA) inhibits the macroautophagy pathway.	Dichloroacetic Acid	81-96	pyruvate dehydrogenase kinase 1	Homo sapiens	32-63
30948782-4	2019	Metabolic stress induced by the pyruvate dehydrogenase kinase-1 (PDK1) inhibitor dichloroacetate (DCA) inhibits the macroautophagy pathway.	Dichloroacetic Acid	81-96	pyruvate dehydrogenase kinase 1	Homo sapiens	65-69
30948782-4	2019	Metabolic stress induced by the pyruvate dehydrogenase kinase-1 (PDK1) inhibitor dichloroacetate (DCA) inhibits the macroautophagy pathway.	Dichloroacetic Acid	98-101	pyruvate dehydrogenase kinase 1	Homo sapiens	32-63
30948782-4	2019	Metabolic stress induced by the pyruvate dehydrogenase kinase-1 (PDK1) inhibitor dichloroacetate (DCA) inhibits the macroautophagy pathway.	Dichloroacetic Acid	98-101	pyruvate dehydrogenase kinase 1	Homo sapiens	65-69
30822618-6	2019	RESULTS: CEM/C1, CCRF/CEM, HL-60, HL-60/MX2 cells were exposed to DCA for 24 h. The sensitivity of each cell line to DCA is different and depends on the concentration.	Dichloroacetic Acid	66-69	MX dynamin like GTPase 2	Homo sapiens	40-43
31032475-8	2019	Administration of the lactate-lowering agent dichloroacetate during exercise training in mice decreases circulating TGF-beta2 levels and reduces exercise-stimulated improvements in glucose tolerance.	Dichloroacetic Acid	45-60	transforming growth factor, beta 2	Mus musculus	116-125
30447284-3	2019	TGA and DSC analysis suggested that sodium DCA was very hygroscopic.	Dichloroacetic Acid	36-46	T-box transcription factor 1	Homo sapiens	0-3
30881027-4	2019	Dichloroacetic acid (DCA) reverses the Warburg effect by inhibition of PDK1 to switch cytoplasmic glucose metabolism to mitochondrial oxidative phosphorylation (OXPHOS).	Dichloroacetic Acid	0-19	pyruvate dehydrogenase kinase 1	Homo sapiens	71-75
30881027-4	2019	Dichloroacetic acid (DCA) reverses the Warburg effect by inhibition of PDK1 to switch cytoplasmic glucose metabolism to mitochondrial oxidative phosphorylation (OXPHOS).	Dichloroacetic Acid	21-24	pyruvate dehydrogenase kinase 1	Homo sapiens	71-75
30881027-11	2019	Treatment of A2780 cells with various concentrations of DCA resulted in decreased expression of UCP2, a metabolic switch from glycolysis to mitochondrial OXPHOS, and an increase in oxidative stress induced by ROS.	Dichloroacetic Acid	56-59	uncoupling protein 2	Homo sapiens	96-100
30881027-12	2019	These effects were not observed in A2780/DDP cells with higher UCP2 expression suggesting that UCP2 might induce changes in mitochondrial functions that result in different sensitivities to DCA.	Dichloroacetic Acid	190-193	uncoupling protein 2	Homo sapiens	95-99
30371859-11	2019	The immunoblotting results showed that DCA treatment triggered cardiac AMPK signaling pathway by increasing the phosphorylation of AMPK"s upstream kinase liver kinase B1 (LKB1) under both sham operations and I/R conditions.	Dichloroacetic Acid	39-42	serine/threonine kinase 11	Mus musculus	154-169
30371859-11	2019	The immunoblotting results showed that DCA treatment triggered cardiac AMPK signaling pathway by increasing the phosphorylation of AMPK"s upstream kinase liver kinase B1 (LKB1) under both sham operations and I/R conditions.	Dichloroacetic Acid	39-42	serine/threonine kinase 11	Mus musculus	171-175
30170182-7	2019	We also observed that overexpression of pyruvate dehydrogenase kinase 4 (PDK4), an important mitochondrial matrix enzyme in cellular energy metabolism, exacerbated beta-GP-induced oxidative stress and subsequent apoptosis in VSMCs but that these effects were suppressed by dichloroacetate, a widely reported PDK4 inhibitor.	Dichloroacetic Acid	273-288	pyruvate dehydrogenase kinase 4	Homo sapiens	40-71
30170182-7	2019	We also observed that overexpression of pyruvate dehydrogenase kinase 4 (PDK4), an important mitochondrial matrix enzyme in cellular energy metabolism, exacerbated beta-GP-induced oxidative stress and subsequent apoptosis in VSMCs but that these effects were suppressed by dichloroacetate, a widely reported PDK4 inhibitor.	Dichloroacetic Acid	273-288	pyruvate dehydrogenase kinase 4	Homo sapiens	73-77
30213498-5	2018	Herein, we utilized a recently reported PDK1 inhibitor 2,2-Dichloro-1-(4-isopropoxy-3-nitrophenyl)ethan-1-one (Cpd64), which was more potent and selective than dichloroacetate (DCA) and/or dichloroacetophenone (DAP), to study the mechanism of PDK1 inhibition in TKi-mediated anti-cancer activity.	Dichloroacetic Acid	160-175	pyruvate dehydrogenase kinase 1	Homo sapiens	40-44
30159850-0	2019	Mitochondrial Modulation by Dichloroacetate Reduces Toxicity of Aberrant Glial Cells and Gliosis in the SOD1G93A Rat Model of Amyotrophic Lateral Sclerosis.	Dichloroacetic Acid	28-43	superoxide dismutase 1	Rattus norvegicus	104-108
30159850-2	2019	Neonatal astrocytes obtained from the SOD1G93A rat model of ALS exhibit mitochondrial dysfunction and neurotoxicity that can be reduced by dichloroacetate (DCA), a metabolic modulator that has been used in humans, and shows beneficial effects on disease outcome in SOD1G93A mice.	Dichloroacetic Acid	139-154	superoxide dismutase 1	Rattus norvegicus	38-42
30159850-2	2019	Neonatal astrocytes obtained from the SOD1G93A rat model of ALS exhibit mitochondrial dysfunction and neurotoxicity that can be reduced by dichloroacetate (DCA), a metabolic modulator that has been used in humans, and shows beneficial effects on disease outcome in SOD1G93A mice.	Dichloroacetic Acid	139-154	superoxide dismutase 1	Homo sapiens	265-269
30159850-2	2019	Neonatal astrocytes obtained from the SOD1G93A rat model of ALS exhibit mitochondrial dysfunction and neurotoxicity that can be reduced by dichloroacetate (DCA), a metabolic modulator that has been used in humans, and shows beneficial effects on disease outcome in SOD1G93A mice.	Dichloroacetic Acid	156-159	superoxide dismutase 1	Rattus norvegicus	38-42
30159850-2	2019	Neonatal astrocytes obtained from the SOD1G93A rat model of ALS exhibit mitochondrial dysfunction and neurotoxicity that can be reduced by dichloroacetate (DCA), a metabolic modulator that has been used in humans, and shows beneficial effects on disease outcome in SOD1G93A mice.	Dichloroacetic Acid	156-159	superoxide dismutase 1	Homo sapiens	265-269
30159850-7	2019	Furthermore, oral DCA administration (100 mg/kg, 10 days) to symptomatic SOD1G93A rats reduced MN degeneration, gliosis, and the number of GFAP/S100beta double-labeled hypertrophic glial cells in the spinal cord.	Dichloroacetic Acid	18-21	superoxide dismutase 1	Rattus norvegicus	73-77
30159850-7	2019	Furthermore, oral DCA administration (100 mg/kg, 10 days) to symptomatic SOD1G93A rats reduced MN degeneration, gliosis, and the number of GFAP/S100beta double-labeled hypertrophic glial cells in the spinal cord.	Dichloroacetic Acid	18-21	glial fibrillary acidic protein	Rattus norvegicus	139-143
30540262-4	2018	The mean and standard deviation of dichloroacetic acid and trichloroacetic acid were estimated as 282 +- 437 and 326 +- 517 mug L-1, respectively, which most often surpassed the WHO guidelines.	Dichloroacetic Acid	35-54	immunoglobulin kappa variable 1-16	Homo sapiens	128-131
30513596-8	2018	Here, we show that glucose deprivation synergizes with propranolol for anti-cancer activity, and that the rational combination of propranolol and dichloroacetate (DCA), a clinically available glycolytic inhibitor, dramatically attenuates tumor cell metabolism and mTOR signaling, inhibits proliferation and colony formation, and induces apoptosis.	Dichloroacetic Acid	146-161	mechanistic target of rapamycin kinase	Homo sapiens	264-268
30513596-8	2018	Here, we show that glucose deprivation synergizes with propranolol for anti-cancer activity, and that the rational combination of propranolol and dichloroacetate (DCA), a clinically available glycolytic inhibitor, dramatically attenuates tumor cell metabolism and mTOR signaling, inhibits proliferation and colony formation, and induces apoptosis.	Dichloroacetic Acid	163-166	mechanistic target of rapamycin kinase	Homo sapiens	264-268
30479587-6	2018	The study results show a significantly reduced RNA expression of Na-K-2Cl co-transporter (NKCC1) in thymus of 4-week DCA-treated rats (P &lt; .03).	Dichloroacetic Acid	117-120	solute carrier family 12 member 2	Rattus norvegicus	90-95
30213498-5	2018	Herein, we utilized a recently reported PDK1 inhibitor 2,2-Dichloro-1-(4-isopropoxy-3-nitrophenyl)ethan-1-one (Cpd64), which was more potent and selective than dichloroacetate (DCA) and/or dichloroacetophenone (DAP), to study the mechanism of PDK1 inhibition in TKi-mediated anti-cancer activity.	Dichloroacetic Acid	177-180	pyruvate dehydrogenase kinase 1	Homo sapiens	40-44
29956736-14	2018	In conclusion, inhibition of the Akt/GSK-3beta pathway improved the pro-apoptotic effect of DCA on human PASMCs, which may be attributed to a reversal of the Warburg effect by blocking the mutual interaction between HIF-1alpha and PDK-1, consequently downregulating HK-2.	Dichloroacetic Acid	92-95	AKT serine/threonine kinase 1	Homo sapiens	33-36
29956736-0	2018	Reversal of the Warburg effect with DCA in PDGF-treated human PASMC is potentiated by pyruvate dehydrogenase kinase-1 inhibition mediated through blocking Akt/GSK-3beta signalling.	Dichloroacetic Acid	36-39	pyruvate dehydrogenase kinase 1	Homo sapiens	86-117
29956736-14	2018	In conclusion, inhibition of the Akt/GSK-3beta pathway improved the pro-apoptotic effect of DCA on human PASMCs, which may be attributed to a reversal of the Warburg effect by blocking the mutual interaction between HIF-1alpha and PDK-1, consequently downregulating HK-2.	Dichloroacetic Acid	92-95	glycogen synthase kinase 3 beta	Homo sapiens	37-46
29956736-0	2018	Reversal of the Warburg effect with DCA in PDGF-treated human PASMC is potentiated by pyruvate dehydrogenase kinase-1 inhibition mediated through blocking Akt/GSK-3beta signalling.	Dichloroacetic Acid	36-39	AKT serine/threonine kinase 1	Homo sapiens	155-158
29956736-14	2018	In conclusion, inhibition of the Akt/GSK-3beta pathway improved the pro-apoptotic effect of DCA on human PASMCs, which may be attributed to a reversal of the Warburg effect by blocking the mutual interaction between HIF-1alpha and PDK-1, consequently downregulating HK-2.	Dichloroacetic Acid	92-95	hypoxia inducible factor 1 subunit alpha	Homo sapiens	216-226
29956736-0	2018	Reversal of the Warburg effect with DCA in PDGF-treated human PASMC is potentiated by pyruvate dehydrogenase kinase-1 inhibition mediated through blocking Akt/GSK-3beta signalling.	Dichloroacetic Acid	36-39	glycogen synthase kinase 3 beta	Homo sapiens	159-168
29956736-14	2018	In conclusion, inhibition of the Akt/GSK-3beta pathway improved the pro-apoptotic effect of DCA on human PASMCs, which may be attributed to a reversal of the Warburg effect by blocking the mutual interaction between HIF-1alpha and PDK-1, consequently downregulating HK-2.	Dichloroacetic Acid	92-95	pyruvate dehydrogenase kinase 1	Homo sapiens	231-236
29956736-10	2018	DCA at 10 mM promoted apoptosis and the upregulation of activated caspase-3 in PASMCs pre-treated with 20 ng/ml PDGF-homeodimer BB (BB).	Dichloroacetic Acid	0-3	caspase 3	Homo sapiens	66-75
29956736-12	2018	However, co-administration of 10 mM DCA with LY294002 significantly decreased the cell proliferation index and induced cell apoptosis and caspase-3 activation.	Dichloroacetic Acid	36-39	caspase 3	Homo sapiens	138-147
29956736-13	2018	The combined administration of LY294002 with DCA significantly decreased lactate concentration, promoted the depolarisation of the DeltaPsim and repressed HIF-1alpha upregulation and HK-2 activation in PASMCs treated with PDGF, which was attributed to the potentiation of DCA-induced PDK-1 inhibition by LY294002 via blockade of the Akt/GSK-3beta/HIF-1alpha signalling pathway.	Dichloroacetic Acid	45-48	hypoxia inducible factor 1 subunit alpha	Homo sapiens	155-165
29956736-13	2018	The combined administration of LY294002 with DCA significantly decreased lactate concentration, promoted the depolarisation of the DeltaPsim and repressed HIF-1alpha upregulation and HK-2 activation in PASMCs treated with PDGF, which was attributed to the potentiation of DCA-induced PDK-1 inhibition by LY294002 via blockade of the Akt/GSK-3beta/HIF-1alpha signalling pathway.	Dichloroacetic Acid	45-48	hexokinase 2	Homo sapiens	183-187
29956736-13	2018	The combined administration of LY294002 with DCA significantly decreased lactate concentration, promoted the depolarisation of the DeltaPsim and repressed HIF-1alpha upregulation and HK-2 activation in PASMCs treated with PDGF, which was attributed to the potentiation of DCA-induced PDK-1 inhibition by LY294002 via blockade of the Akt/GSK-3beta/HIF-1alpha signalling pathway.	Dichloroacetic Acid	45-48	pyruvate dehydrogenase kinase 1	Homo sapiens	284-289
29956736-13	2018	The combined administration of LY294002 with DCA significantly decreased lactate concentration, promoted the depolarisation of the DeltaPsim and repressed HIF-1alpha upregulation and HK-2 activation in PASMCs treated with PDGF, which was attributed to the potentiation of DCA-induced PDK-1 inhibition by LY294002 via blockade of the Akt/GSK-3beta/HIF-1alpha signalling pathway.	Dichloroacetic Acid	45-48	AKT serine/threonine kinase 1	Homo sapiens	333-336
29956736-13	2018	The combined administration of LY294002 with DCA significantly decreased lactate concentration, promoted the depolarisation of the DeltaPsim and repressed HIF-1alpha upregulation and HK-2 activation in PASMCs treated with PDGF, which was attributed to the potentiation of DCA-induced PDK-1 inhibition by LY294002 via blockade of the Akt/GSK-3beta/HIF-1alpha signalling pathway.	Dichloroacetic Acid	45-48	glycogen synthase kinase 3 beta	Homo sapiens	337-346
29956736-13	2018	The combined administration of LY294002 with DCA significantly decreased lactate concentration, promoted the depolarisation of the DeltaPsim and repressed HIF-1alpha upregulation and HK-2 activation in PASMCs treated with PDGF, which was attributed to the potentiation of DCA-induced PDK-1 inhibition by LY294002 via blockade of the Akt/GSK-3beta/HIF-1alpha signalling pathway.	Dichloroacetic Acid	45-48	hypoxia inducible factor 1 subunit alpha	Homo sapiens	347-357
29956736-14	2018	In conclusion, inhibition of the Akt/GSK-3beta pathway improved the pro-apoptotic effect of DCA on human PASMCs, which may be attributed to a reversal of the Warburg effect by blocking the mutual interaction between HIF-1alpha and PDK-1, consequently downregulating HK-2.	Dichloroacetic Acid	92-95	hexokinase 2	Homo sapiens	266-270
29907593-8	2018	Inhibition of PDK4 with dichloroacetate (DCA) resulted in increased PDH activity, reduced cell growth, and G0-G1 phase arrest in bladder cancer cells.	Dichloroacetic Acid	24-39	pyruvate dehydrogenase kinase 4	Homo sapiens	14-18
29907593-8	2018	Inhibition of PDK4 with dichloroacetate (DCA) resulted in increased PDH activity, reduced cell growth, and G0-G1 phase arrest in bladder cancer cells.	Dichloroacetic Acid	41-44	pyruvate dehydrogenase kinase 4	Homo sapiens	14-18
29853471-1	2018	Glutathione transferase zeta1 (GSTZ1) catalyzes glutathione (GSH)-dependent dechlorination of dichloroacetate (DCA), an investigational drug with therapeutic potential in metabolic disorders and cancer.	Dichloroacetic Acid	94-109	glutathione S-transferase zeta 1	Homo sapiens	0-29
30108111-4	2018	PDKs activity in human and mouse platelets was inhibited with dichloroacetic acid (DCA), a potent inhibitor of all 4 forms of PDK.	Dichloroacetic Acid	62-81	pyruvate dehydrogenase kinase, isoenzyme 1	Mus musculus	0-4
30108111-4	2018	PDKs activity in human and mouse platelets was inhibited with dichloroacetic acid (DCA), a potent inhibitor of all 4 forms of PDK.	Dichloroacetic Acid	83-86	pyruvate dehydrogenase kinase, isoenzyme 1	Mus musculus	0-4
30108111-5	2018	Human and mouse platelets pretreated with DCA exhibited decreased platelet aggregation to suboptimal doses of collagen, convulxin, thrombin, and adenosine diphosphate concomitant with decreased glucose uptake.	Dichloroacetic Acid	42-45	coagulation factor II	Mus musculus	131-139
30108111-7	2018	Furthermore, DCA inhibited ATP secretion, thromboxane A2 generation, and tyrosine phosphorylation of Syk and PLCgamma2 in response to collagen or convulxin in human and mouse platelets (P &lt; .05 vs vehicle treated).	Dichloroacetic Acid	13-16	spleen associated tyrosine kinase	Homo sapiens	101-104
30108111-7	2018	Furthermore, DCA inhibited ATP secretion, thromboxane A2 generation, and tyrosine phosphorylation of Syk and PLCgamma2 in response to collagen or convulxin in human and mouse platelets (P &lt; .05 vs vehicle treated).	Dichloroacetic Acid	13-16	phospholipase C gamma 2	Homo sapiens	109-118
29853471-1	2018	Glutathione transferase zeta1 (GSTZ1) catalyzes glutathione (GSH)-dependent dechlorination of dichloroacetate (DCA), an investigational drug with therapeutic potential in metabolic disorders and cancer.	Dichloroacetic Acid	94-109	glutathione S-transferase zeta 1	Homo sapiens	31-36
29853471-1	2018	Glutathione transferase zeta1 (GSTZ1) catalyzes glutathione (GSH)-dependent dechlorination of dichloroacetate (DCA), an investigational drug with therapeutic potential in metabolic disorders and cancer.	Dichloroacetic Acid	111-114	glutathione S-transferase zeta 1	Homo sapiens	0-29
29853471-1	2018	Glutathione transferase zeta1 (GSTZ1) catalyzes glutathione (GSH)-dependent dechlorination of dichloroacetate (DCA), an investigational drug with therapeutic potential in metabolic disorders and cancer.	Dichloroacetic Acid	111-114	glutathione S-transferase zeta 1	Homo sapiens	31-36
29853471-4	2018	GSTZ1 expression and activity with DCA were determined in 103 human hepatic mitochondrial samples prepared from livers of donors aged 1 day to 84 years.	Dichloroacetic Acid	35-38	glutathione S-transferase zeta 1	Homo sapiens	0-5
29626439-0	2018	Regulation of dichloroacetate biotransformation in rat liver and extrahepatic tissues by GSTZ1 expression and chloride concentration.	Dichloroacetic Acid	14-29	glutathione S-transferase zeta 1	Rattus norvegicus	89-94
29626439-1	2018	Biotransformation of dichloroacetate (DCA) to glyoxylate by hepatic glutathione transferase zeta 1 (GSTZ1) is considered the principal determinant of the rate of plasma clearance of the drug.	Dichloroacetic Acid	21-36	glutathione S-transferase zeta 1	Rattus norvegicus	68-98
29626439-1	2018	Biotransformation of dichloroacetate (DCA) to glyoxylate by hepatic glutathione transferase zeta 1 (GSTZ1) is considered the principal determinant of the rate of plasma clearance of the drug.	Dichloroacetic Acid	21-36	glutathione S-transferase zeta 1	Rattus norvegicus	100-105
29626439-1	2018	Biotransformation of dichloroacetate (DCA) to glyoxylate by hepatic glutathione transferase zeta 1 (GSTZ1) is considered the principal determinant of the rate of plasma clearance of the drug.	Dichloroacetic Acid	38-41	glutathione S-transferase zeta 1	Rattus norvegicus	68-98
29626439-1	2018	Biotransformation of dichloroacetate (DCA) to glyoxylate by hepatic glutathione transferase zeta 1 (GSTZ1) is considered the principal determinant of the rate of plasma clearance of the drug.	Dichloroacetic Acid	38-41	glutathione S-transferase zeta 1	Rattus norvegicus	100-105
29626439-5	2018	Hepatic chloride concentrations, which influence the rate of GSTZ1 inactivation by DCA, were lower in rat than in human tissues and rats did not show the age dependence previously seen in humans.	Dichloroacetic Acid	83-86	glutathione S-transferase zeta 1	Rattus norvegicus	61-66
29626439-8	2018	GSTZ1 activity with DCA could not be measured accurately in kidney cell-free homogenates due to rapid depletion of glutathione by gamma-glutamyl transpeptidase.	Dichloroacetic Acid	20-23	glutathione S-transferase zeta 1	Rattus norvegicus	0-5
29626439-9	2018	Following oral administration of DCA, 100 mg/kg, to rats, GSTZ1 expression and activity were reduced in all rat tissues, but chloride concentrations were not affected.	Dichloroacetic Acid	33-36	glutathione S-transferase zeta 1	Rattus norvegicus	58-63
29766157-6	2018	Pt(iv)-DCA compounds determine a substantial increase of ROS production, blockage of oxidative phosphorylation, hypopolarization of the mitochondrial membrane, and caspase-3/7 mediated apoptotic cell death.	Dichloroacetic Acid	7-10	caspase 3	Homo sapiens	164-173
29844702-9	2018	Furthermore, Perifosine, an AKT inhibitor, can greatly weaken the capacity of inducing apoptosis by DCA.	Dichloroacetic Acid	100-103	AKT serine/threonine kinase 1	Homo sapiens	28-31
28846566-9	2018	In addition, DCA reduced the messenger RNA expression of tumor necrosis factor alpha and interleukin 1beta in brain hippocampus and cortex after ROSC.	Dichloroacetic Acid	13-16	tumor necrosis factor	Rattus norvegicus	57-84
28846566-9	2018	In addition, DCA reduced the messenger RNA expression of tumor necrosis factor alpha and interleukin 1beta in brain hippocampus and cortex after ROSC.	Dichloroacetic Acid	13-16	interleukin 1 beta	Rattus norvegicus	89-106
29495001-3	2018	Using sodium dichloroacetate (DCA), a previously reported small molecule inhibitor of AKT, the present studies uncovered an AKT-independent mechanism in regulating vascular calcification.	Dichloroacetic Acid	6-28	AKT serine/threonine kinase 1	Homo sapiens	86-89
29495001-3	2018	Using sodium dichloroacetate (DCA), a previously reported small molecule inhibitor of AKT, the present studies uncovered an AKT-independent mechanism in regulating vascular calcification.	Dichloroacetic Acid	6-28	AKT serine/threonine kinase 1	Homo sapiens	124-127
29495001-3	2018	Using sodium dichloroacetate (DCA), a previously reported small molecule inhibitor of AKT, the present studies uncovered an AKT-independent mechanism in regulating vascular calcification.	Dichloroacetic Acid	30-33	AKT serine/threonine kinase 1	Homo sapiens	86-89
29495001-5	2018	Furthermore, DCA markedly enhanced vascular calcification in atherosclerotic ApoE knockout mice in vivo.	Dichloroacetic Acid	13-16	apolipoprotein E	Mus musculus	77-81
29495001-6	2018	DCA-induced VSMC calcification was associated with increased Runx2, but not via activation of AKT, a key upstream signal that upregulates Runx2 during VSMC calcification.	Dichloroacetic Acid	0-3	RUNX family transcription factor 2	Homo sapiens	61-66
29495001-6	2018	DCA-induced VSMC calcification was associated with increased Runx2, but not via activation of AKT, a key upstream signal that upregulates Runx2 during VSMC calcification.	Dichloroacetic Acid	0-3	RUNX family transcription factor 2	Homo sapiens	138-143
29495001-7	2018	In contrast, DCA inhibited AKT activation and induced activation of p38 MAPK in calcified atherosclerotic lesions in vivo and calcified VSMC in vitro.	Dichloroacetic Acid	13-16	AKT serine/threonine kinase 1	Homo sapiens	27-30
29495001-7	2018	In contrast, DCA inhibited AKT activation and induced activation of p38 MAPK in calcified atherosclerotic lesions in vivo and calcified VSMC in vitro.	Dichloroacetic Acid	13-16	mitogen-activated protein kinase 14	Homo sapiens	68-71
29495001-8	2018	Using a pharmacological inhibitor and shRNA for p38 MAPK, we demonstrated that inhibition of p38 MAPK blocked DCA-induced Runx2 upregulation and VSMC calcification.	Dichloroacetic Acid	110-113	mitogen-activated protein kinase 14	Homo sapiens	48-51
29495001-8	2018	Using a pharmacological inhibitor and shRNA for p38 MAPK, we demonstrated that inhibition of p38 MAPK blocked DCA-induced Runx2 upregulation and VSMC calcification.	Dichloroacetic Acid	110-113	mitogen-activated protein kinase 14	Homo sapiens	93-96
29495001-8	2018	Using a pharmacological inhibitor and shRNA for p38 MAPK, we demonstrated that inhibition of p38 MAPK blocked DCA-induced Runx2 upregulation and VSMC calcification.	Dichloroacetic Acid	110-113	RUNX family transcription factor 2	Homo sapiens	122-127
29495001-9	2018	Furthermore, Runx2 deletion attenuated DCA-induced VSMC calcification.	Dichloroacetic Acid	39-42	RUNX family transcription factor 2	Homo sapiens	13-18
29495001-11	2018	Knockdown p38 MAPK inhibited DCA-induced Runx2 transactivity, supporting the function of p38 MAPK in regulating Runx2 transactivity.	Dichloroacetic Acid	29-32	mitogen-activated protein kinase 14	Homo sapiens	10-13
29495001-11	2018	Knockdown p38 MAPK inhibited DCA-induced Runx2 transactivity, supporting the function of p38 MAPK in regulating Runx2 transactivity.	Dichloroacetic Acid	29-32	RUNX family transcription factor 2	Homo sapiens	41-46
29495001-11	2018	Knockdown p38 MAPK inhibited DCA-induced Runx2 transactivity, supporting the function of p38 MAPK in regulating Runx2 transactivity.	Dichloroacetic Acid	29-32	mitogen-activated protein kinase 14	Homo sapiens	89-92
29495001-11	2018	Knockdown p38 MAPK inhibited DCA-induced Runx2 transactivity, supporting the function of p38 MAPK in regulating Runx2 transactivity.	Dichloroacetic Acid	29-32	RUNX family transcription factor 2	Homo sapiens	112-117
29495001-12	2018	Our studies have uncovered a new function of DCA in regulating vascular calcification, via AKT-independent activation of p38 MAPK.	Dichloroacetic Acid	45-48	AKT serine/threonine kinase 1	Homo sapiens	91-94
29495001-12	2018	Our studies have uncovered a new function of DCA in regulating vascular calcification, via AKT-independent activation of p38 MAPK.	Dichloroacetic Acid	45-48	mitogen-activated protein kinase 14	Homo sapiens	121-124
29844702-10	2018	The results indicate that the AKT-mTOR pathway, a main negative regulator of autophagy, is involved in the DCA-induced inhibition of autophagy.	Dichloroacetic Acid	107-110	AKT serine/threonine kinase 1	Homo sapiens	30-33
