PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
3207683-4	1988	The rate of conversion of methylglyoxal to (S)-D-lactoylglutathione is near optimal, on the basis that the apparent rate constant for the glyoxalase I reaction (kcatEt/Km congruent to 4-20 s-1 for pig, rat, and human erythrocytes) is roughly equal to the apparent rate constant for decomposition of the thiohemiacetals to form glutathione and methylglyoxal [k(obsd) = 11 s-1, pH 7].	Pyruvaldehyde	26-39	lactoylglutathione lyase	Sus scrofa	138-150
3796671-1	1987	Methylglyoxal, at concentrations ranging from 0.16 to 1.5 mM, caused a dose-dependent increase in the frequency of HGPRT-deficient mutants in V79 cells.	Pyruvaldehyde	0-13	hypoxanthine-guanine phosphoribosyltransferase	Cricetulus griseus	115-120
2900825-0	1988	Induction and promotion of gamma-glutamyltranspeptidase-positive foci in the rat liver by methylglyoxal.	Pyruvaldehyde	90-103	gamma-glutamyltransferase 1	Rattus norvegicus	27-55
2900825-1	1988	The effect of pre-(initiation) and post-(promotion) administration of methylglyoxal (MG) on the induction of gamma-glutamyltranspeptidase (GGT)-positive foci in the liver of F344 male rats was investigated.	Pyruvaldehyde	70-83	gamma-glutamyltransferase 1	Rattus norvegicus	109-137
2900825-1	1988	The effect of pre-(initiation) and post-(promotion) administration of methylglyoxal (MG) on the induction of gamma-glutamyltranspeptidase (GGT)-positive foci in the liver of F344 male rats was investigated.	Pyruvaldehyde	70-83	gamma-glutamyltransferase 1	Rattus norvegicus	139-142
2900825-2	1988	GGT-positive foci were produced in dose-related amounts by 0.05 and 0.2% MG in drinking water, either when administered to uninitiated rats or when given in the promotion phase.	Pyruvaldehyde	73-75	gamma-glutamyltransferase 1	Rattus norvegicus	0-3
3325758-8	1987	Cytochrome P-450 content (cyt P-450) and ethoxycoumarin O-deethylase activity (ECD) were also weakly enhanced by MG treatment.	Pyruvaldehyde	113-115	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	0-16
3769094-2	1986	Changes of methylglyoxal level accompanying the changes of glyoxalase I and II activities in mice bearing L1210 leukemia and sarcoma 180.	Pyruvaldehyde	11-24	glyoxalase 1	Mus musculus	59-71
3967340-1	1985	Administration of methylglyoxal at doses of 300-600 mg/kg body weight by gastric tube to male F344 rats induced 100-fold increase in ornithine decarboxylase activity (formation of 682 pmol CO2/30 min/mg protein) within 7 h, 26-fold increase in DNA synthesis (incorporation of 17 800 d.p.m.	Pyruvaldehyde	18-31	ornithine decarboxylase 1	Rattus norvegicus	133-156
3086526-1	1986	Lysozyme was reacted with xylose, methyl linoleate, glyoxal, methylglyoxal and diacetyl in an aqueous system (50 degrees C, pH 6.0), and browning, polymerization, changes of amino acids composition and relative digestibility of the browned lysozyme were investigated.	Pyruvaldehyde	61-74	lysozyme	Homo sapiens	0-8
7350914-7	1980	Mouse liver glyoxalase II is competitively inhibited by the substrate of glyoxalase I (the hemimercaptal of methylglyoxal and glutathione); the Ki is 0.3 mM.	Pyruvaldehyde	108-121	hydroxyacyl glutathione hydrolase	Mus musculus	12-25
6463589-3	1984	Km values for methylglyoxal (glyoxalase I) and S-lactoylglutathione (glyoxalase II) are identical both in normal and pathological subjects, as are the thermostability of the two enzymes.	Pyruvaldehyde	14-27	glyoxalase I	Homo sapiens	29-41
6360161-1	1983	Glyoxalase I (S-lactoyl-glutathione methylglyoxal-lyase (isomerizing), EC 4.4.1.5) was assayed using alcoholic, acidic 2,4-dinitrophenylhydrazine to follow the disappearance of methylglyoxal over time, with the absorbance of formed methylglyoxal bis-hydrazone measured at 432 nm.	Pyruvaldehyde	36-49	glyoxalase I	Homo sapiens	0-12
6305345-1	1983	When the myeloperoxidase-catalyzed peroxidation of acetoacetate proceeds in the presence of piperidinooxy free radical, methyl glyoxal is formed, and the nitroxide group is reduced to the secondary amine.	Pyruvaldehyde	120-134	myeloperoxidase	Homo sapiens	9-24
6305345-4	1983	It is shown that lactoperoxidase, prostaglandin synthetase, and prostacyclin synthetase generate methyl glyoxal with requirements identical to those of myeloperoxidase.	Pyruvaldehyde	97-111	lactoperoxidase	Homo sapiens	17-87
6305345-4	1983	It is shown that lactoperoxidase, prostaglandin synthetase, and prostacyclin synthetase generate methyl glyoxal with requirements identical to those of myeloperoxidase.	Pyruvaldehyde	97-111	myeloperoxidase	Homo sapiens	152-167
6863314-2	1983	Glyoxalase I catalyzes the formation of S-D-lactoyl-glutathione via the hemimercaptal adduct of methylglyoxal and glutathione.	Pyruvaldehyde	96-109	glyoxalase I	Homo sapiens	0-12
7013790-3	1981	175, 361], fructose-1,6-bisphosphate aldolase of rabbit muscle causes the slow formation of inorganic phosphate (Pi) and methylglyoxal when incubated with dihydroxyacetone phosphate (DHAP).	Pyruvaldehyde	121-134	fructose-bisphosphate aldolase B	Oryctolagus cuniculus	11-45
7013791-1	1981	When a mixture of triosephosphate isomerase (rabbit muscle) and dihydroxyacetone phosphate (DHAP) is quenched with acid, a compound is liberated, presumed to be the cis-enediol 3-phosphate, that decomposes to inorganic phosphate (Pi) and methylglyoxal [Iyengar, R., & Rose, I.A.	Pyruvaldehyde	238-251	triosephosphate isomerase	Oryctolagus cuniculus	18-43
7350914-7	1980	Mouse liver glyoxalase II is competitively inhibited by the substrate of glyoxalase I (the hemimercaptal of methylglyoxal and glutathione); the Ki is 0.3 mM.	Pyruvaldehyde	108-121	glyoxalase 1	Mus musculus	12-24
33901606-0	2021	Methylglyoxal influences development of Caenorhabditis elegans via lin-41-dependent pathway.	Pyruvaldehyde	0-13	Protein lin-41	Caenorhabditis elegans	67-73
35531-1	1979	Pig kidney aldehyde reductase is inactivated by 2,3-butanedione, phenylglyoxal, methylglyoxal, and 1,2-cyclohexanedione.	Pyruvaldehyde	80-93	aldo-keto reductase family 1 member B	Sus scrofa	11-29
234222-0	1975	Evidence for the generation of excited methylglyoxal in the myoglobin catalyzed oxidation of acetoacetate.	Pyruvaldehyde	39-52	myoglobin	Homo sapiens	60-69
33933705-0	2021	High-Performance affinity chromatographic studies of repaglinide and nateglinide interactions with normal and glyoxal- or methylglyoxal-modified human albumin serum.	Pyruvaldehyde	122-135	albumin	Homo sapiens	151-158
33933705-1	2021	During diabetes human serum albumin (HSA), an important drug transport protein, can be modified by agents such as glyoxal (Go) and methylglyoxal (MGo) to form advanced glycation end-products.	Pyruvaldehyde	131-144	albumin	Homo sapiens	28-35
33933705-1	2021	During diabetes human serum albumin (HSA), an important drug transport protein, can be modified by agents such as glyoxal (Go) and methylglyoxal (MGo) to form advanced glycation end-products.	Pyruvaldehyde	146-149	albumin	Homo sapiens	28-35
33644826-1	2021	The reactive dicarbonyl metabolite, methylglyoxal (MG), is increased in obesity and diabetes and is implicated in the development of insulin resistance, type 2 diabetes mellitus and vascular complications of diabetes.	Pyruvaldehyde	36-49	insulin	Homo sapiens	133-140
33644826-1	2021	The reactive dicarbonyl metabolite, methylglyoxal (MG), is increased in obesity and diabetes and is implicated in the development of insulin resistance, type 2 diabetes mellitus and vascular complications of diabetes.	Pyruvaldehyde	51-53	insulin	Homo sapiens	133-140
38777-19	1979	The experiments with dihydroxy-acetone phosphate and triose phosphate isomerase have to be carried out at 1 degree C because at 37 degrees C there is conversion into methyl glyoxal and orthophosphate.	Pyruvaldehyde	166-180	triosephosphate isomerase	Oryctolagus cuniculus	53-79
690442-1	1978	Glyoxalase I converts methylglyoxal and glutathione to S-lactoylglutathione and glyoxalase II converts this compound to D-lactic acid, regenerating glutathione in the process.	Pyruvaldehyde	22-35	glyoxalase I	Homo sapiens	0-12
159813-9	1978	The glyoxalase I inhibitor S-(p-bromobenzyl)-glutathione didnot significantly enhance the activity of methylglyoxal against the solid form of the tumour.	Pyruvaldehyde	102-115	glyoxalase 1	Mus musculus	4-16
33644826-8	2021	An effective strategy to counter increased MG is inducing increased expression of glyoxalase-1 (Glo1).	Pyruvaldehyde	43-45	glyoxalase I	Homo sapiens	82-94
33644826-8	2021	An effective strategy to counter increased MG is inducing increased expression of glyoxalase-1 (Glo1).	Pyruvaldehyde	43-45	glyoxalase I	Homo sapiens	96-100
33644826-9	2021	An optimized inducer of Glo1 expression, trans-resveratrol and hesperetin combination, normalized increased MG concentration, corrected insulin resistance and decreased low grade inflammation in overweight and obese subjects.	Pyruvaldehyde	108-110	glyoxalase I	Homo sapiens	24-28
33901606-8	2021	The effect of methylglyoxal on development was in part due to the modulation of lin-41, which encodes a homolog of human TRIM71.	Pyruvaldehyde	14-27	tripartite motif containing 71	Homo sapiens	80-86
33901606-8	2021	The effect of methylglyoxal on development was in part due to the modulation of lin-41, which encodes a homolog of human TRIM71.	Pyruvaldehyde	14-27	tripartite motif containing 71	Homo sapiens	121-127
33901606-9	2021	The mutation of lin-41 could alleviate or abolish the effects of methylglyoxal on growth rate, body size, pumping rate and locomotive activity.	Pyruvaldehyde	65-78	tripartite motif containing 71	Homo sapiens	16-22
33901606-10	2021	In summary, these results suggested that methylglyoxal influenced the development of Caenorhabditis elegans, which is in part via the lin-41-dependent pathway.	Pyruvaldehyde	41-54	Protein lin-41	Caenorhabditis elegans	134-140
33891395-4	2021	During MG-ARP degradation, the formation of glyoxal (GO) and methylglyoxal (MGO) was facilitated by additional Met, through retro-aldolization reaction of C6-alpha-dicarbonyl compounds.	Pyruvaldehyde	61-74	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	10-13
33966256-5	2021	Here, we show that acute MG treatment activated components of the p38 MAPK pathway and enhanced glycolysis in primary murine macrophages.	Pyruvaldehyde	25-27	mitogen-activated protein kinase 14	Mus musculus	66-74
33966051-3	2021	The viability of GLO1 knockout (KO)-hiPSCs decreased and activity of caspase-3 was increased upon addition of methylglyoxal (MGO), a reactive carbonyl compound.	Pyruvaldehyde	110-123	glyoxalase I	Homo sapiens	17-21
33966051-3	2021	The viability of GLO1 knockout (KO)-hiPSCs decreased and activity of caspase-3 was increased upon addition of methylglyoxal (MGO), a reactive carbonyl compound.	Pyruvaldehyde	110-123	caspase 3	Homo sapiens	69-78
33966051-3	2021	The viability of GLO1 knockout (KO)-hiPSCs decreased and activity of caspase-3 was increased upon addition of methylglyoxal (MGO), a reactive carbonyl compound.	Pyruvaldehyde	125-128	glyoxalase I	Homo sapiens	17-21
33966051-3	2021	The viability of GLO1 knockout (KO)-hiPSCs decreased and activity of caspase-3 was increased upon addition of methylglyoxal (MGO), a reactive carbonyl compound.	Pyruvaldehyde	125-128	caspase 3	Homo sapiens	69-78
33966051-4	2021	In the GLO1 KO-hiPSC-derived neurons, MGO administration impaired neurite extension and cell migration.	Pyruvaldehyde	38-41	glyoxalase I	Homo sapiens	7-11
33966051-6	2021	Mitochondrial dysfunction, including diminished membrane potential and dampened respiratory function, was observed in the GLO1 KO-hiPSCs and derived neurons after addition of MGO and hence might be the mechanism underlying the effects of carbonyl stress.	Pyruvaldehyde	175-178	glyoxalase I	Homo sapiens	122-126
33891395-4	2021	During MG-ARP degradation, the formation of glyoxal (GO) and methylglyoxal (MGO) was facilitated by additional Met, through retro-aldolization reaction of C6-alpha-dicarbonyl compounds.	Pyruvaldehyde	76-79	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	10-13
33896363-13	2021	MGO could stimulate the main three ER stress pathways, PERK phosphorylation, IRE1alpha, and ATF6 expressions in a time- and concentration-dependent manner.	Pyruvaldehyde	0-3	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	55-59
33909175-0	2021	Hepatocyte growth factor ameliorates methylglyoxal-induced peritoneal inflammation and fibrosis in mouse model.	Pyruvaldehyde	37-50	hepatocyte growth factor	Mus musculus	0-24
33896363-13	2021	MGO could stimulate the main three ER stress pathways, PERK phosphorylation, IRE1alpha, and ATF6 expressions in a time- and concentration-dependent manner.	Pyruvaldehyde	0-3	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	77-86
33896363-13	2021	MGO could stimulate the main three ER stress pathways, PERK phosphorylation, IRE1alpha, and ATF6 expressions in a time- and concentration-dependent manner.	Pyruvaldehyde	0-3	activating transcription factor 6	Homo sapiens	92-96
33392911-0	2021	The Isothiocyanate Sulforaphane Depends on the Nrf2/gamma-GCL/GSH Axis to Prevent Mitochondrial Dysfunction in Cells Exposed to Methylglyoxal.	Pyruvaldehyde	128-141	NFE2 like bZIP transcription factor 2	Homo sapiens	47-51
33917901-3	2021	In this study, glyoxalase 1(Glo1)-knockout and vitamin B6-deficient mice (KO/VB6 (-) mice), which are susceptible to methylglyoxal (MGO)-induced oxidative damages, were used as a CS-SCZ model to analyze MGO-modified protein and the carbonyl stress status in the brain.	Pyruvaldehyde	132-135	glyoxalase 1	Mus musculus	15-27
33850227-0	2021	Methylglyoxal induces p53 activation and inhibits mTORC1 in human umbilical vein endothelial cells.	Pyruvaldehyde	0-13	tumor protein p53	Homo sapiens	22-25
33850227-0	2021	Methylglyoxal induces p53 activation and inhibits mTORC1 in human umbilical vein endothelial cells.	Pyruvaldehyde	0-13	CREB regulated transcription coactivator 1	Mus musculus	50-56
33850227-2	2021	We have previously reported that MGO induces transcriptional changes compatible with p53 activation in cultured human endothelial cells.	Pyruvaldehyde	33-36	tumor protein p53	Homo sapiens	85-88
33850227-3	2021	To further substantiate this finding and to explore the underlying mechanisms and possible consequences of p53 activation, we aimed (1) to provide direct evidence for p53 activation in MGO-treated human umbilical vein endothelial cells (HUVECs), (2) to assess putative mechanisms by which this occurs, (3) to analyze down-stream effects on mTOR and autophagy pathways, and (4) to assess the potential benefit of carnosine herein.	Pyruvaldehyde	185-188	tumor protein p53	Homo sapiens	107-110
33850227-3	2021	To further substantiate this finding and to explore the underlying mechanisms and possible consequences of p53 activation, we aimed (1) to provide direct evidence for p53 activation in MGO-treated human umbilical vein endothelial cells (HUVECs), (2) to assess putative mechanisms by which this occurs, (3) to analyze down-stream effects on mTOR and autophagy pathways, and (4) to assess the potential benefit of carnosine herein.	Pyruvaldehyde	185-188	tumor protein p53	Homo sapiens	167-170
33850227-3	2021	To further substantiate this finding and to explore the underlying mechanisms and possible consequences of p53 activation, we aimed (1) to provide direct evidence for p53 activation in MGO-treated human umbilical vein endothelial cells (HUVECs), (2) to assess putative mechanisms by which this occurs, (3) to analyze down-stream effects on mTOR and autophagy pathways, and (4) to assess the potential benefit of carnosine herein.	Pyruvaldehyde	185-188	mechanistic target of rapamycin kinase	Homo sapiens	340-344
33850227-4	2021	Exposure of HUVECs to 800 microM of MGO for 5 h induced p53 phosphorylation.	Pyruvaldehyde	36-39	tumor protein p53	Homo sapiens	56-59
33850227-6	2021	Compatible with p53 activation, MGO treatment resulted in cell cycle arrest, inhibition of mTORC1 and induction of autophagy.	Pyruvaldehyde	32-35	tumor protein p53	Homo sapiens	16-19
33850227-6	2021	Compatible with p53 activation, MGO treatment resulted in cell cycle arrest, inhibition of mTORC1 and induction of autophagy.	Pyruvaldehyde	32-35	CREB regulated transcription coactivator 1	Mus musculus	91-97
33850227-8	2021	In conclusion, our results demonstrate that MGO elicits DNA damage and p53 activation in HUVECs, resulting in modulation of downstream pathways, e.g. mTORC1.	Pyruvaldehyde	44-47	tumor protein p53	Homo sapiens	71-74
33850227-8	2021	In conclusion, our results demonstrate that MGO elicits DNA damage and p53 activation in HUVECs, resulting in modulation of downstream pathways, e.g. mTORC1.	Pyruvaldehyde	44-47	CREB regulated transcription coactivator 1	Mus musculus	150-156
32930996-11	2021	Therefore, EM protected the mitochondria by a mechanism dependent on the AMPK/Nrf2/HO-1 signaling pathway in MG-challenged SH-SY5Y cells.	Pyruvaldehyde	109-111	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	73-77
32930996-11	2021	Therefore, EM protected the mitochondria by a mechanism dependent on the AMPK/Nrf2/HO-1 signaling pathway in MG-challenged SH-SY5Y cells.	Pyruvaldehyde	109-111	NFE2 like bZIP transcription factor 2	Homo sapiens	78-82
32930996-11	2021	Therefore, EM protected the mitochondria by a mechanism dependent on the AMPK/Nrf2/HO-1 signaling pathway in MG-challenged SH-SY5Y cells.	Pyruvaldehyde	109-111	heme oxygenase 1	Homo sapiens	83-87
33392911-9	2021	Inhibition of gamma-GCL with buthionine sulfoximine (BSO) or silencing of Nrf2 using small interfering RNA (siRNA) against this transcription factor reduced the levels of GSH and abolished the mitochondrial protection promoted by SFN in the MG-treated cells.	Pyruvaldehyde	241-243	NFE2 like bZIP transcription factor 2	Homo sapiens	74-78
33392911-10	2021	Thus, SFN protected mitochondria of the MG-challenged cells by a mechanism involving the Nrf2/gamma-GCL/GSH axis.	Pyruvaldehyde	40-42	NFE2 like bZIP transcription factor 2	Homo sapiens	89-93
33792156-5	2022	We observed that the accumulation of MGO-derived AGEs in human diabetic wounds increased, whereas the expression of glyoxalase 1 (GLO1), a key metabolic enzyme of MGO, decreased.	Pyruvaldehyde	163-166	glyoxalase I	Homo sapiens	116-128
33792156-5	2022	We observed that the accumulation of MGO-derived AGEs in human diabetic wounds increased, whereas the expression of glyoxalase 1 (GLO1), a key metabolic enzyme of MGO, decreased.	Pyruvaldehyde	163-166	glyoxalase I	Homo sapiens	130-134
33792156-7	2022	In vitro, MGO damaged the phagocytic functions of M1-like macrophages induced by lipopolysaccharide (LPS), but not those of M0-like macrophages induced by PMA or of M2-like macrophages induced by interleukins 4 (IL-4) and 13 (IL-13); the impaired phagocytosis of M1-like macrophages was rescued by PM administration.	Pyruvaldehyde	10-13	interleukin 13	Homo sapiens	226-231