29844702-10	2018	The results indicate that the AKT-mTOR pathway, a main negative regulator of autophagy, is involved in the DCA-induced inhibition of autophagy.	Dichloroacetic Acid	107-110	mechanistic target of rapamycin kinase	Homo sapiens	34-38
29641284-0	2018	Personalized Dosing of Dichloroacetate Using GSTZ1 Clinical Genotyping Assay.	Dichloroacetic Acid	23-38	glutathione S-transferase zeta 1	Homo sapiens	45-50
29740092-4	2018	The unconjugated bile acids CDCA, DCA and UDCA and, to a lesser extent, CA were found to be relatively potent agonists for the GPBAR1 (TGR5) receptor and elicit cAMP release, whereas all glyco- and tauro- conjugated bile acids are weak agonists.	Dichloroacetic Acid	29-32	G protein-coupled bile acid receptor 1	Homo sapiens	127-133
29740092-4	2018	The unconjugated bile acids CDCA, DCA and UDCA and, to a lesser extent, CA were found to be relatively potent agonists for the GPBAR1 (TGR5) receptor and elicit cAMP release, whereas all glyco- and tauro- conjugated bile acids are weak agonists.	Dichloroacetic Acid	29-32	G protein-coupled bile acid receptor 1	Homo sapiens	135-139
29854830-1	2018	We recently have proved that excessive fecal DCA caused by high-fat diet may serve as an endogenous danger-associated molecular pattern to activate NLRP3 inflammasome and thus contributes to the development of inflammatory bowel disease (IBD).	Dichloroacetic Acid	45-48	NLR family, pyrin domain containing 3	Mus musculus	148-153
29854830-2	2018	Moreover, the effect of DCA on inflammasome activation is mainly mediated through bile acid receptor sphingosine-1-phosphate receptor 2 (S1PR2); however, the intermediate process remains unclear.	Dichloroacetic Acid	24-27	sphingosine-1-phosphate receptor 2	Mus musculus	101-135
29854830-2	2018	Moreover, the effect of DCA on inflammasome activation is mainly mediated through bile acid receptor sphingosine-1-phosphate receptor 2 (S1PR2); however, the intermediate process remains unclear.	Dichloroacetic Acid	24-27	sphingosine-1-phosphate receptor 2	Mus musculus	137-142
29854830-4	2018	In this study, we found that DCA could dose dependently upregulate S1PR2 expression.	Dichloroacetic Acid	29-32	sphingosine-1-phosphate receptor 2	Mus musculus	67-72
29854830-5	2018	Meanwhile, DCA-induced NLRP3 inflammasome activation is at least partially achieved through stimulating extracellular regulated protein kinases (ERK) signaling pathway downstream of S1PR2 followed by promoting of lysosomal cathepsin B release.	Dichloroacetic Acid	11-14	NLR family, pyrin domain containing 3	Mus musculus	23-28
29854830-5	2018	Meanwhile, DCA-induced NLRP3 inflammasome activation is at least partially achieved through stimulating extracellular regulated protein kinases (ERK) signaling pathway downstream of S1PR2 followed by promoting of lysosomal cathepsin B release.	Dichloroacetic Acid	11-14	mitogen-activated protein kinase 1	Mus musculus	145-148
29854830-5	2018	Meanwhile, DCA-induced NLRP3 inflammasome activation is at least partially achieved through stimulating extracellular regulated protein kinases (ERK) signaling pathway downstream of S1PR2 followed by promoting of lysosomal cathepsin B release.	Dichloroacetic Acid	11-14	sphingosine-1-phosphate receptor 2	Mus musculus	182-187
29854830-5	2018	Meanwhile, DCA-induced NLRP3 inflammasome activation is at least partially achieved through stimulating extracellular regulated protein kinases (ERK) signaling pathway downstream of S1PR2 followed by promoting of lysosomal cathepsin B release.	Dichloroacetic Acid	11-14	cathepsin B	Mus musculus	223-234
29854830-6	2018	DCA enema significantly aggravated DSS-induced colitis in mice and S1PR2 inhibitor as well as inflammasome inhibition by cathepsin B antagonist substantially reducing the mature IL-1beta production and alleviated colonic inflammation superimposed by DCA.	Dichloroacetic Acid	0-3	sphingosine-1-phosphate receptor 2	Mus musculus	67-72
29854830-6	2018	DCA enema significantly aggravated DSS-induced colitis in mice and S1PR2 inhibitor as well as inflammasome inhibition by cathepsin B antagonist substantially reducing the mature IL-1beta production and alleviated colonic inflammation superimposed by DCA.	Dichloroacetic Acid	0-3	interleukin 1 beta	Mus musculus	178-186
29854830-6	2018	DCA enema significantly aggravated DSS-induced colitis in mice and S1PR2 inhibitor as well as inflammasome inhibition by cathepsin B antagonist substantially reducing the mature IL-1beta production and alleviated colonic inflammation superimposed by DCA.	Dichloroacetic Acid	250-253	cathepsin B	Mus musculus	121-132
29854830-7	2018	Therefore, our findings suggest that S1PR2/ERK1/2/cathepsin B signaling plays a critical role in triggering inflammasome activation by DCA and S1PR2 may represent a new potential therapeutic target for the management of intestinal inflammation in individuals on a high-fat diet.	Dichloroacetic Acid	135-138	sphingosine-1-phosphate receptor 2	Mus musculus	37-42
29854830-7	2018	Therefore, our findings suggest that S1PR2/ERK1/2/cathepsin B signaling plays a critical role in triggering inflammasome activation by DCA and S1PR2 may represent a new potential therapeutic target for the management of intestinal inflammation in individuals on a high-fat diet.	Dichloroacetic Acid	135-138	mitogen-activated protein kinase 3	Mus musculus	43-49
29854830-7	2018	Therefore, our findings suggest that S1PR2/ERK1/2/cathepsin B signaling plays a critical role in triggering inflammasome activation by DCA and S1PR2 may represent a new potential therapeutic target for the management of intestinal inflammation in individuals on a high-fat diet.	Dichloroacetic Acid	135-138	cathepsin B	Mus musculus	50-61
29471628-7	2018	Additionally, culturing IPEC-J2 cells in the presence of 5 mM DCA markedly increased the phosphorylation of PDHA1 and PDH phosphatase 1, but inhibited PDK1 phosphorylation ( P &lt; 0.05).	Dichloroacetic Acid	62-65	pyruvate dehydrogenase E1 component subunit alpha, somatic form, mitochondrial	Sus scrofa	108-113
29471628-7	2018	Additionally, culturing IPEC-J2 cells in the presence of 5 mM DCA markedly increased the phosphorylation of PDHA1 and PDH phosphatase 1, but inhibited PDK1 phosphorylation ( P &lt; 0.05).	Dichloroacetic Acid	62-65	pyruvate dehydrogenase kinase 1	Sus scrofa	151-155
29641284-1	2018	AIMS: Dichloroacetate (DCA) represents the first targeted therapy for pyruvate dehydrogenase complex deficiency; it is metabolized by glutathione transferase zeta1 (GSTZ1).	Dichloroacetic Acid	6-21	glutathione S-transferase zeta 1	Homo sapiens	134-163
29641284-1	2018	AIMS: Dichloroacetate (DCA) represents the first targeted therapy for pyruvate dehydrogenase complex deficiency; it is metabolized by glutathione transferase zeta1 (GSTZ1).	Dichloroacetic Acid	6-21	glutathione S-transferase zeta 1	Homo sapiens	165-170
29641284-1	2018	AIMS: Dichloroacetate (DCA) represents the first targeted therapy for pyruvate dehydrogenase complex deficiency; it is metabolized by glutathione transferase zeta1 (GSTZ1).	Dichloroacetic Acid	23-26	glutathione S-transferase zeta 1	Homo sapiens	134-163
29641284-1	2018	AIMS: Dichloroacetate (DCA) represents the first targeted therapy for pyruvate dehydrogenase complex deficiency; it is metabolized by glutathione transferase zeta1 (GSTZ1).	Dichloroacetic Acid	23-26	glutathione S-transferase zeta 1	Homo sapiens	165-170
29641284-2	2018	Variation in the GSTZ1 haplotype is the principal variable influencing DCA kinetics and dynamics in humans.	Dichloroacetic Acid	71-74	glutathione S-transferase zeta 1	Homo sapiens	17-22
29641284-3	2018	We aimed to develop a sensitive and rapid clinical genetic screening test for determining GSTZ1 haplotype status in individuals who would be treated with DCA, and then apply the test for the investigation of the plasma pharmacokinetics (PK) of DCA as a function of GSTZ1 haplotype.	Dichloroacetic Acid	154-157	glutathione S-transferase zeta 1	Homo sapiens	90-95
29196929-10	2018	CONCLUSIONS: In the context of a high dCa (1.75 mmol/l) and a stable dose of calcitriol, preoperative ALP levels were significantly associated with calcium requirement in patients with CKD5 undergoing PTX.	Dichloroacetic Acid	38-41	alkaline phosphatase, placental	Homo sapiens	102-105
29431735-6	2018	Moreover, the glycemia levels correlated inversely with the level of skeletal glucose uptake, and pharmacological treatment with the glycolysis inhibitor dichloroacetate (DCA), which restored glucose metabolism in Vhl-deficient osteogenic cells in vitro, prevented the development of the systemic metabolic phenotype in the mutant mice.	Dichloroacetic Acid	154-169	von Hippel-Lindau tumor suppressor	Mus musculus	214-217
29431735-6	2018	Moreover, the glycemia levels correlated inversely with the level of skeletal glucose uptake, and pharmacological treatment with the glycolysis inhibitor dichloroacetate (DCA), which restored glucose metabolism in Vhl-deficient osteogenic cells in vitro, prevented the development of the systemic metabolic phenotype in the mutant mice.	Dichloroacetic Acid	171-174	von Hippel-Lindau tumor suppressor	Mus musculus	214-217
28914978-6	2018	A 2-compartment model accounting for saturable clearance and GSTZ1 enzyme turnover successfully characterized the DCA PK in adults and children.	Dichloroacetic Acid	114-117	glutathione S-transferase zeta 1	Homo sapiens	61-66
28914978-7	2018	DCA-induced inactivation of GSTZ1 resulted in phenoconversion of all subjects into slow metabolizers after repeated dosing.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	28-33
28914978-8	2018	However, rate and extent of inactivation was 2-fold higher in subjects without the wild-type EGT allelic variant of GSTZ1, resulting in further phenoconversion into ultraslow metabolizers after repeated DCA administration.	Dichloroacetic Acid	203-206	glutathione S-transferase zeta 1	Homo sapiens	116-121
28914978-9	2018	Furthermore, DCA-induced GSTZ1 inactivation rate and extent was found to be 25- to 30-fold lower in children than in adults, potentially accounting for the observed age-dependent changes in PK.	Dichloroacetic Acid	13-16	glutathione S-transferase zeta 1	Homo sapiens	25-30
29143921-5	2018	Dichloroacetate (DCA) can alter tumor pHi by inhibiting the enzyme pyruvate dehydrogenase kinase causing reduced lactate (increasing pHi), or by decreasing the expression of monocarboxylate transporters and vacuolar ATPase leading to reduced pHi.	Dichloroacetic Acid	0-15	glucose-6-phosphate isomerase 1	Mus musculus	38-41
28915065-0	2018	Targeting Hypoxia-Inducible Factor-1alpha/Pyruvate Dehydrogenase Kinase 1 Axis by Dichloroacetate Suppresses Bleomycin-induced Pulmonary Fibrosis.	Dichloroacetic Acid	82-97	hypoxia inducible factor 1, alpha subunit	Mus musculus	10-41
28915065-0	2018	Targeting Hypoxia-Inducible Factor-1alpha/Pyruvate Dehydrogenase Kinase 1 Axis by Dichloroacetate Suppresses Bleomycin-induced Pulmonary Fibrosis.	Dichloroacetic Acid	82-97	pyruvate dehydrogenase kinase, isoenzyme 1	Mus musculus	42-73
30067423-5	2018	Mechanically, AGK2 and Sirtinol were found to increase the lysine-acetylation and decrease the serine-phosphorylation of PDHA1, which enabled the two inhibitors to synergize with DCA to further activate PDHA1.	Dichloroacetic Acid	179-182	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	121-126
30067423-5	2018	Mechanically, AGK2 and Sirtinol were found to increase the lysine-acetylation and decrease the serine-phosphorylation of PDHA1, which enabled the two inhibitors to synergize with DCA to further activate PDHA1.	Dichloroacetic Acid	179-182	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	203-208
29143921-5	2018	Dichloroacetate (DCA) can alter tumor pHi by inhibiting the enzyme pyruvate dehydrogenase kinase causing reduced lactate (increasing pHi), or by decreasing the expression of monocarboxylate transporters and vacuolar ATPase leading to reduced pHi.	Dichloroacetic Acid	0-15	glucose-6-phosphate isomerase 1	Mus musculus	133-136
29143921-5	2018	Dichloroacetate (DCA) can alter tumor pHi by inhibiting the enzyme pyruvate dehydrogenase kinase causing reduced lactate (increasing pHi), or by decreasing the expression of monocarboxylate transporters and vacuolar ATPase leading to reduced pHi.	Dichloroacetic Acid	0-15	glucose-6-phosphate isomerase 1	Mus musculus	133-136
29143921-5	2018	Dichloroacetate (DCA) can alter tumor pHi by inhibiting the enzyme pyruvate dehydrogenase kinase causing reduced lactate (increasing pHi), or by decreasing the expression of monocarboxylate transporters and vacuolar ATPase leading to reduced pHi.	Dichloroacetic Acid	17-20	glucose-6-phosphate isomerase 1	Mus musculus	38-41
29143921-5	2018	Dichloroacetate (DCA) can alter tumor pHi by inhibiting the enzyme pyruvate dehydrogenase kinase causing reduced lactate (increasing pHi), or by decreasing the expression of monocarboxylate transporters and vacuolar ATPase leading to reduced pHi.	Dichloroacetic Acid	17-20	glucose-6-phosphate isomerase 1	Mus musculus	133-136
29143921-5	2018	Dichloroacetate (DCA) can alter tumor pHi by inhibiting the enzyme pyruvate dehydrogenase kinase causing reduced lactate (increasing pHi), or by decreasing the expression of monocarboxylate transporters and vacuolar ATPase leading to reduced pHi.	Dichloroacetic Acid	17-20	glucose-6-phosphate isomerase 1	Mus musculus	133-136
29143921-6	2018	Since the net in vivo effect of DCA on pHi is difficult to predict, the purpose of this study was to quantify the magnitude of acute pHi change in glioblastoma after a single DCA injection using AACID CEST MRI.	Dichloroacetic Acid	175-178	glucose-6-phosphate isomerase 1	Mus musculus	133-136
29143921-10	2018	One hour after DCA injection there was a significant increase in tumor AACID level by 0.04 +- 0.01 corresponding to a 0.16 decrease in pHi, and no change in AACID in contralateral tissue.	Dichloroacetic Acid	15-18	glucose-6-phosphate isomerase 1	Mus musculus	135-138
28447512-9	2017	Hepatic concentrations of IL-1beta, MCP-1 and TNF-alpha in DCA group were reduced to 68%, 75% and 63% of DC values, respectively.	Dichloroacetic Acid	59-62	interleukin 1 beta	Rattus norvegicus	26-34
28734906-11	2017	The DCA Vantage was able to measure a patient and an EQA sample with an HbA1c value close to 6.5% both accurately and precisely.	Dichloroacetic Acid	4-7	hemoglobin subunit alpha 1	Homo sapiens	72-76
29416681-3	2018	We show here that a metabolic switch to oxidative phosphorylation (OXPHOS), either by treating cells with dichloroacetate (DCA) or by changing the available substrates, reduced expression of ABCB1, ABCC1, ABCC5 and ABCG2 in wild-type p53-expressing cells.	Dichloroacetic Acid	106-121	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	215-220
29416681-3	2018	We show here that a metabolic switch to oxidative phosphorylation (OXPHOS), either by treating cells with dichloroacetate (DCA) or by changing the available substrates, reduced expression of ABCB1, ABCC1, ABCC5 and ABCG2 in wild-type p53-expressing cells.	Dichloroacetic Acid	106-121	tumor protein p53	Homo sapiens	234-237
29416681-3	2018	We show here that a metabolic switch to oxidative phosphorylation (OXPHOS), either by treating cells with dichloroacetate (DCA) or by changing the available substrates, reduced expression of ABCB1, ABCC1, ABCC5 and ABCG2 in wild-type p53-expressing cells.	Dichloroacetic Acid	123-126	ATP binding cassette subfamily C member 5	Homo sapiens	205-210
29416681-3	2018	We show here that a metabolic switch to oxidative phosphorylation (OXPHOS), either by treating cells with dichloroacetate (DCA) or by changing the available substrates, reduced expression of ABCB1, ABCC1, ABCC5 and ABCG2 in wild-type p53-expressing cells.	Dichloroacetic Acid	123-126	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	215-220
29416681-3	2018	We show here that a metabolic switch to oxidative phosphorylation (OXPHOS), either by treating cells with dichloroacetate (DCA) or by changing the available substrates, reduced expression of ABCB1, ABCC1, ABCC5 and ABCG2 in wild-type p53-expressing cells.	Dichloroacetic Acid	123-126	tumor protein p53	Homo sapiens	234-237
28964917-7	2017	Bypass or pharmacological reactivation of PDH by dichloroacetate restored the peroxide removal capability of mitochondria from Nnt-/- mice on a HFD.	Dichloroacetic Acid	49-64	nicotinamide nucleotide transhydrogenase	Mus musculus	127-130
28447512-9	2017	Hepatic concentrations of IL-1beta, MCP-1 and TNF-alpha in DCA group were reduced to 68%, 75% and 63% of DC values, respectively.	Dichloroacetic Acid	59-62	mast cell protease 1-like 1	Rattus norvegicus	36-41
28447512-9	2017	Hepatic concentrations of IL-1beta, MCP-1 and TNF-alpha in DCA group were reduced to 68%, 75% and 63% of DC values, respectively.	Dichloroacetic Acid	59-62	tumor necrosis factor	Rattus norvegicus	46-55
29070699-6	2017	Treatment of explanted human PAH lungs with the PDK inhibitor dichloroacetate (DCA) ex vivo activated PDH and increased mitochondrial respiration.	Dichloroacetic Acid	62-77	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	102-105
29059435-6	2017	Dichloroacetate is the prototypic xenobiotic inhibitor of PDK, thereby maintaining PDC in its unphosphorylated, catalytically active form.	Dichloroacetic Acid	0-15	phosducin	Homo sapiens	83-86
29070699-6	2017	Treatment of explanted human PAH lungs with the PDK inhibitor dichloroacetate (DCA) ex vivo activated PDH and increased mitochondrial respiration.	Dichloroacetic Acid	79-82	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	102-105
28878225-11	2017	In summary, our results indicate that DCA, by inducing OXPHOS, promotes ERK5/MEF2 activation leading to LDLR expression.	Dichloroacetic Acid	38-41	mitogen-activated protein kinase 7	Homo sapiens	72-76
28878225-0	2017	The PDK1 Inhibitor Dichloroacetate Controls Cholesterol Homeostasis Through the ERK5/MEF2 Pathway.	Dichloroacetic Acid	19-34	pyruvate dehydrogenase kinase 1	Homo sapiens	4-8
28878225-0	2017	The PDK1 Inhibitor Dichloroacetate Controls Cholesterol Homeostasis Through the ERK5/MEF2 Pathway.	Dichloroacetic Acid	19-34	mitogen-activated protein kinase 7	Homo sapiens	80-84
28878225-0	2017	The PDK1 Inhibitor Dichloroacetate Controls Cholesterol Homeostasis Through the ERK5/MEF2 Pathway.	Dichloroacetic Acid	19-34	myocyte enhancer factor 2A	Homo sapiens	85-89
28878225-9	2017	DCA induces expression of the MAPK ERK5 that turns on the transcription factor MEF2.	Dichloroacetic Acid	0-3	mitogen-activated protein kinase 7	Homo sapiens	35-39
28878225-9	2017	DCA induces expression of the MAPK ERK5 that turns on the transcription factor MEF2.	Dichloroacetic Acid	0-3	myocyte enhancer factor 2A	Homo sapiens	79-83
28878225-11	2017	In summary, our results indicate that DCA, by inducing OXPHOS, promotes ERK5/MEF2 activation leading to LDLR expression.	Dichloroacetic Acid	38-41	myocyte enhancer factor 2A	Homo sapiens	77-81
28878225-11	2017	In summary, our results indicate that DCA, by inducing OXPHOS, promotes ERK5/MEF2 activation leading to LDLR expression.	Dichloroacetic Acid	38-41	low density lipoprotein receptor	Homo sapiens	104-108
28928817-6	2017	The proliferation of TE-1 cells was markedly inhibited at low concentrations of DCA and 5-FU treatment when subjected to Atg5 mRNA interference, indicating that autophagy performed a protective role in cell survival upon DCA treatment.	Dichloroacetic Acid	80-83	autophagy related 5	Homo sapiens	121-125
28928817-6	2017	The proliferation of TE-1 cells was markedly inhibited at low concentrations of DCA and 5-FU treatment when subjected to Atg5 mRNA interference, indicating that autophagy performed a protective role in cell survival upon DCA treatment.	Dichloroacetic Acid	221-224	autophagy related 5	Homo sapiens	121-125
28928817-8	2017	Notably, the protein kinase B (Akt)-mechanistic target of rapamycin (mTOR) signaling pathway, an important negative regulator of autophagy, was demonstrated to be suppressed by DCA treatment.	Dichloroacetic Acid	177-180	AKT serine/threonine kinase 1	Homo sapiens	31-34
28928817-8	2017	Notably, the protein kinase B (Akt)-mechanistic target of rapamycin (mTOR) signaling pathway, an important negative regulator of autophagy, was demonstrated to be suppressed by DCA treatment.	Dichloroacetic Acid	177-180	mechanistic target of rapamycin kinase	Homo sapiens	69-73
29137417-0	2017	Inhibition of retinoic acid receptor beta signaling confers glycolytic dependence and sensitization to dichloroacetate in melanoma cells.	Dichloroacetic Acid	103-118	retinoic acid receptor beta	Homo sapiens	14-41
28258224-3	2017	Conversely, we also demonstrated that orally ingested synthetic amines, such as monodansylcadaverine (DCA) and biotin-labeled pentylamine, are TG-dependently incorporated into Relish-N, causing the nuclear translocation of modified Relish-N in gut epithelial cells.	Dichloroacetic Acid	102-105	Transglutaminase	Drosophila melanogaster	143-145
29535790-1	2017	Dichloroacetate (DCA) is a simple and small anticancer drug that arouses the activity of the enzyme pyruvate dehydrogenase (PDH) through inhibition of the enzyme pyruvate dehydrogenase kinases (PDK1-4).	Dichloroacetic Acid	0-15	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	100-122
29535790-1	2017	Dichloroacetate (DCA) is a simple and small anticancer drug that arouses the activity of the enzyme pyruvate dehydrogenase (PDH) through inhibition of the enzyme pyruvate dehydrogenase kinases (PDK1-4).	Dichloroacetic Acid	0-15	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	124-127
29535790-1	2017	Dichloroacetate (DCA) is a simple and small anticancer drug that arouses the activity of the enzyme pyruvate dehydrogenase (PDH) through inhibition of the enzyme pyruvate dehydrogenase kinases (PDK1-4).	Dichloroacetic Acid	0-15	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	162-184
29535790-1	2017	Dichloroacetate (DCA) is a simple and small anticancer drug that arouses the activity of the enzyme pyruvate dehydrogenase (PDH) through inhibition of the enzyme pyruvate dehydrogenase kinases (PDK1-4).	Dichloroacetic Acid	0-15	pyruvate dehydrogenase kinase 1	Homo sapiens	194-200
29535790-1	2017	Dichloroacetate (DCA) is a simple and small anticancer drug that arouses the activity of the enzyme pyruvate dehydrogenase (PDH) through inhibition of the enzyme pyruvate dehydrogenase kinases (PDK1-4).	Dichloroacetic Acid	17-20	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	100-122
29535790-1	2017	Dichloroacetate (DCA) is a simple and small anticancer drug that arouses the activity of the enzyme pyruvate dehydrogenase (PDH) through inhibition of the enzyme pyruvate dehydrogenase kinases (PDK1-4).	Dichloroacetic Acid	17-20	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	124-127
29535790-1	2017	Dichloroacetate (DCA) is a simple and small anticancer drug that arouses the activity of the enzyme pyruvate dehydrogenase (PDH) through inhibition of the enzyme pyruvate dehydrogenase kinases (PDK1-4).	Dichloroacetic Acid	17-20	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	162-184
29535790-1	2017	Dichloroacetate (DCA) is a simple and small anticancer drug that arouses the activity of the enzyme pyruvate dehydrogenase (PDH) through inhibition of the enzyme pyruvate dehydrogenase kinases (PDK1-4).	Dichloroacetic Acid	17-20	pyruvate dehydrogenase kinase 1	Homo sapiens	194-200
28881683-0	2017	Inhibition of COX2 enhances the chemosensitivity of dichloroacetate in cervical cancer cells.	Dichloroacetic Acid	52-67	prostaglandin-endoperoxide synthase 2	Homo sapiens	14-18
28881683-4	2017	However, it is still unknown whether COX2 can affect the sensitivity of DCA in cervical cancer cells.	Dichloroacetic Acid	72-75	prostaglandin-endoperoxide synthase 2	Homo sapiens	37-41
28881683-6	2017	Furthermore, we for the first time revealed that DCA could upregulate COX2 which impeded the chemosensitivity of DCA in cervical cancer cells.	Dichloroacetic Acid	49-52	prostaglandin-endoperoxide synthase 2	Homo sapiens	70-74
28881683-6	2017	Furthermore, we for the first time revealed that DCA could upregulate COX2 which impeded the chemosensitivity of DCA in cervical cancer cells.	Dichloroacetic Acid	113-116	prostaglandin-endoperoxide synthase 2	Homo sapiens	70-74
28881683-7	2017	Mechanistic study showed that DCA reduced the level of RNA binding protein quaking (QKI), leading to the decay suppression of COX2 mRNA and the subsequent elevation of COX2 protein.	Dichloroacetic Acid	30-33	QKI, KH domain containing RNA binding	Homo sapiens	75-82
28881683-7	2017	Mechanistic study showed that DCA reduced the level of RNA binding protein quaking (QKI), leading to the decay suppression of COX2 mRNA and the subsequent elevation of COX2 protein.	Dichloroacetic Acid	30-33	QKI, KH domain containing RNA binding	Homo sapiens	84-87
28881683-7	2017	Mechanistic study showed that DCA reduced the level of RNA binding protein quaking (QKI), leading to the decay suppression of COX2 mRNA and the subsequent elevation of COX2 protein.	Dichloroacetic Acid	30-33	prostaglandin-endoperoxide synthase 2	Homo sapiens	126-130
28881683-7	2017	Mechanistic study showed that DCA reduced the level of RNA binding protein quaking (QKI), leading to the decay suppression of COX2 mRNA and the subsequent elevation of COX2 protein.	Dichloroacetic Acid	30-33	prostaglandin-endoperoxide synthase 2	Homo sapiens	168-172
28881683-8	2017	Inhibition of COX2 using celecoxib could sensitize DCA in repressing the growth of cervical cancer cells both in vitro and in vivo.	Dichloroacetic Acid	51-54	prostaglandin-endoperoxide synthase 2	Homo sapiens	14-18
28881683-9	2017	These results indicate that COX2 is a novel resistance factor of DCA, and combination of celecoxib with DCA may be beneficial to the treatment of cervical cancer.	Dichloroacetic Acid	65-68	prostaglandin-endoperoxide synthase 2	Homo sapiens	28-32
28410193-4	2017	To mimic the GBM resistant state, we generated an in vitro TMZ resistant model and demonstrated that dichloroacetate (DCA), a metabolic inhibitor of pyruvate dehydrogenase kinase 1 (PDK1), reverses the Warburg effect.	Dichloroacetic Acid	118-121	pyruvate dehydrogenase kinase 1	Homo sapiens	182-186
28505181-5	2017	Our results further demonstrate that inhibition of PDK1 using small molecule inhibitors dichloroacetic acid (DCA) and dichloroacetophenone (DAP) resulted in reduced cell growth and increased apoptosis.	Dichloroacetic Acid	88-107	pyruvate dehydrogenase kinase 1	Homo sapiens	51-55
28505181-5	2017	Our results further demonstrate that inhibition of PDK1 using small molecule inhibitors dichloroacetic acid (DCA) and dichloroacetophenone (DAP) resulted in reduced cell growth and increased apoptosis.	Dichloroacetic Acid	109-112	pyruvate dehydrogenase kinase 1	Homo sapiens	51-55
28505181-8	2017	Additionally, we show that DCA treatment led to inhibition of PI3K/Akt pathway and reduction in PDK1 protein levels.	Dichloroacetic Acid	27-30	AKT serine/threonine kinase 1	Homo sapiens	67-70
28505181-8	2017	Additionally, we show that DCA treatment led to inhibition of PI3K/Akt pathway and reduction in PDK1 protein levels.	Dichloroacetic Acid	27-30	pyruvate dehydrogenase kinase 1	Homo sapiens	96-100
28339028-9	2017	In addition, the radioresistance, glycolytic state and cell proliferation of 435R cells were also decreased after inhibiting pyruvate dehydrogenase kinase 1 (PDK1) with dichloroacetate (DCA).	Dichloroacetic Acid	169-184	pyruvate dehydrogenase kinase 1	Homo sapiens	125-156
28339028-9	2017	In addition, the radioresistance, glycolytic state and cell proliferation of 435R cells were also decreased after inhibiting pyruvate dehydrogenase kinase 1 (PDK1) with dichloroacetate (DCA).	Dichloroacetic Acid	169-184	pyruvate dehydrogenase kinase 1	Homo sapiens	158-162
28339028-9	2017	In addition, the radioresistance, glycolytic state and cell proliferation of 435R cells were also decreased after inhibiting pyruvate dehydrogenase kinase 1 (PDK1) with dichloroacetate (DCA).	Dichloroacetic Acid	186-189	pyruvate dehydrogenase kinase 1	Homo sapiens	125-156
28339028-9	2017	In addition, the radioresistance, glycolytic state and cell proliferation of 435R cells were also decreased after inhibiting pyruvate dehydrogenase kinase 1 (PDK1) with dichloroacetate (DCA).	Dichloroacetic Acid	186-189	pyruvate dehydrogenase kinase 1	Homo sapiens	158-162
28163135-2	2017	DCA was found to inhibit its own metabolism by irreversibly inactivating glutathione transferase zeta 1 (GSTZ1-1), resulting in nonlinear kinetics and abnormally high accumulation ratio after repeated dosing.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Rattus norvegicus	73-103
28163135-2	2017	DCA was found to inhibit its own metabolism by irreversibly inactivating glutathione transferase zeta 1 (GSTZ1-1), resulting in nonlinear kinetics and abnormally high accumulation ratio after repeated dosing.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Rattus norvegicus	105-112
28163135-4	2017	The maximum rate constant for DCA-induced GSTZ1-1 inactivation is estimated to be 0.96/h, which is 110 times that of the rate constant for GSTZ1-1 natural degradation (0.00875/h).	Dichloroacetic Acid	30-33	glutathione S-transferase zeta 1	Rattus norvegicus	42-49
28163135-4	2017	The maximum rate constant for DCA-induced GSTZ1-1 inactivation is estimated to be 0.96/h, which is 110 times that of the rate constant for GSTZ1-1 natural degradation (0.00875/h).	Dichloroacetic Acid	30-33	glutathione S-transferase zeta 1	Rattus norvegicus	139-146
28258224-5	2017	Here, we used mass spectrometry analysis of a recombinant Relish-N modified with DCA by TG activity after proteolytic digestion and show that the DCA-modified Gln residues are located in the DNA-binding region of Relish-N. TG-catalyzed DCA incorporation inhibited binding of Relish-N to the Rel-responsive element in the NF-kappaB-binding DNA sequence.	Dichloroacetic Acid	81-84	Relish	Drosophila melanogaster	213-219
28258224-5	2017	Here, we used mass spectrometry analysis of a recombinant Relish-N modified with DCA by TG activity after proteolytic digestion and show that the DCA-modified Gln residues are located in the DNA-binding region of Relish-N. TG-catalyzed DCA incorporation inhibited binding of Relish-N to the Rel-responsive element in the NF-kappaB-binding DNA sequence.	Dichloroacetic Acid	81-84	Transglutaminase	Drosophila melanogaster	223-225
28258224-5	2017	Here, we used mass spectrometry analysis of a recombinant Relish-N modified with DCA by TG activity after proteolytic digestion and show that the DCA-modified Gln residues are located in the DNA-binding region of Relish-N. TG-catalyzed DCA incorporation inhibited binding of Relish-N to the Rel-responsive element in the NF-kappaB-binding DNA sequence.	Dichloroacetic Acid	81-84	Relish	Drosophila melanogaster	213-219
28258224-5	2017	Here, we used mass spectrometry analysis of a recombinant Relish-N modified with DCA by TG activity after proteolytic digestion and show that the DCA-modified Gln residues are located in the DNA-binding region of Relish-N. TG-catalyzed DCA incorporation inhibited binding of Relish-N to the Rel-responsive element in the NF-kappaB-binding DNA sequence.	Dichloroacetic Acid	146-149	Relish	Drosophila melanogaster	58-64
28258224-5	2017	Here, we used mass spectrometry analysis of a recombinant Relish-N modified with DCA by TG activity after proteolytic digestion and show that the DCA-modified Gln residues are located in the DNA-binding region of Relish-N. TG-catalyzed DCA incorporation inhibited binding of Relish-N to the Rel-responsive element in the NF-kappaB-binding DNA sequence.	Dichloroacetic Acid	146-149	Relish	Drosophila melanogaster	213-219
28258224-5	2017	Here, we used mass spectrometry analysis of a recombinant Relish-N modified with DCA by TG activity after proteolytic digestion and show that the DCA-modified Gln residues are located in the DNA-binding region of Relish-N. TG-catalyzed DCA incorporation inhibited binding of Relish-N to the Rel-responsive element in the NF-kappaB-binding DNA sequence.	Dichloroacetic Acid	146-149	Transglutaminase	Drosophila melanogaster	223-225
28258224-5	2017	Here, we used mass spectrometry analysis of a recombinant Relish-N modified with DCA by TG activity after proteolytic digestion and show that the DCA-modified Gln residues are located in the DNA-binding region of Relish-N. TG-catalyzed DCA incorporation inhibited binding of Relish-N to the Rel-responsive element in the NF-kappaB-binding DNA sequence.	Dichloroacetic Acid	146-149	Relish	Drosophila melanogaster	213-219
28258224-5	2017	Here, we used mass spectrometry analysis of a recombinant Relish-N modified with DCA by TG activity after proteolytic digestion and show that the DCA-modified Gln residues are located in the DNA-binding region of Relish-N. TG-catalyzed DCA incorporation inhibited binding of Relish-N to the Rel-responsive element in the NF-kappaB-binding DNA sequence.	Dichloroacetic Acid	146-149	Relish	Drosophila melanogaster	58-64
28258224-5	2017	Here, we used mass spectrometry analysis of a recombinant Relish-N modified with DCA by TG activity after proteolytic digestion and show that the DCA-modified Gln residues are located in the DNA-binding region of Relish-N. TG-catalyzed DCA incorporation inhibited binding of Relish-N to the Rel-responsive element in the NF-kappaB-binding DNA sequence.	Dichloroacetic Acid	146-149	Relish	Drosophila melanogaster	213-219
28258224-5	2017	Here, we used mass spectrometry analysis of a recombinant Relish-N modified with DCA by TG activity after proteolytic digestion and show that the DCA-modified Gln residues are located in the DNA-binding region of Relish-N. TG-catalyzed DCA incorporation inhibited binding of Relish-N to the Rel-responsive element in the NF-kappaB-binding DNA sequence.	Dichloroacetic Acid	146-149	Transglutaminase	Drosophila melanogaster	223-225
28258224-5	2017	Here, we used mass spectrometry analysis of a recombinant Relish-N modified with DCA by TG activity after proteolytic digestion and show that the DCA-modified Gln residues are located in the DNA-binding region of Relish-N. TG-catalyzed DCA incorporation inhibited binding of Relish-N to the Rel-responsive element in the NF-kappaB-binding DNA sequence.	Dichloroacetic Acid	146-149	Relish	Drosophila melanogaster	213-219
28258224-7	2017	Of note, natural polyamines, including spermidine and spermine, competitively inhibited TG-dependent DCA incorporation into Relish-N.	Dichloroacetic Acid	101-104	Transglutaminase	Drosophila melanogaster	88-90
28258224-7	2017	Of note, natural polyamines, including spermidine and spermine, competitively inhibited TG-dependent DCA incorporation into Relish-N.	Dichloroacetic Acid	101-104	Relish	Drosophila melanogaster	124-130
28881758-7	2017	Moreover, combining paclitaxel withthe specific PDK2 inhibitor dichloroacetate had a synergistic inhibitory effect on the viability of paclitaxel-resistant lung cancer cells.	Dichloroacetic Acid	63-78	pyruvate dehydrogenase kinase 2	Homo sapiens	48-52
28595656-10	2017	siRNA-mediated knock-down of all PDKs or the use of DCA (a pan-PDK inhibitor) abolished PDH-E1alpha phosphorylation.	Dichloroacetic Acid	52-55	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	88-91
28483502-1	2017	OBJECTIVE: To determine the effects of attenuating oxidative stress with the use of dichloroacetate (DCA) on the expression of key redox enzymes myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) as well as on apoptosis.	Dichloroacetic Acid	84-99	myeloperoxidase	Homo sapiens	145-160
28483502-1	2017	OBJECTIVE: To determine the effects of attenuating oxidative stress with the use of dichloroacetate (DCA) on the expression of key redox enzymes myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) as well as on apoptosis.	Dichloroacetic Acid	84-99	myeloperoxidase	Homo sapiens	162-165
28483502-1	2017	OBJECTIVE: To determine the effects of attenuating oxidative stress with the use of dichloroacetate (DCA) on the expression of key redox enzymes myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) as well as on apoptosis.	Dichloroacetic Acid	84-99	nitric oxide synthase 2	Homo sapiens	171-202
28483502-1	2017	OBJECTIVE: To determine the effects of attenuating oxidative stress with the use of dichloroacetate (DCA) on the expression of key redox enzymes myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) as well as on apoptosis.	Dichloroacetic Acid	84-99	nitric oxide synthase 2	Homo sapiens	204-208
28483502-1	2017	OBJECTIVE: To determine the effects of attenuating oxidative stress with the use of dichloroacetate (DCA) on the expression of key redox enzymes myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) as well as on apoptosis.	Dichloroacetic Acid	101-104	myeloperoxidase	Homo sapiens	145-160
28483502-1	2017	OBJECTIVE: To determine the effects of attenuating oxidative stress with the use of dichloroacetate (DCA) on the expression of key redox enzymes myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) as well as on apoptosis.	Dichloroacetic Acid	101-104	myeloperoxidase	Homo sapiens	162-165
28483502-1	2017	OBJECTIVE: To determine the effects of attenuating oxidative stress with the use of dichloroacetate (DCA) on the expression of key redox enzymes myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) as well as on apoptosis.	Dichloroacetic Acid	101-104	nitric oxide synthase 2	Homo sapiens	171-202
28483502-1	2017	OBJECTIVE: To determine the effects of attenuating oxidative stress with the use of dichloroacetate (DCA) on the expression of key redox enzymes myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) as well as on apoptosis.	Dichloroacetic Acid	101-104	nitric oxide synthase 2	Homo sapiens	204-208
28483502-9	2017	Treatment with the use of DCA decreased MPO, iNOS, and nitrate/nitrite levels and negated the effect of hypoxia in both types of cells.	Dichloroacetic Acid	26-29	myeloperoxidase	Homo sapiens	40-43
28483502-9	2017	Treatment with the use of DCA decreased MPO, iNOS, and nitrate/nitrite levels and negated the effect of hypoxia in both types of cells.	Dichloroacetic Acid	26-29	nitric oxide synthase 2	Homo sapiens	45-49
28258224-3	2017	Conversely, we also demonstrated that orally ingested synthetic amines, such as monodansylcadaverine (DCA) and biotin-labeled pentylamine, are TG-dependently incorporated into Relish-N, causing the nuclear translocation of modified Relish-N in gut epithelial cells.	Dichloroacetic Acid	102-105	Relish	Drosophila melanogaster	176-182
28258224-3	2017	Conversely, we also demonstrated that orally ingested synthetic amines, such as monodansylcadaverine (DCA) and biotin-labeled pentylamine, are TG-dependently incorporated into Relish-N, causing the nuclear translocation of modified Relish-N in gut epithelial cells.	Dichloroacetic Acid	102-105	Relish	Drosophila melanogaster	232-238
28410193-4	2017	To mimic the GBM resistant state, we generated an in vitro TMZ resistant model and demonstrated that dichloroacetate (DCA), a metabolic inhibitor of pyruvate dehydrogenase kinase 1 (PDK1), reverses the Warburg effect.	Dichloroacetic Acid	101-116	pyruvate dehydrogenase kinase 1	Homo sapiens	149-180
28258224-5	2017	Here, we used mass spectrometry analysis of a recombinant Relish-N modified with DCA by TG activity after proteolytic digestion and show that the DCA-modified Gln residues are located in the DNA-binding region of Relish-N. TG-catalyzed DCA incorporation inhibited binding of Relish-N to the Rel-responsive element in the NF-kappaB-binding DNA sequence.	Dichloroacetic Acid	81-84	Relish	Drosophila melanogaster	58-64
28410193-4	2017	To mimic the GBM resistant state, we generated an in vitro TMZ resistant model and demonstrated that dichloroacetate (DCA), a metabolic inhibitor of pyruvate dehydrogenase kinase 1 (PDK1), reverses the Warburg effect.	Dichloroacetic Acid	101-116	pyruvate dehydrogenase kinase 1	Homo sapiens	182-186
28258224-5	2017	Here, we used mass spectrometry analysis of a recombinant Relish-N modified with DCA by TG activity after proteolytic digestion and show that the DCA-modified Gln residues are located in the DNA-binding region of Relish-N. TG-catalyzed DCA incorporation inhibited binding of Relish-N to the Rel-responsive element in the NF-kappaB-binding DNA sequence.	Dichloroacetic Acid	81-84	Transglutaminase	Drosophila melanogaster	88-90
28410193-4	2017	To mimic the GBM resistant state, we generated an in vitro TMZ resistant model and demonstrated that dichloroacetate (DCA), a metabolic inhibitor of pyruvate dehydrogenase kinase 1 (PDK1), reverses the Warburg effect.	Dichloroacetic Acid	118-121	pyruvate dehydrogenase kinase 1	Homo sapiens	149-180
28410193-5	2017	Microarray analysis conducted on the TMZ resistant cells with their subsequent treatment with DCA revealed PDK1 as its sole target.	Dichloroacetic Acid	94-97	pyruvate dehydrogenase kinase 1	Homo sapiens	107-111
28040265-5	2017	Cisplatin-induced suppression of the mitochondrial membrane potential, oxygen consumption rate, expression of electron transport chain components, cytochrome c oxidase activity, and disruption of mitochondrial morphology were noticeably improved in the kidneys of DCA-treated or PDK4 knockout mice.	Dichloroacetic Acid	264-267	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	279-283
28410193-7	2017	Computational homology modeling and docking studies confirmed DCA binding to EGFR, EGFRvIII and PDK1 with high affinity.	Dichloroacetic Acid	62-65	epidermal growth factor receptor	Homo sapiens	77-81
28410193-7	2017	Computational homology modeling and docking studies confirmed DCA binding to EGFR, EGFRvIII and PDK1 with high affinity.	Dichloroacetic Acid	62-65	pyruvate dehydrogenase kinase 1	Homo sapiens	96-100
28428715-11	2017	In multiple regression analysis, the difference in therapy protocol (DCA + ASV or SOF + LDV) was an independent predictor that was significantly associated with the increase in TC and LDL-C at 4 wk of therapy.	Dichloroacetic Acid	69-72	component of oligomeric golgi complex 2	Homo sapiens	184-189
28123081-5	2017	Exposure to dichloroacetate, an inhibitor of PDKs, increased mitochondrial respiration and decreased production of reactive oxygen species in mutant cells, emphasizing PDH as an interesting therapeutic target in HD.	Dichloroacetic Acid	12-27	pyruvate dehydrogenase kinase, isoenzyme 1	Mus musculus	45-49
28040265-6	2017	Additionally, levels of the oxidative stress marker 4-hydroxynonenal and mitochondrial reactive oxygen species were attenuated, whereas superoxide dismutase 2 and catalase expression and glutathione synthetase and glutathione levels were recovered in DCA-treated or PDK4 knockout mice.	Dichloroacetic Acid	251-254	glutathione synthetase	Mus musculus	187-209
28040265-6	2017	Additionally, levels of the oxidative stress marker 4-hydroxynonenal and mitochondrial reactive oxygen species were attenuated, whereas superoxide dismutase 2 and catalase expression and glutathione synthetase and glutathione levels were recovered in DCA-treated or PDK4 knockout mice.	Dichloroacetic Acid	251-254	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	266-270
28040265-7	2017	Interestingly, lipid accumulation was considerably attenuated in DCA-treated or PDK4 knockout mice via recovered expression of peroxisome proliferator-activated receptor-alpha and coactivator PGC-1alpha, which was accompanied by recovery of mitochondrial biogenesis.	Dichloroacetic Acid	65-68	peroxisome proliferator activated receptor alpha	Mus musculus	127-175
28040265-7	2017	Interestingly, lipid accumulation was considerably attenuated in DCA-treated or PDK4 knockout mice via recovered expression of peroxisome proliferator-activated receptor-alpha and coactivator PGC-1alpha, which was accompanied by recovery of mitochondrial biogenesis.	Dichloroacetic Acid	65-68	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	192-202
27514773-5	2016	In this study, we utilized Dichloroacetate (DCA), a widely regarded PDK inhibitor, together with Erlotinib and Gefitinib, two well-known EGFR inhibitors, and demonstrated that the applications of DCA in combination with either Erlotinib or Gefitinib significantly attenuated the viability of EGFR mutant NSCLC cells (NCI-H1975 and NCI-H1650) in a synergistic manner.	Dichloroacetic Acid	44-47	epidermal growth factor receptor	Homo sapiens	292-296
27413020-12	2016	Finally, the preventive effect of GW0742 on oxidative stress and cAMP-induced relaxation were overcome by the pyruvate dehydrogenase kinase 4 (PDK4) inhibitor dichloroacetate (DCA).	Dichloroacetic Acid	159-174	pyruvate dehydrogenase kinase 4	Rattus norvegicus	110-141
27413020-12	2016	Finally, the preventive effect of GW0742 on oxidative stress and cAMP-induced relaxation were overcome by the pyruvate dehydrogenase kinase 4 (PDK4) inhibitor dichloroacetate (DCA).	Dichloroacetic Acid	159-174	pyruvate dehydrogenase kinase 4	Rattus norvegicus	143-147
27413020-12	2016	Finally, the preventive effect of GW0742 on oxidative stress and cAMP-induced relaxation were overcome by the pyruvate dehydrogenase kinase 4 (PDK4) inhibitor dichloroacetate (DCA).	Dichloroacetic Acid	176-179	pyruvate dehydrogenase kinase 4	Rattus norvegicus	110-141
27413020-12	2016	Finally, the preventive effect of GW0742 on oxidative stress and cAMP-induced relaxation were overcome by the pyruvate dehydrogenase kinase 4 (PDK4) inhibitor dichloroacetate (DCA).	Dichloroacetic Acid	176-179	pyruvate dehydrogenase kinase 4	Rattus norvegicus	143-147
27771434-6	2017	The first step in DCA metabolism is conversion to glyoxylate catalyzed by glutathione transferase zeta 1 (GSTZ1), for which DCA is a mechanism-based inactivator.	Dichloroacetic Acid	18-21	glutathione S-transferase zeta 1	Homo sapiens	74-104
27771434-6	2017	The first step in DCA metabolism is conversion to glyoxylate catalyzed by glutathione transferase zeta 1 (GSTZ1), for which DCA is a mechanism-based inactivator.	Dichloroacetic Acid	18-21	glutathione S-transferase zeta 1	Homo sapiens	106-111
27771434-6	2017	The first step in DCA metabolism is conversion to glyoxylate catalyzed by glutathione transferase zeta 1 (GSTZ1), for which DCA is a mechanism-based inactivator.	Dichloroacetic Acid	124-127	glutathione S-transferase zeta 1	Homo sapiens	74-104
27771434-6	2017	The first step in DCA metabolism is conversion to glyoxylate catalyzed by glutathione transferase zeta 1 (GSTZ1), for which DCA is a mechanism-based inactivator.	Dichloroacetic Acid	124-127	glutathione S-transferase zeta 1	Homo sapiens	106-111
27771434-7	2017	The rate of GSTZ1 inactivation by DCA is influenced by age, GSTZ1 haplotype and cellular concentrations of chloride.	Dichloroacetic Acid	34-37	glutathione S-transferase zeta 1	Homo sapiens	12-17
27771434-7	2017	The rate of GSTZ1 inactivation by DCA is influenced by age, GSTZ1 haplotype and cellular concentrations of chloride.	Dichloroacetic Acid	34-37	glutathione S-transferase zeta 1	Homo sapiens	60-65
27668346-4	2016	We will then introduce MCT1 and SLC5A8, which are respective transporter for antitumor agent 3-bromopyruvic acid and dichloroacetic acid, and monochloroacetic acid transporters Deh4p and Dehp2 from a haloacids-degrading bacterium.	Dichloroacetic Acid	117-136	solute carrier family 16 member 1	Homo sapiens	23-27
27668346-4	2016	We will then introduce MCT1 and SLC5A8, which are respective transporter for antitumor agent 3-bromopyruvic acid and dichloroacetic acid, and monochloroacetic acid transporters Deh4p and Dehp2 from a haloacids-degrading bacterium.	Dichloroacetic Acid	117-136	solute carrier family 5 member 8	Homo sapiens	32-38
27514773-5	2016	In this study, we utilized Dichloroacetate (DCA), a widely regarded PDK inhibitor, together with Erlotinib and Gefitinib, two well-known EGFR inhibitors, and demonstrated that the applications of DCA in combination with either Erlotinib or Gefitinib significantly attenuated the viability of EGFR mutant NSCLC cells (NCI-H1975 and NCI-H1650) in a synergistic manner.	Dichloroacetic Acid	27-42	epidermal growth factor receptor	Homo sapiens	292-296
27388934-7	2016	This hyper-phosphorylation can be reversed by treating the PDK3(R158H) fibroblasts with the PDK inhibitor dichloroacetate (DCA).	Dichloroacetic Acid	106-121	pyruvate dehydrogenase kinase 3	Homo sapiens	59-63
27388934-7	2016	This hyper-phosphorylation can be reversed by treating the PDK3(R158H) fibroblasts with the PDK inhibitor dichloroacetate (DCA).	Dichloroacetic Acid	123-126	pyruvate dehydrogenase kinase 3	Homo sapiens	59-63
27514773-5	2016	In this study, we utilized Dichloroacetate (DCA), a widely regarded PDK inhibitor, together with Erlotinib and Gefitinib, two well-known EGFR inhibitors, and demonstrated that the applications of DCA in combination with either Erlotinib or Gefitinib significantly attenuated the viability of EGFR mutant NSCLC cells (NCI-H1975 and NCI-H1650) in a synergistic manner.	Dichloroacetic Acid	196-199	epidermal growth factor receptor	Homo sapiens	137-141
27514773-5	2016	In this study, we utilized Dichloroacetate (DCA), a widely regarded PDK inhibitor, together with Erlotinib and Gefitinib, two well-known EGFR inhibitors, and demonstrated that the applications of DCA in combination with either Erlotinib or Gefitinib significantly attenuated the viability of EGFR mutant NSCLC cells (NCI-H1975 and NCI-H1650) in a synergistic manner.	Dichloroacetic Acid	196-199	epidermal growth factor receptor	Homo sapiens	292-296
27569287-0	2016	TRAIL restores DCA/metformin-mediated cell death in hypoxia.	Dichloroacetic Acid	15-18	TNF superfamily member 10	Homo sapiens	0-5
27569287-3	2016	In the present study, we found that TRAIL can overcome the effect of hypoxia on the cell death induced by treatment of DCA and metformin in breast cancer cells.	Dichloroacetic Acid	119-122	TNF superfamily member 10	Homo sapiens	36-41
27569287-4	2016	Unexpectedly, DR5 is upregulated in the cells treated with DCA/metformin, and sustained under hypoxia.	Dichloroacetic Acid	59-62	TNF receptor superfamily member 10b	Homo sapiens	14-17
27569287-5	2016	Blocking DR5 by siRNA inhibited DCA/metformin/TRAIL-induced cell death, indicating that DR5 upregulation plays an important role in sensitizing cancer cells to TRAIL-induced cell death.	Dichloroacetic Acid	32-35	TNF receptor superfamily member 10b	Homo sapiens	9-12
27569287-5	2016	Blocking DR5 by siRNA inhibited DCA/metformin/TRAIL-induced cell death, indicating that DR5 upregulation plays an important role in sensitizing cancer cells to TRAIL-induced cell death.	Dichloroacetic Acid	32-35	TNF superfamily member 10	Homo sapiens	46-51
27569287-5	2016	Blocking DR5 by siRNA inhibited DCA/metformin/TRAIL-induced cell death, indicating that DR5 upregulation plays an important role in sensitizing cancer cells to TRAIL-induced cell death.	Dichloroacetic Acid	32-35	TNF receptor superfamily member 10b	Homo sapiens	88-91
27569287-5	2016	Blocking DR5 by siRNA inhibited DCA/metformin/TRAIL-induced cell death, indicating that DR5 upregulation plays an important role in sensitizing cancer cells to TRAIL-induced cell death.	Dichloroacetic Acid	32-35	TNF superfamily member 10	Homo sapiens	160-165
27569287-6	2016	Furthermore, we found that activation of JNK and c-Jun is responsible for upregulation of DR5 induced by DCA/metformin.	Dichloroacetic Acid	105-108	mitogen-activated protein kinase 8	Homo sapiens	41-44