32746708-7	2021	GO and MGO increased production of pro-inflammatory such as interleukin (IL)-1beta and IL-6) and MUC5AC/5B.	Pyruvaldehyde	7-10	interleukin 1 alpha	Homo sapiens	60-82
33859775-0	2021	Cudrania tricuspidata Root Extract Prevents Methylglyoxal-Induced Inflammation and Oxidative Stress via Regulation of the PKC-NOX4 Pathway in Human Kidney Cells.	Pyruvaldehyde	44-57	proline rich transmembrane protein 2	Homo sapiens	122-125
33859775-0	2021	Cudrania tricuspidata Root Extract Prevents Methylglyoxal-Induced Inflammation and Oxidative Stress via Regulation of the PKC-NOX4 Pathway in Human Kidney Cells.	Pyruvaldehyde	44-57	NADPH oxidase 4	Homo sapiens	126-130
33859775-8	2021	MGO induced the expression of NADPH oxidase 4 (NOX4); CTRE pretreatment inhibited this induction.	Pyruvaldehyde	0-3	NADPH oxidase 4	Homo sapiens	47-51
33859775-10	2021	Collectively, our data suggest that CTRE attenuates MGO-induced inflammation and oxidative stress via inhibition of PKC activation and NOX4 expression, as well as upregulating the Nrf2-antioxidant enzyme pathway in HK-2 cells.	Pyruvaldehyde	52-55	proline rich transmembrane protein 2	Homo sapiens	116-119
33859775-10	2021	Collectively, our data suggest that CTRE attenuates MGO-induced inflammation and oxidative stress via inhibition of PKC activation and NOX4 expression, as well as upregulating the Nrf2-antioxidant enzyme pathway in HK-2 cells.	Pyruvaldehyde	52-55	NADPH oxidase 4	Homo sapiens	135-139
33741073-13	2021	In dialysis-induced peritoneal fibrosis, peritoneal mesothelial cells secrete transforming growth factor-beta1 (TGF-beta1) when exposed to methylglyoxal (MGO)-containing peritoneal dialysate.	Pyruvaldehyde	139-152	transforming growth factor, beta 1	Rattus norvegicus	78-110
33741073-13	2021	In dialysis-induced peritoneal fibrosis, peritoneal mesothelial cells secrete transforming growth factor-beta1 (TGF-beta1) when exposed to methylglyoxal (MGO)-containing peritoneal dialysate.	Pyruvaldehyde	139-152	transforming growth factor, beta 1	Rattus norvegicus	112-121
33741073-13	2021	In dialysis-induced peritoneal fibrosis, peritoneal mesothelial cells secrete transforming growth factor-beta1 (TGF-beta1) when exposed to methylglyoxal (MGO)-containing peritoneal dialysate.	Pyruvaldehyde	154-157	transforming growth factor, beta 1	Rattus norvegicus	78-110
33741073-13	2021	In dialysis-induced peritoneal fibrosis, peritoneal mesothelial cells secrete transforming growth factor-beta1 (TGF-beta1) when exposed to methylglyoxal (MGO)-containing peritoneal dialysate.	Pyruvaldehyde	154-157	transforming growth factor, beta 1	Rattus norvegicus	112-121
33741073-15	2021	The dominant peritoneal tissue M2 macrophages, marked by upregulated Arg-1 expression, account for the attenuation of MGO-induced dedifferentiation of peritoneal mesothelial cells to maintain epithelial integrity.	Pyruvaldehyde	118-121	arginase 1	Rattus norvegicus	69-74
32746708-7	2021	GO and MGO increased production of pro-inflammatory such as interleukin (IL)-1beta and IL-6) and MUC5AC/5B.	Pyruvaldehyde	7-10	interleukin 6	Homo sapiens	87-91
32746708-8	2021	Additionally, GO and MGO significantly activated extracellular signal-regulated kinase 1/2 (ERK1/2), p38 MAPK, and NF-kappaB.	Pyruvaldehyde	21-24	mitogen-activated protein kinase 1	Homo sapiens	49-90
32746708-8	2021	Additionally, GO and MGO significantly activated extracellular signal-regulated kinase 1/2 (ERK1/2), p38 MAPK, and NF-kappaB.	Pyruvaldehyde	21-24	mitogen-activated protein kinase 3	Homo sapiens	92-98
32746708-8	2021	Additionally, GO and MGO significantly activated extracellular signal-regulated kinase 1/2 (ERK1/2), p38 MAPK, and NF-kappaB.	Pyruvaldehyde	21-24	nuclear factor kappa B subunit 1	Homo sapiens	115-124
32746708-9	2021	Whether ERK1/2, p38 MAPK, and NF-kappaB signaling pathway were involved in GO and MGO-induced production of pro-inflammatory cytokines (IL-1beta and IL-6) and MUC5AC/5B, we used specific inhibitors and siRNA transfection.	Pyruvaldehyde	82-85	mitogen-activated protein kinase 3	Homo sapiens	8-14
32746708-9	2021	Whether ERK1/2, p38 MAPK, and NF-kappaB signaling pathway were involved in GO and MGO-induced production of pro-inflammatory cytokines (IL-1beta and IL-6) and MUC5AC/5B, we used specific inhibitors and siRNA transfection.	Pyruvaldehyde	82-85	nuclear factor kappa B subunit 1	Homo sapiens	30-39
32746708-9	2021	Whether ERK1/2, p38 MAPK, and NF-kappaB signaling pathway were involved in GO and MGO-induced production of pro-inflammatory cytokines (IL-1beta and IL-6) and MUC5AC/5B, we used specific inhibitors and siRNA transfection.	Pyruvaldehyde	82-85	interleukin 1 alpha	Homo sapiens	136-144
32746708-9	2021	Whether ERK1/2, p38 MAPK, and NF-kappaB signaling pathway were involved in GO and MGO-induced production of pro-inflammatory cytokines (IL-1beta and IL-6) and MUC5AC/5B, we used specific inhibitors and siRNA transfection.	Pyruvaldehyde	82-85	interleukin 6	Homo sapiens	149-153
32746708-10	2021	These significantly repressed GO- and MGO-induced expression of pro-inflammatory cytokines (IL-1beta and IL-6) and MUC5AC/5B.	Pyruvaldehyde	38-41	interleukin 1 alpha	Homo sapiens	92-100
32746708-10	2021	These significantly repressed GO- and MGO-induced expression of pro-inflammatory cytokines (IL-1beta and IL-6) and MUC5AC/5B.	Pyruvaldehyde	38-41	interleukin 6	Homo sapiens	105-109
32746708-10	2021	These significantly repressed GO- and MGO-induced expression of pro-inflammatory cytokines (IL-1beta and IL-6) and MUC5AC/5B.	Pyruvaldehyde	38-41	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	115-121
32746708-11	2021	CONCLUSIONS: GO and MGO induced pro-inflammatory cytokines and MUC5AC/5B expression via ERK1/2, p38 MAPK, and NF-kappaB in human nasal epithelial cells.	Pyruvaldehyde	20-23	mitogen-activated protein kinase 3	Homo sapiens	88-94
32746708-11	2021	CONCLUSIONS: GO and MGO induced pro-inflammatory cytokines and MUC5AC/5B expression via ERK1/2, p38 MAPK, and NF-kappaB in human nasal epithelial cells.	Pyruvaldehyde	20-23	nuclear factor kappa B subunit 1	Homo sapiens	110-119
33411218-10	2021	Thus, CA promoted mitochondrial protection by a PI3K/Akt/Nrf2/gamma-GCL/GSH axis in MG-treated SH-SY5Y cells.	Pyruvaldehyde	84-86	AKT serine/threonine kinase 1	Homo sapiens	53-56
32678947-0	2021	Classically activated mouse macrophages produce methylglyoxal that induces a TLR4- and RAGE-independent proinflammatory response.	Pyruvaldehyde	48-61	toll-like receptor 4	Mus musculus	77-81
32678947-0	2021	Classically activated mouse macrophages produce methylglyoxal that induces a TLR4- and RAGE-independent proinflammatory response.	Pyruvaldehyde	48-61	advanced glycosylation end product-specific receptor	Mus musculus	87-91
32678947-8	2021	Macrophages treated with LPS and IFN-gamma also exhibited decreased expression of glyoxalase 1 (Glo1), an enzyme that metabolizes MG.	Pyruvaldehyde	130-132	interferon gamma	Mus musculus	33-42
32678947-8	2021	Macrophages treated with LPS and IFN-gamma also exhibited decreased expression of glyoxalase 1 (Glo1), an enzyme that metabolizes MG.	Pyruvaldehyde	130-132	glyoxalase 1	Mus musculus	82-94
32678947-8	2021	Macrophages treated with LPS and IFN-gamma also exhibited decreased expression of glyoxalase 1 (Glo1), an enzyme that metabolizes MG.	Pyruvaldehyde	130-132	glyoxalase 1	Mus musculus	96-100
32678947-10	2021	Despite prior evidence that MG adducts may signal through "receptor for advanced glycation endproducts" (RAGE), MG-mediated cell death and cytokine induction by exogenous MG was RAGE-independent in primary macrophages.	Pyruvaldehyde	28-30	advanced glycosylation end product-specific receptor	Mus musculus	105-109
32678947-10	2021	Despite prior evidence that MG adducts may signal through "receptor for advanced glycation endproducts" (RAGE), MG-mediated cell death and cytokine induction by exogenous MG was RAGE-independent in primary macrophages.	Pyruvaldehyde	112-114	advanced glycosylation end product-specific receptor	Mus musculus	178-182
32678947-10	2021	Despite prior evidence that MG adducts may signal through "receptor for advanced glycation endproducts" (RAGE), MG-mediated cell death and cytokine induction by exogenous MG was RAGE-independent in primary macrophages.	Pyruvaldehyde	112-114	advanced glycosylation end product-specific receptor	Mus musculus	178-182
32678947-12	2021	Overall, our evidence suggests that MG may be produced by M1 macrophages during sepsis, following IFN-gamma-dependent down-regulation of Glo1, contributing to over-exuberant inflammation.	Pyruvaldehyde	36-38	interferon gamma	Mus musculus	98-107
32678947-12	2021	Overall, our evidence suggests that MG may be produced by M1 macrophages during sepsis, following IFN-gamma-dependent down-regulation of Glo1, contributing to over-exuberant inflammation.	Pyruvaldehyde	36-38	glyoxalase 1	Mus musculus	137-141
33411218-10	2021	Thus, CA promoted mitochondrial protection by a PI3K/Akt/Nrf2/gamma-GCL/GSH axis in MG-treated SH-SY5Y cells.	Pyruvaldehyde	84-86	NFE2 like bZIP transcription factor 2	Homo sapiens	57-61
33359687-4	2021	Here, we comprehensively investigate age-related accumulation of AGEs and dicarbonyls, including methylglyoxal (MG), glyoxal (GO), and 3-deoxyglucosone (3-DG), and the effects of mitochondrial reactive oxygen species (ROS) on cerebral AGEs accumulation, mitochondrial function, and oxidative stress in the aging human and mouse brain.	Pyruvaldehyde	97-110	renin binding protein	Homo sapiens	37-40
33671767-3	2021	The efficiency of the glyoxalase system, consisting of glyoxalase 1 (GlxI) and glyoxalase 2 (GlxII), is crucial for turning the accumulated MG into nontoxic metabolites.	Pyruvaldehyde	140-142	glyoxalase I	Homo sapiens	69-73
33671767-3	2021	The efficiency of the glyoxalase system, consisting of glyoxalase 1 (GlxI) and glyoxalase 2 (GlxII), is crucial for turning the accumulated MG into nontoxic metabolites.	Pyruvaldehyde	140-142	hydroxyacylglutathione hydrolase	Homo sapiens	93-98
33671767-6	2021	The insulin-induced accumulation of MG and S-d-lactoylglutathione were efficiently removed by the treatment of metformin, possibly via affecting the glyoxalase system.	Pyruvaldehyde	36-38	insulin	Homo sapiens	4-11
33671767-8	2021	While insulin induced an influx of extracellular MG, metformin inhibited the trafficking of MG across the plasma membrane.	Pyruvaldehyde	49-51	insulin	Homo sapiens	6-13
33671767-11	2021	Overall, alternative biochemical regulation of the glyoxalase system mediated by insulin signaling or molecules like biguanides may control cellular MG homeostasis.	Pyruvaldehyde	149-151	insulin	Homo sapiens	81-88
33841846-0	2021	Effect of methylglyoxal on the alteration in structure and digestibility of alpha-lactalbumin, and the formation of advanced glycation end products under simulated thermal processing.	Pyruvaldehyde	10-23	lactalbumin alpha	Homo sapiens	76-93
33841846-3	2021	In this study, methylglyoxal (MG), the most abundant alpha-DCs, was selected to investigate the alteration effects on the structure and digestibility of alpha-lactalbumin (alphaLA) under thermal processing (60-100 C).	Pyruvaldehyde	15-28	lactalbumin alpha	Homo sapiens	153-170
33841846-3	2021	In this study, methylglyoxal (MG), the most abundant alpha-DCs, was selected to investigate the alteration effects on the structure and digestibility of alpha-lactalbumin (alphaLA) under thermal processing (60-100 C).	Pyruvaldehyde	30-32	lactalbumin alpha	Homo sapiens	153-170
33359687-4	2021	Here, we comprehensively investigate age-related accumulation of AGEs and dicarbonyls, including methylglyoxal (MG), glyoxal (GO), and 3-deoxyglucosone (3-DG), and the effects of mitochondrial reactive oxygen species (ROS) on cerebral AGEs accumulation, mitochondrial function, and oxidative stress in the aging human and mouse brain.	Pyruvaldehyde	112-114	renin binding protein	Homo sapiens	37-40
33223150-4	2021	In this study, immunoextraction based on polyclonal anti-HSA antibodies was used with high-performance affinity microcolumns to see how AGE-related modifications produced by glyoxal (Go) and methylglyoxal (MGo) affected the binding of HSA to several first- and second-generation sulfonylureas, a class of drugs used to treat type II diabetes and known to bind to HSA.	Pyruvaldehyde	206-209	albumin	Homo sapiens	235-238
33223150-4	2021	In this study, immunoextraction based on polyclonal anti-HSA antibodies was used with high-performance affinity microcolumns to see how AGE-related modifications produced by glyoxal (Go) and methylglyoxal (MGo) affected the binding of HSA to several first- and second-generation sulfonylureas, a class of drugs used to treat type II diabetes and known to bind to HSA.	Pyruvaldehyde	206-209	albumin	Homo sapiens	235-238
33223150-4	2021	In this study, immunoextraction based on polyclonal anti-HSA antibodies was used with high-performance affinity microcolumns to see how AGE-related modifications produced by glyoxal (Go) and methylglyoxal (MGo) affected the binding of HSA to several first- and second-generation sulfonylureas, a class of drugs used to treat type II diabetes and known to bind to HSA.	Pyruvaldehyde	191-204	albumin	Homo sapiens	57-60
33223150-8	2021	Both Go- and MGo-related modifications at clinically relevant levels were found by this method to create significant changes in the binding by some sulfonylureas with HSA.	Pyruvaldehyde	13-16	albumin	Homo sapiens	167-170
33223150-4	2021	In this study, immunoextraction based on polyclonal anti-HSA antibodies was used with high-performance affinity microcolumns to see how AGE-related modifications produced by glyoxal (Go) and methylglyoxal (MGo) affected the binding of HSA to several first- and second-generation sulfonylureas, a class of drugs used to treat type II diabetes and known to bind to HSA.	Pyruvaldehyde	191-204	renin binding protein	Homo sapiens	136-139
33223150-4	2021	In this study, immunoextraction based on polyclonal anti-HSA antibodies was used with high-performance affinity microcolumns to see how AGE-related modifications produced by glyoxal (Go) and methylglyoxal (MGo) affected the binding of HSA to several first- and second-generation sulfonylureas, a class of drugs used to treat type II diabetes and known to bind to HSA.	Pyruvaldehyde	191-204	albumin	Homo sapiens	235-238
33223150-4	2021	In this study, immunoextraction based on polyclonal anti-HSA antibodies was used with high-performance affinity microcolumns to see how AGE-related modifications produced by glyoxal (Go) and methylglyoxal (MGo) affected the binding of HSA to several first- and second-generation sulfonylureas, a class of drugs used to treat type II diabetes and known to bind to HSA.	Pyruvaldehyde	191-204	albumin	Homo sapiens	235-238
33223150-4	2021	In this study, immunoextraction based on polyclonal anti-HSA antibodies was used with high-performance affinity microcolumns to see how AGE-related modifications produced by glyoxal (Go) and methylglyoxal (MGo) affected the binding of HSA to several first- and second-generation sulfonylureas, a class of drugs used to treat type II diabetes and known to bind to HSA.	Pyruvaldehyde	206-209	albumin	Homo sapiens	57-60
33223150-4	2021	In this study, immunoextraction based on polyclonal anti-HSA antibodies was used with high-performance affinity microcolumns to see how AGE-related modifications produced by glyoxal (Go) and methylglyoxal (MGo) affected the binding of HSA to several first- and second-generation sulfonylureas, a class of drugs used to treat type II diabetes and known to bind to HSA.	Pyruvaldehyde	206-209	renin binding protein	Homo sapiens	136-139
33011857-2	2021	Cell culture studies reported that MGO could impair the glyoxalase, thioredoxin, and glutathione systems.	Pyruvaldehyde	35-38	thioredoxin 1	Mus musculus	68-79
33540757-1	2021	Glyoxalase 1 (Glo1) is the rate-limiting enzyme in the detoxification of methylglyoxal (MGO) into D-lactate.	Pyruvaldehyde	73-86	glyoxalase I	Homo sapiens	0-12
33540757-1	2021	Glyoxalase 1 (Glo1) is the rate-limiting enzyme in the detoxification of methylglyoxal (MGO) into D-lactate.	Pyruvaldehyde	73-86	glyoxalase I	Homo sapiens	14-18
33540757-1	2021	Glyoxalase 1 (Glo1) is the rate-limiting enzyme in the detoxification of methylglyoxal (MGO) into D-lactate.	Pyruvaldehyde	88-91	glyoxalase I	Homo sapiens	0-12
33540757-1	2021	Glyoxalase 1 (Glo1) is the rate-limiting enzyme in the detoxification of methylglyoxal (MGO) into D-lactate.	Pyruvaldehyde	88-91	glyoxalase I	Homo sapiens	14-18
33011857-7	2021	Increased DARPP32 Thr75/Thr34 phosphorylation ratio was observed, suggesting a suppression of phosphatase 1 inhibition, which may be involved in behavioral responses to MGO.	Pyruvaldehyde	169-172	protein phosphatase 1, regulatory inhibitor subunit 1B	Mus musculus	10-17
33095439-7	2021	In addition, hippocampal glutamate uptake decreased and glutamine synthetase activity and glutathione levels diminished during seventy-two hours after infusion of MG.	Pyruvaldehyde	163-165	glutamate-ammonia ligase	Rattus norvegicus	56-76
33727737-10	2021	Methylglyoxal is a physiological substrate of the glyoxalase system, and the accelerated accumulation of this compound lowers the glyoxalase I activity.	Pyruvaldehyde	0-13	glyoxalase I	Homo sapiens	130-142
33059495-5	2021	The toxicity of MG was more pronounced in the strains with deletion in genes engaged with DNA repair checkpoint proteins, namely Rad23 and Rad50.	Pyruvaldehyde	16-18	Rad23p	Saccharomyces cerevisiae S288C	129-134
33360689-1	2021	Glyoxalase 1 (encoded by GLO1) is a glutathione-dependent enzyme detoxifying the glycolytic byproduct methylglyoxal (MG), an oncometabolite involved in metabolic reprogramming.	Pyruvaldehyde	102-115	glyoxalase I	Homo sapiens	25-29
33360689-1	2021	Glyoxalase 1 (encoded by GLO1) is a glutathione-dependent enzyme detoxifying the glycolytic byproduct methylglyoxal (MG), an oncometabolite involved in metabolic reprogramming.	Pyruvaldehyde	117-119	glyoxalase I	Homo sapiens	25-29
33059495-5	2021	The toxicity of MG was more pronounced in the strains with deletion in genes engaged with DNA repair checkpoint proteins, namely Rad23 and Rad50.	Pyruvaldehyde	16-18	MRX complex DNA-binding subunit	Saccharomyces cerevisiae S288C	139-144
33460343-9	2021	RESULTS: MG increased malondialdehyde, albuminuria, Nrf2, miR-192 and miR-204 expression in diabetic groups and GA decreased them.	Pyruvaldehyde	9-11	nuclear factor, erythroid derived 2, like 2	Mus musculus	52-56
33460343-9	2021	RESULTS: MG increased malondialdehyde, albuminuria, Nrf2, miR-192 and miR-204 expression in diabetic groups and GA decreased them.	Pyruvaldehyde	9-11	microRNA 192	Mus musculus	58-65