27569287-6	2016	Furthermore, we found that activation of JNK and c-Jun is responsible for upregulation of DR5 induced by DCA/metformin.	Dichloroacetic Acid	105-108	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	49-54
27569287-6	2016	Furthermore, we found that activation of JNK and c-Jun is responsible for upregulation of DR5 induced by DCA/metformin.	Dichloroacetic Acid	105-108	TNF receptor superfamily member 10b	Homo sapiens	90-93
27449090-5	2016	Interestingly, we for the first time revealed that Met sensitized DCA via dramatically attenuating DCA-induced Mcl-1 protein and protective autophagy, while DCA sensitized Met through markedly alleviating Met-induced excessive lactate accumulation and glucose consumption.	Dichloroacetic Acid	66-69	myeloid cell leukemia sequence 1	Mus musculus	111-116
27449090-5	2016	Interestingly, we for the first time revealed that Met sensitized DCA via dramatically attenuating DCA-induced Mcl-1 protein and protective autophagy, while DCA sensitized Met through markedly alleviating Met-induced excessive lactate accumulation and glucose consumption.	Dichloroacetic Acid	99-102	myeloid cell leukemia sequence 1	Mus musculus	111-116
27449090-5	2016	Interestingly, we for the first time revealed that Met sensitized DCA via dramatically attenuating DCA-induced Mcl-1 protein and protective autophagy, while DCA sensitized Met through markedly alleviating Met-induced excessive lactate accumulation and glucose consumption.	Dichloroacetic Acid	99-102	myeloid cell leukemia sequence 1	Mus musculus	111-116
27494858-0	2016	Dichloroacetate potentiates tamoxifen-induced cell death in breast cancer cells via downregulation of the epidermal growth factor receptor.	Dichloroacetic Acid	0-15	epidermal growth factor receptor	Homo sapiens	106-138
27494858-5	2016	In the present study, we found that DCA sensitized MCF7 breast cancer cells to tamoxifen-induced cell death by decreasing epidermal growth factor receptor (EGFR) expression.	Dichloroacetic Acid	36-39	epidermal growth factor receptor	Homo sapiens	122-154
27494858-5	2016	In the present study, we found that DCA sensitized MCF7 breast cancer cells to tamoxifen-induced cell death by decreasing epidermal growth factor receptor (EGFR) expression.	Dichloroacetic Acid	36-39	epidermal growth factor receptor	Homo sapiens	156-160
27494858-7	2016	Furthermore, p38 mitogen-activated protein kinase played an important role in DCA/tamoxifen-induced EGFR degradation.	Dichloroacetic Acid	78-81	mitogen-activated protein kinase 14	Homo sapiens	13-16
27494858-7	2016	Furthermore, p38 mitogen-activated protein kinase played an important role in DCA/tamoxifen-induced EGFR degradation.	Dichloroacetic Acid	78-81	epidermal growth factor receptor	Homo sapiens	100-104
27494858-9	2016	In summary, our results suggest that DCA is an attractive potential drug that sensitizes cells to tamoxifen-induced cell death and overcome tamoxifen resistance via downregulation of EGFR expression in breast cancer cells.	Dichloroacetic Acid	37-40	epidermal growth factor receptor	Homo sapiens	183-187
27685525-13	2016	High antitumor activity of DCA + 2DG was associated with 31% decrease (p &lt; 0.05) of lactate content in tumor tissue and 120% increase (p &lt; 0.01) of ROS production in CD14(+) cells recruited to the region of tumor growth.	Dichloroacetic Acid	27-30	CD14 antigen	Mus musculus	172-176
27471054-8	2016	Furthermore, when co-administered with IFN-alpha or ribavirin, DCA further inhibited viral replication.	Dichloroacetic Acid	63-66	interferon alpha 1	Homo sapiens	39-48
27264935-6	2016	Inhibition of Pdk2 in lkb1 mutants with dichloroacetate, a promising anticancer drug, rescued the lactate production to wild-type level, suggesting the lkb1 mutant may be used to screen compounds targeting aerobic glycolysis in cancer therapy.	Dichloroacetic Acid	40-55	pyruvate dehydrogenase kinase 2b	Danio rerio	14-18
27264935-6	2016	Inhibition of Pdk2 in lkb1 mutants with dichloroacetate, a promising anticancer drug, rescued the lactate production to wild-type level, suggesting the lkb1 mutant may be used to screen compounds targeting aerobic glycolysis in cancer therapy.	Dichloroacetic Acid	40-55	serine/threonine kinase 11	Danio rerio	22-26
27264935-6	2016	Inhibition of Pdk2 in lkb1 mutants with dichloroacetate, a promising anticancer drug, rescued the lactate production to wild-type level, suggesting the lkb1 mutant may be used to screen compounds targeting aerobic glycolysis in cancer therapy.	Dichloroacetic Acid	40-55	serine/threonine kinase 11	Danio rerio	152-156
27151823-2	2016	Compound is a mononuclear species where the cobalt(ii) ion is six-coordinate with four bim molecules in the equatorial positions [Co-Nbim = 2.1546(15) and 2.1489(15) A] and two trans-positioned dca ligands [Co-Ndca = 2.1575(18) A] in the axial sites of a somewhat distorted octahedral surrounding.	Dichloroacetic Acid	194-197	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	51-53
27151823-3	2016	The structures of and consist of two-dimensional grids of cobalt(ii) ions where each metal atom is linked to the other four metal centres by single dca bridges exhibiting the mu1,5-dca coordination mode [Co-Ndca = 2.190(3)-2.220(3) () and 2.127(3)-2.153(3) A ()].	Dichloroacetic Acid	148-151	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	65-67
27323896-2	2016	Through molecular docking studies mono- and dihaloacetates are identified as potent PDK2 binders and matched their efficiency with dichloroacetic acid.	Dichloroacetic Acid	131-150	pyruvate dehydrogenase kinase 2	Homo sapiens	84-88
27153546-5	2016	DCA treatment also significantly reduced subcortical white matter injury as indicated by myelin basic protein staining (p = 0.018).	Dichloroacetic Acid	0-3	myelin basic protein	Mus musculus	89-109
26850694-0	2016	GSTZ1 expression and chloride concentrations modulate sensitivity of cancer cells to dichloroacetate.	Dichloroacetic Acid	85-100	glutathione S-transferase zeta 1	Homo sapiens	0-5
26850694-3	2016	Here we show that expression of glutathione transferase zeta 1 (GSTZ1), the enzyme responsible for conversion of DCA to its inactive metabolite, glyoxylate, is downregulated in liver cancer and upregulated in some breast cancers, leading to abnormal expression of the protein.	Dichloroacetic Acid	113-116	glutathione S-transferase zeta 1	Homo sapiens	32-62
26850694-3	2016	Here we show that expression of glutathione transferase zeta 1 (GSTZ1), the enzyme responsible for conversion of DCA to its inactive metabolite, glyoxylate, is downregulated in liver cancer and upregulated in some breast cancers, leading to abnormal expression of the protein.	Dichloroacetic Acid	113-116	glutathione S-transferase zeta 1	Homo sapiens	64-69
26850694-4	2016	The cellular concentration of chloride, an ion that influences the stability of GSTZ1 in the presence of DCA, was also found to be abnormal in tumors, with consistently higher concentrations in hepatocellular carcinoma than in surrounding non-tumor tissue.	Dichloroacetic Acid	105-108	glutathione S-transferase zeta 1	Homo sapiens	80-85
26850694-5	2016	Finally, results from experiments employing two- and three-dimensional cultures of HepG2 cells, parental and transduced to express GSTZ1, demonstrate that high levels of GSTZ1 expression confers resistance to the effect of high concentrations of DCA on cell viability.	Dichloroacetic Acid	246-249	glutathione S-transferase zeta 1	Homo sapiens	131-136
26850694-5	2016	Finally, results from experiments employing two- and three-dimensional cultures of HepG2 cells, parental and transduced to express GSTZ1, demonstrate that high levels of GSTZ1 expression confers resistance to the effect of high concentrations of DCA on cell viability.	Dichloroacetic Acid	246-249	glutathione S-transferase zeta 1	Homo sapiens	170-175
27153546-6	2016	Apoptotic cell death in the cortex, as indicated by counting the cells that were positive for apoptosis-inducing factor (p = 0.018) and active caspase-3 (p = 0.021), was significantly reduced after DCA treatment.	Dichloroacetic Acid	198-201	caspase 3	Mus musculus	143-152
27115471-10	2016	Reduced expression of heat shock proteins (HSPs) was observed in AA cells, whereas DCA induced expression of CHOP, C/EBP, HSP60, and HSP90 in CA cells.	Dichloroacetic Acid	83-86	DNA damage inducible transcript 3	Homo sapiens	109-113
27115471-10	2016	Reduced expression of heat shock proteins (HSPs) was observed in AA cells, whereas DCA induced expression of CHOP, C/EBP, HSP60, and HSP90 in CA cells.	Dichloroacetic Acid	83-86	CCAAT enhancer binding protein alpha	Homo sapiens	115-120
27115471-10	2016	Reduced expression of heat shock proteins (HSPs) was observed in AA cells, whereas DCA induced expression of CHOP, C/EBP, HSP60, and HSP90 in CA cells.	Dichloroacetic Acid	83-86	heat shock protein family D (Hsp60) member 1	Homo sapiens	122-127
27115471-10	2016	Reduced expression of heat shock proteins (HSPs) was observed in AA cells, whereas DCA induced expression of CHOP, C/EBP, HSP60, and HSP90 in CA cells.	Dichloroacetic Acid	83-86	heat shock protein 90 alpha family class A member 1	Homo sapiens	133-138
27143230-4	2016	This is because conversion of DCA to glyoxylate is catalyzed by one enzyme, glutathione transferase zeta 1 (GSTZ1-1), which is inactivated by DCA.	Dichloroacetic Acid	30-33	glutathione S-transferase zeta 1	Homo sapiens	76-106
27143230-4	2016	This is because conversion of DCA to glyoxylate is catalyzed by one enzyme, glutathione transferase zeta 1 (GSTZ1-1), which is inactivated by DCA.	Dichloroacetic Acid	30-33	glutathione S-transferase zeta 1	Homo sapiens	108-115
27143230-4	2016	This is because conversion of DCA to glyoxylate is catalyzed by one enzyme, glutathione transferase zeta 1 (GSTZ1-1), which is inactivated by DCA.	Dichloroacetic Acid	142-145	glutathione S-transferase zeta 1	Homo sapiens	76-106
27143230-4	2016	This is because conversion of DCA to glyoxylate is catalyzed by one enzyme, glutathione transferase zeta 1 (GSTZ1-1), which is inactivated by DCA.	Dichloroacetic Acid	142-145	glutathione S-transferase zeta 1	Homo sapiens	108-115
27143230-5	2016	SNPs in the GSTZ1 gene result in expression of polymorphic variants of the enzyme that differ in activity and rates of inactivation by DCA under physiological conditions: these properties lead to considerable variation between people in the pharmacokinetics of DCA.	Dichloroacetic Acid	135-138	glutathione S-transferase zeta 1	Homo sapiens	12-17
27143230-5	2016	SNPs in the GSTZ1 gene result in expression of polymorphic variants of the enzyme that differ in activity and rates of inactivation by DCA under physiological conditions: these properties lead to considerable variation between people in the pharmacokinetics of DCA.	Dichloroacetic Acid	261-264	glutathione S-transferase zeta 1	Homo sapiens	12-17
27006991-3	2016	For the first time, we have successfully developed DCA derived inhibitors that preferentially bind to the adenosine triphosphate (ATP) pocket of PDK isoform 1 (PDK1).	Dichloroacetic Acid	51-54	pyruvate dehydrogenase kinase 1	Homo sapiens	145-158
27006991-3	2016	For the first time, we have successfully developed DCA derived inhibitors that preferentially bind to the adenosine triphosphate (ATP) pocket of PDK isoform 1 (PDK1).	Dichloroacetic Acid	51-54	pyruvate dehydrogenase kinase 1	Homo sapiens	160-164
26935268-0	2016	In human alloreactive CD4+ T-cells, dichloroacetate inhibits aerobic glycolysis, induces apoptosis and favors differentiation towards the regulatory T-cell subset instead of effector T-cell subsets.	Dichloroacetic Acid	36-51	CD4 molecule	Homo sapiens	22-25
26959881-0	2016	Metformin combined with sodium dichloroacetate promotes B leukemic cell death by suppressing anti-apoptotic protein Mcl-1.	Dichloroacetic Acid	24-46	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	116-121
26433571-10	2016	DCA reactivated mitochondrial function (increased respiration, Krebs cycle metabolites such as alpha-ketoglutarate [cofactor of factor inhibiting HIF], and mitochondrial reactive oxygen species), increased p53 activity and apoptosis, and decreased proliferation in 786-O cells.	Dichloroacetic Acid	0-3	tumor protein p53	Homo sapiens	206-209
26935268-4	2016	As DCA inhibits aerobic glycolysis, which is a prerequisite for CD4+ T-cell proliferation and differentiation into effector T-cells, its possible immunosuppressive role in mixed lymphocyte reaction (MLR), a model of alloreactivity, was investigated.	Dichloroacetic Acid	3-6	CD4 molecule	Homo sapiens	64-67
26935268-8	2016	In CD4+ T-cells, DCA induced apoptosis, and decreased the expression of glucose trasporter-1, hexokinase II, lactate dehydrogenase-A and phosphorylated pyruvate dehydrogenase, while it increased total pyruvate dehydrogenase.	Dichloroacetic Acid	17-20	CD4 molecule	Homo sapiens	3-6
26935268-8	2016	In CD4+ T-cells, DCA induced apoptosis, and decreased the expression of glucose trasporter-1, hexokinase II, lactate dehydrogenase-A and phosphorylated pyruvate dehydrogenase, while it increased total pyruvate dehydrogenase.	Dichloroacetic Acid	17-20	lactate dehydrogenase A	Homo sapiens	109-132
26935268-9	2016	In addition, DCA increased the expression of transcription factor forkhead box P3, whereas it decreased the expression of T-box transcription factor TBX21, trans-acting T-cell-specific transcription factor GATA-3 and retinoic acid receptor related orphan receptor-gammat.	Dichloroacetic Acid	13-16	forkhead box P3	Homo sapiens	66-81
26935268-9	2016	In addition, DCA increased the expression of transcription factor forkhead box P3, whereas it decreased the expression of T-box transcription factor TBX21, trans-acting T-cell-specific transcription factor GATA-3 and retinoic acid receptor related orphan receptor-gammat.	Dichloroacetic Acid	13-16	T-box transcription factor 21	Homo sapiens	149-154
26607904-11	2016	High glycolysis and PDK2 overexpression are closely linked to cisplatin resistance in HNC cells; the latter can be overcome by DCA.	Dichloroacetic Acid	127-130	pyruvate dehydrogenase kinase 2	Homo sapiens	20-24
26194612-7	2016	DCA revealed that the multivariable models with the addition of PHI or PCA3 showed a greater net benefit and performed better than the reference models.	Dichloroacetic Acid	0-3	prostate cancer associated 3	Homo sapiens	71-75
26871475-11	2016	Honokiol DCA and hexafluoro inhibited the phosphorylation of DRP1, thus stimulating a phenotype suggestive of respiration through mitochondrial normalization.	Dichloroacetic Acid	9-12	collapsin response mediator protein 1	Homo sapiens	61-65
26958021-9	2015	Furthermore, DCA+GDCA can show stronger inhibition towards the secretion of IL-10 than DCA and GDCA.	Dichloroacetic Acid	18-21	interleukin 10	Homo sapiens	76-81
26958021-7	2015	Furthermore, the biological function was investigated for the inhibition of DCA and GDCA towards the secretion of IL-10 by CD4+CD25- T cells.	Dichloroacetic Acid	76-79	interleukin 10	Homo sapiens	114-119
26958021-8	2015	Both DCA and GDCA significantly inhibited the secretion of IL-10 by CD4+CD25- T cells.	Dichloroacetic Acid	5-8	interleukin 10	Homo sapiens	59-64
26958021-9	2015	Furthermore, DCA+GDCA can show stronger inhibition towards the secretion of IL-10 than DCA and GDCA.	Dichloroacetic Acid	13-16	interleukin 10	Homo sapiens	76-81
26616058-0	2016	Targeting HIF-1alpha is a prerequisite for cell sensitivity to dichloroacetate (DCA) and metformin.	Dichloroacetic Acid	63-78	hypoxia inducible factor 1 subunit alpha	Homo sapiens	10-20
26616058-0	2016	Targeting HIF-1alpha is a prerequisite for cell sensitivity to dichloroacetate (DCA) and metformin.	Dichloroacetic Acid	80-83	hypoxia inducible factor 1 subunit alpha	Homo sapiens	10-20
26616058-4	2016	Interestingly, HIF-1alpha activation markedly suppressed DCA/metformin-induced cell death and recovered the expressions of glycolytic enzymes that were decreased by two drugs.	Dichloroacetic Acid	57-60	hypoxia inducible factor 1 subunit alpha	Homo sapiens	15-25
26958021-10	2015	CONCLUSION: The inhibition of IL-10 secretion by elevated DCA and GDCA components in nasopharyngeal carcinoma patients is the inducer for nasopharyngeal carcinoma.	Dichloroacetic Acid	58-61	interleukin 10	Homo sapiens	30-35
26461057-9	2015	Furthermore, exposure of cells to DCA, a bile acid component of gastric refluxate and known tumour promoter for oesophageal cancer, causes disassembly of the Golgi structure into ministacks, resulting in cleavage and secretion of GOLPH2.	Dichloroacetic Acid	34-37	golgi membrane protein 1	Homo sapiens	230-236
26215756-12	2015	RESULT(S): Dichloroacetate increased apoptosis, SOD3 messenger RNA, iNOS messenger RNA, and NO levels in fibroblasts from peritoneum and adhesions.	Dichloroacetic Acid	11-26	superoxide dismutase 3	Homo sapiens	48-52
26215756-12	2015	RESULT(S): Dichloroacetate increased apoptosis, SOD3 messenger RNA, iNOS messenger RNA, and NO levels in fibroblasts from peritoneum and adhesions.	Dichloroacetic Acid	11-26	nitric oxide synthase 2	Homo sapiens	68-72
26052022-4	2015	All HAAs studied, and DCAA and DBAA in particular (at lower concentrations than those, which caused necrosis) induced apoptotic changes, which was confirmed by analysis of alterations in cell membrane permeability and caspase 8, 9 and 3 activation.	Dichloroacetic Acid	22-26	caspase 8	Homo sapiens	218-227
26095603-5	2015	Reversal of the glycolytic switch by dichloracetate induced apoptosis and reduced cell growth, particularly in the S100A4 stimulated cells.	Dichloroacetic Acid	37-51	S100 calcium binding protein A4	Homo sapiens	115-121
26231043-3	2015	We found that DCA induces the AMP-activated protein kinase (AMPK)/p53 pathway with increased efficacy in tumors expressing wild type (wt p53).	Dichloroacetic Acid	14-17	tumor protein p53	Homo sapiens	66-69
25601413-4	2015	Moreover, docking studies revealed putative binding sites of phenylbutyrate on PDK2 and 3 that are located on different sites compared to dichloroacetate (DCA), a previously known PDK inhibitor.	Dichloroacetic Acid	138-153	pyruvate dehydrogenase kinase 2	Homo sapiens	79-89
25601413-4	2015	Moreover, docking studies revealed putative binding sites of phenylbutyrate on PDK2 and 3 that are located on different sites compared to dichloroacetate (DCA), a previously known PDK inhibitor.	Dichloroacetic Acid	155-158	pyruvate dehydrogenase kinase 2	Homo sapiens	79-89
26343699-5	2015	The results showed that TCE and its oxidative metabolites, TCA and DCA, significantly enhanced IL-2 releasing and the expression of T cell activation markers, CD25 and CD69.	Dichloroacetic Acid	67-70	interleukin 2	Homo sapiens	95-99
26343699-5	2015	The results showed that TCE and its oxidative metabolites, TCA and DCA, significantly enhanced IL-2 releasing and the expression of T cell activation markers, CD25 and CD69.	Dichloroacetic Acid	67-70	interleukin 2 receptor subunit alpha	Homo sapiens	159-163
26343699-5	2015	The results showed that TCE and its oxidative metabolites, TCA and DCA, significantly enhanced IL-2 releasing and the expression of T cell activation markers, CD25 and CD69.	Dichloroacetic Acid	67-70	CD69 molecule	Homo sapiens	168-172
26422103-2	2015	Therefore, the aim of this work is the study of capability of aconitine-containing antiangiogenic agent BC1 to enhance anticancer activity of DCA against Ehrlich carcinoma.	Dichloroacetic Acid	142-145	brain cytoplasmic RNA 1	Mus musculus	104-107
26231043-3	2015	We found that DCA induces the AMP-activated protein kinase (AMPK)/p53 pathway with increased efficacy in tumors expressing wild type (wt p53).	Dichloroacetic Acid	14-17	tumor protein p53	Homo sapiens	137-140
26231043-4	2015	Clinically relevant, low concentrations of doxorubicin synergize in vitro and in vivo with DCA to further enhance p53 activation and to block tumor progression.	Dichloroacetic Acid	91-94	tumor protein p53	Homo sapiens	114-117
26231043-6	2015	However, DCA synergized with the Hsp90 inhibitor 17-AAG to specifically eliminate these cells.	Dichloroacetic Acid	9-12	heat shock protein 90 alpha family class A member 1	Homo sapiens	33-38
26231043-6	2015	However, DCA synergized with the Hsp90 inhibitor 17-AAG to specifically eliminate these cells.	Dichloroacetic Acid	9-12	N-methylpurine DNA glycosylase	Homo sapiens	52-55
26045167-7	2015	Notably, pharmacological activation of PDH by cell exposure to dichloroacetate (DCA) increased production of hyperpolarized 5-(13)C-glutamate in IDH1 mutant cells.	Dichloroacetic Acid	63-78	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	39-42
25795215-6	2015	Twenty-eight days of treatment with dichloroacetate restored PDH flux to normal levels (0.018 +- 0.002 s(-1)), reversed diastolic dysfunction (E/E" 14 +- 1), and normalized blood glucose levels (7.5 +- 0.7 mmol/L).	Dichloroacetic Acid	36-51	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	61-64
26177448-3	2015	Recently, GPBAR1 (TGR5) a G-protein coupled receptor has been shown to mediate itching caused by intradermal administration of DCA and LCA.	Dichloroacetic Acid	127-130	G protein-coupled bile acid receptor 1	Mus musculus	10-16
26177448-3	2015	Recently, GPBAR1 (TGR5) a G-protein coupled receptor has been shown to mediate itching caused by intradermal administration of DCA and LCA.	Dichloroacetic Acid	127-130	G protein-coupled bile acid receptor 1	Mus musculus	18-22
26177448-3	2015	Recently, GPBAR1 (TGR5) a G-protein coupled receptor has been shown to mediate itching caused by intradermal administration of DCA and LCA.	Dichloroacetic Acid	127-130	G protein-coupled receptor 34	Mus musculus	26-52
26177448-6	2015	RESULTS: In naive mice skin application of DCA, TLCA, 6-ECDCA, oleanolic and betulinic acid induces a GPBAR1 dependent pruritogenic response that could be desensitized by re-challenging the mice with the same GPBAR1 agonist.	Dichloroacetic Acid	43-46	G protein-coupled bile acid receptor 1	Mus musculus	102-108
26177448-6	2015	RESULTS: In naive mice skin application of DCA, TLCA, 6-ECDCA, oleanolic and betulinic acid induces a GPBAR1 dependent pruritogenic response that could be desensitized by re-challenging the mice with the same GPBAR1 agonist.	Dichloroacetic Acid	43-46	G protein-coupled bile acid receptor 1	Mus musculus	209-215
26177448-7	2015	In wild type and GPBAR1-/- mice cholestasis induced by ANIT fails to induce spontaneous itching and abrogates scratching behavior caused by intradermal administration of DCA.	Dichloroacetic Acid	170-173	G protein-coupled bile acid receptor 1	Mus musculus	17-23
26147621-8	2015	Interestingly, we were also able to describe a possible pathway that involves Hif-1alpha and p53 during DCA-induced loss of pluripotency.	Dichloroacetic Acid	104-107	hypoxia inducible factor 1 subunit alpha	Homo sapiens	78-88
26147621-8	2015	Interestingly, we were also able to describe a possible pathway that involves Hif-1alpha and p53 during DCA-induced loss of pluripotency.	Dichloroacetic Acid	104-107	tumor protein p53	Homo sapiens	93-96
25471732-0	2015	Inhibition of S6K1 enhances dichloroacetate-induced cell death.	Dichloroacetic Acid	28-43	ribosomal protein S6 kinase B1	Homo sapiens	14-18
25471732-3	2015	In the present study, we investigated the effects of S6 kinase 1 (S6K1) inhibition on DCA-induced cell death and the underlying mechanisms in breast cancer cells.	Dichloroacetic Acid	86-89	ribosomal protein S6 kinase B1	Homo sapiens	53-64
25471732-3	2015	In the present study, we investigated the effects of S6 kinase 1 (S6K1) inhibition on DCA-induced cell death and the underlying mechanisms in breast cancer cells.	Dichloroacetic Acid	86-89	ribosomal protein S6 kinase B1	Homo sapiens	66-70
25471732-8	2015	RESULTS: PF4708671, a selective inhibitor of S6K1, and knockdown of S6K1 with specific siRNA enhanced DCA-induced cell death.	Dichloroacetic Acid	102-105	ribosomal protein S6 kinase B1	Homo sapiens	68-72
25471732-12	2015	CONCLUSIONS: Based on these findings, we propose that inhibition of S6K1, in combination with the glycolytic inhibitor, DCA, provides effective cancer therapy.	Dichloroacetic Acid	120-123	ribosomal protein S6 kinase B1	Homo sapiens	68-72
25995437-8	2015	Pretreatment of SQ20B cells with dichloroacetate (DCA), which inhibits PDH-E1alpha phosphorylation by inhibiting dehydrogenase kinases (PDK), reversed the decrease in OCR in response to PI3K/Akt/mTOR inhibition.	Dichloroacetic Acid	33-48	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	71-74
25995437-8	2015	Pretreatment of SQ20B cells with dichloroacetate (DCA), which inhibits PDH-E1alpha phosphorylation by inhibiting dehydrogenase kinases (PDK), reversed the decrease in OCR in response to PI3K/Akt/mTOR inhibition.	Dichloroacetic Acid	33-48	AKT serine/threonine kinase 1	Homo sapiens	191-194
25995437-8	2015	Pretreatment of SQ20B cells with dichloroacetate (DCA), which inhibits PDH-E1alpha phosphorylation by inhibiting dehydrogenase kinases (PDK), reversed the decrease in OCR in response to PI3K/Akt/mTOR inhibition.	Dichloroacetic Acid	33-48	mechanistic target of rapamycin kinase	Homo sapiens	195-199
25995437-8	2015	Pretreatment of SQ20B cells with dichloroacetate (DCA), which inhibits PDH-E1alpha phosphorylation by inhibiting dehydrogenase kinases (PDK), reversed the decrease in OCR in response to PI3K/Akt/mTOR inhibition.	Dichloroacetic Acid	50-53	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	71-74
25995437-8	2015	Pretreatment of SQ20B cells with dichloroacetate (DCA), which inhibits PDH-E1alpha phosphorylation by inhibiting dehydrogenase kinases (PDK), reversed the decrease in OCR in response to PI3K/Akt/mTOR inhibition.	Dichloroacetic Acid	50-53	AKT serine/threonine kinase 1	Homo sapiens	191-194