33460343-9	2021	RESULTS: MG increased malondialdehyde, albuminuria, Nrf2, miR-192 and miR-204 expression in diabetic groups and GA decreased them.	Pyruvaldehyde	9-11	microRNA 204	Mus musculus	70-77
33392167-6	2020	In further studies, we showed that methylglyoxal (MGO), the main form of advanced glycation end products (AGEs), accumulated significantly and caused the destabilization of HIF-1alpha in the diabetic state.	Pyruvaldehyde	35-48	hypoxia inducible factor 1 subunit alpha	Homo sapiens	173-183
33315368-1	2021	Glyoxalase I (GlxI) is an important enzyme that catalyzes the detoxification of methylglyoxal (MG) with the help of glutathione (H-SG).	Pyruvaldehyde	80-93	glyoxalase I	Homo sapiens	0-12
33509461-10	2021	Some of fruit extracts were able to inhibit alpha-glucosidase and glycation in methylglyoxal and fructose models, whereas none of them was active for lipase and alpha-amylase.	Pyruvaldehyde	79-92	sucrase-isomaltase	Homo sapiens	44-61
32809100-13	2021	Direct AGE inhibitors currently investigated include pyridoxamine and epalrestat, the inhibition of the formation of reactive dicarbonyls such as methylglyoxal as an important precursor of AGEs via increased activation of the detoxifying enzyme Glo-1 and inhibitors of NOX-derived ROS to reduce the AGE/RAGE signalling.	Pyruvaldehyde	146-159	glyoxalase I	Homo sapiens	245-250
32809100-13	2021	Direct AGE inhibitors currently investigated include pyridoxamine and epalrestat, the inhibition of the formation of reactive dicarbonyls such as methylglyoxal as an important precursor of AGEs via increased activation of the detoxifying enzyme Glo-1 and inhibitors of NOX-derived ROS to reduce the AGE/RAGE signalling.	Pyruvaldehyde	146-159	advanced glycosylation end-product specific receptor	Homo sapiens	303-307
30900959-11	2021	NGEN also increased neurite length and enhanced IGF-1R and p-Akt in MG-treated NSC34 cells.	Pyruvaldehyde	68-70	insulin-like growth factor I receptor	Mus musculus	48-54
30900959-12	2021	Furthermore, NGEN attenuated MG-induced apoptotic death accompanied with down-regulation of cleaved-poly (ADP-ribose) polymerase (PARP) and up-regulation of B-cell lymphoma-2 (Bcl-2).	Pyruvaldehyde	29-31	poly (ADP-ribose) polymerase family, member 1	Mus musculus	100-128
30900959-12	2021	Furthermore, NGEN attenuated MG-induced apoptotic death accompanied with down-regulation of cleaved-poly (ADP-ribose) polymerase (PARP) and up-regulation of B-cell lymphoma-2 (Bcl-2).	Pyruvaldehyde	29-31	B cell leukemia/lymphoma 2	Mus musculus	157-174
30900959-12	2021	Furthermore, NGEN attenuated MG-induced apoptotic death accompanied with down-regulation of cleaved-poly (ADP-ribose) polymerase (PARP) and up-regulation of B-cell lymphoma-2 (Bcl-2).	Pyruvaldehyde	29-31	B cell leukemia/lymphoma 2	Mus musculus	176-181
30900959-13	2021	However, AG1024, an IGF-1R antagonist, attenuated the anti-oxidative and anti-apoptotic effects of NGEN in MG-treated cells.	Pyruvaldehyde	107-109	insulin-like growth factor I receptor	Mus musculus	20-26
33379155-6	2020	An increase in MGO level also occurs under oxidative stress (OxS) conditions probably due to several events among which the decrease in GSH level and/or the bottleneck of glycolysis caused by the reversible S-glutathionylation and inhibition of glyceraldehyde-3-phosphate dehydrogenase.	Pyruvaldehyde	15-18	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	245-285
33379155-8	2020	Moreover, it is highlighted how the products of MGO metabolism, S-D-lactoylglutathione (SLG) and D-lactate, which can be taken up and metabolized by mitochondria, could play important roles in cell response to OxS, contributing to cytosol-mitochondria crosstalk, cytosolic and mitochondrial GSH pools, energy production, and the restoration of the GSH/GSSG ratio.	Pyruvaldehyde	48-51	sialic acid binding Ig like lectin 12	Homo sapiens	88-91
33392167-6	2020	In further studies, we showed that methylglyoxal (MGO), the main form of advanced glycation end products (AGEs), accumulated significantly and caused the destabilization of HIF-1alpha in the diabetic state.	Pyruvaldehyde	50-53	hypoxia inducible factor 1 subunit alpha	Homo sapiens	173-183
33392167-7	2020	Insulin could alleviate the MGO-induced HIF-1alpha unstable state and promote HIF-1alpha target gene expression and its downstream biological effect such as angiogenesis and wound extracellular matrix deposition.	Pyruvaldehyde	28-31	insulin	Homo sapiens	0-7
33392167-7	2020	Insulin could alleviate the MGO-induced HIF-1alpha unstable state and promote HIF-1alpha target gene expression and its downstream biological effect such as angiogenesis and wound extracellular matrix deposition.	Pyruvaldehyde	28-31	hypoxia inducible factor 1 subunit alpha	Homo sapiens	40-50
33046246-0	2020	Comparison of the reaction of methylglyoxal (MGO) with murine and human amyloid beta (Abeta): Insights into a mechanism of Alzheimer"s disease (AD).	Pyruvaldehyde	30-43	amyloid beta precursor protein	Homo sapiens	72-84
33255888-1	2020	Methylglyoxal (MG), a potent precursor of advanced glycation end-products (AGE), is increased in metabolic disorders such as diabetes and obesity.	Pyruvaldehyde	0-13	renin binding protein	Rattus norvegicus	75-78
33046246-0	2020	Comparison of the reaction of methylglyoxal (MGO) with murine and human amyloid beta (Abeta): Insights into a mechanism of Alzheimer"s disease (AD).	Pyruvaldehyde	30-43	amyloid beta precursor protein	Homo sapiens	86-91
33046246-0	2020	Comparison of the reaction of methylglyoxal (MGO) with murine and human amyloid beta (Abeta): Insights into a mechanism of Alzheimer"s disease (AD).	Pyruvaldehyde	45-48	amyloid beta precursor protein	Homo sapiens	72-84
33046246-0	2020	Comparison of the reaction of methylglyoxal (MGO) with murine and human amyloid beta (Abeta): Insights into a mechanism of Alzheimer"s disease (AD).	Pyruvaldehyde	45-48	amyloid beta precursor protein	Homo sapiens	86-91
33046246-2	2020	The reactions of MGO with mAbeta(R13H), hAbeta(H13F), Nalpha-acetyl-l-lysine, and Nalpha-acetyl-l-arginine implied that the lack of His13 in mAbeta prohibits its Lys16 residue from reacting to produce cross-linked reaction products and O2 -.	Pyruvaldehyde	17-20	amyloid beta precursor protein	Homo sapiens	40-51
33161365-8	2020	Herein, we report an analogue of NAP, 1,8-diamino naphthalene (DAN) is an efficient chemosensor for highly sensitive detection of FA, MGO and GO with minimum detection limits of 0.95-3.97 muM.	Pyruvaldehyde	134-137	catenin beta like 1	Homo sapiens	33-36
33255888-1	2020	Methylglyoxal (MG), a potent precursor of advanced glycation end-products (AGE), is increased in metabolic disorders such as diabetes and obesity.	Pyruvaldehyde	15-17	renin binding protein	Rattus norvegicus	75-78
33255888-4	2020	Compared to SHR wild-type animals, SHR-Glo1+/- rats showed significantly reduced Glo1 expression and lower GLO1 activity in tissues associated with increased MG levels.	Pyruvaldehyde	158-160	glyoxalase 1	Rattus norvegicus	39-43
33024240-7	2021	In addition, the ability in methylglyoxal (MGO) detoxification and deglycation was almost abolished in the mutation of DJ-1 DeltaC3 and point mutant L187E compared with wild-type DJ-1 (DJ-1 WT).	Pyruvaldehyde	28-41	Parkinsonism associated deglycase	Homo sapiens	119-123
33166134-4	2020	This study aims to evaluate the roles of glyoxalase 1 (GLO1)-methylglyoxal (MG)-gamma-aminobutyric acid (GABA) signaling in ASD using a valproic acid (VPA)-induced animal model of autism.	Pyruvaldehyde	61-74	glyoxalase 1	Mus musculus	41-53
33166134-4	2020	This study aims to evaluate the roles of glyoxalase 1 (GLO1)-methylglyoxal (MG)-gamma-aminobutyric acid (GABA) signaling in ASD using a valproic acid (VPA)-induced animal model of autism.	Pyruvaldehyde	61-74	glyoxalase I	Homo sapiens	55-59
33166134-4	2020	This study aims to evaluate the roles of glyoxalase 1 (GLO1)-methylglyoxal (MG)-gamma-aminobutyric acid (GABA) signaling in ASD using a valproic acid (VPA)-induced animal model of autism.	Pyruvaldehyde	76-78	glyoxalase 1	Mus musculus	41-53
33166134-4	2020	This study aims to evaluate the roles of glyoxalase 1 (GLO1)-methylglyoxal (MG)-gamma-aminobutyric acid (GABA) signaling in ASD using a valproic acid (VPA)-induced animal model of autism.	Pyruvaldehyde	76-78	glyoxalase I	Homo sapiens	55-59
32858501-2	2020	It consists of glyoxalase 1 (GLO1), glyoxalase 2 (GLO2), and reduced glutathione (GSH), which perform an essential metabolic function in cells by detoxifying methylglyoxal (MG) and other endogenous harmful metabolites into non-toxic d-lactate.	Pyruvaldehyde	158-171	glyoxalase I	Homo sapiens	29-33
32858501-2	2020	It consists of glyoxalase 1 (GLO1), glyoxalase 2 (GLO2), and reduced glutathione (GSH), which perform an essential metabolic function in cells by detoxifying methylglyoxal (MG) and other endogenous harmful metabolites into non-toxic d-lactate.	Pyruvaldehyde	158-171	hydroxyacylglutathione hydrolase	Homo sapiens	50-54
32858501-2	2020	It consists of glyoxalase 1 (GLO1), glyoxalase 2 (GLO2), and reduced glutathione (GSH), which perform an essential metabolic function in cells by detoxifying methylglyoxal (MG) and other endogenous harmful metabolites into non-toxic d-lactate.	Pyruvaldehyde	173-175	glyoxalase I	Homo sapiens	29-33
32858501-2	2020	It consists of glyoxalase 1 (GLO1), glyoxalase 2 (GLO2), and reduced glutathione (GSH), which perform an essential metabolic function in cells by detoxifying methylglyoxal (MG) and other endogenous harmful metabolites into non-toxic d-lactate.	Pyruvaldehyde	173-175	hydroxyacylglutathione hydrolase	Homo sapiens	50-54
32835595-9	2020	The putative PdGLX1 genes were also able to complement the loss-of-function MG hypersensitive GLO1 (YML004C) yeast mutants and promote growth by enhancing MG detoxification and reducing the accumulation of reactive oxygen species (ROS) under stress conditions as indicated by flow cytometry.	Pyruvaldehyde	76-78	lactoylglutathione lyase GLO1	Saccharomyces cerevisiae S288C	94-98
32101837-11	2020	Methylglyoxal, a precursor of advanced glycation end products, increased the expressions of ICAM-1 and p22phox in HUVECs (P<0.05, both).	Pyruvaldehyde	0-13	intercellular adhesion molecule 1	Mus musculus	92-98
32101837-11	2020	Methylglyoxal, a precursor of advanced glycation end products, increased the expressions of ICAM-1 and p22phox in HUVECs (P<0.05, both).	Pyruvaldehyde	0-13	cytochrome b-245, alpha polypeptide	Mus musculus	103-110
32101837-12	2020	Methylglyoxal also decreased the phosphorylation of eNOSSer1177 and Akt but increased the phosphorylation of eNOSThr495 and p38 MAPK in HUVECs.	Pyruvaldehyde	0-13	mitogen-activated protein kinase 14	Mus musculus	124-132
32942016-1	2020	Methylglyoxal was shown to impair adipose tissue capillarization and insulin sensitivity in obese models.	Pyruvaldehyde	0-13	insulin	Homo sapiens	69-76
33024240-7	2021	In addition, the ability in methylglyoxal (MGO) detoxification and deglycation was almost abolished in the mutation of DJ-1 DeltaC3 and point mutant L187E compared with wild-type DJ-1 (DJ-1 WT).	Pyruvaldehyde	28-41	Parkinsonism associated deglycase	Homo sapiens	179-183
33024240-7	2021	In addition, the ability in methylglyoxal (MGO) detoxification and deglycation was almost abolished in the mutation of DJ-1 DeltaC3 and point mutant L187E compared with wild-type DJ-1 (DJ-1 WT).	Pyruvaldehyde	43-46	Parkinsonism associated deglycase	Homo sapiens	119-123
33024240-7	2021	In addition, the ability in methylglyoxal (MGO) detoxification and deglycation was almost abolished in the mutation of DJ-1 DeltaC3 and point mutant L187E compared with wild-type DJ-1 (DJ-1 WT).	Pyruvaldehyde	43-46	Parkinsonism associated deglycase	Homo sapiens	179-183
32980661-2	2020	In zebrafish, knockout of the main MG detoxifying system Glyoxalase 1, led to limited MG elevation but significantly elevated aldehyde dehydrogenases (ALDH) activity and aldh3a1 expression, suggesting the compensatory role of Aldh3a1 in diabetes.	Pyruvaldehyde	35-37	glyoxalase 1	Danio rerio	57-69
32980661-2	2020	In zebrafish, knockout of the main MG detoxifying system Glyoxalase 1, led to limited MG elevation but significantly elevated aldehyde dehydrogenases (ALDH) activity and aldh3a1 expression, suggesting the compensatory role of Aldh3a1 in diabetes.	Pyruvaldehyde	35-37	aldehyde dehydrogenase 3 family, member A1	Danio rerio	170-177
32980661-2	2020	In zebrafish, knockout of the main MG detoxifying system Glyoxalase 1, led to limited MG elevation but significantly elevated aldehyde dehydrogenases (ALDH) activity and aldh3a1 expression, suggesting the compensatory role of Aldh3a1 in diabetes.	Pyruvaldehyde	35-37	aldehyde dehydrogenase 3 family, member A1	Danio rerio	226-233
32913257-5	2020	Methylglyoxal treatment also significantly decreased the mRNA expression of the slit diaphragm markers ZO-1 and NEPH1 and significantly increased the mRNA expression of the oxidative stress marker HO-1.	Pyruvaldehyde	0-13	tight junction protein 1	Homo sapiens	103-107
33043179-1	2020	Methylglyoxal (MG), a glycolytic intermediate and reactive dicarbonyl, is responsible for exacerbation of insulin resistance and diabetic complication.	Pyruvaldehyde	0-13	insulin	Homo sapiens	106-113
33043179-1	2020	Methylglyoxal (MG), a glycolytic intermediate and reactive dicarbonyl, is responsible for exacerbation of insulin resistance and diabetic complication.	Pyruvaldehyde	15-17	insulin	Homo sapiens	106-113
32913257-5	2020	Methylglyoxal treatment also significantly decreased the mRNA expression of the slit diaphragm markers ZO-1 and NEPH1 and significantly increased the mRNA expression of the oxidative stress marker HO-1.	Pyruvaldehyde	0-13	kirre like nephrin family adhesion molecule 1	Homo sapiens	112-117
32913257-5	2020	Methylglyoxal treatment also significantly decreased the mRNA expression of the slit diaphragm markers ZO-1 and NEPH1 and significantly increased the mRNA expression of the oxidative stress marker HO-1.	Pyruvaldehyde	0-13	heme oxygenase 1	Homo sapiens	197-201
32731097-9	2020	Methylglyoxal (MG) production was increased by Cr but reduced by NaHS through a mechanism which could be based on glutathione-S-transferase (GST) detoxification.	Pyruvaldehyde	0-13	glutathione S-transferase	Zea mays	114-139
32899154-0	2020	Methylglyoxal-Induced Dysfunction in Brain Endothelial Cells via the Suppression of Akt/HIF-1alpha Pathway and Activation of Mitophagy Associated with Increased Reactive Oxygen Species.	Pyruvaldehyde	0-13	AKT serine/threonine kinase 1	Homo sapiens	84-87
32899154-0	2020	Methylglyoxal-Induced Dysfunction in Brain Endothelial Cells via the Suppression of Akt/HIF-1alpha Pathway and Activation of Mitophagy Associated with Increased Reactive Oxygen Species.	Pyruvaldehyde	0-13	hypoxia inducible factor 1 subunit alpha	Homo sapiens	88-98
32731097-9	2020	Methylglyoxal (MG) production was increased by Cr but reduced by NaHS through a mechanism which could be based on glutathione-S-transferase (GST) detoxification.	Pyruvaldehyde	0-13	glutathione S-transferase	Zea mays	141-144
32731097-9	2020	Methylglyoxal (MG) production was increased by Cr but reduced by NaHS through a mechanism which could be based on glutathione-S-transferase (GST) detoxification.	Pyruvaldehyde	15-17	glutathione S-transferase	Zea mays	114-139
32731097-9	2020	Methylglyoxal (MG) production was increased by Cr but reduced by NaHS through a mechanism which could be based on glutathione-S-transferase (GST) detoxification.	Pyruvaldehyde	15-17	glutathione S-transferase	Zea mays	141-144
32807835-0	2020	Methylglyoxal inhibits nuclear division through alterations in vacuolar morphology and accumulation of Atg18 on the vacuolar membrane in Saccharomyces cerevisiae.	Pyruvaldehyde	0-13	phosphoinositide binding protein ATG18	Saccharomyces cerevisiae S288C	103-108
32825285-2	2020	The viability of INS-1 cells was maintained upon pre-treating with CA before exposure to MG.	Pyruvaldehyde	89-91	insulin 1	Rattus norvegicus	17-22
32474849-7	2020	In addition, MG and NaHS alone or in combination also separately modulated the metabolism of osmolytes (proline, trehalose, glycine betaine, and total soluble sugar), H2S (L-cysteine desulfhydrase and O-acetylserine (thione) lyase), and MG (glyoxalase I, glyoxalase II, and MG reductase).	Pyruvaldehyde	13-15	glyoxylase 1	Zea mays	241-253
32878255-6	2020	In addition, MG reduced the expression of transcription factor Nrf2 (p < 0.01), which controls antioxidant and lipogenic genes.	Pyruvaldehyde	13-15	NFE2 like bZIP transcription factor 2	Rattus norvegicus	63-67
32795389-4	2020	Metabolic pathways related to the glycolytic by-product methylglyoxal (MGO) are rewired in Alkbh7-/- mice, along with elevated levels of MGO protein adducts.	Pyruvaldehyde	56-69	alkB homolog 7	Mus musculus	91-97
32795389-4	2020	Metabolic pathways related to the glycolytic by-product methylglyoxal (MGO) are rewired in Alkbh7-/- mice, along with elevated levels of MGO protein adducts.	Pyruvaldehyde	71-74	alkB homolog 7	Mus musculus	91-97
32795389-6	2020	Integrating these observations, we propose ALKBH7 regulates glyoxal metabolism, and that protection against necrosis and cardiac IR injury bought on by ALKBH7 deficiency originates from the signaling response to elevated MGO stress.	Pyruvaldehyde	221-224	alkB homolog 7	Mus musculus	43-49
32795389-6	2020	Integrating these observations, we propose ALKBH7 regulates glyoxal metabolism, and that protection against necrosis and cardiac IR injury bought on by ALKBH7 deficiency originates from the signaling response to elevated MGO stress.	Pyruvaldehyde	221-224	alkB homolog 7	Mus musculus	152-158
32807835-4	2020	Here, we show that increase in the levels of phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P2) is crucial for the inhibitory effects of MG on nuclear division, and the deletion of PtdIns(3,5)P2-effector Atg18 alleviated the MG-mediated inhibitory effects.	Pyruvaldehyde	140-142	phosphoinositide binding protein ATG18	Saccharomyces cerevisiae S288C	207-212
32807835-8	2020	Our results suggest that both the accumulation of Atg18 on the vacuolar membrane and alterations in vacuolar morphology are necessary for the MG-induced inhibition of nuclear division.	Pyruvaldehyde	142-144	phosphoinositide binding protein ATG18	Saccharomyces cerevisiae S288C	50-55
32636256-4	2020	Importantly, we found that low MG-producing E. coli mutants, Deltahns E. coli, extended the lifespan of C. elegans through activation of the DAF-16/FOXO family transcription factor and the mitochondrial unfolded protein response (UPRmt).	Pyruvaldehyde	31-33	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	141-147
32698053-8	2020	Our results suggested that MG induced metabolic changes typically associated with aerobic glycolysis, including a lowered expression of proteins involved in oxidative metabolism and increased expression of the glycolytic enzymes L-lactate dehydrogenase and glyceraldehyde-3-phosphate dehydrogenase.	Pyruvaldehyde	27-29	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	257-297
32636256-8	2020	Finally, we demonstrate that MG enhances the phosphorylation of hSGK1 and accelerates cellular senescence in human dermal fibroblasts, suggesting the conserved role of MG in controlling longevity across species.	Pyruvaldehyde	29-31	serum/glucocorticoid regulated kinase 1	Homo sapiens	64-69
32573222-5	2020	Mechanistically, genistein upregulated the expressions of glyoxalase I and II, and aldose reductase to detoxify MGO, and genistein and its microbial metabolites, dihydrogenistein and 6"-hydroxy-O-demethylangolensin, were able to trap endogenous MGO via formation of MGO conjugates.	Pyruvaldehyde	112-115	glyoxalase 1	Mus musculus	58-77
32298726-7	2020	In vitro experiments supported the minor relevance of Glo1 in the detoxification of circulating MG but the important role of plasma albumin as an MG scavenger.	Pyruvaldehyde	96-98	glyoxalase 1	Mus musculus	54-58
32679775-7	2020	The highly increased permeability and loss of noncovalent interactions of deamidated TIM were found to play a central role in the process of selective enzyme inactivation and methylglyoxal production.	Pyruvaldehyde	175-188	triosephosphate isomerase 1	Homo sapiens	85-88
32640624-1	2020	Accumulation of methylglyoxal (MG) arising from downregulation of its primary degrading enzyme glyoxalase-1 (Glo1) is an underlying cause of diabetic cardiomyopathy (DC).	Pyruvaldehyde	16-29	glyoxalase 1	Rattus norvegicus	95-107
32640624-1	2020	Accumulation of methylglyoxal (MG) arising from downregulation of its primary degrading enzyme glyoxalase-1 (Glo1) is an underlying cause of diabetic cardiomyopathy (DC).	Pyruvaldehyde	16-29	glyoxalase 1	Rattus norvegicus	109-113
32640624-1	2020	Accumulation of methylglyoxal (MG) arising from downregulation of its primary degrading enzyme glyoxalase-1 (Glo1) is an underlying cause of diabetic cardiomyopathy (DC).	Pyruvaldehyde	31-33	glyoxalase 1	Rattus norvegicus	95-107
32640624-1	2020	Accumulation of methylglyoxal (MG) arising from downregulation of its primary degrading enzyme glyoxalase-1 (Glo1) is an underlying cause of diabetic cardiomyopathy (DC).	Pyruvaldehyde	31-33	glyoxalase 1	Rattus norvegicus	109-113
32640624-6	2020	A single injection of AAV2/9 Endo-Glo1 (1.7 x 1012 viron particles/kg) one week after onset of T1DM, potentiated GSH, and blunted MG accumulation, carbonyl/oxidative stress, microvascular leakage, inflammation, fibrosis, and impairments in cardiac and myocyte functions that develop after eight weeks of T1DM.	Pyruvaldehyde	130-132	glyoxalase I	Homo sapiens	34-38
32649695-11	2020	Western blotting confirmed that superoxide dismutase 1 (SOD-1) and parkinson disease protein 7 (DJ-1) are upregulated and may participate with MG in CDDP-induced AKI.	Pyruvaldehyde	143-145	superoxide dismutase 1, soluble	Mus musculus	32-54
32649695-11	2020	Western blotting confirmed that superoxide dismutase 1 (SOD-1) and parkinson disease protein 7 (DJ-1) are upregulated and may participate with MG in CDDP-induced AKI.	Pyruvaldehyde	143-145	superoxide dismutase 1, soluble	Mus musculus	56-61
32649695-11	2020	Western blotting confirmed that superoxide dismutase 1 (SOD-1) and parkinson disease protein 7 (DJ-1) are upregulated and may participate with MG in CDDP-induced AKI.	Pyruvaldehyde	143-145	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	96-100
32298726-6	2020	Mice simultaneously deficient in the receptor for AGEs (RAGE) and overexpressing Glo1 exhibited higher basal plasma MG levels and did generally not respond to long-term MG intake.	Pyruvaldehyde	116-118	glyoxalase 1	Mus musculus	81-85
32560521-7	2020	Isosamidin prevented MGO-induced apoptosis in HUVECs by downregulating the expression of Bax and upregulating the expression of Bcl-2.	Pyruvaldehyde	21-24	BCL2 associated X, apoptosis regulator	Homo sapiens	89-92
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	60-73	insulin like growth factor 1 receptor	Homo sapiens	174-211
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	60-73	insulin like growth factor 1 receptor	Homo sapiens	213-219
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	60-73	AKT serine/threonine kinase 1	Homo sapiens	224-227
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	60-73	glycogen synthase kinase 3 alpha	Homo sapiens	231-239
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	60-73	glucagon like peptide 1 receptor	Homo sapiens	241-273
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	60-73	glucagon like peptide 1 receptor	Homo sapiens	275-281
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	60-73	brain derived neurotrophic factor	Homo sapiens	288-321
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	60-73	brain derived neurotrophic factor	Homo sapiens	323-327
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	75-77	insulin like growth factor 1 receptor	Homo sapiens	174-211
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	75-77	insulin like growth factor 1 receptor	Homo sapiens	213-219
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	75-77	AKT serine/threonine kinase 1	Homo sapiens	224-227
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	75-77	glycogen synthase kinase 3 alpha	Homo sapiens	231-239
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	75-77	glucagon like peptide 1 receptor	Homo sapiens	241-273
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	75-77	glucagon like peptide 1 receptor	Homo sapiens	275-281
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	75-77	brain derived neurotrophic factor	Homo sapiens	288-321
32599797-8	2020	In human dopaminergic SH-SY5Y cells treated with or without methylglyoxal (MG), a toxic endogenous by-product of glycolysis, AN07 up-regulated neurotrophic signals including insulin-like growth factor 1 receptor (IGF-1R), p-Akt, p-GSK3beta, glucagon-like peptide 1 receptor (GLP-1R), and brain-derived neurotrophic factor (BDNF).	Pyruvaldehyde	75-77	brain derived neurotrophic factor	Homo sapiens	323-327
32599797-9	2020	AN07 attenuated MG-induced apoptosis by up-regulating the B-cell lymphoma 2 (Bcl-2) protein and down-regulating the cytosolic expression of cytochrome c.	Pyruvaldehyde	16-18	BCL2 apoptosis regulator	Homo sapiens	58-75
32599797-9	2020	AN07 attenuated MG-induced apoptosis by up-regulating the B-cell lymphoma 2 (Bcl-2) protein and down-regulating the cytosolic expression of cytochrome c.	Pyruvaldehyde	16-18	BCL2 apoptosis regulator	Homo sapiens	77-82
32599797-9	2020	AN07 attenuated MG-induced apoptosis by up-regulating the B-cell lymphoma 2 (Bcl-2) protein and down-regulating the cytosolic expression of cytochrome c.	Pyruvaldehyde	16-18	cytochrome c, somatic	Homo sapiens	140-152
32599797-10	2020	AN07 also attenuated MG-induced neurite damage via down-regulating the Rho-associated protein kinase 2 (ROCK2)/phosphorylated LIM kinase 1 (p-LIMK1) pathway.	Pyruvaldehyde	21-23	Rho associated coiled-coil containing protein kinase 2	Homo sapiens	71-102
32599797-10	2020	AN07 also attenuated MG-induced neurite damage via down-regulating the Rho-associated protein kinase 2 (ROCK2)/phosphorylated LIM kinase 1 (p-LIMK1) pathway.	Pyruvaldehyde	21-23	Rho associated coiled-coil containing protein kinase 2	Homo sapiens	104-109
32591537-0	2020	Protein arginine deiminase 4 antagonizes methylglyoxal-induced histone glycation.	Pyruvaldehyde	41-54	peptidyl arginine deiminase 4	Homo sapiens	0-28
32500907-1	2020	calyxes ameliorate methylglyoxal-induced oxidative stress via modulation of RAGE expression: identification of active phytometabolites by GC-MS analysis.	Pyruvaldehyde	19-32	advanced glycosylation end-product specific receptor	Homo sapiens	76-80
32599797-10	2020	AN07 also attenuated MG-induced neurite damage via down-regulating the Rho-associated protein kinase 2 (ROCK2)/phosphorylated LIM kinase 1 (p-LIMK1) pathway.	Pyruvaldehyde	21-23	LIM domain kinase 1	Homo sapiens	142-147
32599797-11	2020	Moreover, AN07 ameliorated the MG-induced down-regulation of neuroprotective Parkinsonism-associated proteins parkin, pink1, and DJ-1.	Pyruvaldehyde	31-33	PTEN induced kinase 1	Homo sapiens	118-123
32599797-11	2020	Moreover, AN07 ameliorated the MG-induced down-regulation of neuroprotective Parkinsonism-associated proteins parkin, pink1, and DJ-1.	Pyruvaldehyde	31-33	Parkinsonism associated deglycase	Homo sapiens	129-133
32560521-7	2020	Isosamidin prevented MGO-induced apoptosis in HUVECs by downregulating the expression of Bax and upregulating the expression of Bcl-2.	Pyruvaldehyde	21-24	BCL2 apoptosis regulator	Homo sapiens	128-133
32503323-10	2020	Both the extract and major compounds also inhibited the expression of p-p53 and Bax and increased the levels of Bcl-2 that had been previously reduced by MG treatment.	Pyruvaldehyde	154-156	BCL2 apoptosis regulator	Homo sapiens	112-117
32566104-5	2020	Moreover, MGO upregulated the autophagy markers p62 and LC3-II.	Pyruvaldehyde	10-13	nucleoporin 62	Homo sapiens	48-51
32566104-5	2020	Moreover, MGO upregulated the autophagy markers p62 and LC3-II.	Pyruvaldehyde	10-13	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	56-59
32566104-6	2020	Apoptosis caused by MGO was increased in ATG5-knockdown cells compared to that in wild-type cells.	Pyruvaldehyde	20-23	autophagy related 5	Homo sapiens	41-45
31955977-7	2020	Mechanistically, the exposure to HG/MG resulted in reactive oxygen species (ROS) accumulation which is secondary to the impairment of thioredoxin (Trx) activity in these cells.	Pyruvaldehyde	36-38	thioredoxin	Homo sapiens	134-145
32325188-0	2020	The protective effects of moscatilin against methylglyoxal-induced neurotoxicity via the regulation of p38/JNK MAPK pathways in PC12 neuron-like cells.	Pyruvaldehyde	45-58	mitogen activated protein kinase 14	Rattus norvegicus	103-106
32325188-0	2020	The protective effects of moscatilin against methylglyoxal-induced neurotoxicity via the regulation of p38/JNK MAPK pathways in PC12 neuron-like cells.	Pyruvaldehyde	45-58	mitogen-activated protein kinase 8	Rattus norvegicus	107-110
32325188-6	2020	MGO induced cell apoptosis via the upregulation of p53, caspases 3 and poly(ADP-ribose)polymerase, enhancement of cytochrome c release, and interruption of the Bax/Bcl-2 balance; these detrimental effects were ameliorated by moscatilin.	Pyruvaldehyde	0-3	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	51-54
32325188-6	2020	MGO induced cell apoptosis via the upregulation of p53, caspases 3 and poly(ADP-ribose)polymerase, enhancement of cytochrome c release, and interruption of the Bax/Bcl-2 balance; these detrimental effects were ameliorated by moscatilin.	Pyruvaldehyde	0-3	poly (ADP-ribose) polymerase 1	Rattus norvegicus	71-97
32325188-6	2020	MGO induced cell apoptosis via the upregulation of p53, caspases 3 and poly(ADP-ribose)polymerase, enhancement of cytochrome c release, and interruption of the Bax/Bcl-2 balance; these detrimental effects were ameliorated by moscatilin.	Pyruvaldehyde	0-3	BCL2 associated X, apoptosis regulator	Rattus norvegicus	160-163
32325188-6	2020	MGO induced cell apoptosis via the upregulation of p53, caspases 3 and poly(ADP-ribose)polymerase, enhancement of cytochrome c release, and interruption of the Bax/Bcl-2 balance; these detrimental effects were ameliorated by moscatilin.	Pyruvaldehyde	0-3	BCL2, apoptosis regulator	Rattus norvegicus	164-169
32325188-7	2020	Furthermore, moscatilin inhibited MGO-induced activation of MAP kinase (MAPK) superfamily, including p38 and c-Jun N-terminal kinases (JNKs).	Pyruvaldehyde	34-37	mitogen activated protein kinase 14	Rattus norvegicus	101-104
32325188-8	2020	In conclusion, we found that the neuroprotective effect of moscatilin is due to a reduction of MGO-induced damage to mitochondria function through modulating the p38 and JNK stress-activated MAPK cascades pathway.	Pyruvaldehyde	95-98	mitogen activated protein kinase 14	Rattus norvegicus	162-165
32325188-8	2020	In conclusion, we found that the neuroprotective effect of moscatilin is due to a reduction of MGO-induced damage to mitochondria function through modulating the p38 and JNK stress-activated MAPK cascades pathway.	Pyruvaldehyde	95-98	mitogen-activated protein kinase 8	Rattus norvegicus	170-173
31955977-7	2020	Mechanistically, the exposure to HG/MG resulted in reactive oxygen species (ROS) accumulation which is secondary to the impairment of thioredoxin (Trx) activity in these cells.	Pyruvaldehyde	36-38	thioredoxin	Homo sapiens	147-150
31955977-9	2020	Functional supplementation of Trx using thioredoxin mimetic peptides (TMP) reversed the HG/MG-induced ROS generation, improved the migration, proliferation, survival and restored VEGF-A-induced chemotaxis and sprouting angiogenesis of hyperglycemic ECs.	Pyruvaldehyde	91-93	thioredoxin	Homo sapiens	30-33
31955977-9	2020	Functional supplementation of Trx using thioredoxin mimetic peptides (TMP) reversed the HG/MG-induced ROS generation, improved the migration, proliferation, survival and restored VEGF-A-induced chemotaxis and sprouting angiogenesis of hyperglycemic ECs.	Pyruvaldehyde	91-93	thioredoxin	Homo sapiens	40-51
32550794-6	2020	In DCFH and MGO treated cells, Oncoglabrinol C (20 mug/ml) effectively downregulated caspase 3/7 activity by ~33% and ~43.5%, respectively.	Pyruvaldehyde	12-15	caspase 3	Homo sapiens	85-96
32547400-0	2020	Stimulation of GLP-1 Receptor Inhibits Methylglyoxal-Induced Mitochondrial Dysfunctions in H9c2 Cardiomyoblasts: Potential Role of Epac/PI3K/Akt Pathway.	Pyruvaldehyde	39-52	glucagon-like peptide 1 receptor	Rattus norvegicus	15-29
32547400-7	2020	GLP-1R stimulation also improved the alterations of mitochondrial membrane potential (MMP) and expressions of genes related to mitochondrial functions and dynamics induced by MG.	Pyruvaldehyde	175-177	glucagon-like peptide 1 receptor	Rattus norvegicus	0-6
32114052-10	2020	In in vitro studies, methylglyoxal (MGO), a precursor of AGEs, significantly increased the expression of inflammatory molecules such as MCP-1 and TNF-alpha in a murine macrophage cell line, RAW264.7.	Pyruvaldehyde	21-34	mast cell protease 1	Mus musculus	136-141
32467587-9	2020	We observed that MGO-induced autophagic cell death and inhibited the ROS-mediated Akt/mTOR signaling pathway.	Pyruvaldehyde	17-20	AKT serine/threonine kinase 1	Homo sapiens	82-85
32467587-9	2020	We observed that MGO-induced autophagic cell death and inhibited the ROS-mediated Akt/mTOR signaling pathway.	Pyruvaldehyde	17-20	mechanistic target of rapamycin kinase	Homo sapiens	86-90
32467587-10	2020	MGO also triggered apoptosis by elevating the cleaved caspase-3 to Bax/Bcl-2 ratio and through activation of the ROS-mediated MAPKs (p-JNK, p-p38, and p-ERK) signaling pathway.	Pyruvaldehyde	0-3	caspase 3	Homo sapiens	54-63
32467587-10	2020	MGO also triggered apoptosis by elevating the cleaved caspase-3 to Bax/Bcl-2 ratio and through activation of the ROS-mediated MAPKs (p-JNK, p-p38, and p-ERK) signaling pathway.	Pyruvaldehyde	0-3	BCL2 associated X, apoptosis regulator	Homo sapiens	67-70
32467587-10	2020	MGO also triggered apoptosis by elevating the cleaved caspase-3 to Bax/Bcl-2 ratio and through activation of the ROS-mediated MAPKs (p-JNK, p-p38, and p-ERK) signaling pathway.	Pyruvaldehyde	0-3	BCL2 apoptosis regulator	Homo sapiens	71-76
32467587-10	2020	MGO also triggered apoptosis by elevating the cleaved caspase-3 to Bax/Bcl-2 ratio and through activation of the ROS-mediated MAPKs (p-JNK, p-p38, and p-ERK) signaling pathway.	Pyruvaldehyde	0-3	mitogen-activated protein kinase 8	Homo sapiens	135-138
32467587-10	2020	MGO also triggered apoptosis by elevating the cleaved caspase-3 to Bax/Bcl-2 ratio and through activation of the ROS-mediated MAPKs (p-JNK, p-p38, and p-ERK) signaling pathway.	Pyruvaldehyde	0-3	mitogen-activated protein kinase 14	Homo sapiens	142-145
32467587-10	2020	MGO also triggered apoptosis by elevating the cleaved caspase-3 to Bax/Bcl-2 ratio and through activation of the ROS-mediated MAPKs (p-JNK, p-p38, and p-ERK) signaling pathway.	Pyruvaldehyde	0-3	mitogen-activated protein kinase 1	Homo sapiens	153-156
32467587-11	2020	Collectively, these findings suggest that autophagy and apoptosis inhibit angiogenesis via the ROS-mediated Akt/mTOR and MAPKs signaling pathways, respectively, when HAoEC are treated with MGO.	Pyruvaldehyde	189-192	AKT serine/threonine kinase 1	Homo sapiens	108-111
32467587-11	2020	Collectively, these findings suggest that autophagy and apoptosis inhibit angiogenesis via the ROS-mediated Akt/mTOR and MAPKs signaling pathways, respectively, when HAoEC are treated with MGO.	Pyruvaldehyde	189-192	mechanistic target of rapamycin kinase	Homo sapiens	112-116
32453778-2	2020	Glyoxalase I (GLYI) and Glyoxalase II (GLYII), the two core enzymes of this pathway work together to neutralize methylglyoxal (MG), a dicarbonyl molecule with detrimental cytotoxicity at higher concentrations.	Pyruvaldehyde	112-125	glyoxalase/bleomycin resistance protein/dioxygenase superfamily protein	Arabidopsis thaliana	0-12
32453778-2	2020	Glyoxalase I (GLYI) and Glyoxalase II (GLYII), the two core enzymes of this pathway work together to neutralize methylglyoxal (MG), a dicarbonyl molecule with detrimental cytotoxicity at higher concentrations.	Pyruvaldehyde	112-125	glyoxalase/bleomycin resistance protein/dioxygenase superfamily protein	Arabidopsis thaliana	14-18
32453778-2	2020	Glyoxalase I (GLYI) and Glyoxalase II (GLYII), the two core enzymes of this pathway work together to neutralize methylglyoxal (MG), a dicarbonyl molecule with detrimental cytotoxicity at higher concentrations.	Pyruvaldehyde	112-125	glyoxalase 2-1	Arabidopsis thaliana	24-37
32453778-2	2020	Glyoxalase I (GLYI) and Glyoxalase II (GLYII), the two core enzymes of this pathway work together to neutralize methylglyoxal (MG), a dicarbonyl molecule with detrimental cytotoxicity at higher concentrations.	Pyruvaldehyde	112-125	glyoxalase 2-1	Arabidopsis thaliana	39-44
32453778-2	2020	Glyoxalase I (GLYI) and Glyoxalase II (GLYII), the two core enzymes of this pathway work together to neutralize methylglyoxal (MG), a dicarbonyl molecule with detrimental cytotoxicity at higher concentrations.	Pyruvaldehyde	127-129	glyoxalase/bleomycin resistance protein/dioxygenase superfamily protein	Arabidopsis thaliana	0-12