25995437-8	2015	Pretreatment of SQ20B cells with dichloroacetate (DCA), which inhibits PDH-E1alpha phosphorylation by inhibiting dehydrogenase kinases (PDK), reversed the decrease in OCR in response to PI3K/Akt/mTOR inhibition.	Dichloroacetic Acid	50-53	mechanistic target of rapamycin kinase	Homo sapiens	195-199
26045167-7	2015	Notably, pharmacological activation of PDH by cell exposure to dichloroacetate (DCA) increased production of hyperpolarized 5-(13)C-glutamate in IDH1 mutant cells.	Dichloroacetic Acid	63-78	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	145-149
26045167-7	2015	Notably, pharmacological activation of PDH by cell exposure to dichloroacetate (DCA) increased production of hyperpolarized 5-(13)C-glutamate in IDH1 mutant cells.	Dichloroacetic Acid	80-83	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	39-42
26045167-7	2015	Notably, pharmacological activation of PDH by cell exposure to dichloroacetate (DCA) increased production of hyperpolarized 5-(13)C-glutamate in IDH1 mutant cells.	Dichloroacetic Acid	80-83	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	145-149
26045167-8	2015	Furthermore, DCA treatment also abrogated the clonogenic advantage conferred by IDH1 mutation.	Dichloroacetic Acid	13-16	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	80-84
25982179-3	2015	To this end, we tested whether a short-time treatment of AML cells, including cells with FLT3-ITD mutation, with sub-lethal dose of dichloroacetate (DCA) (priming) followed by pharmacologic dose of arsenic trioxide (ATO) in presence of low-dose DCA could produce insurmountable level of oxidative damage that kill AML cells.	Dichloroacetic Acid	132-147	fms related receptor tyrosine kinase 3	Homo sapiens	89-93
25762000-16	2015	Conclusions The RP2D of oral DCA is 6.25 mg/kg BID.	Dichloroacetic Acid	29-32	BH3 interacting domain death agonist	Homo sapiens	47-50
25976231-5	2015	Melanoma cell lines treated with DCA showed a shift in metabolism, that is, a decrease in glucose consumption and lactate production, downregulation of proliferation, an increase of apoptosis and a decrease in mTOR pathway activation.	Dichloroacetic Acid	33-36	mechanistic target of rapamycin kinase	Homo sapiens	210-214
25820275-8	2015	Further, inhibition of pyruvate dehydrogenase kinase 4 activity with dichloroacetate delayed symptom onset while improving mitochondrial dysfunction and ameliorating muscle denervation.	Dichloroacetic Acid	69-84	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	23-54
28962410-7	2015	Further, as TCA and DCA, the ligand of peroxisome proliferator activated receptor alpha (PPARA), are involved in the process of hepatocarcinogenesis in rodents, we examined expression of PPARA mRNA and let-7c miRNA in the workers.	Dichloroacetic Acid	20-23	peroxisome proliferator activated receptor alpha	Homo sapiens	39-87
28962410-7	2015	Further, as TCA and DCA, the ligand of peroxisome proliferator activated receptor alpha (PPARA), are involved in the process of hepatocarcinogenesis in rodents, we examined expression of PPARA mRNA and let-7c miRNA in the workers.	Dichloroacetic Acid	20-23	peroxisome proliferator activated receptor alpha	Homo sapiens	89-94
28962410-7	2015	Further, as TCA and DCA, the ligand of peroxisome proliferator activated receptor alpha (PPARA), are involved in the process of hepatocarcinogenesis in rodents, we examined expression of PPARA mRNA and let-7c miRNA in the workers.	Dichloroacetic Acid	20-23	peroxisome proliferator activated receptor alpha	Homo sapiens	187-192
28962410-7	2015	Further, as TCA and DCA, the ligand of peroxisome proliferator activated receptor alpha (PPARA), are involved in the process of hepatocarcinogenesis in rodents, we examined expression of PPARA mRNA and let-7c miRNA in the workers.	Dichloroacetic Acid	20-23	microRNA let-7c	Homo sapiens	202-208
25748576-1	2015	We recently reported that, in a concentration-dependent manner, chloride protects hepatic glutathione transferase zeta 1 from inactivation by dichloroacetate, an investigational drug used in treating various acquired and congenital metabolic diseases.	Dichloroacetic Acid	142-157	glutathione S-transferase zeta 1	Homo sapiens	90-120
25738370-2	2015	Haplotype variability in GSTZ1 influences the kinetics and, possibly, the toxicity of DCA.	Dichloroacetic Acid	86-89	glutathione S-transferase zeta 1	Homo sapiens	25-30
25738370-3	2015	DCA metabolism correlates with expression of the GSTZ1 protein, so it is important to document variables that affect expression.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	49-54
25738370-10	2015	CONCLUSION: We conclude that the lower expression of GSTZ1 in Whites who possess the K carrier haplotype results in lower enzymatic activity and slower metabolism of DCA, compared with those who possess the non-K carrier haplotype.	Dichloroacetic Acid	166-169	glutathione S-transferase zeta 1	Homo sapiens	53-58
25649989-5	2015	Thus elongated anions such as Tf2N(-) and DCA(-) that can interact with two different metal sites tend to lower IRMOF stability compared to spherical anions such as Br(-) and PF6(-).	Dichloroacetic Acid	42-45	sperm associated antigen 17	Homo sapiens	175-178
25502361-7	2015	Inhibition of PDK1 expression was observed when oral cancer cells were treated with the PDK1 inhibitor dichloroacetate (DCA).	Dichloroacetic Acid	103-118	pyruvate dehydrogenase kinase 1	Homo sapiens	14-18
25502361-7	2015	Inhibition of PDK1 expression was observed when oral cancer cells were treated with the PDK1 inhibitor dichloroacetate (DCA).	Dichloroacetic Acid	103-118	pyruvate dehydrogenase kinase 1	Homo sapiens	88-92
25502361-7	2015	Inhibition of PDK1 expression was observed when oral cancer cells were treated with the PDK1 inhibitor dichloroacetate (DCA).	Dichloroacetic Acid	120-123	pyruvate dehydrogenase kinase 1	Homo sapiens	14-18
25502361-7	2015	Inhibition of PDK1 expression was observed when oral cancer cells were treated with the PDK1 inhibitor dichloroacetate (DCA).	Dichloroacetic Acid	120-123	pyruvate dehydrogenase kinase 1	Homo sapiens	88-92
25283137-0	2015	Chloral hydrate, through biotransformation to dichloroacetate, inhibits maleylacetoacetate isomerase and tyrosine catabolism in humans.	Dichloroacetic Acid	46-61	glutathione S-transferase zeta 1	Homo sapiens	72-100
25283137-2	2015	DCA is further metabolized by glutathione transferase zeta 1 (GSTZ1), which is identical to maleylacetoacetate isomerase (MAAI), the penultimate enzyme in tyrosine catabolism.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	30-60
25283137-2	2015	DCA is further metabolized by glutathione transferase zeta 1 (GSTZ1), which is identical to maleylacetoacetate isomerase (MAAI), the penultimate enzyme in tyrosine catabolism.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	62-67
25283137-2	2015	DCA is further metabolized by glutathione transferase zeta 1 (GSTZ1), which is identical to maleylacetoacetate isomerase (MAAI), the penultimate enzyme in tyrosine catabolism.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	92-120
25283137-2	2015	DCA is further metabolized by glutathione transferase zeta 1 (GSTZ1), which is identical to maleylacetoacetate isomerase (MAAI), the penultimate enzyme in tyrosine catabolism.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	122-126
25283137-3	2015	DCA inhibits its own metabolism through depletion/inactivation of GSTZ1/MAAI with repeated exposure, resulting in lower plasma clearance of the drug and the accumulation of the urinary biomarker maleylacetone (MA), a metabolite of tyrosine.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	66-71
25283137-3	2015	DCA inhibits its own metabolism through depletion/inactivation of GSTZ1/MAAI with repeated exposure, resulting in lower plasma clearance of the drug and the accumulation of the urinary biomarker maleylacetone (MA), a metabolite of tyrosine.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	72-76
25283137-12	2015	CONCLUSIONS: These data indicate that the amount of DCA produced from clinically relevant doses of CH, although insufficient to alter DCA kinetics, is sufficient to inhibit MAAI and tyrosine catabolism, as evidenced by the accumulation of urinary MA.	Dichloroacetic Acid	52-55	glutathione S-transferase zeta 1	Homo sapiens	173-177
25531406-9	2015	For example, the concentrations of trihalomethanes (THMs), dichloroacetic acid (DCAA) and chloropicrin (CP) were substantially higher in the hot water tap than in the cold water time-variable SDS samples.	Dichloroacetic Acid	80-84	nuclear RNA export factor 1	Homo sapiens	151-154
25544776-0	2015	The anti-leukemic activity of sodium dichloroacetate in p53mutated/null cells is mediated by a p53-independent ILF3/p21 pathway.	Dichloroacetic Acid	30-52	tumor protein p53	Homo sapiens	56-59
25544776-0	2015	The anti-leukemic activity of sodium dichloroacetate in p53mutated/null cells is mediated by a p53-independent ILF3/p21 pathway.	Dichloroacetic Acid	30-52	tumor protein p53	Homo sapiens	95-98
25544776-0	2015	The anti-leukemic activity of sodium dichloroacetate in p53mutated/null cells is mediated by a p53-independent ILF3/p21 pathway.	Dichloroacetic Acid	30-52	interleukin enhancer binding factor 3	Homo sapiens	111-115
25544776-0	2015	The anti-leukemic activity of sodium dichloroacetate in p53mutated/null cells is mediated by a p53-independent ILF3/p21 pathway.	Dichloroacetic Acid	30-52	H3 histone pseudogene 16	Homo sapiens	116-119
25544776-2	2015	Having recently demonstrated that the mitochondria-targeting small molecule sodium dichloroacetate (DCA) exhibits anti-leukemic activity in p53wild-type B-CLL cells, the aim of this study was to evaluate the effect of DCA in p53mutated B-CLL cells and in p53mutated/null leukemic cell lines.	Dichloroacetic Acid	76-98	tumor protein p53	Homo sapiens	140-143
25544776-2	2015	Having recently demonstrated that the mitochondria-targeting small molecule sodium dichloroacetate (DCA) exhibits anti-leukemic activity in p53wild-type B-CLL cells, the aim of this study was to evaluate the effect of DCA in p53mutated B-CLL cells and in p53mutated/null leukemic cell lines.	Dichloroacetic Acid	76-98	tumor protein p53	Homo sapiens	225-228
25544776-2	2015	Having recently demonstrated that the mitochondria-targeting small molecule sodium dichloroacetate (DCA) exhibits anti-leukemic activity in p53wild-type B-CLL cells, the aim of this study was to evaluate the effect of DCA in p53mutated B-CLL cells and in p53mutated/null leukemic cell lines.	Dichloroacetic Acid	100-103	tumor protein p53	Homo sapiens	140-143
25544776-2	2015	Having recently demonstrated that the mitochondria-targeting small molecule sodium dichloroacetate (DCA) exhibits anti-leukemic activity in p53wild-type B-CLL cells, the aim of this study was to evaluate the effect of DCA in p53mutated B-CLL cells and in p53mutated/null leukemic cell lines.	Dichloroacetic Acid	100-103	tumor protein p53	Homo sapiens	225-228
25544776-3	2015	DCA exhibited comparable cytotoxicity in p53wild-type and p53mutated B-CLL patient cell cultures, as well as in p53mutated B leukemic cell lines (MAVER, MEC-1, MEC-2).	Dichloroacetic Acid	0-3	tumor protein p53	Homo sapiens	41-44
25544776-3	2015	DCA exhibited comparable cytotoxicity in p53wild-type and p53mutated B-CLL patient cell cultures, as well as in p53mutated B leukemic cell lines (MAVER, MEC-1, MEC-2).	Dichloroacetic Acid	0-3	tumor protein p53	Homo sapiens	58-61
25544776-3	2015	DCA exhibited comparable cytotoxicity in p53wild-type and p53mutated B-CLL patient cell cultures, as well as in p53mutated B leukemic cell lines (MAVER, MEC-1, MEC-2).	Dichloroacetic Acid	0-3	tumor protein p53	Homo sapiens	58-61
25544776-3	2015	DCA exhibited comparable cytotoxicity in p53wild-type and p53mutated B-CLL patient cell cultures, as well as in p53mutated B leukemic cell lines (MAVER, MEC-1, MEC-2).	Dichloroacetic Acid	0-3	ATR serine/threonine kinase	Homo sapiens	153-158
25544776-5	2015	By using a proteomic approach, we demonstrated that DCA up-regulated the ILF3 transcription factor, which is a known regulator of p21 expression.	Dichloroacetic Acid	52-55	interleukin enhancer binding factor 3	Homo sapiens	73-77
25544776-5	2015	By using a proteomic approach, we demonstrated that DCA up-regulated the ILF3 transcription factor, which is a known regulator of p21 expression.	Dichloroacetic Acid	52-55	H3 histone pseudogene 16	Homo sapiens	130-133
25544776-6	2015	The role of the ILF3/p21 axis in mediating the DCA anti-leukemic activity was underscored by knocking-down experiments.	Dichloroacetic Acid	47-50	interleukin enhancer binding factor 3	Homo sapiens	16-20
25544776-6	2015	The role of the ILF3/p21 axis in mediating the DCA anti-leukemic activity was underscored by knocking-down experiments.	Dichloroacetic Acid	47-50	H3 histone pseudogene 16	Homo sapiens	21-24
25544776-7	2015	Indeed, transfection with ILF3 and p21 siRNAs significantly decreased both the DCA-induced p21 expression and the DCA-mediated cytotoxicity.	Dichloroacetic Acid	79-82	interleukin enhancer binding factor 3	Homo sapiens	26-30
25544776-7	2015	Indeed, transfection with ILF3 and p21 siRNAs significantly decreased both the DCA-induced p21 expression and the DCA-mediated cytotoxicity.	Dichloroacetic Acid	79-82	H3 histone pseudogene 16	Homo sapiens	35-38
25544776-7	2015	Indeed, transfection with ILF3 and p21 siRNAs significantly decreased both the DCA-induced p21 expression and the DCA-mediated cytotoxicity.	Dichloroacetic Acid	79-82	H3 histone pseudogene 16	Homo sapiens	91-94
25544776-7	2015	Indeed, transfection with ILF3 and p21 siRNAs significantly decreased both the DCA-induced p21 expression and the DCA-mediated cytotoxicity.	Dichloroacetic Acid	114-117	interleukin enhancer binding factor 3	Homo sapiens	26-30
25544776-7	2015	Indeed, transfection with ILF3 and p21 siRNAs significantly decreased both the DCA-induced p21 expression and the DCA-mediated cytotoxicity.	Dichloroacetic Acid	114-117	H3 histone pseudogene 16	Homo sapiens	35-38
25544776-8	2015	Taken together, our results emphasize that DCA is a small molecule that merits further evaluation as a therapeutic agent also for p53mutated leukemic cells, by acting through the induction of a p53-independent pathway.	Dichloroacetic Acid	43-46	tumor protein p53	Homo sapiens	130-133
25544776-8	2015	Taken together, our results emphasize that DCA is a small molecule that merits further evaluation as a therapeutic agent also for p53mutated leukemic cells, by acting through the induction of a p53-independent pathway.	Dichloroacetic Acid	43-46	tumor protein p53	Homo sapiens	194-197
25536473-0	2015	Pyruvate dehydrogenase kinase expression and metabolic changes following dichloroacetate exposure in anoxic human colorectal cancer cells.	Dichloroacetic Acid	73-88	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	0-22
25536473-1	2015	Dichloroacetate (DCA) is a small molecule that inhibits pyruvate dehydrogenase kinase (PDK) to constrain the aerobic glycolytic pathway observed in many cancer cells and effectively kill them with limited cytotoxicity on normal cells.	Dichloroacetic Acid	0-15	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	56-78
25536473-1	2015	Dichloroacetate (DCA) is a small molecule that inhibits pyruvate dehydrogenase kinase (PDK) to constrain the aerobic glycolytic pathway observed in many cancer cells and effectively kill them with limited cytotoxicity on normal cells.	Dichloroacetic Acid	17-20	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	56-78
25536473-6	2015	We show evidence of differential regulation in PDH phosphorylation between different human CRC cells leading to differences in mitochondrial activity following DCA exposure.	Dichloroacetic Acid	160-163	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	47-50
25544754-6	2015	DCA treatment of the three OSCC cell lines, at pharmacological concentrations, resulted in stimulation of the respiratory activity and caused a remarkably distinctive pro-apoptotic/cytostatic effect on HSC-2 and HSC-3.	Dichloroacetic Acid	0-3	DnaJ heat shock protein family (Hsp40) member B7	Homo sapiens	212-217
25644430-14	2015	As an alternative, we used DCA in combination with miR-206 to increase the flux of pyruvate into the mitochondrion by reactivating PDH.	Dichloroacetic Acid	27-30	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	131-134
25973318-4	2015	Therefore, the purpose of this study was to shift tumor cells from aerobic glycolysis to oxidative phosphorylation using dichloroacetate (DCA), an inhibitor of PDH-kinase.	Dichloroacetic Acid	121-136	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	160-163
25973318-4	2015	Therefore, the purpose of this study was to shift tumor cells from aerobic glycolysis to oxidative phosphorylation using dichloroacetate (DCA), an inhibitor of PDH-kinase.	Dichloroacetic Acid	138-141	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	160-163
25585916-0	2015	A potent tumoricidal co-drug "Bet-CA"--an ester derivative of betulinic acid and dichloroacetate selectively and synergistically kills cancer cells.	Dichloroacetic Acid	81-96	delta/notch like EGF repeat containing	Homo sapiens	30-33
25585916-3	2015	Here, we report synthesis, characterization and tumoricidal potential of a co-drug Bet-CA, where a DCA molecule has been appended on C-3 hydroxyl group of BA to generate an ester derivative for increased solubility and subsequent cleavage by internal esterase(s) to release one unit each of BA and DCA.	Dichloroacetic Acid	99-102	delta/notch like EGF repeat containing	Homo sapiens	83-86
25585916-3	2015	Here, we report synthesis, characterization and tumoricidal potential of a co-drug Bet-CA, where a DCA molecule has been appended on C-3 hydroxyl group of BA to generate an ester derivative for increased solubility and subsequent cleavage by internal esterase(s) to release one unit each of BA and DCA.	Dichloroacetic Acid	298-301	delta/notch like EGF repeat containing	Homo sapiens	83-86
25344893-6	2015	Treatment with 20 mM DCA did not increase apoptosis, despite decreasing levels of anti-apoptotic protein Mcl-1 after 6 h, in any of the cell lines observed.	Dichloroacetic Acid	21-24	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	105-110
25344893-8	2015	A decrease in Mcl-1 correlated with a decrease in proliferation, both of which showed dose-dependence in DCA treated cells.	Dichloroacetic Acid	105-108	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	14-19
25344893-10	2015	These data suggest that a reduction in the prosurvival Bcl-2 family member Mcl-1 due to increased proteasomal degradation is correlated with the ability of DCA to reduce proliferation of HCT116 human colorectal cancer cells without causing apoptosis.	Dichloroacetic Acid	156-159	BCL2 apoptosis regulator	Homo sapiens	55-60
25344893-10	2015	These data suggest that a reduction in the prosurvival Bcl-2 family member Mcl-1 due to increased proteasomal degradation is correlated with the ability of DCA to reduce proliferation of HCT116 human colorectal cancer cells without causing apoptosis.	Dichloroacetic Acid	156-159	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	75-80
26301238-5	2015	Increasing DCA concentration alone does not affect total glutathione or its redox ratio but does increase activity in the SOD/CAT oxidative stress defense pathway.	Dichloroacetic Acid	11-14	catalase	Rattus norvegicus	126-129
26301238-6	2015	These data suggest that alveolar type II cells rely on SOD and CAT more than glutathione to combat DCA-induced stress.	Dichloroacetic Acid	99-102	catalase	Rattus norvegicus	63-66
25644430-15	2015	DCA enhanced the inhibition of RMS cell growth induced by miR-206, and sustained it upon miR-206 de-induction.	Dichloroacetic Acid	0-3	microRNA 206	Homo sapiens	58-65
25644430-15	2015	DCA enhanced the inhibition of RMS cell growth induced by miR-206, and sustained it upon miR-206 de-induction.	Dichloroacetic Acid	0-3	microRNA 206	Homo sapiens	89-96
25791820-0	2015	Synergistic anticancer potential of dichloroacetate and estradiol analogue exerting their effect via ROS-JNK-Bcl-2-mediated signalling pathways.	Dichloroacetic Acid	36-51	mitogen-activated protein kinase 8	Homo sapiens	105-108
25180822-11	2015	Dichloroacetic acid, trichloroacetic acid, and bromochloroacetic acid were the major HAAs detected in most of the tap water, and accounted for 29%, 20% and 19% of the total HAAs, respectively.	Dichloroacetic Acid	0-19	nuclear RNA export factor 1	Homo sapiens	114-117
25791820-0	2015	Synergistic anticancer potential of dichloroacetate and estradiol analogue exerting their effect via ROS-JNK-Bcl-2-mediated signalling pathways.	Dichloroacetic Acid	36-51	BCL2 apoptosis regulator	Homo sapiens	109-114
25791820-12	2015	Antimitotic compound C9 in combination with a glycolytic inhibitor dichloroacetate eradicates breast cancer cells through ROS-JNK-Bcl-2-mediated signalling pathways in vitro and it is argued that autophagy acts as protective mechanism in the treated cells before apoptosis occurs.	Dichloroacetic Acid	67-82	mitogen-activated protein kinase 8	Homo sapiens	126-129
25791820-12	2015	Antimitotic compound C9 in combination with a glycolytic inhibitor dichloroacetate eradicates breast cancer cells through ROS-JNK-Bcl-2-mediated signalling pathways in vitro and it is argued that autophagy acts as protective mechanism in the treated cells before apoptosis occurs.	Dichloroacetic Acid	67-82	BCL2 apoptosis regulator	Homo sapiens	130-135
25846762-8	2015	In all groups, DCA caused a decrease in cell viability, an induction of autophagy in a dose-dependent manner and a decrease in Tim23, FIS1 and PARKIN protein expression, leading to profound morphological changes in the mitochondrial network resulting in shorter and more fragmented filaments.	Dichloroacetic Acid	15-18	translocase of inner mitochondrial membrane 23	Homo sapiens	127-132
25846762-8	2015	In all groups, DCA caused a decrease in cell viability, an induction of autophagy in a dose-dependent manner and a decrease in Tim23, FIS1 and PARKIN protein expression, leading to profound morphological changes in the mitochondrial network resulting in shorter and more fragmented filaments.	Dichloroacetic Acid	15-18	fission, mitochondrial 1	Homo sapiens	134-138
25079374-0	2015	Haplotype variations in glutathione transferase zeta 1 influence the kinetics and dynamics of chronic dichloroacetate in children.	Dichloroacetic Acid	102-117	glutathione S-transferase zeta 1	Homo sapiens	24-54
25079374-6	2015	However, chronic DCA exposure did not lead to progressive accumulation of plasma drug concentration; instead, kinetics parameters plateaued, consistent with the hypothesis that equipoise is established between the inhibitory effect of DCA on GSTZ1/MAAI and new enzyme synthesis.	Dichloroacetic Acid	235-238	glutathione S-transferase zeta 1	Homo sapiens	242-247
25418122-8	2015	RESULTS: In this study, results show that triggering TGR5 with the specific agonist betulinic acid (BA), and the bile acids CDCA or DCA, activated both the main MAP kinases ERK1/2, p38 and JNK, and the NF-kappaB signaling pathway.	Dichloroacetic Acid	125-128	G protein-coupled bile acid receptor 1	Homo sapiens	53-57
25418122-8	2015	RESULTS: In this study, results show that triggering TGR5 with the specific agonist betulinic acid (BA), and the bile acids CDCA or DCA, activated both the main MAP kinases ERK1/2, p38 and JNK, and the NF-kappaB signaling pathway.	Dichloroacetic Acid	125-128	mitogen-activated protein kinase 3	Homo sapiens	173-179
25418122-8	2015	RESULTS: In this study, results show that triggering TGR5 with the specific agonist betulinic acid (BA), and the bile acids CDCA or DCA, activated both the main MAP kinases ERK1/2, p38 and JNK, and the NF-kappaB signaling pathway.	Dichloroacetic Acid	125-128	mitogen-activated protein kinase 1	Homo sapiens	181-184
25418122-8	2015	RESULTS: In this study, results show that triggering TGR5 with the specific agonist betulinic acid (BA), and the bile acids CDCA or DCA, activated both the main MAP kinases ERK1/2, p38 and JNK, and the NF-kappaB signaling pathway.	Dichloroacetic Acid	125-128	mitogen-activated protein kinase 8	Homo sapiens	189-192
25418122-8	2015	RESULTS: In this study, results show that triggering TGR5 with the specific agonist betulinic acid (BA), and the bile acids CDCA or DCA, activated both the main MAP kinases ERK1/2, p38 and JNK, and the NF-kappaB signaling pathway.	Dichloroacetic Acid	125-128	nuclear factor kappa B subunit 1	Homo sapiens	202-211
25424544-8	2015	Serum and hepatic levels of TCA and DCA were correlated with increased transcription of peroxisome proliferator-marker genes Cyp4a10 and Acox1 but not with degree of induction in hepatocellular proliferation.	Dichloroacetic Acid	36-39	cytochrome P450, family 4, subfamily a, polypeptide 10	Mus musculus	125-132
25424544-8	2015	Serum and hepatic levels of TCA and DCA were correlated with increased transcription of peroxisome proliferator-marker genes Cyp4a10 and Acox1 but not with degree of induction in hepatocellular proliferation.	Dichloroacetic Acid	36-39	acyl-Coenzyme A oxidase 1, palmitoyl	Mus musculus	137-142
25424545-5	2015	The quantitative relationship was evaluated between strain-, dose, and time-dependent formation of TCE metabolites from cytochrome P-450-mediated oxidation (trichloroacetic acid [TCA], dichloroacetic acid [DCA], and trichloroethanol) and glutathione conjugation [S-(1,2-dichlorovinyl)-L-cysteine and S-(1,2-dichlorovinyl)glutathione], and various kidney toxicity phenotypes.	Dichloroacetic Acid	185-204	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	120-136