32453778-2	2020	Glyoxalase I (GLYI) and Glyoxalase II (GLYII), the two core enzymes of this pathway work together to neutralize methylglyoxal (MG), a dicarbonyl molecule with detrimental cytotoxicity at higher concentrations.	Pyruvaldehyde	127-129	glyoxalase/bleomycin resistance protein/dioxygenase superfamily protein	Arabidopsis thaliana	14-18
32453778-2	2020	Glyoxalase I (GLYI) and Glyoxalase II (GLYII), the two core enzymes of this pathway work together to neutralize methylglyoxal (MG), a dicarbonyl molecule with detrimental cytotoxicity at higher concentrations.	Pyruvaldehyde	127-129	glyoxalase 2-1	Arabidopsis thaliana	24-37
32453778-2	2020	Glyoxalase I (GLYI) and Glyoxalase II (GLYII), the two core enzymes of this pathway work together to neutralize methylglyoxal (MG), a dicarbonyl molecule with detrimental cytotoxicity at higher concentrations.	Pyruvaldehyde	127-129	glyoxalase 2-1	Arabidopsis thaliana	39-44
32453778-3	2020	The first step towards the detoxification of MG is catalyzed by GLYI, a metalloenzyme that requires divalent metal ions (either Zn2+ as seen in eukaryotes or Ni2+ as in prokaryotes).	Pyruvaldehyde	45-47	glyoxalase/bleomycin resistance protein/dioxygenase superfamily protein	Arabidopsis thaliana	64-68
32453778-8	2020	Further, lack in germination of Arabidopsis AtGLYI2 mutants in presence of exogenous MG indicates the direct involvement of Zn2+ dependent GLYI in MG detoxification, suggesting Zn2+ dependent GLYI as the main enzyme responsible for MG detoxification and salinity stress tolerance.	Pyruvaldehyde	85-87	glyoxalase/bleomycin resistance protein/dioxygenase superfamily protein	Arabidopsis thaliana	46-50
32453778-8	2020	Further, lack in germination of Arabidopsis AtGLYI2 mutants in presence of exogenous MG indicates the direct involvement of Zn2+ dependent GLYI in MG detoxification, suggesting Zn2+ dependent GLYI as the main enzyme responsible for MG detoxification and salinity stress tolerance.	Pyruvaldehyde	85-87	glyoxalase/bleomycin resistance protein/dioxygenase superfamily protein	Arabidopsis thaliana	139-143
32453778-8	2020	Further, lack in germination of Arabidopsis AtGLYI2 mutants in presence of exogenous MG indicates the direct involvement of Zn2+ dependent GLYI in MG detoxification, suggesting Zn2+ dependent GLYI as the main enzyme responsible for MG detoxification and salinity stress tolerance.	Pyruvaldehyde	147-149	glyoxalase/bleomycin resistance protein/dioxygenase superfamily protein	Arabidopsis thaliana	139-143
32453778-8	2020	Further, lack in germination of Arabidopsis AtGLYI2 mutants in presence of exogenous MG indicates the direct involvement of Zn2+ dependent GLYI in MG detoxification, suggesting Zn2+ dependent GLYI as the main enzyme responsible for MG detoxification and salinity stress tolerance.	Pyruvaldehyde	147-149	glyoxalase/bleomycin resistance protein/dioxygenase superfamily protein	Arabidopsis thaliana	139-143
32114052-10	2020	In in vitro studies, methylglyoxal (MGO), a precursor of AGEs, significantly increased the expression of inflammatory molecules such as MCP-1 and TNF-alpha in a murine macrophage cell line, RAW264.7.	Pyruvaldehyde	21-34	tumor necrosis factor	Mus musculus	146-155
32114052-10	2020	In in vitro studies, methylglyoxal (MGO), a precursor of AGEs, significantly increased the expression of inflammatory molecules such as MCP-1 and TNF-alpha in a murine macrophage cell line, RAW264.7.	Pyruvaldehyde	36-39	mast cell protease 1	Mus musculus	136-141
32114052-10	2020	In in vitro studies, methylglyoxal (MGO), a precursor of AGEs, significantly increased the expression of inflammatory molecules such as MCP-1 and TNF-alpha in a murine macrophage cell line, RAW264.7.	Pyruvaldehyde	36-39	tumor necrosis factor	Mus musculus	146-155
32259355-6	2020	Upon treating cells with increasing amounts of methylglyoxal, we found that the levels of Hsp27 decreased in a dose-dependent manner.	Pyruvaldehyde	47-60	heat shock protein 2	Mus musculus	90-95
32413970-2	2020	Glyoxalase 1 (GLO1) is a ubiquitous cellular enzyme involved in detoxification of methylglyoxal (MG), a cytotoxic byproduct of glycolysis whose excess can produce oxidative stress.	Pyruvaldehyde	82-95	glyoxalase I	Homo sapiens	0-12
32413970-2	2020	Glyoxalase 1 (GLO1) is a ubiquitous cellular enzyme involved in detoxification of methylglyoxal (MG), a cytotoxic byproduct of glycolysis whose excess can produce oxidative stress.	Pyruvaldehyde	82-95	glyoxalase I	Homo sapiens	14-18
32413970-2	2020	Glyoxalase 1 (GLO1) is a ubiquitous cellular enzyme involved in detoxification of methylglyoxal (MG), a cytotoxic byproduct of glycolysis whose excess can produce oxidative stress.	Pyruvaldehyde	97-99	glyoxalase I	Homo sapiens	0-12
32413970-2	2020	Glyoxalase 1 (GLO1) is a ubiquitous cellular enzyme involved in detoxification of methylglyoxal (MG), a cytotoxic byproduct of glycolysis whose excess can produce oxidative stress.	Pyruvaldehyde	97-99	glyoxalase I	Homo sapiens	14-18
32198181-9	2020	Application of MGO together with bradykinin or prostaglandin E2 resulted in an over-additive effect on iCGRP release, whereas MGO applied at a pH of 5.2 resulted in reduced release, probably due to an MGO-mediated inhibition of TRPV1 receptors.	Pyruvaldehyde	15-18	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	228-233
32147098-9	2020	In conclusion, MGO enhances the production of VEGF and suppresses the production of PDGF-BB, potentially leading to disturbance of angiogenesis in the peritoneal membrane.	Pyruvaldehyde	15-18	vascular endothelial growth factor A	Homo sapiens	46-50
32384625-0	2020	Cyanidin Attenuates Methylglyoxal-Induced Oxidative Stress and Apoptosis in INS-1 Pancreatic beta-Cells by Increasing Glyoxalase-1 Activity.	Pyruvaldehyde	20-33	insulin 1	Rattus norvegicus	76-81
32384625-0	2020	Cyanidin Attenuates Methylglyoxal-Induced Oxidative Stress and Apoptosis in INS-1 Pancreatic beta-Cells by Increasing Glyoxalase-1 Activity.	Pyruvaldehyde	20-33	glyoxalase 1	Rattus norvegicus	118-130
32384625-2	2020	In this study, we investigated the protective effect of cyanidin against MG-induced oxidative stress and apoptosis in rat INS-1 pancreatic beta-cells.	Pyruvaldehyde	73-75	insulin 1	Rattus norvegicus	122-127
32384625-5	2020	In the cotreatment condition, cyanidin (33.3 and 100 muM) also decreased MG-induced apoptosis as determined by caspase-3 activity.	Pyruvaldehyde	73-75	caspase 3	Rattus norvegicus	111-120
32384625-6	2020	Furthermore, INS-1 cells treated with MG increased the generation of reactive oxygen species (ROS) during a 6 h exposure.	Pyruvaldehyde	38-40	insulin 1	Rattus norvegicus	13-18
32384625-8	2020	Furthermore, MG diminished the activity of glyoxalase 1 (Glo-1) and its gene expression as well as the level of total glutathione.	Pyruvaldehyde	13-15	glyoxalase 1	Rattus norvegicus	43-55
32384625-8	2020	Furthermore, MG diminished the activity of glyoxalase 1 (Glo-1) and its gene expression as well as the level of total glutathione.	Pyruvaldehyde	13-15	glyoxalase 1	Rattus norvegicus	57-62
32384625-9	2020	In contrast, cyanidin reversed the inhibitory effect of MG on Glo-1 activity and glutathione levels.	Pyruvaldehyde	56-58	glyoxalase 1	Rattus norvegicus	62-67
32384625-11	2020	These findings suggest that cyanidin exerts a protective effect against MG-induced oxidative stress and apoptosis in pancreatic beta-cells by increasing the activity of Glo-1.	Pyruvaldehyde	72-74	glyoxalase 1	Rattus norvegicus	169-174
32259355-9	2020	Remarkably, increasing the levels of Hsp27 suppressed the deleterious effects induced by MGO.	Pyruvaldehyde	89-92	heat shock protein 2	Mus musculus	37-42
32353034-0	2020	Analyzing structural alterations of mitochondrial intermembrane space superoxide scavengers cytochrome-c and SOD1 after methylglyoxal treatment.	Pyruvaldehyde	120-133	cytochrome c, somatic	Homo sapiens	92-104
32353034-0	2020	Analyzing structural alterations of mitochondrial intermembrane space superoxide scavengers cytochrome-c and SOD1 after methylglyoxal treatment.	Pyruvaldehyde	120-133	superoxide dismutase 1	Homo sapiens	109-113
32353034-8	2020	In this study, we investigated the susceptibility of SOD1 and cytochrome-c to in vitro glycation by the dicarbonyl methylglyoxal (MGO) and the resulting effects on their structure.	Pyruvaldehyde	130-133	superoxide dismutase 1	Homo sapiens	53-57
32353034-8	2020	In this study, we investigated the susceptibility of SOD1 and cytochrome-c to in vitro glycation by the dicarbonyl methylglyoxal (MGO) and the resulting effects on their structure.	Pyruvaldehyde	130-133	cytochrome c, somatic	Homo sapiens	62-74
32353034-12	2020	Subjecting SOD1 to MGO does not influence its secondary structure.	Pyruvaldehyde	19-22	superoxide dismutase 1	Homo sapiens	11-15
32353034-14	2020	Furthermore, the appearance of a second peak in the calorimetry diagram indirectly suggests de-metallation of SOD1 when high MGO levels are used.	Pyruvaldehyde	125-128	superoxide dismutase 1	Homo sapiens	110-114
32233480-0	2020	MG-HCr, the Methylglyoxal-Derived Hydroimidazolone of Creatine, is a Biomarker for the Dietary Intake of Animal Source Food.	Pyruvaldehyde	12-25	coiled-coil alpha-helical rod protein 1	Homo sapiens	3-6
32353034-15	2020	In conclusion, our data demonstrate that MGO has the potential to alter several structural parameters in important proteins of energy metabolism (cytochrome-c) and antioxidant defense (cytochrome-c, SOD1).	Pyruvaldehyde	41-44	cytochrome c, somatic	Homo sapiens	146-158
32353034-15	2020	In conclusion, our data demonstrate that MGO has the potential to alter several structural parameters in important proteins of energy metabolism (cytochrome-c) and antioxidant defense (cytochrome-c, SOD1).	Pyruvaldehyde	41-44	cytochrome c, somatic	Homo sapiens	185-197
32353034-15	2020	In conclusion, our data demonstrate that MGO has the potential to alter several structural parameters in important proteins of energy metabolism (cytochrome-c) and antioxidant defense (cytochrome-c, SOD1).	Pyruvaldehyde	41-44	superoxide dismutase 1	Homo sapiens	199-203
32257229-1	2020	Glyoxalase I (Gly I) is the first enzyme in the glutathionine-dependent glyoxalase pathway for detoxification of methylglyoxal (MG) under stress conditions.	Pyruvaldehyde	113-126	lactoylglutathione lyase	Solanum lycopersicum	0-12
32317986-8	2020	Additionally, MGO exposure induced upregulation of TRPA1 and down-regulation of TRPV1 and TRPV4 in bladder tissues.	Pyruvaldehyde	14-17	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	51-56
32317986-8	2020	Additionally, MGO exposure induced upregulation of TRPA1 and down-regulation of TRPV1 and TRPV4 in bladder tissues.	Pyruvaldehyde	14-17	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	80-85
32317986-8	2020	Additionally, MGO exposure induced upregulation of TRPA1 and down-regulation of TRPV1 and TRPV4 in bladder tissues.	Pyruvaldehyde	14-17	transient receptor potential cation channel, subfamily V, member 4	Mus musculus	90-95
32317986-9	2020	Methylglyoxal did not change the mRNA expression of the advanced glycation end products receptor (RAGE), but markedly increased its downstream NF-kappaB - iNOS signaling.	Pyruvaldehyde	0-13	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	143-152
32317986-9	2020	Methylglyoxal did not change the mRNA expression of the advanced glycation end products receptor (RAGE), but markedly increased its downstream NF-kappaB - iNOS signaling.	Pyruvaldehyde	0-13	nitric oxide synthase 2, inducible	Mus musculus	155-159
32317986-11	2020	Altogether, our data show that 4-week MGO intake in mice produces an overactive bladder phenotype in addition to bladder inflammation and increased NF-kB/iNOS signaling.	Pyruvaldehyde	38-41	nitric oxide synthase 2, inducible	Mus musculus	154-158
32317986-12	2020	TRPA1 up-regulation and TRPV1/TRPV4 down-regulation may account for the MGO-induced bladder overactivity.	Pyruvaldehyde	72-75	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	0-5
32317986-12	2020	TRPA1 up-regulation and TRPV1/TRPV4 down-regulation may account for the MGO-induced bladder overactivity.	Pyruvaldehyde	72-75	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	24-29
32317986-12	2020	TRPA1 up-regulation and TRPV1/TRPV4 down-regulation may account for the MGO-induced bladder overactivity.	Pyruvaldehyde	72-75	transient receptor potential cation channel, subfamily V, member 4	Mus musculus	30-35
32332750-3	2020	Here, we show that methylglyoxal, a glycolytic intermediate metabolite, modulates Notch signalling to regulate NPC fate decision.	Pyruvaldehyde	19-32	notch receptor 1	Homo sapiens	82-87
32332750-5	2020	Interestingly, methylglyoxal inhibits the enzymatic activity of GAPDH and engages it as an RNA-binding protein to suppress Notch1 translation.	Pyruvaldehyde	15-28	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	64-69
32332750-5	2020	Interestingly, methylglyoxal inhibits the enzymatic activity of GAPDH and engages it as an RNA-binding protein to suppress Notch1 translation.	Pyruvaldehyde	15-28	notch receptor 1	Homo sapiens	123-129
32332750-6	2020	Reducing GAPDH levels or restoring Notch signalling rescues methylglyoxal-induced NPC depletion and premature differentiation in the developing mouse cortex.	Pyruvaldehyde	60-73	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	9-14
32332750-6	2020	Reducing GAPDH levels or restoring Notch signalling rescues methylglyoxal-induced NPC depletion and premature differentiation in the developing mouse cortex.	Pyruvaldehyde	60-73	notch receptor 1	Homo sapiens	35-40
31939094-0	2020	Inhibition of thioredoxin 2 by intracellular methylglyoxal accumulation leads to mitochondrial dysfunction and apoptosis in INS-1 cells.	Pyruvaldehyde	45-58	thioredoxin 2	Rattus norvegicus	14-27
31939094-0	2020	Inhibition of thioredoxin 2 by intracellular methylglyoxal accumulation leads to mitochondrial dysfunction and apoptosis in INS-1 cells.	Pyruvaldehyde	45-58	insulin 1	Rattus norvegicus	124-129
31939094-1	2020	PURPOSE: To investigate the role of thioredoxin 2 (Trx2) inhibition induced by intracellular methylglyoxal (MGO) in pancreatic beta-cell mitochondrial dysfunction and apoptosis.	Pyruvaldehyde	93-106	thioredoxin 2	Rattus norvegicus	36-49
31939094-1	2020	PURPOSE: To investigate the role of thioredoxin 2 (Trx2) inhibition induced by intracellular methylglyoxal (MGO) in pancreatic beta-cell mitochondrial dysfunction and apoptosis.	Pyruvaldehyde	93-106	thioredoxin 2	Rattus norvegicus	51-55
31939094-1	2020	PURPOSE: To investigate the role of thioredoxin 2 (Trx2) inhibition induced by intracellular methylglyoxal (MGO) in pancreatic beta-cell mitochondrial dysfunction and apoptosis.	Pyruvaldehyde	108-111	thioredoxin 2	Rattus norvegicus	36-49
31939094-1	2020	PURPOSE: To investigate the role of thioredoxin 2 (Trx2) inhibition induced by intracellular methylglyoxal (MGO) in pancreatic beta-cell mitochondrial dysfunction and apoptosis.	Pyruvaldehyde	108-111	thioredoxin 2	Rattus norvegicus	51-55
31939094-2	2020	METHODS: Rat pancreatic beta-cell line INS-1 cells were treated with Glo1 siRNAs or exogenous MGO to increase intracellular MGO.	Pyruvaldehyde	94-97	insulin 1	Rattus norvegicus	39-44
31939094-2	2020	METHODS: Rat pancreatic beta-cell line INS-1 cells were treated with Glo1 siRNAs or exogenous MGO to increase intracellular MGO.	Pyruvaldehyde	124-127	glyoxalase 1	Rattus norvegicus	69-73
31939094-6	2020	RESULTS: The increase of intracellular MGO by Glo1 blockage or MGO treatment led to advanced glycation end products (AGEs) overproduction, mitochondrial ROS increase, and insulin secretion paralysis.	Pyruvaldehyde	39-42	glyoxalase 1	Rattus norvegicus	46-50
31939094-7	2020	These were probably due to MGO-induced inhibition of mitochondrial Trx2.	Pyruvaldehyde	27-30	thioredoxin 2	Rattus norvegicus	67-71
31939094-8	2020	Trx2 inhibition by blockage of either Glo1 or Trx2 impaired mitochondrial integrity, inhibited cytochrome C oxidases subunit 1 and 4 (Cox1 and Cox4) expression and further reduced ATP generation, and all of these might lead to insulin paralysis; whereas Trx2 overexpression partially reversed MGO-induced oxidative stress, attenuated insulin secretion by preventing mitochondrial damage.	Pyruvaldehyde	293-296	thioredoxin 2	Rattus norvegicus	0-4
31939094-8	2020	Trx2 inhibition by blockage of either Glo1 or Trx2 impaired mitochondrial integrity, inhibited cytochrome C oxidases subunit 1 and 4 (Cox1 and Cox4) expression and further reduced ATP generation, and all of these might lead to insulin paralysis; whereas Trx2 overexpression partially reversed MGO-induced oxidative stress, attenuated insulin secretion by preventing mitochondrial damage.	Pyruvaldehyde	293-296	glyoxalase 1	Rattus norvegicus	38-42
31939094-9	2020	Trx2 overexpression also retarded MGO-induced apoptosis of INS-1 cell through inhibiting ASK1 activation and downregulation of the ASK1-p38 MAPK pathway.	Pyruvaldehyde	34-37	thioredoxin 2	Rattus norvegicus	0-4
31939094-9	2020	Trx2 overexpression also retarded MGO-induced apoptosis of INS-1 cell through inhibiting ASK1 activation and downregulation of the ASK1-p38 MAPK pathway.	Pyruvaldehyde	34-37	insulin 1	Rattus norvegicus	59-64
31939094-9	2020	Trx2 overexpression also retarded MGO-induced apoptosis of INS-1 cell through inhibiting ASK1 activation and downregulation of the ASK1-p38 MAPK pathway.	Pyruvaldehyde	34-37	mitogen-activated protein kinase kinase kinase 5	Rattus norvegicus	89-93
31939094-9	2020	Trx2 overexpression also retarded MGO-induced apoptosis of INS-1 cell through inhibiting ASK1 activation and downregulation of the ASK1-p38 MAPK pathway.	Pyruvaldehyde	34-37	mitogen-activated protein kinase kinase kinase 5	Rattus norvegicus	131-135
31939094-10	2020	CONCLUSIONS: Our results reveal a possible mechanism for beta-cell oxidative damage upon intracellular MGO-induced Trx2 inactivation and mitochondrial dysfunction and apoptosis.	Pyruvaldehyde	103-106	thioredoxin 2	Rattus norvegicus	115-119
32007798-3	2020	This study aimed to evaluate the effects of long-term oral intake of MGO on ovalbumin-induced eosinophil inflammation.	Pyruvaldehyde	69-72	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	76-85
32007798-6	2020	In MGO-treated mice, OVA challenge significantly increased the peribronchiolar infiltrations of inflammatory cells and eosinophils compared with control group.	Pyruvaldehyde	3-6	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	21-24
32007798-7	2020	Higher levels of IL-4, IL-5, and eotaxin in BAL fluid were also detected in MGO compared with control group.	Pyruvaldehyde	76-79	interleukin 4	Mus musculus	17-21
32007798-7	2020	Higher levels of IL-4, IL-5, and eotaxin in BAL fluid were also detected in MGO compared with control group.	Pyruvaldehyde	76-79	interleukin 5	Mus musculus	23-27