25079374-7	2015	GSTZ1/MAAI haplotype variability affects DCA kinetics and biotransformation.	Dichloroacetic Acid	41-44	glutathione S-transferase zeta 1	Homo sapiens	0-5
25079374-7	2015	GSTZ1/MAAI haplotype variability affects DCA kinetics and biotransformation.	Dichloroacetic Acid	41-44	glutathione S-transferase zeta 1	Homo sapiens	6-10
25079374-1	2015	Dichloroacetate (DCA) is biotransformed by glutathione transferase zeta 1 (GSTZ1), a bifunctional enzyme that, as maleylacetoacetate isomerase (MAAI), catalyzes the penultimate step in tyrosine catabolism.	Dichloroacetic Acid	0-15	glutathione S-transferase zeta 1	Homo sapiens	43-73
25079374-1	2015	Dichloroacetate (DCA) is biotransformed by glutathione transferase zeta 1 (GSTZ1), a bifunctional enzyme that, as maleylacetoacetate isomerase (MAAI), catalyzes the penultimate step in tyrosine catabolism.	Dichloroacetic Acid	0-15	glutathione S-transferase zeta 1	Homo sapiens	75-80
25079374-1	2015	Dichloroacetate (DCA) is biotransformed by glutathione transferase zeta 1 (GSTZ1), a bifunctional enzyme that, as maleylacetoacetate isomerase (MAAI), catalyzes the penultimate step in tyrosine catabolism.	Dichloroacetic Acid	0-15	glutathione S-transferase zeta 1	Homo sapiens	114-142
25079374-1	2015	Dichloroacetate (DCA) is biotransformed by glutathione transferase zeta 1 (GSTZ1), a bifunctional enzyme that, as maleylacetoacetate isomerase (MAAI), catalyzes the penultimate step in tyrosine catabolism.	Dichloroacetic Acid	0-15	glutathione S-transferase zeta 1	Homo sapiens	144-148
25079374-1	2015	Dichloroacetate (DCA) is biotransformed by glutathione transferase zeta 1 (GSTZ1), a bifunctional enzyme that, as maleylacetoacetate isomerase (MAAI), catalyzes the penultimate step in tyrosine catabolism.	Dichloroacetic Acid	17-20	glutathione S-transferase zeta 1	Homo sapiens	43-73
25079374-1	2015	Dichloroacetate (DCA) is biotransformed by glutathione transferase zeta 1 (GSTZ1), a bifunctional enzyme that, as maleylacetoacetate isomerase (MAAI), catalyzes the penultimate step in tyrosine catabolism.	Dichloroacetic Acid	17-20	glutathione S-transferase zeta 1	Homo sapiens	75-80
25079374-1	2015	Dichloroacetate (DCA) is biotransformed by glutathione transferase zeta 1 (GSTZ1), a bifunctional enzyme that, as maleylacetoacetate isomerase (MAAI), catalyzes the penultimate step in tyrosine catabolism.	Dichloroacetic Acid	17-20	glutathione S-transferase zeta 1	Homo sapiens	114-142
25079374-1	2015	Dichloroacetate (DCA) is biotransformed by glutathione transferase zeta 1 (GSTZ1), a bifunctional enzyme that, as maleylacetoacetate isomerase (MAAI), catalyzes the penultimate step in tyrosine catabolism.	Dichloroacetic Acid	17-20	glutathione S-transferase zeta 1	Homo sapiens	144-148
25079374-2	2015	DCA inhibits GSTZ1/MAAI, leading to delayed plasma drug clearance and to accumulation of potentially toxic tyrosine intermediates.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	13-18
25079374-2	2015	DCA inhibits GSTZ1/MAAI, leading to delayed plasma drug clearance and to accumulation of potentially toxic tyrosine intermediates.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	19-23
25079374-3	2015	Haplotype variability in GSTZ1 influences short-term DCA kinetics in healthy adults, but the impact of genotype in children treated chronically with DCA is unknown.	Dichloroacetic Acid	53-56	glutathione S-transferase zeta 1	Homo sapiens	25-30
25079374-6	2015	However, chronic DCA exposure did not lead to progressive accumulation of plasma drug concentration; instead, kinetics parameters plateaued, consistent with the hypothesis that equipoise is established between the inhibitory effect of DCA on GSTZ1/MAAI and new enzyme synthesis.	Dichloroacetic Acid	17-20	glutathione S-transferase zeta 1	Homo sapiens	242-247
25212175-12	2014	Metformin-induced oxidative damage is enhanced by DCA through PDK1 inhibition which also diminishes metformin promoted lactate production.	Dichloroacetic Acid	50-53	pyruvate dehydrogenase kinase 1	Homo sapiens	62-66
25234313-7	2014	PCK rats are an orthologous model of human autosomal recessive PKD and were treated with 75 mg/l DCA in their drinking water.	Dichloroacetic Acid	97-100	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	0-3
25234313-9	2014	Only male PCK rats were adversely affected by DCA treatment, with an increase in the severity of renal cystic disease evinced by an increase in cystic enlargement and proteinuria.	Dichloroacetic Acid	46-49	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	10-13
25320679-9	2014	However, unlike TNF-alpha- , butyrate-stimulated lipolysis was not associated with increased lactate release or inhibited by activation of pyruvate dehydrogenase (PDH) with dichloroacetate.	Dichloroacetic Acid	173-188	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	139-161
25320679-9	2014	However, unlike TNF-alpha- , butyrate-stimulated lipolysis was not associated with increased lactate release or inhibited by activation of pyruvate dehydrogenase (PDH) with dichloroacetate.	Dichloroacetic Acid	173-188	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	163-166
24892448-2	2014	METHODS: We investigated the cellular and metabolic responses to DCA treatment and recovery in human colorectal (HT29, HCT116 WT and HCT116 Bax-ko), prostate carcinoma cells (PC3) and HT29 xenografts by flow cytometry, western blotting, electron microscopy, (1)H and hyperpolarised (13)C-magnetic resonance spectroscopy.	Dichloroacetic Acid	65-68	BCL2 associated X, apoptosis regulator	Homo sapiens	140-143
25110234-10	2014	Furthermore, preventive treatment with DCA significantly increased the activity of copper/zinc superoxide dismutase (Cu/Zn SOD activity, 88+-4.2 vs. 53+-2.7 U/mgprot; P&lt;0.05) and promoted the degradation of ROS (106+-4.7 vs. 79+-13.3 U/mgprot; P&lt;0.05), which was compromised in the delayed intervention group.	Dichloroacetic Acid	39-42	superoxide dismutase 1	Rattus norvegicus	117-126
25110234-11	2014	Therefore, DCA is effective to prevent the formation of intimal lesions, which may be attributed to the induction of the upregulation of Cu/Zn SOD activity and the suppression of HIF-1alpha activation.	Dichloroacetic Acid	11-14	superoxide dismutase 1	Rattus norvegicus	137-146
25110234-11	2014	Therefore, DCA is effective to prevent the formation of intimal lesions, which may be attributed to the induction of the upregulation of Cu/Zn SOD activity and the suppression of HIF-1alpha activation.	Dichloroacetic Acid	11-14	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	179-189
24892448-4	2014	We observed increased production of reactive oxygen species (ROS) and mTOR inhibition (decreased pS6 ribosomal protein and p4E-BP1 expression) as well as increased expression of MCT1 following DCA treatment.	Dichloroacetic Acid	193-196	solute carrier family 16 member 1	Homo sapiens	178-182
24892448-8	2014	CONCLUSIONS: DCA induces autophagy in cancer cells accompanied by ROS production and mTOR inhibition, reduced lactate excretion, reduced k(PL) and increased NAD(+)/NADH ratio.	Dichloroacetic Acid	13-16	mechanistic target of rapamycin kinase	Homo sapiens	85-89
24535708-6	2014	We observed mild OS and induction of antioxidant defense system in 20.0 mug/ml DCA-exposed organism after 24 h. After prolonged exposure to DCA, exposed organism exhibited improved survival, elevated expression of hsp27, gclc, and gclm concomitant with lower ROS generation and GSH depletion and improved locomotor performance.	Dichloroacetic Acid	79-82	Heat shock protein 27	Drosophila melanogaster	214-219
24962518-0	2014	Sodium dichloroacetate exhibits anti-leukemic activity in B-chronic lymphocytic leukemia (B-CLL) and synergizes with the p53 activator Nutlin-3.	Dichloroacetic Acid	0-22	tumor protein p53	Homo sapiens	121-124
24962518-5	2014	Indeed, transfection of leukemic cells with p21 siRNAs significantly decreased the DCA+Nutlin-3-induced cytotoxicity.	Dichloroacetic Acid	83-86	H3 histone pseudogene 16	Homo sapiens	44-47
24535708-6	2014	We observed mild OS and induction of antioxidant defense system in 20.0 mug/ml DCA-exposed organism after 24 h. After prolonged exposure to DCA, exposed organism exhibited improved survival, elevated expression of hsp27, gclc, and gclm concomitant with lower ROS generation and GSH depletion and improved locomotor performance.	Dichloroacetic Acid	79-82	Glutamate-cysteine ligase catalytic subunit	Drosophila melanogaster	221-225
24535708-6	2014	We observed mild OS and induction of antioxidant defense system in 20.0 mug/ml DCA-exposed organism after 24 h. After prolonged exposure to DCA, exposed organism exhibited improved survival, elevated expression of hsp27, gclc, and gclm concomitant with lower ROS generation and GSH depletion and improved locomotor performance.	Dichloroacetic Acid	79-82	Glutamate-cysteine ligase modifier subunit	Drosophila melanogaster	231-235
24535708-6	2014	We observed mild OS and induction of antioxidant defense system in 20.0 mug/ml DCA-exposed organism after 24 h. After prolonged exposure to DCA, exposed organism exhibited improved survival, elevated expression of hsp27, gclc, and gclm concomitant with lower ROS generation and GSH depletion and improved locomotor performance.	Dichloroacetic Acid	140-143	Heat shock protein 27	Drosophila melanogaster	214-219
24535708-6	2014	We observed mild OS and induction of antioxidant defense system in 20.0 mug/ml DCA-exposed organism after 24 h. After prolonged exposure to DCA, exposed organism exhibited improved survival, elevated expression of hsp27, gclc, and gclm concomitant with lower ROS generation and GSH depletion and improved locomotor performance.	Dichloroacetic Acid	140-143	Glutamate-cysteine ligase catalytic subunit	Drosophila melanogaster	221-225
24535708-6	2014	We observed mild OS and induction of antioxidant defense system in 20.0 mug/ml DCA-exposed organism after 24 h. After prolonged exposure to DCA, exposed organism exhibited improved survival, elevated expression of hsp27, gclc, and gclm concomitant with lower ROS generation and GSH depletion and improved locomotor performance.	Dichloroacetic Acid	140-143	Glutamate-cysteine ligase modifier subunit	Drosophila melanogaster	231-235
24535708-8	2014	The study provides evidence for the attenuation of cellular and functional decline in aged Drosophila after prolonged DCA exposure and the effect of hsp27 modulation which further incites studies towards the therapeutic application of DCA.	Dichloroacetic Acid	235-238	Heat shock protein 27	Drosophila melanogaster	149-154
24747400-5	2014	Pharmacologic PDK2 blockade with dichloroacetate or lentiviral PDK2 knockdown prevented DeltaPsim hyperpolarization, facilitated apoptosis and reduced myointima formation in injured human mammary and coronary arteries, rat aortas, rabbit iliac arteries and swine (pig) coronary arteries.	Dichloroacetic Acid	33-48	pyruvate dehydrogenase kinase 2	Homo sapiens	14-18
24297161-6	2014	Dosing was based on haplotype variation in glutathione transferase zeta 1/maleylacetoacetate isomerase (GSTZ1/MAAI), which participates in DCA and tyrosine catabolism.	Dichloroacetic Acid	139-142	glutathione S-transferase zeta 1	Homo sapiens	104-109
24297161-6	2014	Dosing was based on haplotype variation in glutathione transferase zeta 1/maleylacetoacetate isomerase (GSTZ1/MAAI), which participates in DCA and tyrosine catabolism.	Dichloroacetic Acid	139-142	glutathione S-transferase zeta 1	Homo sapiens	110-114
24527778-8	2014	In turn, the effects induced by the agonists were suppressed when HUVEC were also incubated with the PPARbeta antagonist GSK0660, the pyruvate dehydrogenase kinase (PDK)4 inhibitor dichloroacetate or after knockdown of both PPARbeta and PDK4 with siRNA.	Dichloroacetic Acid	181-196	peroxisome proliferator-activated receptor delta	Rattus norvegicus	101-109
24527778-8	2014	In turn, the effects induced by the agonists were suppressed when HUVEC were also incubated with the PPARbeta antagonist GSK0660, the pyruvate dehydrogenase kinase (PDK)4 inhibitor dichloroacetate or after knockdown of both PPARbeta and PDK4 with siRNA.	Dichloroacetic Acid	181-196	pyruvate dehydrogenase kinase 4	Rattus norvegicus	165-170
24527778-8	2014	In turn, the effects induced by the agonists were suppressed when HUVEC were also incubated with the PPARbeta antagonist GSK0660, the pyruvate dehydrogenase kinase (PDK)4 inhibitor dichloroacetate or after knockdown of both PPARbeta and PDK4 with siRNA.	Dichloroacetic Acid	181-196	peroxisome proliferator-activated receptor delta	Rattus norvegicus	224-232
24527778-8	2014	In turn, the effects induced by the agonists were suppressed when HUVEC were also incubated with the PPARbeta antagonist GSK0660, the pyruvate dehydrogenase kinase (PDK)4 inhibitor dichloroacetate or after knockdown of both PPARbeta and PDK4 with siRNA.	Dichloroacetic Acid	181-196	pyruvate dehydrogenase kinase 4	Rattus norvegicus	237-241
24632415-0	2014	Chloride and other anions inhibit dichloroacetate-induced inactivation of human liver GSTZ1 in a haplotype-dependent manner.	Dichloroacetic Acid	34-49	glutathione S-transferase zeta 1	Homo sapiens	86-91
24632415-1	2014	The in vivo elimination rate of dichloroacetate (DCA), an investigational drug; is determined by the rate of its biotransformation to glyoxylate, catalyzed by glutathione transferase zeta1 (GSTZ1).	Dichloroacetic Acid	32-47	glutathione S-transferase zeta 1	Homo sapiens	159-188
24632415-1	2014	The in vivo elimination rate of dichloroacetate (DCA), an investigational drug; is determined by the rate of its biotransformation to glyoxylate, catalyzed by glutathione transferase zeta1 (GSTZ1).	Dichloroacetic Acid	32-47	glutathione S-transferase zeta 1	Homo sapiens	190-195
24632415-1	2014	The in vivo elimination rate of dichloroacetate (DCA), an investigational drug; is determined by the rate of its biotransformation to glyoxylate, catalyzed by glutathione transferase zeta1 (GSTZ1).	Dichloroacetic Acid	49-52	glutathione S-transferase zeta 1	Homo sapiens	159-188
24632415-1	2014	The in vivo elimination rate of dichloroacetate (DCA), an investigational drug; is determined by the rate of its biotransformation to glyoxylate, catalyzed by glutathione transferase zeta1 (GSTZ1).	Dichloroacetic Acid	49-52	glutathione S-transferase zeta 1	Homo sapiens	190-195
24632415-2	2014	DCA is a mechanism-based inactivator of GSTZ1, thus elimination of DCA is slowed with repeated dosing.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	40-45
24632415-2	2014	DCA is a mechanism-based inactivator of GSTZ1, thus elimination of DCA is slowed with repeated dosing.	Dichloroacetic Acid	67-70	glutathione S-transferase zeta 1	Homo sapiens	40-45
24632415-3	2014	We observed that chloride, a physiologically important anion, attenuated DCA-induced GSTZ1 inactivation in human liver cytosol in a concentration and GSTZ1 haplotype-dependent way.	Dichloroacetic Acid	73-76	glutathione S-transferase zeta 1	Homo sapiens	85-90
24632415-3	2014	We observed that chloride, a physiologically important anion, attenuated DCA-induced GSTZ1 inactivation in human liver cytosol in a concentration and GSTZ1 haplotype-dependent way.	Dichloroacetic Acid	73-76	glutathione S-transferase zeta 1	Homo sapiens	150-155
24632415-4	2014	In the absence of chloride, incubation with 0.5mM DCA resulted in inactivation of GSTZ1 with a half-life of 0.4h (samples with the KRT haplotype) to 0.5h (EGT haplotype).	Dichloroacetic Acid	50-53	glutathione S-transferase zeta 1	Homo sapiens	82-87
24632415-4	2014	In the absence of chloride, incubation with 0.5mM DCA resulted in inactivation of GSTZ1 with a half-life of 0.4h (samples with the KRT haplotype) to 0.5h (EGT haplotype).	Dichloroacetic Acid	50-53	keratin 126, pseudogene	Homo sapiens	131-134
24632415-6	2014	The chloride concentration that protected 50% of the GSTZ1 activity following 2-h incubation with 0.5mM DCA (EC50) was 15.0+-3.1mM (mean+-S.D., n=3) for EGT samples and 36.2+-2.2mM for KRT samples.	Dichloroacetic Acid	104-107	glutathione S-transferase zeta 1	Homo sapiens	53-58
24632415-7	2014	Bromide, iodide and sulfite also protected GSTZ1 from inactivation by DCA, however fluoride, sulfate, carbonate, acetate, cyanide did not.	Dichloroacetic Acid	70-73	glutathione S-transferase zeta 1	Homo sapiens	43-48
24632415-10	2014	Because the in vivo half-life of DCA is determined by the fraction of active GSTZ1 in the liver, identifying factors that regulate GSTZ1 activity is important in determining appropriate DCA dosing in humans.	Dichloroacetic Acid	33-36	glutathione S-transferase zeta 1	Homo sapiens	77-82
24632415-10	2014	Because the in vivo half-life of DCA is determined by the fraction of active GSTZ1 in the liver, identifying factors that regulate GSTZ1 activity is important in determining appropriate DCA dosing in humans.	Dichloroacetic Acid	33-36	glutathione S-transferase zeta 1	Homo sapiens	131-136
24632415-10	2014	Because the in vivo half-life of DCA is determined by the fraction of active GSTZ1 in the liver, identifying factors that regulate GSTZ1 activity is important in determining appropriate DCA dosing in humans.	Dichloroacetic Acid	186-189	glutathione S-transferase zeta 1	Homo sapiens	131-136
24785472-3	2014	The SFG results indicate that both [BMIM](+) and [DCA](-) can be detected specifically on the graphene-coated BaF2 (111) surface, without coating only [DCA](-) are observed.	Dichloroacetic Acid	50-53	BANF family member 2	Homo sapiens	110-114
24785472-4	2014	[DCA](-) anions are attracted to the positively charged BaF2 (111) surface and occupy the first layer at the solid-liquid interface.	Dichloroacetic Acid	1-4	BANF family member 2	Homo sapiens	56-60
24639007-9	2014	This effect was probably related to the absence of the LDH-B subunit in LNCaP-LN3 cells, and could have a bearing on cancer treatment with DCA and related compounds.	Dichloroacetic Acid	139-142	lactate dehydrogenase B	Homo sapiens	55-60
22705712-4	2012	DCA treatment also altered expression of HIF1-alpha and pH regulators: VATPase and MCT1 and production of cytokines: IL-10, IL-6 and IFN-gamma.	Dichloroacetic Acid	0-3	hypoxia inducible factor 1, alpha subunit	Mus musculus	41-51
24342832-6	2014	Moreover, the addition of 20mM DCA only increased the sensitivity of these cells to 5-FU under hypoxic conditions, and the resistance to 5-FU under hypoxia was also attenuated in PDK1 knockdown cell lines.	Dichloroacetic Acid	31-34	pyruvate dehydrogenase kinase 1	Homo sapiens	179-183
25482950-3	2014	Dichloroacetate (DCA) is a pyruvate dehydrogenase kinase (PDK) inhibitor that can reverse the Warburg effect.	Dichloroacetic Acid	0-15	pyruvate dehydrogenase kinase 2	Homo sapiens	58-61
25482950-3	2014	Dichloroacetate (DCA) is a pyruvate dehydrogenase kinase (PDK) inhibitor that can reverse the Warburg effect.	Dichloroacetic Acid	17-20	pyruvate dehydrogenase kinase 2	Homo sapiens	58-61
23872533-7	2013	The relative STARD5 affinity for the different bile acids studied is: DCA&gt;LCA&gt;CDCA&gt;GDCA&gt;TDCA&gt;CA&gt;UDCA.	Dichloroacetic Acid	70-73	StAR related lipid transfer domain containing 5	Homo sapiens	13-19
23929671-6	2013	The severity of the yeast respiratory phenotypes partly correlated with the different clinical presentations observed in MTO1 mutant patients, although the clinical outcome was highly variable in patients with the same mutation and seemed also to depend on timely start of pharmacological treatment, centered on the control of lactic acidosis by dichloroacetate.	Dichloroacetic Acid	346-361	tRNA modification protein MTO1	Saccharomyces cerevisiae S288C	121-125
24199158-6	2013	However, life style intervention such as exercise, which is the most potent physiological activator of muscle PDC, along with pharmacological intervention such as administration of dichloroacetate or L-carnitine can prove to be viable strategies for treating muscle insulin resistance in obesity and T2D as they can potentially restore whole body glucose disposal.	Dichloroacetic Acid	181-196	insulin	Homo sapiens	266-273
23420584-6	2013	We show that dichloroacetate (DCA), an inhibitor of pyruvate dehydrogenase kinases, targets macrophages to suppress activation of the IL-23/IL-17 pathway and the expression of ARG1 by lactic acid.	Dichloroacetic Acid	13-28	interleukin 23, alpha subunit p19	Mus musculus	134-139
23420584-6	2013	We show that dichloroacetate (DCA), an inhibitor of pyruvate dehydrogenase kinases, targets macrophages to suppress activation of the IL-23/IL-17 pathway and the expression of ARG1 by lactic acid.	Dichloroacetic Acid	13-28	interleukin 17A	Mus musculus	140-145
23420584-6	2013	We show that dichloroacetate (DCA), an inhibitor of pyruvate dehydrogenase kinases, targets macrophages to suppress activation of the IL-23/IL-17 pathway and the expression of ARG1 by lactic acid.	Dichloroacetic Acid	13-28	arginase, liver	Mus musculus	176-180
23420584-6	2013	We show that dichloroacetate (DCA), an inhibitor of pyruvate dehydrogenase kinases, targets macrophages to suppress activation of the IL-23/IL-17 pathway and the expression of ARG1 by lactic acid.	Dichloroacetic Acid	30-33	interleukin 23, alpha subunit p19	Mus musculus	134-139
23420584-6	2013	We show that dichloroacetate (DCA), an inhibitor of pyruvate dehydrogenase kinases, targets macrophages to suppress activation of the IL-23/IL-17 pathway and the expression of ARG1 by lactic acid.	Dichloroacetic Acid	30-33	interleukin 17A	Mus musculus	140-145
23420584-6	2013	We show that dichloroacetate (DCA), an inhibitor of pyruvate dehydrogenase kinases, targets macrophages to suppress activation of the IL-23/IL-17 pathway and the expression of ARG1 by lactic acid.	Dichloroacetic Acid	30-33	arginase, liver	Mus musculus	176-180
23471124-10	2013	Similar to DCA, activation of PKM2 in many cancers results in increased mitochondrial function and decreased tumor growth.	Dichloroacetic Acid	11-14	pyruvate kinase M1/2	Homo sapiens	30-34
23247844-0	2013	FOXO1-mediated upregulation of pyruvate dehydrogenase kinase-4 (PDK4) decreases glucose oxidation and impairs right ventricular function in pulmonary hypertension: therapeutic benefits of dichloroacetate.	Dichloroacetic Acid	188-203	forkhead box O1	Homo sapiens	0-5
23247844-0	2013	FOXO1-mediated upregulation of pyruvate dehydrogenase kinase-4 (PDK4) decreases glucose oxidation and impairs right ventricular function in pulmonary hypertension: therapeutic benefits of dichloroacetate.	Dichloroacetic Acid	188-203	pyruvate dehydrogenase kinase 4	Homo sapiens	31-62
23247844-0	2013	FOXO1-mediated upregulation of pyruvate dehydrogenase kinase-4 (PDK4) decreases glucose oxidation and impairs right ventricular function in pulmonary hypertension: therapeutic benefits of dichloroacetate.	Dichloroacetic Acid	188-203	pyruvate dehydrogenase kinase 4	Homo sapiens	64-68
23247844-3	2013	We hypothesize that FOXO1-mediated PDK4 upregulation causes bioenergetic impairment and RV dysfunction, which can be reversed by dichloroacetate.	Dichloroacetic Acid	129-144	forkhead box O1	Homo sapiens	20-25
23247844-3	2013	We hypothesize that FOXO1-mediated PDK4 upregulation causes bioenergetic impairment and RV dysfunction, which can be reversed by dichloroacetate.	Dichloroacetic Acid	129-144	pyruvate dehydrogenase kinase 4	Homo sapiens	35-39
23247844-13	2013	Chronically dichloroacetate decreased PDK4 and FOXO1, thereby activating PDH and increasing GO in FHR.	Dichloroacetic Acid	12-27	pyruvate dehydrogenase kinase 4	Homo sapiens	38-42
23247844-13	2013	Chronically dichloroacetate decreased PDK4 and FOXO1, thereby activating PDH and increasing GO in FHR.	Dichloroacetic Acid	12-27	forkhead box O1	Homo sapiens	47-52
23247844-13	2013	Chronically dichloroacetate decreased PDK4 and FOXO1, thereby activating PDH and increasing GO in FHR.	Dichloroacetic Acid	12-27	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	73-76
23247844-15	2013	Chronic dichloroacetate inhibits FOXO1-induced PDK4 upregulation and restores GO, leading to improved bioenergetics and RV function in RVH.	Dichloroacetic Acid	8-23	forkhead box O1	Homo sapiens	33-38
23247844-15	2013	Chronic dichloroacetate inhibits FOXO1-induced PDK4 upregulation and restores GO, leading to improved bioenergetics and RV function in RVH.	Dichloroacetic Acid	8-23	pyruvate dehydrogenase kinase 4	Homo sapiens	47-51
23755715-7	2013	In conclusion, the DCA Vantage underestimates HbA1c levels; however it met the acceptance criteria of having a coefficient of variation &lt; 3%.	Dichloroacetic Acid	19-22	hemoglobin subunit alpha 1	Homo sapiens	46-50
23135628-7	2013	However,             DCA treatment reduced lactate production and increased responsiveness to 5-FU             in MKN45 cells, which expressed high levels of PDK-1 in comparison to the other             cell lines.	Dichloroacetic Acid	21-24	pyruvate dehydrogenase kinase 1	Homo sapiens	158-163
23135628-9	2013	In addition, PDK-1 inhibitors such as DCA may be considered             an additional treatment option for patients with PDK-1-expressing gastric cancers.	Dichloroacetic Acid	38-41	pyruvate dehydrogenase kinase 1	Homo sapiens	13-18
23135628-9	2013	In addition, PDK-1 inhibitors such as DCA may be considered             an additional treatment option for patients with PDK-1-expressing gastric cancers.	Dichloroacetic Acid	38-41	pyruvate dehydrogenase kinase 1	Homo sapiens	121-126
23515860-4	2013	DCA can inhibit the expression of heat shock proteins 70 (Hsp70) in a dose-dependent and time-dependent manner (P &lt; 0.01).	Dichloroacetic Acid	0-3	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	34-56