32257229-1	2020	Glyoxalase I (Gly I) is the first enzyme in the glutathionine-dependent glyoxalase pathway for detoxification of methylglyoxal (MG) under stress conditions.	Pyruvaldehyde	128-130	lactoylglutathione lyase	Solanum lycopersicum	0-12
32914122-0	2020	Monitoring of methylglyoxal/indole interaction by ATR-FTIR spectroscopy and qTOF/MS/MS analysis.	Pyruvaldehyde	14-27	ATR serine/threonine kinase	Homo sapiens	50-53
32007798-7	2020	Higher levels of IL-4, IL-5, and eotaxin in BAL fluid were also detected in MGO compared with control group.	Pyruvaldehyde	76-79	chemokine (C-C motif) ligand 11	Mus musculus	33-40
32007798-8	2020	In addition, lung tissue of MGO-treated mice displayed significant increases in mRNA expressions of NF-kappaB and iNOS whereas COX-2 expression remained unchanged.	Pyruvaldehyde	28-31	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	100-109
32007798-8	2020	In addition, lung tissue of MGO-treated mice displayed significant increases in mRNA expressions of NF-kappaB and iNOS whereas COX-2 expression remained unchanged.	Pyruvaldehyde	28-31	nitric oxide synthase 2, inducible	Mus musculus	114-118
32007798-8	2020	In addition, lung tissue of MGO-treated mice displayed significant increases in mRNA expressions of NF-kappaB and iNOS whereas COX-2 expression remained unchanged.	Pyruvaldehyde	28-31	cytochrome c oxidase II, mitochondrial	Mus musculus	127-132
32007798-10	2020	In MGO group, OVA-challenge increased significantly the NOX-2 and NOX-4 mRNA expressions, without affecting the NOX-1 expression.	Pyruvaldehyde	3-6	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	14-17
32007798-10	2020	In MGO group, OVA-challenge increased significantly the NOX-2 and NOX-4 mRNA expressions, without affecting the NOX-1 expression.	Pyruvaldehyde	3-6	cytochrome b-245, beta polypeptide	Mus musculus	56-61
32007798-10	2020	In MGO group, OVA-challenge increased significantly the NOX-2 and NOX-4 mRNA expressions, without affecting the NOX-1 expression.	Pyruvaldehyde	3-6	NADPH oxidase 4	Mus musculus	66-71
32007798-12	2020	In conclusion, 12-week intake of MGO exacerbates Th2-mediated airway eosinophil infiltration by activation of NF-kB/iNOS-dependent signaling pathway and positive regulation of NOX-2 and NOX-4 in the lung tissues.	Pyruvaldehyde	33-36	heart and neural crest derivatives expressed 2	Mus musculus	49-52
32007798-12	2020	In conclusion, 12-week intake of MGO exacerbates Th2-mediated airway eosinophil infiltration by activation of NF-kB/iNOS-dependent signaling pathway and positive regulation of NOX-2 and NOX-4 in the lung tissues.	Pyruvaldehyde	33-36	nitric oxide synthase 2, inducible	Mus musculus	116-120
32007798-12	2020	In conclusion, 12-week intake of MGO exacerbates Th2-mediated airway eosinophil infiltration by activation of NF-kB/iNOS-dependent signaling pathway and positive regulation of NOX-2 and NOX-4 in the lung tissues.	Pyruvaldehyde	33-36	cytochrome b-245, beta polypeptide	Mus musculus	176-181
32007798-12	2020	In conclusion, 12-week intake of MGO exacerbates Th2-mediated airway eosinophil infiltration by activation of NF-kB/iNOS-dependent signaling pathway and positive regulation of NOX-2 and NOX-4 in the lung tissues.	Pyruvaldehyde	33-36	NADPH oxidase 4	Mus musculus	186-191
31953836-5	2020	Methylglyoxal was the major alpha-DC affected during storage, its relative content decreasing from 233.71 to 44.12 mug mL-1 in the glucose-lysine system.	Pyruvaldehyde	0-13	L1 cell adhesion molecule	Mus musculus	119-123
32114742-0	2020	miR-450a-5p Eliminates MGO-Induced Insulin Resistance via Targeting CREB.	Pyruvaldehyde	23-26	insulin	Homo sapiens	35-42
32114742-0	2020	miR-450a-5p Eliminates MGO-Induced Insulin Resistance via Targeting CREB.	Pyruvaldehyde	23-26	cAMP responsive element binding protein 1	Homo sapiens	68-72
32114742-10	2020	Moreover, MGO inhibited eNOS/AKT pathway activation and NO release mediated by insulin, and such effects were reversed by up-regulation of miR-450a-5p.	Pyruvaldehyde	10-13	AKT serine/threonine kinase 1	Homo sapiens	29-32
32114742-10	2020	Moreover, MGO inhibited eNOS/AKT pathway activation and NO release mediated by insulin, and such effects were reversed by up-regulation of miR-450a-5p.	Pyruvaldehyde	10-13	insulin	Homo sapiens	79-86
32114742-12	2020	Conclusions: Up-regulated miR-450a-5p eliminates MGO-induced insulin resistance via targeting CREB, and therefore could be used as a potential target to improve insulin resistance and treat patients with diabetes-related diseases.	Pyruvaldehyde	49-52	insulin	Homo sapiens	61-68
32114742-12	2020	Conclusions: Up-regulated miR-450a-5p eliminates MGO-induced insulin resistance via targeting CREB, and therefore could be used as a potential target to improve insulin resistance and treat patients with diabetes-related diseases.	Pyruvaldehyde	49-52	cAMP responsive element binding protein 1	Homo sapiens	94-98
32114742-12	2020	Conclusions: Up-regulated miR-450a-5p eliminates MGO-induced insulin resistance via targeting CREB, and therefore could be used as a potential target to improve insulin resistance and treat patients with diabetes-related diseases.	Pyruvaldehyde	49-52	insulin	Homo sapiens	161-168
32914122-4	2020	In this study, the trapping of methylglyoxal by indole was monitored at various temperatures either by (a) ATR-FTIR spectroscopy or (b) in-solution using qTOF/MS/MS analysis.	Pyruvaldehyde	31-44	ATR serine/threonine kinase	Homo sapiens	107-110
32011880-1	2020	Glyoxalase I (GlxI) is a member of the glyoxalase system, which is important in cell detoxification and converts hemithioacetals of methylglyoxal (a cytotoxic byproduct of sugar metabolism that may react with DNA or proteins and introduce nucleic acid strand breaks, elevated mutation frequencies, and structural or functional changes of the proteins) and glutathione into d-lactate.	Pyruvaldehyde	132-145	glyoxalase I	Homo sapiens	0-12
32011880-1	2020	Glyoxalase I (GlxI) is a member of the glyoxalase system, which is important in cell detoxification and converts hemithioacetals of methylglyoxal (a cytotoxic byproduct of sugar metabolism that may react with DNA or proteins and introduce nucleic acid strand breaks, elevated mutation frequencies, and structural or functional changes of the proteins) and glutathione into d-lactate.	Pyruvaldehyde	132-145	glyoxalase I	Homo sapiens	14-18
31879183-1	2020	Glyoxalase I (GLO1) is a homodimeric Zn2+-metalloenzyme that catalyses the transformation of methylglyoxal (MG) to d-lacate through the intermediate S-d-lactoylglutathione.	Pyruvaldehyde	93-106	glyoxalase I	Homo sapiens	0-12
31879183-1	2020	Glyoxalase I (GLO1) is a homodimeric Zn2+-metalloenzyme that catalyses the transformation of methylglyoxal (MG) to d-lacate through the intermediate S-d-lactoylglutathione.	Pyruvaldehyde	93-106	glyoxalase I	Homo sapiens	14-18
31879183-1	2020	Glyoxalase I (GLO1) is a homodimeric Zn2+-metalloenzyme that catalyses the transformation of methylglyoxal (MG) to d-lacate through the intermediate S-d-lactoylglutathione.	Pyruvaldehyde	108-110	glyoxalase I	Homo sapiens	0-12
31879183-1	2020	Glyoxalase I (GLO1) is a homodimeric Zn2+-metalloenzyme that catalyses the transformation of methylglyoxal (MG) to d-lacate through the intermediate S-d-lactoylglutathione.	Pyruvaldehyde	108-110	glyoxalase I	Homo sapiens	14-18
31608441-7	2020	We found that T1-IFNs were able to boost interferon-gamma and granzyme B production in 5-amino-6-d-ribitylaminouracil/methylglyoxal-stimulated MAIT cells.	Pyruvaldehyde	118-131	interferon gamma	Homo sapiens	41-57
31909963-2	2020	Through sequential reactions, reduced glutathione (GSH), glyoxalase I (glo-1), and glyoxalase II (glo-2) convert MG into D-lactate.	Pyruvaldehyde	113-115	glyoxalase 1	Mus musculus	57-69
31909963-2	2020	Through sequential reactions, reduced glutathione (GSH), glyoxalase I (glo-1), and glyoxalase II (glo-2) convert MG into D-lactate.	Pyruvaldehyde	113-115	glyoxalase 1	Mus musculus	71-76
31909963-2	2020	Through sequential reactions, reduced glutathione (GSH), glyoxalase I (glo-1), and glyoxalase II (glo-2) convert MG into D-lactate.	Pyruvaldehyde	113-115	hydroxyacyl glutathione hydrolase	Mus musculus	83-96
31909963-2	2020	Through sequential reactions, reduced glutathione (GSH), glyoxalase I (glo-1), and glyoxalase II (glo-2) convert MG into D-lactate.	Pyruvaldehyde	113-115	hydroxyacyl glutathione hydrolase	Mus musculus	98-103
32023458-0	2020	Methylglyoxal Scavengers Resensitize KRAS-Mutated Colorectal Tumors to Cetuximab.	Pyruvaldehyde	0-13	KRAS proto-oncogene, GTPase	Homo sapiens	37-41
32023458-5	2020	Mutant KRAS cells under MGO stress show AKT-dependent survival when compared with wild-type KRAS isogenic CRC cells.	Pyruvaldehyde	24-27	KRAS proto-oncogene, GTPase	Homo sapiens	7-11
32023458-5	2020	Mutant KRAS cells under MGO stress show AKT-dependent survival when compared with wild-type KRAS isogenic CRC cells.	Pyruvaldehyde	24-27	AKT serine/threonine kinase 1	Homo sapiens	40-43
32023458-6	2020	MGO induces AKT activation through phosphatidylinositol 3-kinase (PI3K)/mammalian target of rapamycin 2 (mTORC2) and Hsp27 regulation.	Pyruvaldehyde	0-3	AKT serine/threonine kinase 1	Homo sapiens	12-15
32023458-6	2020	MGO induces AKT activation through phosphatidylinositol 3-kinase (PI3K)/mammalian target of rapamycin 2 (mTORC2) and Hsp27 regulation.	Pyruvaldehyde	0-3	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	35-64
32023458-6	2020	MGO induces AKT activation through phosphatidylinositol 3-kinase (PI3K)/mammalian target of rapamycin 2 (mTORC2) and Hsp27 regulation.	Pyruvaldehyde	0-3	CREB regulated transcription coactivator 2	Mus musculus	105-111
32023458-6	2020	MGO induces AKT activation through phosphatidylinositol 3-kinase (PI3K)/mammalian target of rapamycin 2 (mTORC2) and Hsp27 regulation.	Pyruvaldehyde	0-3	heat shock protein family B (small) member 1	Homo sapiens	117-122
32023458-7	2020	Importantly, the sole induction of MGO stress in sensitive wild-type KRAS cells renders them resistant to cetuximab.	Pyruvaldehyde	35-38	KRAS proto-oncogene, GTPase	Homo sapiens	69-73
32023458-8	2020	MGO scavengers inhibit AKT and resensitize KRAS-mutated CRC cells to cetuximab in vivo.	Pyruvaldehyde	0-3	AKT serine/threonine kinase 1	Homo sapiens	23-26
32023458-8	2020	MGO scavengers inhibit AKT and resensitize KRAS-mutated CRC cells to cetuximab in vivo.	Pyruvaldehyde	0-3	KRAS proto-oncogene, GTPase	Homo sapiens	43-47
32023458-9	2020	This study establishes a link between MGO and AKT activation and pinpoints this oncometabolite as a potential target to tackle EGFR-targeted therapy resistance in CRC.	Pyruvaldehyde	38-41	AKT serine/threonine kinase 1	Homo sapiens	46-49
32023458-9	2020	This study establishes a link between MGO and AKT activation and pinpoints this oncometabolite as a potential target to tackle EGFR-targeted therapy resistance in CRC.	Pyruvaldehyde	38-41	epidermal growth factor receptor	Homo sapiens	127-131
31608441-7	2020	We found that T1-IFNs were able to boost interferon-gamma and granzyme B production in 5-amino-6-d-ribitylaminouracil/methylglyoxal-stimulated MAIT cells.	Pyruvaldehyde	118-131	granzyme B	Homo sapiens	62-72
31931282-0	2020	Methylglyoxal interaction with superoxide dismutase 1.	Pyruvaldehyde	0-13	superoxide dismutase 1	Homo sapiens	31-53
31786717-8	2020	An interesting finding was a marked decrease in dopamine levels in the prefrontal cortex of mice treated with 50 mg/kg MGO for 11 days, along with a ~ 25% decrease in the Glo1 content.	Pyruvaldehyde	119-122	glyoxalase 1	Mus musculus	171-175
31899224-11	2020	Furthermore, PCr pretreatment significantly decreased p-ERK expression of MGO-induced injury in NRK-52E cells transfected with p-ERK cDNA.	Pyruvaldehyde	74-77	Eph receptor B1	Rattus norvegicus	56-59
31899224-11	2020	Furthermore, PCr pretreatment significantly decreased p-ERK expression of MGO-induced injury in NRK-52E cells transfected with p-ERK cDNA.	Pyruvaldehyde	74-77	Eph receptor B1	Rattus norvegicus	129-132
31931282-4	2020	Among the proteins affected by glycation, MG has been found to react with superoxide dismutase 1 (SOD1), a fundamental anti-oxidant enzyme that is abundantly expressed in neurons.	Pyruvaldehyde	42-44	superoxide dismutase 1	Homo sapiens	74-96
31931282-4	2020	Among the proteins affected by glycation, MG has been found to react with superoxide dismutase 1 (SOD1), a fundamental anti-oxidant enzyme that is abundantly expressed in neurons.	Pyruvaldehyde	42-44	superoxide dismutase 1	Homo sapiens	98-102
31931282-5	2020	Considering the high neuronal susceptibility to MG-induced oxidative stress, we sought to investigate by mass spectrometry and NMR spectroscopy which are the structural modifications induced on SOD1 by the reaction with MG.	Pyruvaldehyde	48-50	superoxide dismutase 1	Homo sapiens	194-198
31931282-5	2020	Considering the high neuronal susceptibility to MG-induced oxidative stress, we sought to investigate by mass spectrometry and NMR spectroscopy which are the structural modifications induced on SOD1 by the reaction with MG.	Pyruvaldehyde	220-222	superoxide dismutase 1	Homo sapiens	194-198
31931282-6	2020	We show that MG reacts preferentially with the disulfide-reduced, demetallated form of SOD1, gradually causing its unfolding, and to a lesser extent, with the intermediate state of maturation - the reduced, zinc-bound homodimer - causing its gradual monomerization.	Pyruvaldehyde	13-15	superoxide dismutase 1	Homo sapiens	87-91
31931282-7	2020	These results suggest that MG could impair the correct maturation of SOD1 in vivo, thus both increasing cellular oxidative stress and promoting the cytotoxic misfolding and aggregation process of SOD1.	Pyruvaldehyde	27-29	superoxide dismutase 1	Homo sapiens	69-73
31931282-7	2020	These results suggest that MG could impair the correct maturation of SOD1 in vivo, thus both increasing cellular oxidative stress and promoting the cytotoxic misfolding and aggregation process of SOD1.	Pyruvaldehyde	27-29	superoxide dismutase 1	Homo sapiens	196-200
31968011-11	2020	The renal protective mechanism might be associated with down-regulation of GLO1 via reducing the contents of methylglyoxal derived from glycolysis.	Pyruvaldehyde	109-122	glyoxalase 1	Mus musculus	75-79
31905169-6	2020	Advanced glycation end products formation, receptor for AGE (RAGE) protein expression, and its downstream inflammatory cytokines and fibrotic factors in kidney tissue, were significantly suppressed in the DPP4-def-STZ compared to the WT-STZ with increasing glyoxalase-1 (GLO-1) expression responsible for the detoxification of methylglyoxal (MGO).	Pyruvaldehyde	327-340	dipeptidylpeptidase 4	Rattus norvegicus	205-209
31947651-8	2020	Overall, present findings demonstrate that MG-dependent glycative stress is involved in ovarian dysfunctions associated to PCOS and support the hypothesis of a SIRT1-dependent adaptive response.	Pyruvaldehyde	43-45	sirtuin 1	Mus musculus	160-165
31905169-6	2020	Advanced glycation end products formation, receptor for AGE (RAGE) protein expression, and its downstream inflammatory cytokines and fibrotic factors in kidney tissue, were significantly suppressed in the DPP4-def-STZ compared to the WT-STZ with increasing glyoxalase-1 (GLO-1) expression responsible for the detoxification of methylglyoxal (MGO).	Pyruvaldehyde	342-345	dipeptidylpeptidase 4	Rattus norvegicus	205-209
31905169-7	2020	In vitro, exendin-4 suppressed MGO-induced AGEs production by enhancing the expression of GLO-1 and nuclear factor-erythroid 2 p45 subunit-related factor 2, resulting in decreasing pro-inflammatory cytokine levels.	Pyruvaldehyde	31-34	glyoxalase 1	Rattus norvegicus	90-155
33350989-4	2020	Here, we investigated the role of RAGE on the memory impairment induced by MGO.	Pyruvaldehyde	75-78	advanced glycosylation end product-specific receptor	Mus musculus	34-38
33350989-9	2020	Since the addition of RAGE antagonist in co-treatment with MGO protected mice from the aversive and working memory deficits, AGEs generated by the MGO treatment would be involved in the memory impairment due to RAGE activation.	Pyruvaldehyde	59-62	advanced glycosylation end product-specific receptor	Mus musculus	22-26
33350989-9	2020	Since the addition of RAGE antagonist in co-treatment with MGO protected mice from the aversive and working memory deficits, AGEs generated by the MGO treatment would be involved in the memory impairment due to RAGE activation.	Pyruvaldehyde	147-150	advanced glycosylation end product-specific receptor	Mus musculus	22-26
33350989-9	2020	Since the addition of RAGE antagonist in co-treatment with MGO protected mice from the aversive and working memory deficits, AGEs generated by the MGO treatment would be involved in the memory impairment due to RAGE activation.	Pyruvaldehyde	147-150	advanced glycosylation end product-specific receptor	Mus musculus	211-215
33350989-10	2020	Therefore, further studies are required to establish the involvement of RAGE in the MGO-induced memory impairment.	Pyruvaldehyde	84-87	advanced glycosylation end product-specific receptor	Mus musculus	72-76
31526867-4	2020	Pro-inflammatory ligands of RAGE are also methylglyoxal-derived advanced glycation end-products, which depend in their quantity, at least in part, on the activity of the methylglyoxal-detoxifying enzyme glyoxalase-1 (Glo1).	Pyruvaldehyde	42-55	advanced glycosylation end product-specific receptor	Mus musculus	28-32
31526867-4	2020	Pro-inflammatory ligands of RAGE are also methylglyoxal-derived advanced glycation end-products, which depend in their quantity, at least in part, on the activity of the methylglyoxal-detoxifying enzyme glyoxalase-1 (Glo1).	Pyruvaldehyde	42-55	glyoxalase 1	Mus musculus	203-215
32368974-7	2020	Glyoxalase-1 (GLO-1) acts as a part of the anti-glycation defense system by carrying out detoxification of GO and MGO.	Pyruvaldehyde	114-117	glyoxalase I	Homo sapiens	0-12
31526867-4	2020	Pro-inflammatory ligands of RAGE are also methylglyoxal-derived advanced glycation end-products, which depend in their quantity, at least in part, on the activity of the methylglyoxal-detoxifying enzyme glyoxalase-1 (Glo1).	Pyruvaldehyde	42-55	glyoxalase 1	Mus musculus	217-221
31244422-3	2020	OBJECTIVE: This comparative study focuses on methylglyoxal induced glycoxidative damage suffered by immunoglobulin G (IgG) and fibrinogen, and to unveil implication of structural modification of serum proteins in diabetes associated secondary complications.	Pyruvaldehyde	45-58	fibrinogen beta chain	Homo sapiens	127-137
32368974-7	2020	Glyoxalase-1 (GLO-1) acts as a part of the anti-glycation defense system by carrying out detoxification of GO and MGO.	Pyruvaldehyde	114-117	glyoxalase I	Homo sapiens	14-19
31678323-3	2020	Interestingly, we noticed that hyperosmotic (NaCl) and carbonyl (methylglyoxal, MGO) stresses in HT22 neuronal cells produced a rapid loss of TXNIP (half-life ~12 min), prompting us to search for possible mechanisms controlling this TXNIP loss, including pH change, serum deprivation, calcium metabolism and inhibition of the proteasome and other proteases, autophagy and MAPKs.	Pyruvaldehyde	65-83	thioredoxin interacting protein	Mus musculus	142-147
32524572-1	2020	Glyoxalase 1 (Glo1) is a glutathione (GSH)-dependent enzyme that catalyzes the isomerization of the hemithioacetal formed non-enzymatically from methylglyoxal (MG) and GSH to S-D-lactoylglutathione (SLG).	Pyruvaldehyde	145-158	glyoxalase I	Homo sapiens	0-12
32524572-1	2020	Glyoxalase 1 (Glo1) is a glutathione (GSH)-dependent enzyme that catalyzes the isomerization of the hemithioacetal formed non-enzymatically from methylglyoxal (MG) and GSH to S-D-lactoylglutathione (SLG).	Pyruvaldehyde	145-158	glyoxalase I	Homo sapiens	14-18
32524572-1	2020	Glyoxalase 1 (Glo1) is a glutathione (GSH)-dependent enzyme that catalyzes the isomerization of the hemithioacetal formed non-enzymatically from methylglyoxal (MG) and GSH to S-D-lactoylglutathione (SLG).	Pyruvaldehyde	145-158	sialic acid binding Ig like lectin 12	Homo sapiens	199-202
32524572-1	2020	Glyoxalase 1 (Glo1) is a glutathione (GSH)-dependent enzyme that catalyzes the isomerization of the hemithioacetal formed non-enzymatically from methylglyoxal (MG) and GSH to S-D-lactoylglutathione (SLG).	Pyruvaldehyde	160-162	glyoxalase I	Homo sapiens	0-12
32524572-1	2020	Glyoxalase 1 (Glo1) is a glutathione (GSH)-dependent enzyme that catalyzes the isomerization of the hemithioacetal formed non-enzymatically from methylglyoxal (MG) and GSH to S-D-lactoylglutathione (SLG).	Pyruvaldehyde	160-162	glyoxalase I	Homo sapiens	14-18
32524572-1	2020	Glyoxalase 1 (Glo1) is a glutathione (GSH)-dependent enzyme that catalyzes the isomerization of the hemithioacetal formed non-enzymatically from methylglyoxal (MG) and GSH to S-D-lactoylglutathione (SLG).	Pyruvaldehyde	160-162	sialic acid binding Ig like lectin 12	Homo sapiens	199-202
31678323-3	2020	Interestingly, we noticed that hyperosmotic (NaCl) and carbonyl (methylglyoxal, MGO) stresses in HT22 neuronal cells produced a rapid loss of TXNIP (half-life ~12 min), prompting us to search for possible mechanisms controlling this TXNIP loss, including pH change, serum deprivation, calcium metabolism and inhibition of the proteasome and other proteases, autophagy and MAPKs.	Pyruvaldehyde	65-83	thioredoxin interacting protein	Mus musculus	233-238
31629029-0	2019	Ginsenoside Rb1 mitigates oxidative stress and apoptosis induced by methylglyoxal in SH-SY5Y cells via the PI3K/Akt pathway.	Pyruvaldehyde	68-81	RB transcriptional corepressor 1	Homo sapiens	12-15
31794195-0	2019	Imaging Tumorous Methylglyoxal by an Activatable Near-Infrared Fluorescent Probe for Monitoring Glyoxalase 1 Activity.	Pyruvaldehyde	17-30	glyoxalase I	Homo sapiens	96-108
31794195-1	2019	The accurate detection of tumorous methylglyoxal (MGO) and its detoxifier glyoxalase 1 (GLO1) in living systems is critical for understanding their roles in tumor initiation and progression.	Pyruvaldehyde	35-48	glyoxalase I	Homo sapiens	74-86
31794195-1	2019	The accurate detection of tumorous methylglyoxal (MGO) and its detoxifier glyoxalase 1 (GLO1) in living systems is critical for understanding their roles in tumor initiation and progression.	Pyruvaldehyde	35-48	glyoxalase I	Homo sapiens	88-92
31811113-4	2019	RESULTS Cells predisposed to MG demonstrated an increase in oxidative stress with augmented (P&lt;0.01) inflammatory cytokines such as cyclooxygenase (COX)-2, chemokine receptor CXCR4, interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule 1 (ICAM-1) genes.	Pyruvaldehyde	29-31	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	135-157
31811113-4	2019	RESULTS Cells predisposed to MG demonstrated an increase in oxidative stress with augmented (P&lt;0.01) inflammatory cytokines such as cyclooxygenase (COX)-2, chemokine receptor CXCR4, interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule 1 (ICAM-1) genes.	Pyruvaldehyde	29-31	C-X-C motif chemokine receptor 4	Homo sapiens	178-183
31811113-4	2019	RESULTS Cells predisposed to MG demonstrated an increase in oxidative stress with augmented (P&lt;0.01) inflammatory cytokines such as cyclooxygenase (COX)-2, chemokine receptor CXCR4, interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule 1 (ICAM-1) genes.	Pyruvaldehyde	29-31	interleukin 6	Homo sapiens	185-203
31811113-4	2019	RESULTS Cells predisposed to MG demonstrated an increase in oxidative stress with augmented (P&lt;0.01) inflammatory cytokines such as cyclooxygenase (COX)-2, chemokine receptor CXCR4, interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule 1 (ICAM-1) genes.	Pyruvaldehyde	29-31	C-X-C motif chemokine ligand 8	Homo sapiens	205-209
31811113-4	2019	RESULTS Cells predisposed to MG demonstrated an increase in oxidative stress with augmented (P&lt;0.01) inflammatory cytokines such as cyclooxygenase (COX)-2, chemokine receptor CXCR4, interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule 1 (ICAM-1) genes.	Pyruvaldehyde	29-31	C-C motif chemokine ligand 2	Homo sapiens	211-245
31811113-4	2019	RESULTS Cells predisposed to MG demonstrated an increase in oxidative stress with augmented (P&lt;0.01) inflammatory cytokines such as cyclooxygenase (COX)-2, chemokine receptor CXCR4, interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule 1 (ICAM-1) genes.	Pyruvaldehyde	29-31	C-C motif chemokine ligand 2	Homo sapiens	247-252
31811113-4	2019	RESULTS Cells predisposed to MG demonstrated an increase in oxidative stress with augmented (P&lt;0.01) inflammatory cytokines such as cyclooxygenase (COX)-2, chemokine receptor CXCR4, interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule 1 (ICAM-1) genes.	Pyruvaldehyde	29-31	intercellular adhesion molecule 1	Homo sapiens	259-292
31811113-4	2019	RESULTS Cells predisposed to MG demonstrated an increase in oxidative stress with augmented (P&lt;0.01) inflammatory cytokines such as cyclooxygenase (COX)-2, chemokine receptor CXCR4, interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule 1 (ICAM-1) genes.	Pyruvaldehyde	29-31	intercellular adhesion molecule 1	Homo sapiens	294-300
31811113-5	2019	In addition, the expression of aldose reductase (AR) was increased to 2-fold with accumulated sorbitol in MG exposed cells compared to control.	Pyruvaldehyde	106-108	aldo-keto reductase family 1 member B	Homo sapiens	31-47
31811113-5	2019	In addition, the expression of aldose reductase (AR) was increased to 2-fold with accumulated sorbitol in MG exposed cells compared to control.	Pyruvaldehyde	106-108	aldo-keto reductase family 1 member B	Homo sapiens	49-51
31811113-6	2019	On the other hand, cells exposed to MG evidenced a 3-fold increase in RAGE (receptor for advanced glycation end products) and a 2-fold increase in NF-kappaB (nuclear factor kappa-light-chain-enhancer of activated B cells) expression compared to control cells.	Pyruvaldehyde	36-38	advanced glycosylation end-product specific receptor	Homo sapiens	70-74
31811113-6	2019	On the other hand, cells exposed to MG evidenced a 3-fold increase in RAGE (receptor for advanced glycation end products) and a 2-fold increase in NF-kappaB (nuclear factor kappa-light-chain-enhancer of activated B cells) expression compared to control cells.	Pyruvaldehyde	36-38	advanced glycosylation end-product specific receptor	Homo sapiens	76-120
31494842-8	2020	Moreover, silencing of the transcription factor nuclear factor E2-related factor 2 (Nrf2) suppressed the mitochondrial protection promoted by KW in the MG-challenged cells.	Pyruvaldehyde	152-154	NFE2 like bZIP transcription factor 2	Homo sapiens	84-88
32151743-0	2020	Methylglyoxal-induced miR-223 suppresses rat vascular KATP channel activity by downregulating Kir6.1 mRNA in carbonyl stress.	Pyruvaldehyde	0-13	microRNA 223	Rattus norvegicus	22-29
32151743-0	2020	Methylglyoxal-induced miR-223 suppresses rat vascular KATP channel activity by downregulating Kir6.1 mRNA in carbonyl stress.	Pyruvaldehyde	0-13	potassium inwardly-rectifying channel, subfamily J, member 8	Rattus norvegicus	94-100
32151743-2	2020	Our previous studies have shown that both Kir6.1 and SUB2B are post-transcriptionally downregulated by methylglyoxal (MGO) which is a reactive carbonyl specie and can cause disruption of vascular tone regulation under diabetic conditions.	Pyruvaldehyde	103-116	potassium inwardly-rectifying channel, subfamily J, member 8	Rattus norvegicus	42-48
32151743-2	2020	Our previous studies have shown that both Kir6.1 and SUB2B are post-transcriptionally downregulated by methylglyoxal (MGO) which is a reactive carbonyl specie and can cause disruption of vascular tone regulation under diabetic conditions.	Pyruvaldehyde	118-121	potassium inwardly-rectifying channel, subfamily J, member 8	Rattus norvegicus	42-48
32151743-6	2020	Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) analysis showed augmentation of miR-223 expression in the cultured SMCs after 300 muM MGO exposure by 5-6 folds.	Pyruvaldehyde	157-160	microRNA 223	Rattus norvegicus	103-110
32151743-7	2020	miR-223 overexpression down-regulated Kir6.1 mRNA levels by ~2.6 times while miR-223 knockdown diminished the effect of 300 muM MGO by ~50% in the SMCs.	Pyruvaldehyde	128-131	microRNA 223	Rattus norvegicus	77-84
32151743-10	2020	These results therefore suggest that miR-223 is induced by MGO exposure, which subsequently downregulates the Kir6.1 mRNA, suppresses KATP channel function, and impairs functional regulation of vascular tones.	Pyruvaldehyde	59-62	microRNA 223	Rattus norvegicus	37-44
32151743-10	2020	These results therefore suggest that miR-223 is induced by MGO exposure, which subsequently downregulates the Kir6.1 mRNA, suppresses KATP channel function, and impairs functional regulation of vascular tones.	Pyruvaldehyde	59-62	potassium inwardly-rectifying channel, subfamily J, member 8	Rattus norvegicus	110-116
32151743-13	2020	miR-223 knockdown alleviated the effect of MGO.	Pyruvaldehyde	43-46	microRNA 223	Rattus norvegicus	0-7
31976027-1	2019	Seed Extract</compound-id> Attenuates Methylglyoxal-Induced Insulin Resistance by Inhibition of Advanced Glycation End Product Formation.	Pyruvaldehyde	38-51	insulin	Homo sapiens	60-67
31976027-3	2019	Methylglyoxal (MGO), a major precursor of AGEs, has been reported to induce insulin resistance in both in vitro and in vivo studies.	Pyruvaldehyde	0-13	insulin	Homo sapiens	76-83
31976027-3	2019	Methylglyoxal (MGO), a major precursor of AGEs, has been reported to induce insulin resistance in both in vitro and in vivo studies.	Pyruvaldehyde	15-18	insulin	Homo sapiens	76-83
31976027-5	2019	This study is aimed at investigating whether PCS extract could attenuate insulin resistance induced by MGO.	Pyruvaldehyde	103-106	insulin	Homo sapiens	73-80
31976027-7	2019	We observed that both 200 and 500 mg/kg PCS extract treatment significantly improved glucose tolerance and insulin sensitivity and markedly restored p-Akt and p-IRS1/2 expression in the livers of the MGO-administered mice.	Pyruvaldehyde	200-203	thymoma viral proto-oncogene 1	Mus musculus	151-154
31976027-7	2019	We observed that both 200 and 500 mg/kg PCS extract treatment significantly improved glucose tolerance and insulin sensitivity and markedly restored p-Akt and p-IRS1/2 expression in the livers of the MGO-administered mice.	Pyruvaldehyde	200-203	insulin receptor substrate 1	Mus musculus	161-167
31976027-8	2019	Additionally, the PCS extract significantly increased the phosphorylation of Akt and IRS-1/2 and glucose uptake in MGO-treated HepG2 cells.	Pyruvaldehyde	115-118	AKT serine/threonine kinase 1	Homo sapiens	77-80
31976027-8	2019	Additionally, the PCS extract significantly increased the phosphorylation of Akt and IRS-1/2 and glucose uptake in MGO-treated HepG2 cells.	Pyruvaldehyde	115-118	insulin receptor substrate 1	Homo sapiens	85-92
31976027-11	2019	The PCS extract significantly decreased the phosphorylation of ERK, p38, and NF-kappaB and suppressed the mRNA expression of proinflammatory molecules including TNF-alpha and IL-1beta and iNOS in MGO-administered mice.	Pyruvaldehyde	196-199	tumor necrosis factor	Mus musculus	161-170
31976027-11	2019	The PCS extract significantly decreased the phosphorylation of ERK, p38, and NF-kappaB and suppressed the mRNA expression of proinflammatory molecules including TNF-alpha and IL-1beta and iNOS in MGO-administered mice.	Pyruvaldehyde	196-199	interleukin 1 alpha	Mus musculus	175-183
31976027-11	2019	The PCS extract significantly decreased the phosphorylation of ERK, p38, and NF-kappaB and suppressed the mRNA expression of proinflammatory molecules including TNF-alpha and IL-1beta and iNOS in MGO-administered mice.	Pyruvaldehyde	196-199	nitric oxide synthase 2, inducible	Mus musculus	188-192
31976027-13	2019	Thus, PCS extract ameliorated the MGO-induced insulin resistance in HepG2 cells and in mice by reducing oxidative stress via the inhibition of AGE formation.	Pyruvaldehyde	34-37	insulin	Homo sapiens	46-53
31794195-5	2019	The probe could sense GLO1 activity and monitor the therapeutic effect of GLO1 inhibitors by imaging tumorous MGO in a both a real-time and in situ manner, demonstrating that the biological effect of GLO1 inhibitors is dependent on the GLO1 activity.	Pyruvaldehyde	110-113	glyoxalase I	Homo sapiens	22-26
31794195-5	2019	The probe could sense GLO1 activity and monitor the therapeutic effect of GLO1 inhibitors by imaging tumorous MGO in a both a real-time and in situ manner, demonstrating that the biological effect of GLO1 inhibitors is dependent on the GLO1 activity.	Pyruvaldehyde	110-113	glyoxalase I	Homo sapiens	74-78
31794195-5	2019	The probe could sense GLO1 activity and monitor the therapeutic effect of GLO1 inhibitors by imaging tumorous MGO in a both a real-time and in situ manner, demonstrating that the biological effect of GLO1 inhibitors is dependent on the GLO1 activity.	Pyruvaldehyde	110-113	glyoxalase I	Homo sapiens	74-78
31794195-5	2019	The probe could sense GLO1 activity and monitor the therapeutic effect of GLO1 inhibitors by imaging tumorous MGO in a both a real-time and in situ manner, demonstrating that the biological effect of GLO1 inhibitors is dependent on the GLO1 activity.	Pyruvaldehyde	110-113	glyoxalase I	Homo sapiens	74-78
31794195-6	2019	Furthermore, MEBTD enables the visualization of tumorous MGO induced by GLO1 inhibitors in vivo.	Pyruvaldehyde	57-60	glyoxalase I	Homo sapiens	72-76
31653696-0	2019	The apparent deglycase activity of DJ-1 results from the conversion of free methylglyoxal present in fast equilibrium with hemithioacetals and hemiaminals.	Pyruvaldehyde	76-89	Parkinsonism associated deglycase	Homo sapiens	35-39
31653696-2	2019	The molecular mechanisms underlying this neuroprotection are unclear; however, DJ-1 has been suggested to be a GSH-independent glyoxalase that detoxifies methylglyoxal (MGO) by converting it into lactate.	Pyruvaldehyde	154-167	Parkinsonism associated deglycase	Homo sapiens	79-83
31653696-2	2019	The molecular mechanisms underlying this neuroprotection are unclear; however, DJ-1 has been suggested to be a GSH-independent glyoxalase that detoxifies methylglyoxal (MGO) by converting it into lactate.	Pyruvaldehyde	169-172	Parkinsonism associated deglycase	Homo sapiens	79-83
31653696-3	2019	It has also been suggested that DJ-1 serves as a deglycase that catalyzes hydrolysis of hemithioacetals and hemiaminals formed by reactions of MGO with the thiol and amino groups of proteins.	Pyruvaldehyde	143-146	Parkinsonism associated deglycase	Homo sapiens	32-36
31653696-5	2019	We found that removal of free MGO by DJ-1"s glyoxalase activity forces immediate spontaneous decomposition of hemithioacetals due to the shift in equilibrium position.	Pyruvaldehyde	30-33	Parkinsonism associated deglycase	Homo sapiens	37-41
31653696-7	2019	Furthermore, we demonstrate that higher initial concentrations of hemithioacetals are associated with lower rates of DJ-1-mediated conversion of MGO, ruling out the possibility that hemithioacetals are DJ-1 substrates.	Pyruvaldehyde	145-148	Parkinsonism associated deglycase	Homo sapiens	117-121
31629029-0	2019	Ginsenoside Rb1 mitigates oxidative stress and apoptosis induced by methylglyoxal in SH-SY5Y cells via the PI3K/Akt pathway.	Pyruvaldehyde	68-81	AKT serine/threonine kinase 1	Homo sapiens	112-115
31629029-4	2019	Therefore, this study aimed to investigate the effects of Rb1 on MGO-induced damage in SH-SY5Y cells and the related mechanism.	Pyruvaldehyde	65-68	RB transcriptional corepressor 1	Homo sapiens	58-61
31629029-10	2019	As a result, Rb1 alleviated the injury induced by MGO by increasing the activities of superoxide dismutase, catalase and total glutathione, decreasing the level of malondialdehyde, and alleviating mitochondrial damage and ROS production.	Pyruvaldehyde	50-53	RB transcriptional corepressor 1	Homo sapiens	13-16
31629029-10	2019	As a result, Rb1 alleviated the injury induced by MGO by increasing the activities of superoxide dismutase, catalase and total glutathione, decreasing the level of malondialdehyde, and alleviating mitochondrial damage and ROS production.	Pyruvaldehyde	50-53	catalase	Homo sapiens	108-116
31629029-12	2019	Moreover, the protective effects of Rb1 against MGO-induced apoptosis were partly abolished by LY294002, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K) phosphorylation.	Pyruvaldehyde	48-51	RB transcriptional corepressor 1	Homo sapiens	36-39
31629029-13	2019	Our results demonstrated that Rb1 ameliorated MGO-induced oxidative stress and apoptosis in SH-SY5Y cells via activating the PI3K/Akt signaling pathway.	Pyruvaldehyde	46-49	RB transcriptional corepressor 1	Homo sapiens	30-33
31629029-13	2019	Our results demonstrated that Rb1 ameliorated MGO-induced oxidative stress and apoptosis in SH-SY5Y cells via activating the PI3K/Akt signaling pathway.	Pyruvaldehyde	46-49	AKT serine/threonine kinase 1	Homo sapiens	130-133
32419966-0	2020	Methylglyoxal-derived advanced glycation end products induce matrix metalloproteinases through activation of ERK/JNK/NF-kappaB pathway in kidney proximal epithelial cells.	Pyruvaldehyde	0-13	mitogen-activated protein kinase 8	Rattus norvegicus	113-116
31369791-0	2019	Effect of bergenin on RANKL-induced osteoclast differentiation in the presence of methylglyoxal.	Pyruvaldehyde	82-95	TNF superfamily member 11	Homo sapiens	22-27
31369791-5	2019	Quantitative RT-PCR revealed that bergenin decreased the expression of ERK1, Akt2, MMP-9, and OSTM1 genes in the presence of MG.	Pyruvaldehyde	125-127	mitogen-activated protein kinase 3	Homo sapiens	71-75