23515860-4	2013	DCA can inhibit the expression of heat shock proteins 70 (Hsp70) in a dose-dependent and time-dependent manner (P &lt; 0.01).	Dichloroacetic Acid	0-3	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	58-63
23662191-8	2013	Reactivation of PDH can be achieved directly by PDK inhibition (using dichloroacetate), or indirectly via activating the Randle cycle, using inhibitors of fatty acid oxidation (FAO), trimetazidine and ranolazine.	Dichloroacetic Acid	70-85	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	16-19
22865452-5	2012	Inhibiting PDK3 activity by dichloroacetate (DCA) or siRNA-mediated attenuation was sufficient to increase pyruvate dehydrogenase activity, oxidative phosphorylation, and mitochondrial reactive oxygen species generation.	Dichloroacetic Acid	28-43	pyruvate dehydrogenase kinase 3	Homo sapiens	11-15
22995818-2	2012	The dichloroacetate 14 is an excellent antitumor active agent acting by an apoptose inducing pathway as demonstrated by OA/PI staining, DNA laddering experiments as well as by an annexin V binding assay.	Dichloroacetic Acid	4-19	annexin A5	Homo sapiens	179-188
24338950-10	2014	RESULTS: HNK and its dichloroacetate analog (HDCA) were relatively more effective in suppressing cell viability and AR protein level than honokiol epoxide or biseugenol.	Dichloroacetic Acid	21-36	androgen receptor	Homo sapiens	116-118
24532971-9	2014	In addition, DCA significantly enhanced interferon (IFN)-gamma but not interleukin (IL)-17 production levels in unstimulated and stimulated mouse spleen cells.	Dichloroacetic Acid	13-16	interferon gamma	Mus musculus	40-62
24532971-10	2014	To investigate the mechanism of DCA on IFN-gamma production, DCA cytokine modulatory effect was tested on unstimulated macrophages, T-cells, and natural killer cells.	Dichloroacetic Acid	32-35	interferon gamma	Mus musculus	39-48
24532971-12	2014	Moreover, the DCA-enhancing effect on IFN-gamma production was reversed by anti-IL-12 antibody.	Dichloroacetic Acid	14-17	interferon gamma	Mus musculus	38-47
24532971-14	2014	DCA restored PMA-lowered IFN-gamma and IL-12 levels and normalized PMA-increased transforming growth factor-beta level, but it inhibited IL-10 levels even further (P&lt;0.05).	Dichloroacetic Acid	0-3	interferon gamma	Mus musculus	25-34
24532971-14	2014	DCA restored PMA-lowered IFN-gamma and IL-12 levels and normalized PMA-increased transforming growth factor-beta level, but it inhibited IL-10 levels even further (P&lt;0.05).	Dichloroacetic Acid	0-3	interleukin 10	Mus musculus	137-142
24481450-5	2014	The small molecule Dichloroacetate (DCA), a pyruvate dehydrogenase kinase inhibitor, increases the amount of PKM2/Oct4 complexes and thus inhibited Oct4-dependent gene expression.	Dichloroacetic Acid	19-34	pyruvate kinase M1/2	Rattus norvegicus	109-113
24481450-5	2014	The small molecule Dichloroacetate (DCA), a pyruvate dehydrogenase kinase inhibitor, increases the amount of PKM2/Oct4 complexes and thus inhibited Oct4-dependent gene expression.	Dichloroacetic Acid	36-39	pyruvate kinase M1/2	Rattus norvegicus	109-113
24038869-4	2013	The activity and expression of glutathione transferase zeta 1 (GSTZ1), which biotransforms DCA to glyoxylate, were determined from liver biopsies at baseline and after 27 days.	Dichloroacetic Acid	91-94	glutathione S-transferase zeta 1	Canis lupus familiaris	63-68
24201812-0	2013	Dichloroacetate induces protective autophagy in LoVo cells: involvement of cathepsin D/thioredoxin-like protein 1 and Akt-mTOR-mediated signaling.	Dichloroacetic Acid	0-15	cathepsin D	Homo sapiens	75-86
24201812-0	2013	Dichloroacetate induces protective autophagy in LoVo cells: involvement of cathepsin D/thioredoxin-like protein 1 and Akt-mTOR-mediated signaling.	Dichloroacetic Acid	0-15	thioredoxin like 1	Homo sapiens	87-113
24201812-0	2013	Dichloroacetate induces protective autophagy in LoVo cells: involvement of cathepsin D/thioredoxin-like protein 1 and Akt-mTOR-mediated signaling.	Dichloroacetic Acid	0-15	AKT serine/threonine kinase 1	Homo sapiens	118-121
24201812-0	2013	Dichloroacetate induces protective autophagy in LoVo cells: involvement of cathepsin D/thioredoxin-like protein 1 and Akt-mTOR-mediated signaling.	Dichloroacetic Acid	0-15	mechanistic target of rapamycin kinase	Homo sapiens	122-126
24201812-2	2013	In this study, we demonstrated that DCA could induce autophagy in LoVo cells, which were confirmed by the formation of autophagosomes, appearance of punctate patterns of LC3 immunoreactivity and activation of autophagy associated proteins.	Dichloroacetic Acid	36-39	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	170-173
24201812-3	2013	Moreover, autophagy inhibition by 3-methyladenine (3-MA) or Atg7 siRNA treatment can significantly enhance DCA-induced apoptosis.	Dichloroacetic Acid	107-110	autophagy related 7	Homo sapiens	60-64
24201812-8	2013	Finally, we demonstrated that the Akt-mTOR signaling pathway, a major negative regulator of autophagy, was suppressed by DCA treatment.	Dichloroacetic Acid	121-124	AKT serine/threonine kinase 1	Homo sapiens	34-37
24201812-8	2013	Finally, we demonstrated that the Akt-mTOR signaling pathway, a major negative regulator of autophagy, was suppressed by DCA treatment.	Dichloroacetic Acid	121-124	mechanistic target of rapamycin kinase	Homo sapiens	38-42
24201812-9	2013	To our knowledge, it was the first study to show that DCA induced protective autophagy in LoVo cells, and the potential mechanisms were involved in ROS imbalance and Akt-mTOR signaling pathway suppression.	Dichloroacetic Acid	54-57	AKT serine/threonine kinase 1	Homo sapiens	166-169
24201812-9	2013	To our knowledge, it was the first study to show that DCA induced protective autophagy in LoVo cells, and the potential mechanisms were involved in ROS imbalance and Akt-mTOR signaling pathway suppression.	Dichloroacetic Acid	54-57	mechanistic target of rapamycin kinase	Homo sapiens	170-174
22614004-4	2013	We hypothesized that DCA will also reverse the "pseudohypoxic" mitochondrial signals that lead to HIF1alpha activation in cancer, even in the absence of hypoxia and inhibit cancer angiogenesis.	Dichloroacetic Acid	21-24	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	98-107
22614004-6	2013	Using pharmacologic and molecular approaches that suppress the prolyl-hydroxylase (PHD)-mediated inhibition of HIF1alpha, we show that DCA inhibits HIF1alpha by both a PHD-dependent mechanism (that involves a DCA-induced increase in the production of mitochondria-derived alpha-ketoglutarate) and a PHD-independent mechanism, involving activation of p53 via mitochondrial-derived H(2)O(2), as well as activation of GSK3beta.	Dichloroacetic Acid	135-138	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	111-120
22614004-6	2013	Using pharmacologic and molecular approaches that suppress the prolyl-hydroxylase (PHD)-mediated inhibition of HIF1alpha, we show that DCA inhibits HIF1alpha by both a PHD-dependent mechanism (that involves a DCA-induced increase in the production of mitochondria-derived alpha-ketoglutarate) and a PHD-independent mechanism, involving activation of p53 via mitochondrial-derived H(2)O(2), as well as activation of GSK3beta.	Dichloroacetic Acid	135-138	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	148-157
22614004-6	2013	Using pharmacologic and molecular approaches that suppress the prolyl-hydroxylase (PHD)-mediated inhibition of HIF1alpha, we show that DCA inhibits HIF1alpha by both a PHD-dependent mechanism (that involves a DCA-induced increase in the production of mitochondria-derived alpha-ketoglutarate) and a PHD-independent mechanism, involving activation of p53 via mitochondrial-derived H(2)O(2), as well as activation of GSK3beta.	Dichloroacetic Acid	135-138	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	350-353
22614004-6	2013	Using pharmacologic and molecular approaches that suppress the prolyl-hydroxylase (PHD)-mediated inhibition of HIF1alpha, we show that DCA inhibits HIF1alpha by both a PHD-dependent mechanism (that involves a DCA-induced increase in the production of mitochondria-derived alpha-ketoglutarate) and a PHD-independent mechanism, involving activation of p53 via mitochondrial-derived H(2)O(2), as well as activation of GSK3beta.	Dichloroacetic Acid	135-138	glycogen synthase kinase 3 beta	Rattus norvegicus	415-423
22614004-6	2013	Using pharmacologic and molecular approaches that suppress the prolyl-hydroxylase (PHD)-mediated inhibition of HIF1alpha, we show that DCA inhibits HIF1alpha by both a PHD-dependent mechanism (that involves a DCA-induced increase in the production of mitochondria-derived alpha-ketoglutarate) and a PHD-independent mechanism, involving activation of p53 via mitochondrial-derived H(2)O(2), as well as activation of GSK3beta.	Dichloroacetic Acid	209-212	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	111-120
23257894-11	2013	DCA markedly sensitised sorafenib-resistant HCC cells to sorafenib-induced apoptosis (sub-G1 (combination vs sorafenib): Hep3B, 65.4+-8.4% vs 13+-2.9%; Huh-7 R, 25.3+- 5.7% vs 4.3+-1.5%; each P&lt;0.0001), whereas siRNA of HK2 did not.	Dichloroacetic Acid	0-3	hexokinase 2	Mus musculus	223-226
23612652-10	2013	Finally, DCA markedly increased the production of IL-10 and the expression of FOXP3.	Dichloroacetic Acid	9-12	interleukin 10	Homo sapiens	50-55
23612652-10	2013	Finally, DCA markedly increased the production of IL-10 and the expression of FOXP3.	Dichloroacetic Acid	9-12	forkhead box P3	Homo sapiens	78-83
23045346-6	2012	Simvastatin with DCA maintained body mass gain and food intake, abrogated the myopathy, decreased muscle PDK4 mRNA and protein, MAFbx and cathepsin-L mRNA, increased activity of PDC and reduced proteasome activity compared with simvastatin.	Dichloroacetic Acid	17-20	pyruvate dehydrogenase kinase 4	Rattus norvegicus	105-109
23045346-6	2012	Simvastatin with DCA maintained body mass gain and food intake, abrogated the myopathy, decreased muscle PDK4 mRNA and protein, MAFbx and cathepsin-L mRNA, increased activity of PDC and reduced proteasome activity compared with simvastatin.	Dichloroacetic Acid	17-20	F-box protein 32	Rattus norvegicus	128-133
23045346-6	2012	Simvastatin with DCA maintained body mass gain and food intake, abrogated the myopathy, decreased muscle PDK4 mRNA and protein, MAFbx and cathepsin-L mRNA, increased activity of PDC and reduced proteasome activity compared with simvastatin.	Dichloroacetic Acid	17-20	cathepsin L	Rattus norvegicus	138-149
22865452-5	2012	Inhibiting PDK3 activity by dichloroacetate (DCA) or siRNA-mediated attenuation was sufficient to increase pyruvate dehydrogenase activity, oxidative phosphorylation, and mitochondrial reactive oxygen species generation.	Dichloroacetic Acid	45-48	pyruvate dehydrogenase kinase 3	Homo sapiens	11-15
22782899-5	2012	However, DCA, associated with etoposide or irradiation, induced a Bax-dependent apoptosis in CSCs in vitro and decreased their proliferation in vivo.	Dichloroacetic Acid	9-12	BCL2 associated X, apoptosis regulator	Rattus norvegicus	66-69
22782899-6	2012	The former phenomenon is related to DCA-induced Foxo3 and p53 expression, resulting in the overexpression of BH3-only proteins (Bad, Noxa, and Puma), which in turn facilitates Bax-dependent apoptosis.	Dichloroacetic Acid	36-39	BCL2 associated X, apoptosis regulator	Rattus norvegicus	176-179
22705712-4	2012	DCA treatment also altered expression of HIF1-alpha and pH regulators: VATPase and MCT1 and production of cytokines: IL-10, IL-6 and IFN-gamma.	Dichloroacetic Acid	0-3	ATPase, H+ transporting, lysosomal V0 subunit D2	Mus musculus	71-78
22705712-4	2012	DCA treatment also altered expression of HIF1-alpha and pH regulators: VATPase and MCT1 and production of cytokines: IL-10, IL-6 and IFN-gamma.	Dichloroacetic Acid	0-3	modifier of curly tail 1	Mus musculus	83-87
22705712-4	2012	DCA treatment also altered expression of HIF1-alpha and pH regulators: VATPase and MCT1 and production of cytokines: IL-10, IL-6 and IFN-gamma.	Dichloroacetic Acid	0-3	interleukin 10	Mus musculus	117-122
22705712-4	2012	DCA treatment also altered expression of HIF1-alpha and pH regulators: VATPase and MCT1 and production of cytokines: IL-10, IL-6 and IFN-gamma.	Dichloroacetic Acid	0-3	interleukin 6	Mus musculus	124-128
22705712-4	2012	DCA treatment also altered expression of HIF1-alpha and pH regulators: VATPase and MCT1 and production of cytokines: IL-10, IL-6 and IFN-gamma.	Dichloroacetic Acid	0-3	interferon gamma	Mus musculus	133-142
21642471-5	2012	Atomic modeling revealed that GSTz1/MAAI variants associated with the slowest rates of DCA metabolism induced structural changes in the enzyme homodimer, predicting protein instability or abnormal protein-protein interactions.	Dichloroacetic Acid	87-90	glutathione S-transferase zeta 1	Homo sapiens	30-35
21642471-5	2012	Atomic modeling revealed that GSTz1/MAAI variants associated with the slowest rates of DCA metabolism induced structural changes in the enzyme homodimer, predicting protein instability or abnormal protein-protein interactions.	Dichloroacetic Acid	87-90	glutathione S-transferase zeta 1	Homo sapiens	36-40
21642471-6	2012	Knowledge of the GSTz1/MAAI haplotype can be used prospectively to identify individuals at potential risk of DCA"s adverse side effects from environmental or clinical exposure or who may exhibit aberrant amino acid metabolism in response to dietary protein.	Dichloroacetic Acid	109-112	glutathione S-transferase zeta 1	Homo sapiens	17-22
21642471-6	2012	Knowledge of the GSTz1/MAAI haplotype can be used prospectively to identify individuals at potential risk of DCA"s adverse side effects from environmental or clinical exposure or who may exhibit aberrant amino acid metabolism in response to dietary protein.	Dichloroacetic Acid	109-112	glutathione S-transferase zeta 1	Homo sapiens	23-27
22080752-10	2012	Dichloroacetate (DCA), an inhibitor of aerobic glycolysis, inhibited lactate production, proliferation of T cells, and production of IL-5, IL-17, and IFN-gamma, but it stimulated production of IL-10 and induction of Foxp3.	Dichloroacetic Acid	0-15	interleukin 5	Mus musculus	133-137
21642471-0	2012	Human polymorphisms in the glutathione transferase zeta 1/maleylacetoacetate isomerase gene influence the toxicokinetics of dichloroacetate.	Dichloroacetic Acid	124-139	glutathione S-transferase zeta 1	Homo sapiens	58-86
21642471-1	2012	Dichloroacetate (DCA), a chemical relevant to environmental science and allopathic medicine, is dehalogenated by the bifunctional enzyme glutathione transferase zeta (GSTz1)/maleylacetoacetate isomerase (MAAI), the penultimate enzyme in the phenylalanine/tyrosine catabolic pathway.	Dichloroacetic Acid	0-15	glutathione S-transferase zeta 1	Homo sapiens	167-172
21642471-1	2012	Dichloroacetate (DCA), a chemical relevant to environmental science and allopathic medicine, is dehalogenated by the bifunctional enzyme glutathione transferase zeta (GSTz1)/maleylacetoacetate isomerase (MAAI), the penultimate enzyme in the phenylalanine/tyrosine catabolic pathway.	Dichloroacetic Acid	0-15	glutathione S-transferase zeta 1	Homo sapiens	174-202
21642471-1	2012	Dichloroacetate (DCA), a chemical relevant to environmental science and allopathic medicine, is dehalogenated by the bifunctional enzyme glutathione transferase zeta (GSTz1)/maleylacetoacetate isomerase (MAAI), the penultimate enzyme in the phenylalanine/tyrosine catabolic pathway.	Dichloroacetic Acid	0-15	glutathione S-transferase zeta 1	Homo sapiens	204-208
21642471-1	2012	Dichloroacetate (DCA), a chemical relevant to environmental science and allopathic medicine, is dehalogenated by the bifunctional enzyme glutathione transferase zeta (GSTz1)/maleylacetoacetate isomerase (MAAI), the penultimate enzyme in the phenylalanine/tyrosine catabolic pathway.	Dichloroacetic Acid	17-20	glutathione S-transferase zeta 1	Homo sapiens	167-172
21642471-1	2012	Dichloroacetate (DCA), a chemical relevant to environmental science and allopathic medicine, is dehalogenated by the bifunctional enzyme glutathione transferase zeta (GSTz1)/maleylacetoacetate isomerase (MAAI), the penultimate enzyme in the phenylalanine/tyrosine catabolic pathway.	Dichloroacetic Acid	17-20	glutathione S-transferase zeta 1	Homo sapiens	174-202
21642471-1	2012	Dichloroacetate (DCA), a chemical relevant to environmental science and allopathic medicine, is dehalogenated by the bifunctional enzyme glutathione transferase zeta (GSTz1)/maleylacetoacetate isomerase (MAAI), the penultimate enzyme in the phenylalanine/tyrosine catabolic pathway.	Dichloroacetic Acid	17-20	glutathione S-transferase zeta 1	Homo sapiens	204-208
21642471-2	2012	The authors postulated that polymorphisms in GSTz1/MAAI modify the toxicokinetics of DCA.	Dichloroacetic Acid	85-88	glutathione S-transferase zeta 1	Homo sapiens	45-50
21642471-2	2012	The authors postulated that polymorphisms in GSTz1/MAAI modify the toxicokinetics of DCA.	Dichloroacetic Acid	85-88	glutathione S-transferase zeta 1	Homo sapiens	51-55
22080752-10	2012	Dichloroacetate (DCA), an inhibitor of aerobic glycolysis, inhibited lactate production, proliferation of T cells, and production of IL-5, IL-17, and IFN-gamma, but it stimulated production of IL-10 and induction of Foxp3.	Dichloroacetic Acid	0-15	interleukin 17A	Mus musculus	139-144
22080752-10	2012	Dichloroacetate (DCA), an inhibitor of aerobic glycolysis, inhibited lactate production, proliferation of T cells, and production of IL-5, IL-17, and IFN-gamma, but it stimulated production of IL-10 and induction of Foxp3.	Dichloroacetic Acid	0-15	interferon gamma	Mus musculus	150-159
22080752-10	2012	Dichloroacetate (DCA), an inhibitor of aerobic glycolysis, inhibited lactate production, proliferation of T cells, and production of IL-5, IL-17, and IFN-gamma, but it stimulated production of IL-10 and induction of Foxp3.	Dichloroacetic Acid	0-15	interleukin 10	Mus musculus	193-198
22080752-10	2012	Dichloroacetate (DCA), an inhibitor of aerobic glycolysis, inhibited lactate production, proliferation of T cells, and production of IL-5, IL-17, and IFN-gamma, but it stimulated production of IL-10 and induction of Foxp3.	Dichloroacetic Acid	0-15	forkhead box P3	Mus musculus	216-221
22080752-10	2012	Dichloroacetate (DCA), an inhibitor of aerobic glycolysis, inhibited lactate production, proliferation of T cells, and production of IL-5, IL-17, and IFN-gamma, but it stimulated production of IL-10 and induction of Foxp3.	Dichloroacetic Acid	17-20	interleukin 5	Mus musculus	133-137
22080752-10	2012	Dichloroacetate (DCA), an inhibitor of aerobic glycolysis, inhibited lactate production, proliferation of T cells, and production of IL-5, IL-17, and IFN-gamma, but it stimulated production of IL-10 and induction of Foxp3.	Dichloroacetic Acid	17-20	interleukin 17A	Mus musculus	139-144
22080752-10	2012	Dichloroacetate (DCA), an inhibitor of aerobic glycolysis, inhibited lactate production, proliferation of T cells, and production of IL-5, IL-17, and IFN-gamma, but it stimulated production of IL-10 and induction of Foxp3.	Dichloroacetic Acid	17-20	interferon gamma	Mus musculus	150-159
22080752-10	2012	Dichloroacetate (DCA), an inhibitor of aerobic glycolysis, inhibited lactate production, proliferation of T cells, and production of IL-5, IL-17, and IFN-gamma, but it stimulated production of IL-10 and induction of Foxp3.	Dichloroacetic Acid	17-20	interleukin 10	Mus musculus	193-198
22080752-10	2012	Dichloroacetate (DCA), an inhibitor of aerobic glycolysis, inhibited lactate production, proliferation of T cells, and production of IL-5, IL-17, and IFN-gamma, but it stimulated production of IL-10 and induction of Foxp3.	Dichloroacetic Acid	17-20	forkhead box P3	Mus musculus	216-221
22127296-2	2012	However, DCA can create a deficiency of glutathione transferase Zeta (GSTZ1-1).	Dichloroacetic Acid	9-12	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	70-77
26286408-4	2012	[BMIM](+) cations adhere closely via Coulombic interactions to the negatively charged NaCl{100} surface, while [DCA](-) anions subsequently have a strong electrostatic affinity to the positively charged BaF2(111) surface.	Dichloroacetic Acid	112-115	BANF family member 2	Homo sapiens	203-207
22028318-1	2012	Glutathione transferase zeta 1 (GSTZ1), also known as maleylacetoacetate isomerase, catalyzes the penultimate step of tyrosine catabolism and metabolizes several alpha-halocarboxylic acids, including dichloroacetic acid (DCA), an investigational drug used for lactic acidosis and, recently, solid tumors.	Dichloroacetic Acid	200-219	glutathione S-transferase zeta 1	Homo sapiens	0-30
22028318-1	2012	Glutathione transferase zeta 1 (GSTZ1), also known as maleylacetoacetate isomerase, catalyzes the penultimate step of tyrosine catabolism and metabolizes several alpha-halocarboxylic acids, including dichloroacetic acid (DCA), an investigational drug used for lactic acidosis and, recently, solid tumors.	Dichloroacetic Acid	200-219	glutathione S-transferase zeta 1	Homo sapiens	32-37
22028318-1	2012	Glutathione transferase zeta 1 (GSTZ1), also known as maleylacetoacetate isomerase, catalyzes the penultimate step of tyrosine catabolism and metabolizes several alpha-halocarboxylic acids, including dichloroacetic acid (DCA), an investigational drug used for lactic acidosis and, recently, solid tumors.	Dichloroacetic Acid	200-219	glutathione S-transferase zeta 1	Homo sapiens	54-82
22028318-1	2012	Glutathione transferase zeta 1 (GSTZ1), also known as maleylacetoacetate isomerase, catalyzes the penultimate step of tyrosine catabolism and metabolizes several alpha-halocarboxylic acids, including dichloroacetic acid (DCA), an investigational drug used for lactic acidosis and, recently, solid tumors.	Dichloroacetic Acid	221-224	glutathione S-transferase zeta 1	Homo sapiens	0-30
22028318-1	2012	Glutathione transferase zeta 1 (GSTZ1), also known as maleylacetoacetate isomerase, catalyzes the penultimate step of tyrosine catabolism and metabolizes several alpha-halocarboxylic acids, including dichloroacetic acid (DCA), an investigational drug used for lactic acidosis and, recently, solid tumors.	Dichloroacetic Acid	221-224	glutathione S-transferase zeta 1	Homo sapiens	32-37
22028318-1	2012	Glutathione transferase zeta 1 (GSTZ1), also known as maleylacetoacetate isomerase, catalyzes the penultimate step of tyrosine catabolism and metabolizes several alpha-halocarboxylic acids, including dichloroacetic acid (DCA), an investigational drug used for lactic acidosis and, recently, solid tumors.	Dichloroacetic Acid	221-224	glutathione S-transferase zeta 1	Homo sapiens	54-82
22028318-3	2012	Here, we investigated the cytosolic GSTZ1 developmental expression pattern and the influence of haplotype on GSTZ1 activity with DCA by using human livers from donors between 10 weeks gestation and 74 years.	Dichloroacetic Acid	129-132	glutathione S-transferase zeta 1	Homo sapiens	109-114
22028318-7	2012	GSTZ1 activity with DCA was strongly associated with haplotype and expression level.	Dichloroacetic Acid	20-23	glutathione S-transferase zeta 1	Homo sapiens	0-5
22028318-13	2012	Haplotype influenced GSTZ1 activity with DCA but not protein expression.	Dichloroacetic Acid	41-44	glutathione S-transferase zeta 1	Homo sapiens	21-26
22127296-7	2012	This protection is most likely due to an increased capacity for the liver to synthesize GSH, since DCA increased the expression and activity of glutamate-cysteine ligase GCL, the rate-limiting enzyme of GSH synthesis.	Dichloroacetic Acid	99-102	germ cell-less, spermatogenesis associated 1	Mus musculus	170-173
22318358-0	2012	Flow cytometric evaluation of the effects of 3-bromopyruvate (3BP) and dichloracetate (DCA) on THP-1 cells: a multiparameter analysis.	Dichloroacetic Acid	71-85	GLI family zinc finger 2	Homo sapiens	95-100
22509356-7	2012	Notably, DCA completely prevented the toxicity of SOD1(G93A) astrocytes to motor neurons in coculture conditions.	Dichloroacetic Acid	9-12	superoxide dismutase 1	Rattus norvegicus	50-54
22508045-2	2012	Dichloroacetate (DCA) is a drug which is able to shift pyruvate metabolism from lactate to acetyl-CoA (tricarboxylic acid cycle) by indirect activation of pyruvate dehydrogenase (PDH).	Dichloroacetic Acid	0-15	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	155-177
22508045-2	2012	Dichloroacetate (DCA) is a drug which is able to shift pyruvate metabolism from lactate to acetyl-CoA (tricarboxylic acid cycle) by indirect activation of pyruvate dehydrogenase (PDH).	Dichloroacetic Acid	0-15	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	179-182
22508045-2	2012	Dichloroacetate (DCA) is a drug which is able to shift pyruvate metabolism from lactate to acetyl-CoA (tricarboxylic acid cycle) by indirect activation of pyruvate dehydrogenase (PDH).	Dichloroacetic Acid	17-20	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	155-177
22508045-2	2012	Dichloroacetate (DCA) is a drug which is able to shift pyruvate metabolism from lactate to acetyl-CoA (tricarboxylic acid cycle) by indirect activation of pyruvate dehydrogenase (PDH).	Dichloroacetic Acid	17-20	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	179-182
22509356-8	2012	Chronic administration of DCA (500 mg/L) in the drinking water of mice expressing the SOD1(G93A) mutation increased survival by 2 weeks compared to untreated mice.	Dichloroacetic Acid	26-29	superoxide dismutase 1, soluble	Mus musculus	86-90
22509356-9	2012	Systemic DCA also normalized the reduced RCR value measured in lumbar spinal cord tissue of diseased SOD1(G93A) mice.	Dichloroacetic Acid	9-12	superoxide dismutase 1, soluble	Mus musculus	101-105
22509356-11	2012	Systemic DCA also decreased astrocyte reactivity and prevented motor neuron loss in SOD1(G93A) mice.	Dichloroacetic Acid	9-12	superoxide dismutase 1, soluble	Mus musculus	84-88
21701041-4	2011	Dichloroacetate (DCA) converts anaerobic to aerobic metabolism and thus was utilized to determine the effects on apoptosis, iNOS, MPO, extracellular SOD (SOD-3), and HIF-1a, in EOC cells.	Dichloroacetic Acid	0-15	superoxide dismutase 3	Homo sapiens	154-159
22217710-3	2011	RESULTS: SDA treatment of S37-bearing mice resulted in the reduced activities of total SOD, SOD isoforms (especially Mn-SOD), Cat, GP and significantly decreased GSH content on the background of LP intensification in tumor tissue.	Dichloroacetic Acid	9-12	superoxide dismutase 2, mitochondrial	Mus musculus	87-90
22217710-3	2011	RESULTS: SDA treatment of S37-bearing mice resulted in the reduced activities of total SOD, SOD isoforms (especially Mn-SOD), Cat, GP and significantly decreased GSH content on the background of LP intensification in tumor tissue.	Dichloroacetic Acid	9-12	superoxide dismutase 2, mitochondrial	Mus musculus	92-95
22217710-3	2011	RESULTS: SDA treatment of S37-bearing mice resulted in the reduced activities of total SOD, SOD isoforms (especially Mn-SOD), Cat, GP and significantly decreased GSH content on the background of LP intensification in tumor tissue.	Dichloroacetic Acid	9-12	superoxide dismutase 2, mitochondrial	Mus musculus	117-123
22217710-3	2011	RESULTS: SDA treatment of S37-bearing mice resulted in the reduced activities of total SOD, SOD isoforms (especially Mn-SOD), Cat, GP and significantly decreased GSH content on the background of LP intensification in tumor tissue.	Dichloroacetic Acid	9-12	catalase	Mus musculus	126-129
21701041-4	2011	Dichloroacetate (DCA) converts anaerobic to aerobic metabolism and thus was utilized to determine the effects on apoptosis, iNOS, MPO, extracellular SOD (SOD-3), and HIF-1a, in EOC cells.	Dichloroacetic Acid	0-15	hypoxia inducible factor 1 subunit alpha	Homo sapiens	166-172
21701041-7	2011	Dichloroacetate induced apoptosis, reduced MPO, iNOS, and HIF-1a, whereas increased SOD, in both EOC cell lines.	Dichloroacetic Acid	0-15	myeloperoxidase	Homo sapiens	43-46
21701041-7	2011	Dichloroacetate induced apoptosis, reduced MPO, iNOS, and HIF-1a, whereas increased SOD, in both EOC cell lines.	Dichloroacetic Acid	0-15	nitric oxide synthase 2	Homo sapiens	48-52
21701041-7	2011	Dichloroacetate induced apoptosis, reduced MPO, iNOS, and HIF-1a, whereas increased SOD, in both EOC cell lines.	Dichloroacetic Acid	0-15	hypoxia inducible factor 1 subunit alpha	Homo sapiens	58-64
21701041-7	2011	Dichloroacetate induced apoptosis, reduced MPO, iNOS, and HIF-1a, whereas increased SOD, in both EOC cell lines.	Dichloroacetic Acid	0-15	superoxide dismutase 3	Homo sapiens	84-87
21328317-2	2011	The DCA-Hb conjugate carries approximately 12 DCA molecules per Hb tetramer, and binds to haptoglobin (Hp) forming stable DCA-Hb-Hp complexes, in a similar manner to unmodified Hb.	Dichloroacetic Acid	4-7	haptoglobin	Homo sapiens	90-101
22093145-6	2011	The potentiation of ATO cytotoxicity by DCA is correlated with strong suppression of the expression of c-Myc and HIF-1alpha, and decreased expression of the survival protein Bcl-2.	Dichloroacetic Acid	40-43	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	103-108
22093145-6	2011	The potentiation of ATO cytotoxicity by DCA is correlated with strong suppression of the expression of c-Myc and HIF-1alpha, and decreased expression of the survival protein Bcl-2.	Dichloroacetic Acid	40-43	hypoxia inducible factor 1 subunit alpha	Homo sapiens	113-123
22093145-6	2011	The potentiation of ATO cytotoxicity by DCA is correlated with strong suppression of the expression of c-Myc and HIF-1alpha, and decreased expression of the survival protein Bcl-2.	Dichloroacetic Acid	40-43	BCL2 apoptosis regulator	Homo sapiens	174-179
21499304-0	2011	Role of SLC5A8, a plasma membrane transporter and a tumor suppressor, in the antitumor activity of dichloroacetate.	Dichloroacetic Acid	99-114	solute carrier family 5 member 8	Homo sapiens	8-14
21499304-7	2011	Here we show that SLC5A8 transports DCA very effectively with high affinity.	Dichloroacetic Acid	36-39	solute carrier family 5 member 8	Homo sapiens	18-24
21499304-14	2011	As silencing of SLC5A8 in tumors involves DNA methylation and its expression can be induced by treatment with DNA methylation inhibitors, our findings suggest that combining DCA with a DNA methylation inhibitor would offer a means to reduce the doses of DCA to avoid detrimental effects associated with high doses but without compromising antitumor activity.	Dichloroacetic Acid	174-177	solute carrier family 5 member 8	Homo sapiens	16-22
21499304-14	2011	As silencing of SLC5A8 in tumors involves DNA methylation and its expression can be induced by treatment with DNA methylation inhibitors, our findings suggest that combining DCA with a DNA methylation inhibitor would offer a means to reduce the doses of DCA to avoid detrimental effects associated with high doses but without compromising antitumor activity.	Dichloroacetic Acid	254-257	solute carrier family 5 member 8	Homo sapiens	16-22
21143697-4	2011	We show that upregulation of the two NF-kB target genes show differences in pH preference, with IL-8 being preferentially upregulated by DCA at neutral pH, and IkB being upregulated by neutral DCA, acidic DCA, and acid alone.	Dichloroacetic Acid	137-140	C-X-C motif chemokine ligand 8	Homo sapiens	96-100
21143697-4	2011	We show that upregulation of the two NF-kB target genes show differences in pH preference, with IL-8 being preferentially upregulated by DCA at neutral pH, and IkB being upregulated by neutral DCA, acidic DCA, and acid alone.	Dichloroacetic Acid	193-196	C-X-C motif chemokine ligand 8	Homo sapiens	96-100
21143697-4	2011	We show that upregulation of the two NF-kB target genes show differences in pH preference, with IL-8 being preferentially upregulated by DCA at neutral pH, and IkB being upregulated by neutral DCA, acidic DCA, and acid alone.	Dichloroacetic Acid	193-196	C-X-C motif chemokine ligand 8	Homo sapiens	96-100
21303221-8	2011	DCA was shown to be a k(cat) inactivator of human, rat, and mouse GSTZ1-1; human GSTZ1-1 was more resistant to inactivation than mouse or rat GSTZ1-1.	Dichloroacetic Acid	0-3	glutathione transferase zeta 1 (maleylacetoacetate isomerase)	Mus musculus	66-73
21303221-9	2011	Proteomic analysis showed that hGSTZ1-1 was inactivated when Cys-16 was modified by glutathione and the carbon skeleton of DCA.	Dichloroacetic Acid	123-126	glutathione S-transferase zeta 1	Homo sapiens	31-39
20920954-9	2011	DCA is a suicide inhibitor of GSTz1/MAAI, which can result in delayed plasma clearance of DCA and the accumulation of potentially toxic tyrosine intermediates.	Dichloroacetic Acid	90-93	glutathione S-transferase zeta 1	Homo sapiens	30-35
20920954-8	2011	DCA is primarily biotransformed to glyoxylate by the bifunctional enzyme glutathione transferase zeta1 and maleylacetoacetate isomerase (GSTz1/MAAI), which also catalyzes the penultimate step in the phenylalanine and tyrosine catabolic pathway.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	73-102
20920954-9	2011	DCA is a suicide inhibitor of GSTz1/MAAI, which can result in delayed plasma clearance of DCA and the accumulation of potentially toxic tyrosine intermediates.	Dichloroacetic Acid	90-93	glutathione S-transferase zeta 1	Homo sapiens	36-40
20920954-8	2011	DCA is primarily biotransformed to glyoxylate by the bifunctional enzyme glutathione transferase zeta1 and maleylacetoacetate isomerase (GSTz1/MAAI), which also catalyzes the penultimate step in the phenylalanine and tyrosine catabolic pathway.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	107-135
20920954-10	2011	Age and GSTz1/MAAI haplotype can markedly affect the toxicokinetics of DCA in humans and rodents.	Dichloroacetic Acid	71-74	glutathione S-transferase zeta 1	Homo sapiens	8-13
20920954-8	2011	DCA is primarily biotransformed to glyoxylate by the bifunctional enzyme glutathione transferase zeta1 and maleylacetoacetate isomerase (GSTz1/MAAI), which also catalyzes the penultimate step in the phenylalanine and tyrosine catabolic pathway.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	137-142
20920954-8	2011	DCA is primarily biotransformed to glyoxylate by the bifunctional enzyme glutathione transferase zeta1 and maleylacetoacetate isomerase (GSTz1/MAAI), which also catalyzes the penultimate step in the phenylalanine and tyrosine catabolic pathway.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	143-147
20920954-10	2011	Age and GSTz1/MAAI haplotype can markedly affect the toxicokinetics of DCA in humans and rodents.	Dichloroacetic Acid	71-74	glutathione S-transferase zeta 1	Homo sapiens	14-18
20920954-9	2011	DCA is a suicide inhibitor of GSTz1/MAAI, which can result in delayed plasma clearance of DCA and the accumulation of potentially toxic tyrosine intermediates.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	30-35
21283817-8	2011	Notably, treatment with dichloroacetate, a PDK2 inhibitor, also decreased the HIF1alpha expression as well as cell proliferation in chronic CSE treated OKF6 cells.	Dichloroacetic Acid	24-39	pyruvate dehydrogenase kinase 2	Homo sapiens	43-47
20920954-9	2011	DCA is a suicide inhibitor of GSTz1/MAAI, which can result in delayed plasma clearance of DCA and the accumulation of potentially toxic tyrosine intermediates.	Dichloroacetic Acid	0-3	glutathione S-transferase zeta 1	Homo sapiens	36-40
21170174-0	2011	Dichloroacetate- and Trichloroacetate-Induced Modulation of Superoxide Dismutase, Catalase, and Glutathione Peroxidase Activities and Glutathione Level in the livers of Mice after Subacute and Subchronic exposure.	Dichloroacetic Acid	0-15	catalase	Mus musculus	82-90
21283817-8	2011	Notably, treatment with dichloroacetate, a PDK2 inhibitor, also decreased the HIF1alpha expression as well as cell proliferation in chronic CSE treated OKF6 cells.	Dichloroacetic Acid	24-39	hypoxia inducible factor 1 subunit alpha	Homo sapiens	78-87
21919068-8	2011	The HbA1c EQA results collected and analyzed over a 9-year period showed that the DCA POCT devices used either by professional laboratories or medical offices had better reproducibility than laboratory devices (other than POCT) and that a general improvement of yearly precision performances was observed, especially when frequent EQA schemes were organized.	Dichloroacetic Acid	82-85	hemoglobin subunit alpha 1	Homo sapiens	4-8
21304220-2	2011	METHODS: The PDC activator, dichloroacetate (DCA), was administered as an intravenous infusion in healthy male subjects at a rate of 50 mg kg(-1) min(-1), for 90 min.	Dichloroacetic Acid	28-43	CD59 molecule (CD59 blood group)	Homo sapiens	146-152
21304220-8	2011	Carbohydrate oxidation was increased by DCA, 0.037 +- 0.017 g min(-1) (p &lt; 0.05) at 3 h with no change observed in CON.	Dichloroacetic Acid	40-43	CD59 molecule (CD59 blood group)	Homo sapiens	62-68
21304220-9	2011	UCP3 and PGC1alpha mRNA expression were induced in CON (as a response to continued fasting) but this was attenuated by DCA.	Dichloroacetic Acid	119-122	uncoupling protein 3	Homo sapiens	0-4
21304220-9	2011	UCP3 and PGC1alpha mRNA expression were induced in CON (as a response to continued fasting) but this was attenuated by DCA.	Dichloroacetic Acid	119-122	PPARG coactivator 1 alpha	Homo sapiens	9-18
21403907-9	2011	Moreover, compared with 5-FU alone, the apoptosis of CRC cells treated with DCA and 5-FU was enhanced and demonstrated with the changes of Bcl-2, Bax, and caspase-3 proteins.	Dichloroacetic Acid	76-79	BCL2 apoptosis regulator	Homo sapiens	139-144
21403907-9	2011	Moreover, compared with 5-FU alone, the apoptosis of CRC cells treated with DCA and 5-FU was enhanced and demonstrated with the changes of Bcl-2, Bax, and caspase-3 proteins.	Dichloroacetic Acid	76-79	BCL2 associated X, apoptosis regulator	Homo sapiens	146-149
21403907-9	2011	Moreover, compared with 5-FU alone, the apoptosis of CRC cells treated with DCA and 5-FU was enhanced and demonstrated with the changes of Bcl-2, Bax, and caspase-3 proteins.	Dichloroacetic Acid	76-79	caspase 3	Homo sapiens	155-164
20537792-3	2010	DCA treatment caused significant apoptosis under normoxia in SW480 and Caco-2 cells, but these cells displayed decreased apoptosis when treated with DCA combined with hypoxia, possibly through HIF-1alpha dependent pathways.	Dichloroacetic Acid	0-3	hypoxia inducible factor 1 subunit alpha	Homo sapiens	193-203
20884751-9	2011	Rats administered DCA at a dose of 500 mg/kg/day for 8 weeks showed reduced hepatic GSTZ1 activity and expression of ~10% of control levels in both cytosol and mitochondria.	Dichloroacetic Acid	18-21	glutathione S-transferase zeta 1	Rattus norvegicus	84-89
20884751-10	2011	We conclude that the mitochondrion is a novel site of DCA biotransformation catalyzed by GSTZ1, an enzyme colocalized in cytosol and mitochondrial matrix.	Dichloroacetic Acid	54-57	glutathione S-transferase zeta 1	Rattus norvegicus	89-94
20884751-0	2011	Mitochondrion as a novel site of dichloroacetate biotransformation by glutathione transferase zeta 1.	Dichloroacetic Acid	33-48	glutathione S-transferase zeta 1	Rattus norvegicus	70-100
20884751-2	2011	Repeated doses of DCA result in reduced drug clearance, probably through inhibition of glutathione transferase zeta1 (GSTZ1), a cytosolic enzyme that converts DCA to glyoxylate.	Dichloroacetic Acid	18-21	glutathione S-transferase zeta 1	Rattus norvegicus	87-116
20884751-2	2011	Repeated doses of DCA result in reduced drug clearance, probably through inhibition of glutathione transferase zeta1 (GSTZ1), a cytosolic enzyme that converts DCA to glyoxylate.	Dichloroacetic Acid	18-21	glutathione S-transferase zeta 1	Rattus norvegicus	118-123
20884751-2	2011	Repeated doses of DCA result in reduced drug clearance, probably through inhibition of glutathione transferase zeta1 (GSTZ1), a cytosolic enzyme that converts DCA to glyoxylate.	Dichloroacetic Acid	159-162	glutathione S-transferase zeta 1	Rattus norvegicus	87-116
20884751-2	2011	Repeated doses of DCA result in reduced drug clearance, probably through inhibition of glutathione transferase zeta1 (GSTZ1), a cytosolic enzyme that converts DCA to glyoxylate.	Dichloroacetic Acid	159-162	glutathione S-transferase zeta 1	Rattus norvegicus	118-123
20884751-7	2011	The specific activity of GSTZ1-catalyzed dechlorination of DCA was 2.5- to 3-fold higher in cytosol than in whole mitochondria and was directly proportional to GSTZ1 protein expression in the two compartments.	Dichloroacetic Acid	59-62	glutathione S-transferase zeta 1	Rattus norvegicus	25-30
20884751-7	2011	The specific activity of GSTZ1-catalyzed dechlorination of DCA was 2.5- to 3-fold higher in cytosol than in whole mitochondria and was directly proportional to GSTZ1 protein expression in the two compartments.	Dichloroacetic Acid	59-62	glutathione S-transferase zeta 1	Rattus norvegicus	160-165
20533281-8	2010	However, DCA was found to have selective activity against rho(0) cells [mitochondrial DNA (mtDNA) deficient] and to synergize with 2-deoxyglucose in complex IV deficient HCT116 p53(-/-) cells.	Dichloroacetic Acid	9-12	tumor protein p53	Homo sapiens	177-180
20537792-3	2010	DCA treatment caused significant apoptosis under normoxia in SW480 and Caco-2 cells, but these cells displayed decreased apoptosis when treated with DCA combined with hypoxia, possibly through HIF-1alpha dependent pathways.	Dichloroacetic Acid	149-152	hypoxia inducible factor 1 subunit alpha	Homo sapiens	193-203
21346867-1	2010	Dichloroacetate (DCA) is a synthetic compound that promotes the activity of pyruvate dehydrogenase (PDH) by inhibiting its repressor protein called pyruvate dehydrogenase kinase (PDHK).	Dichloroacetic Acid	0-15	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	76-98
21346867-1	2010	Dichloroacetate (DCA) is a synthetic compound that promotes the activity of pyruvate dehydrogenase (PDH) by inhibiting its repressor protein called pyruvate dehydrogenase kinase (PDHK).	Dichloroacetic Acid	0-15	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	100-103
21346867-1	2010	Dichloroacetate (DCA) is a synthetic compound that promotes the activity of pyruvate dehydrogenase (PDH) by inhibiting its repressor protein called pyruvate dehydrogenase kinase (PDHK).	Dichloroacetic Acid	0-15	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	148-170
21346867-1	2010	Dichloroacetate (DCA) is a synthetic compound that promotes the activity of pyruvate dehydrogenase (PDH) by inhibiting its repressor protein called pyruvate dehydrogenase kinase (PDHK).	Dichloroacetic Acid	17-20	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	76-98
21346867-1	2010	Dichloroacetate (DCA) is a synthetic compound that promotes the activity of pyruvate dehydrogenase (PDH) by inhibiting its repressor protein called pyruvate dehydrogenase kinase (PDHK).	Dichloroacetic Acid	17-20	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	100-103
21346867-1	2010	Dichloroacetate (DCA) is a synthetic compound that promotes the activity of pyruvate dehydrogenase (PDH) by inhibiting its repressor protein called pyruvate dehydrogenase kinase (PDHK).	Dichloroacetic Acid	17-20	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	148-170
21346867-2	2010	The activation of PDH leads to a reduction in ambient cellular lactate concentrations both in vitro and in vivo which contributes to the therapeutic use of DCA in the treatment of systemic lactic acidosis in humans.	Dichloroacetic Acid	156-159	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	18-21
20463368-7	2010	DCA therapy also inhibited the hypoxia-inducible factor-1alpha, promoted p53 activation, and suppressed angiogenesis both in vivo and in vitro.	Dichloroacetic Acid	0-3	hypoxia inducible factor 1 subunit alpha	Homo sapiens	31-62
20165905-0	2010	Dichloroacetate (DCA) enhances tumor cell death in combination with oncolytic adenovirus armed with MDA-7/IL-24.	Dichloroacetic Acid	0-15	interleukin 24	Homo sapiens	106-111
20165905-0	2010	Dichloroacetate (DCA) enhances tumor cell death in combination with oncolytic adenovirus armed with MDA-7/IL-24.	Dichloroacetic Acid	17-20	interleukin 24	Homo sapiens	106-111
20463368-7	2010	DCA therapy also inhibited the hypoxia-inducible factor-1alpha, promoted p53 activation, and suppressed angiogenesis both in vivo and in vitro.	Dichloroacetic Acid	0-3	tumor protein p53	Homo sapiens	73-76
20426967-0	2010	[Cytotoxicity of dichloroacetic acid in lymphocyte and expression of chemokine receptor CXCR2 and chemokine receptor CXCR3 mRNA].	Dichloroacetic Acid	17-36	C-X-C motif chemokine receptor 2	Homo sapiens	88-93
20391627-5	2010	DCA and TCA produced significant and dose-dependent increases in SA and TNF-alpha production and in MPO activity, but the increases in response to the high doses of the compounds (&gt;77 mg/kg/day) in the 13-week treatment period were less significant than those produced in the 4-week treatment period.	Dichloroacetic Acid	0-3	tumor necrosis factor	Mus musculus	72-81
20391627-5	2010	DCA and TCA produced significant and dose-dependent increases in SA and TNF-alpha production and in MPO activity, but the increases in response to the high doses of the compounds (&gt;77 mg/kg/day) in the 13-week treatment period were less significant than those produced in the 4-week treatment period.	Dichloroacetic Acid	0-3	myeloperoxidase	Mus musculus	100-103
20426967-0	2010	[Cytotoxicity of dichloroacetic acid in lymphocyte and expression of chemokine receptor CXCR2 and chemokine receptor CXCR3 mRNA].	Dichloroacetic Acid	17-36	C-X-C motif chemokine receptor 3	Homo sapiens	117-122
20426967-8	2010	At 48 h after the DCA of 0.5 mmol/L and 10.00 mmol/L was used, CXCR2 and CXCR3 mRNA were 10.34, 5.66-fold and 19.43, 8.75-fold of those in the control group (P &lt; 0.01).	Dichloroacetic Acid	18-21	C-X-C motif chemokine receptor 2	Homo sapiens	63-68
20426967-8	2010	At 48 h after the DCA of 0.5 mmol/L and 10.00 mmol/L was used, CXCR2 and CXCR3 mRNA were 10.34, 5.66-fold and 19.43, 8.75-fold of those in the control group (P &lt; 0.01).	Dichloroacetic Acid	18-21	C-X-C motif chemokine receptor 3	Homo sapiens	73-78
19787680-10	2009	Taking ITA haplotype as reference, multivariate regression analysis confirmed the negative (ITG), and positive (DCG, DTG, DCA and DTA) association of specific ACE haplotypes with DN, after adjusting for potential nephropathy-linked covariates.	Dichloroacetic Acid	122-125	angiotensin I converting enzyme	Homo sapiens	159-162
19920111-4	2009	We have used these cells in vitro to determine the effect of HIF1 on cellular sensitivity to the hypoxic cytotoxin PR-104, and its role in cellular oxygen consumption in response to the pyruvate dehydrogenase kinase inhibitor dichloroacetate (DCA).	Dichloroacetic Acid	243-246	hypoxia inducible factor 1 subunit alpha	Homo sapiens	61-65
19920111-5	2009	We have further used these cells in vivo in xenografted tumors to determine the role of HIF1 in regulating tumor hypoxia in response to DCA using (18)F-fluoroazomycin arabinoside positron emission tomography, and its role in regulating tumor sensitivity to the combination of DCA and PR-104.	Dichloroacetic Acid	136-139	hypoxia inducible factor 1 subunit alpha	Homo sapiens	88-92
19592162-5	2009	Decreasing the pH lower than the pH(zpc) increased the DCAA adsorption capacities of these adsorbents due to electrostatic interaction and hydrogen bonding caused by protonation of the hydronium ion.	Dichloroacetic Acid	55-59	zona pellucida glycoprotein 3	Homo sapiens	36-39
19833728-3	2009	In the present study, we investigated the role of the invariant C-terminal DW-motif in inhibition of human PDK2 by dichloroacetate (DCA).	Dichloroacetic Acid	115-130	pyruvate dehydrogenase kinase 2	Homo sapiens	107-111
19833728-3	2009	In the present study, we investigated the role of the invariant C-terminal DW-motif in inhibition of human PDK2 by dichloroacetate (DCA).	Dichloroacetic Acid	132-135	pyruvate dehydrogenase kinase 2	Homo sapiens	107-111
19833728-11	2009	This signaling network locks PDK2 in the inactive closed conformation, which is in equilibrium with the active open conformation without DCA and ADP.	Dichloroacetic Acid	137-140	pyruvate dehydrogenase kinase 2	Homo sapiens	29-33
19679640-0	2009	Dichloroacetate treatment partially regresses established pulmonary hypertension in mice with SM22alpha-targeted overexpression of the serotonin transporter.	Dichloroacetic Acid	0-15	transgelin	Mus musculus	94-103
19679640-3	2009	Dichloroacetate (DCA) inhibits chronic hypoxia- or monocrotaline-induced PAH by inhibiting nuclear factor of activated T-cells (NFAT)c2 and increasing Kv1.5.	Dichloroacetic Acid	0-15	potassium voltage-gated channel, shaker-related subfamily, member 5	Mus musculus	151-156
19679640-3	2009	Dichloroacetate (DCA) inhibits chronic hypoxia- or monocrotaline-induced PAH by inhibiting nuclear factor of activated T-cells (NFAT)c2 and increasing Kv1.5.	Dichloroacetic Acid	17-20	potassium voltage-gated channel, shaker-related subfamily, member 5	Mus musculus	151-156
19694452-2	2009	As a reference reaction, we monitored the well-characterized regulation of pyruvate dehydrogenase (PDH) activity via phosphorylation/dephosphorylation by pyruvate dehydrogenase kinase/pyruvate dehydrogenase phosphatase in response to dichloroacetate, de-energization and Ca2+.	Dichloroacetic Acid	234-249	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	75-97
19694452-2	2009	As a reference reaction, we monitored the well-characterized regulation of pyruvate dehydrogenase (PDH) activity via phosphorylation/dephosphorylation by pyruvate dehydrogenase kinase/pyruvate dehydrogenase phosphatase in response to dichloroacetate, de-energization and Ca2+.	Dichloroacetic Acid	234-249	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	99-102
19694452-2	2009	As a reference reaction, we monitored the well-characterized regulation of pyruvate dehydrogenase (PDH) activity via phosphorylation/dephosphorylation by pyruvate dehydrogenase kinase/pyruvate dehydrogenase phosphatase in response to dichloroacetate, de-energization and Ca2+.	Dichloroacetic Acid	234-249	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	154-176
19694452-2	2009	As a reference reaction, we monitored the well-characterized regulation of pyruvate dehydrogenase (PDH) activity via phosphorylation/dephosphorylation by pyruvate dehydrogenase kinase/pyruvate dehydrogenase phosphatase in response to dichloroacetate, de-energization and Ca2+.	Dichloroacetic Acid	234-249	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	154-176
19694452-4	2009	Dephosphorylation at Ser292 (i.e., the inhibitory site) with DCA correlated with an activation of PDH activity as previously reported, consistent with our de-energization data.	Dichloroacetic Acid	61-64	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	98-101
19694452-7	2009	Among them, four proteins exhibited phosphorylation changes with these physiological stimuli: (1) BCKDH-E1alpha subunit increased phosphorylation at Ser337 with DCA and de-energization; (2) apoptosis-inducing factor phosphorylation was elevated at Ser345 with calcium; (3) ATP synthase F1 complex alpha subunit and (4) mitofilin dephosphorylated at Ser65 and Ser264 upon de-energization.	Dichloroacetic Acid	161-164	branched chain keto acid dehydrogenase E1 subunit alpha	Homo sapiens	98-111
19395583-12	2009	Plasma interleukin (IL)-6 levels significantly increased 2 h after exercise only in the DCA condition (p &lt; 0.01).	Dichloroacetic Acid	88-91	interleukin 6	Homo sapiens	7-25