31369791-6	2019	Bergenin pretreatment yielded significant increases in intracellular calcium concentration, mitochondrial mass, mitochondrial membrane potential, and glyoxalase I reduced by MG.	Pyruvaldehyde	174-176	glyoxalase I	Homo sapiens	150-162
32419966-0	2020	Methylglyoxal-derived advanced glycation end products induce matrix metalloproteinases through activation of ERK/JNK/NF-kappaB pathway in kidney proximal epithelial cells.	Pyruvaldehyde	0-13	Eph receptor B1	Rattus norvegicus	109-112
31767834-2	2019	A recent study has shown that phosphoglycerate kinase 1 (PGK1) inhibition/depletion will lead to Kelch-like ECH-associated protein 1 (Keap1) methylglyoxal modification, thereby activating Nrf2 signaling cascade.	Pyruvaldehyde	141-154	phosphoglycerate kinase 1	Homo sapiens	30-55
31767834-2	2019	A recent study has shown that phosphoglycerate kinase 1 (PGK1) inhibition/depletion will lead to Kelch-like ECH-associated protein 1 (Keap1) methylglyoxal modification, thereby activating Nrf2 signaling cascade.	Pyruvaldehyde	141-154	phosphoglycerate kinase 1	Homo sapiens	57-61
31767834-2	2019	A recent study has shown that phosphoglycerate kinase 1 (PGK1) inhibition/depletion will lead to Kelch-like ECH-associated protein 1 (Keap1) methylglyoxal modification, thereby activating Nrf2 signaling cascade.	Pyruvaldehyde	141-154	kelch like ECH associated protein 1	Homo sapiens	97-132
31767834-2	2019	A recent study has shown that phosphoglycerate kinase 1 (PGK1) inhibition/depletion will lead to Kelch-like ECH-associated protein 1 (Keap1) methylglyoxal modification, thereby activating Nrf2 signaling cascade.	Pyruvaldehyde	141-154	kelch like ECH associated protein 1	Homo sapiens	134-139
31767834-2	2019	A recent study has shown that phosphoglycerate kinase 1 (PGK1) inhibition/depletion will lead to Kelch-like ECH-associated protein 1 (Keap1) methylglyoxal modification, thereby activating Nrf2 signaling cascade.	Pyruvaldehyde	141-154	NFE2 like bZIP transcription factor 2	Homo sapiens	188-192
31738028-1	2019	BACKGROUNDS: Glyoxalase I (GLO1), a ubiquitous enzyme involved in the process of detoxification of methylglyoxal in the cellular glycolysis pathway, was reported to be highly expressed in human tumor.	Pyruvaldehyde	99-112	glyoxalase I	Homo sapiens	13-25
31748248-6	2019	Pleiotropic roles for Yap1 in diverse biological processes were supported by transcriptome data showing that 162 genes are differentially regulated by Yap1, with further analysis revealing that Yap1 promotes cellular resistance to toxic cellular metabolites produced during glycolysis, such as methylglyoxal.	Pyruvaldehyde	294-307	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	22-26
31748248-6	2019	Pleiotropic roles for Yap1 in diverse biological processes were supported by transcriptome data showing that 162 genes are differentially regulated by Yap1, with further analysis revealing that Yap1 promotes cellular resistance to toxic cellular metabolites produced during glycolysis, such as methylglyoxal.	Pyruvaldehyde	294-307	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	151-155
31748248-6	2019	Pleiotropic roles for Yap1 in diverse biological processes were supported by transcriptome data showing that 162 genes are differentially regulated by Yap1, with further analysis revealing that Yap1 promotes cellular resistance to toxic cellular metabolites produced during glycolysis, such as methylglyoxal.	Pyruvaldehyde	294-307	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	151-155
31738028-1	2019	BACKGROUNDS: Glyoxalase I (GLO1), a ubiquitous enzyme involved in the process of detoxification of methylglyoxal in the cellular glycolysis pathway, was reported to be highly expressed in human tumor.	Pyruvaldehyde	99-112	glyoxalase I	Homo sapiens	27-31
31661534-3	2019	Methylglyoxal is detoxified by Glyoxalase I (GLO1).	Pyruvaldehyde	0-13	glyoxalase I	Homo sapiens	31-43
31219946-2	2019	MG could be a mediator of diabetes-induced neuropathic pain through TRPA1 activation and sensitization of the voltage-gated sodium channel subtype 1.8.	Pyruvaldehyde	0-2	transient receptor potential cation channel subfamily A member 1	Homo sapiens	68-73
31219946-5	2019	Involvement of the transduction channels TRPA1 and TRPV1 in MG-induced pain sensation was investigated with specific ion channel blockers.	Pyruvaldehyde	60-62	transient receptor potential cation channel subfamily A member 1	Homo sapiens	41-46
31219946-5	2019	Involvement of the transduction channels TRPA1 and TRPV1 in MG-induced pain sensation was investigated with specific ion channel blockers.	Pyruvaldehyde	60-62	transient receptor potential cation channel subfamily V member 1	Homo sapiens	51-56
31219946-8	2019	Selective pharmacological blockade of TRPA1 or TRPV1 showed that TRPA1 is crucially involved in MG-induced chemical pain sensation and heat hyperalgesia.	Pyruvaldehyde	96-98	transient receptor potential cation channel subfamily A member 1	Homo sapiens	38-43
31219946-8	2019	Selective pharmacological blockade of TRPA1 or TRPV1 showed that TRPA1 is crucially involved in MG-induced chemical pain sensation and heat hyperalgesia.	Pyruvaldehyde	96-98	transient receptor potential cation channel subfamily V member 1	Homo sapiens	47-52
31219946-8	2019	Selective pharmacological blockade of TRPA1 or TRPV1 showed that TRPA1 is crucially involved in MG-induced chemical pain sensation and heat hyperalgesia.	Pyruvaldehyde	96-98	transient receptor potential cation channel subfamily A member 1	Homo sapiens	65-70
31219946-9	2019	In conclusion, the actions of MG through TRPA1 activation on predominantly mechano-insensitive C fibers might be involved in spontaneously perceived pain in diabetic neuropathy and hyperalgesia as well as allodynia.	Pyruvaldehyde	30-32	transient receptor potential cation channel subfamily A member 1	Homo sapiens	41-46
31661534-3	2019	Methylglyoxal is detoxified by Glyoxalase I (GLO1).	Pyruvaldehyde	0-13	glyoxalase I	Homo sapiens	45-49
31667263-0	2019	The dataset of methylglyoxal activating p38 and p44/42 pathway in osteoclast.	Pyruvaldehyde	15-28	mitogen-activated protein kinase 14	Homo sapiens	40-43
31652571-0	2019	GLYI4 Plays A Role in Methylglyoxal Detoxification and Jasmonate-Mediated Stress Responses in Arabidopsis thaliana.	Pyruvaldehyde	22-35	Lactoylglutathione lyase / glyoxalase I family protein	Arabidopsis thaliana	0-5
31652571-3	2019	MG is mostly detoxified by the combined actions of the enzymes glyoxalase I (GLYI) and glyoxalase II (GLYII) that make up the glyoxalase system.	Pyruvaldehyde	0-2	glyoxalase/bleomycin resistance protein/dioxygenase superfamily protein	Arabidopsis thaliana	63-75
31652571-3	2019	MG is mostly detoxified by the combined actions of the enzymes glyoxalase I (GLYI) and glyoxalase II (GLYII) that make up the glyoxalase system.	Pyruvaldehyde	0-2	glyoxalase/bleomycin resistance protein/dioxygenase superfamily protein	Arabidopsis thaliana	77-81
31652571-3	2019	MG is mostly detoxified by the combined actions of the enzymes glyoxalase I (GLYI) and glyoxalase II (GLYII) that make up the glyoxalase system.	Pyruvaldehyde	0-2	glyoxalase 2-1	Arabidopsis thaliana	87-100
31652571-5	2019	Here, we investigated the impact of GLYI4 knock-down on MG scavenging and on JA pathway.	Pyruvaldehyde	56-58	Lactoylglutathione lyase / glyoxalase I family protein	Arabidopsis thaliana	36-41
31652571-6	2019	In glyI4 mutant plants, we observed a general stress phenotype, characterized by compromised MG scavenging, accumulation of reactive oxygen species (ROS), stomatal closure, and reduced fitness.	Pyruvaldehyde	93-95	Lactoylglutathione lyase / glyoxalase I family protein	Arabidopsis thaliana	3-8
31652571-7	2019	Accumulation of MG in glyI4 plants led to lower efficiency of the JA pathway, as highlighted by the increased susceptibility of the plants to the pathogenic fungus Plectospherella cucumerina.	Pyruvaldehyde	16-18	Lactoylglutathione lyase / glyoxalase I family protein	Arabidopsis thaliana	22-27
31652571-8	2019	Moreover, MG accumulation brought about a localization of GLYI4 to the plasma membrane, while MeJA stimulus induced a translocation of the protein into the cytoplasmic compartment.	Pyruvaldehyde	10-12	Lactoylglutathione lyase / glyoxalase I family protein	Arabidopsis thaliana	58-63
31652571-9	2019	Collectively, the results are consistent with the hypothesis that GLYI4 is a hub in the MG and JA pathways.	Pyruvaldehyde	88-90	Lactoylglutathione lyase / glyoxalase I family protein	Arabidopsis thaliana	66-71
31614723-2	2019	We tested the hypotheses in Pin1 silenced cells (SH-SY5Y) treated with 2-deoxy-d-glucose (2DG) and methylglyoxal (MG), stressors causing altered glucose trafficking, glucotoxicity and protein glycation.	Pyruvaldehyde	99-112	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	28-32
31614723-2	2019	We tested the hypotheses in Pin1 silenced cells (SH-SY5Y) treated with 2-deoxy-d-glucose (2DG) and methylglyoxal (MG), stressors causing altered glucose trafficking, glucotoxicity and protein glycation.	Pyruvaldehyde	114-116	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	28-32
31351151-0	2019	Characterization of methylglyoxal induced advanced glycation end products and aggregates of human transferrin: Biophysical and microscopic insight.	Pyruvaldehyde	20-33	transferrin	Homo sapiens	98-109
31351151-2	2019	The purpose of our study was to have an insight into AGEs and aggregates formation of human transferrin (hTF) in the presence of methylglyoxal (MG) employing intrinsic, ANS, Thioflavin T fluorescence, circular dichroism (CD) spectroscopy, docking studies and microscopy.	Pyruvaldehyde	129-142	transferrin	Homo sapiens	92-103
31359290-0	2019	Tanshinone I Induces Mitochondrial Protection by a Mechanism Involving the Nrf2/GSH Axis in the Human Neuroblastoma SH-SY5Y Cells Exposed to Methylglyoxal.	Pyruvaldehyde	141-154	NFE2 like bZIP transcription factor 2	Homo sapiens	75-79
31359290-13	2019	Therefore, T-I induced mitochondrial protection by a mechanism involving the Nrf2/GSH axis in MG-challenged SH-SY5Y cells.	Pyruvaldehyde	94-96	NFE2 like bZIP transcription factor 2	Homo sapiens	77-81
31557885-6	2019	The activity of glyoxalase 1 was not affected by MGO, but was enhanced by Brazilian propolis in EDL muscles.	Pyruvaldehyde	49-52	glyoxalase 1	Mus musculus	16-28
31557885-7	2019	MGO treatment increased mRNA expression of inflammation-related molecules, interleukin (IL)-1beta, IL-6, and toll-like receptor 4 (TLR4).	Pyruvaldehyde	0-3	interleukin 1 beta	Mus musculus	75-97
31557885-7	2019	MGO treatment increased mRNA expression of inflammation-related molecules, interleukin (IL)-1beta, IL-6, and toll-like receptor 4 (TLR4).	Pyruvaldehyde	0-3	interleukin 6	Mus musculus	99-103
31557885-7	2019	MGO treatment increased mRNA expression of inflammation-related molecules, interleukin (IL)-1beta, IL-6, and toll-like receptor 4 (TLR4).	Pyruvaldehyde	0-3	toll-like receptor 4	Mus musculus	109-129
31557885-7	2019	MGO treatment increased mRNA expression of inflammation-related molecules, interleukin (IL)-1beta, IL-6, and toll-like receptor 4 (TLR4).	Pyruvaldehyde	0-3	toll-like receptor 4	Mus musculus	131-135
31667263-0	2019	The dataset of methylglyoxal activating p38 and p44/42 pathway in osteoclast.	Pyruvaldehyde	15-28	interferon induced protein 44	Homo sapiens	48-51
31667263-11	2019	These data implied that MG activated the p38 and p44/42, which was reported to regulate proliferation and differentiation of osteoclast.	Pyruvaldehyde	24-26	mitogen-activated protein kinase 14	Homo sapiens	41-44
31667263-11	2019	These data implied that MG activated the p38 and p44/42, which was reported to regulate proliferation and differentiation of osteoclast.	Pyruvaldehyde	24-26	interferon induced protein 44	Homo sapiens	49-52
31667263-13	2019	The effects of MG to other osteoclast markers through p38 and p44/42 would be worth to be investigated.	Pyruvaldehyde	15-17	mitogen-activated protein kinase 14	Homo sapiens	54-57
31667263-13	2019	The effects of MG to other osteoclast markers through p38 and p44/42 would be worth to be investigated.	Pyruvaldehyde	15-17	interferon induced protein 44	Homo sapiens	62-65
31667263-14	2019	For more insight please see Methylglyoxal Activates Osteoclasts through JNK Pathway leading to Osteoporosis.	Pyruvaldehyde	28-41	mitogen-activated protein kinase 8	Homo sapiens	72-75
31254498-6	2019	The cells were pretreated (for 2 h) with NGN (at 10-80 muM) and then challenged with MG at 500 muM for 24 h. NGN significantly attenuated the effects of MG on the mitochondrial function and redox environment in this experimental model.	Pyruvaldehyde	85-87	latexin	Homo sapiens	95-98
31377450-12	2019	Methylglyoxal elicited pain hypersensitivity and alteration of p53/parkin expression, similar to STZ.	Pyruvaldehyde	0-13	transformation related protein 53, pseudogene	Mus musculus	63-66
31377450-14	2019	Alteration of p53/parkin expression produces mitochondrial dysfunction and ROS accumulation, leading to pain hypersensitivity in diabetic or methylglyoxal treated mice.	Pyruvaldehyde	141-154	transformation related protein 53, pseudogene	Mus musculus	14-17
31480513-8	2019	Interestingly, RSV failed to induce effective response to HG cytotoxicity when EX527 was present, thus suggesting that the upregulation of SIRT1 is essential for RSV to activate the major antiglycative and antioxidative defense and avoid MG- and ROS-dependent molecular damages in HG environment.	Pyruvaldehyde	238-240	sirtuin 1	Homo sapiens	139-144
31254498-10	2019	Therefore, NGN caused mitochondrial protection by an Nrf2/GSH-dependent manner in SH-SY5Y cells exposed to MG.	Pyruvaldehyde	107-109	NFE2 like bZIP transcription factor 2	Homo sapiens	53-57
31438528-2	2019	Glyoxalase-1 (Glo-1) is a ubiquitous cellular enzyme that participates in the detoxification of methylglyoxal (MGO), a cytotoxic byproduct of glycolysis that induces protein modification (advanced glycation end-products, AGEs) and inflammation.	Pyruvaldehyde	96-109	glyoxalase I	Homo sapiens	14-19
31630312-1	2019	The glyoxalase-I (GLO-I) enzyme, which is the initial enzyme of the glyoxalase system that is responsible for the detoxification of cytotoxic alpha-ketoaldehydes, such as methylglyoxal, has been approved as a valid target in cancer therapy.	Pyruvaldehyde	171-184	glyoxalase I	Homo sapiens	4-16
31630312-1	2019	The glyoxalase-I (GLO-I) enzyme, which is the initial enzyme of the glyoxalase system that is responsible for the detoxification of cytotoxic alpha-ketoaldehydes, such as methylglyoxal, has been approved as a valid target in cancer therapy.	Pyruvaldehyde	171-184	glyoxalase I	Homo sapiens	18-23
31517069-2	2019	It is unclear whether PFSE and its stilbene derivatives inhibit cancer cell proliferation via human glyoxalase I (GLO I), the rate-limiting enzyme for detoxification of methylglyoxal.	Pyruvaldehyde	169-182	glyoxalase I	Homo sapiens	100-112
31517069-2	2019	It is unclear whether PFSE and its stilbene derivatives inhibit cancer cell proliferation via human glyoxalase I (GLO I), the rate-limiting enzyme for detoxification of methylglyoxal.	Pyruvaldehyde	169-182	glyoxalase I	Homo sapiens	114-119
31438528-2	2019	Glyoxalase-1 (Glo-1) is a ubiquitous cellular enzyme that participates in the detoxification of methylglyoxal (MGO), a cytotoxic byproduct of glycolysis that induces protein modification (advanced glycation end-products, AGEs) and inflammation.	Pyruvaldehyde	96-109	glyoxalase I	Homo sapiens	0-12
31438528-2	2019	Glyoxalase-1 (Glo-1) is a ubiquitous cellular enzyme that participates in the detoxification of methylglyoxal (MGO), a cytotoxic byproduct of glycolysis that induces protein modification (advanced glycation end-products, AGEs) and inflammation.	Pyruvaldehyde	111-114	glyoxalase I	Homo sapiens	0-12
31438528-2	2019	Glyoxalase-1 (Glo-1) is a ubiquitous cellular enzyme that participates in the detoxification of methylglyoxal (MGO), a cytotoxic byproduct of glycolysis that induces protein modification (advanced glycation end-products, AGEs) and inflammation.	Pyruvaldehyde	111-114	glyoxalase I	Homo sapiens	14-19
31438528-4	2019	ST-I4C attenuated the MGO-induced expression of inflammatory-related genes, such as tumor necrosis factor (TNF)-alpha and IFN-gamma by activating nuclear factor-kappa B (NF-kappaB) without toxicity in HepG2 cells.	Pyruvaldehyde	22-25	tumor necrosis factor	Homo sapiens	84-117
31438528-4	2019	ST-I4C attenuated the MGO-induced expression of inflammatory-related genes, such as tumor necrosis factor (TNF)-alpha and IFN-gamma by activating nuclear factor-kappa B (NF-kappaB) without toxicity in HepG2 cells.	Pyruvaldehyde	22-25	interferon gamma	Homo sapiens	122-131
31438528-4	2019	ST-I4C attenuated the MGO-induced expression of inflammatory-related genes, such as tumor necrosis factor (TNF)-alpha and IFN-gamma by activating nuclear factor-kappa B (NF-kappaB) without toxicity in HepG2 cells.	Pyruvaldehyde	22-25	nuclear factor kappa B subunit 1	Homo sapiens	146-168
31438528-4	2019	ST-I4C attenuated the MGO-induced expression of inflammatory-related genes, such as tumor necrosis factor (TNF)-alpha and IFN-gamma by activating nuclear factor-kappa B (NF-kappaB) without toxicity in HepG2 cells.	Pyruvaldehyde	22-25	nuclear factor kappa B subunit 1	Homo sapiens	170-179
31438528-6	2019	Interestingly, both the mRNA and protein expression levels of Glo-1 increased following ST-I4C treatment, and the decrease in Glo-1 mRNA expression caused by MGO exposure was rescued by ST-I4C pretreatment.	Pyruvaldehyde	158-161	glyoxalase I	Homo sapiens	62-67
31438528-6	2019	Interestingly, both the mRNA and protein expression levels of Glo-1 increased following ST-I4C treatment, and the decrease in Glo-1 mRNA expression caused by MGO exposure was rescued by ST-I4C pretreatment.	Pyruvaldehyde	158-161	glyoxalase I	Homo sapiens	126-131
31426466-10	2019	Since methylglyoxal (MGO) content, a precursor of advanced glycation endproducts (AGE), was augmented in the three tissues in the fructose-fed mothers and has been related to interfere with the functioning of many proteins, the role of MGO in XBP1s migration should not be discarded.	Pyruvaldehyde	6-19	X-box binding protein 1	Rattus norvegicus	243-247
31482070-1	2019	Background: Glyoxalase-I (Glo-I) is essential for detoxification of methylglyoxal (MGO), a byproduct of glycolysis.	Pyruvaldehyde	68-81	glyoxalase I	Homo sapiens	12-24
31482070-1	2019	Background: Glyoxalase-I (Glo-I) is essential for detoxification of methylglyoxal (MGO), a byproduct of glycolysis.	Pyruvaldehyde	68-81	glyoxalase I	Homo sapiens	26-31
31482070-1	2019	Background: Glyoxalase-I (Glo-I) is essential for detoxification of methylglyoxal (MGO), a byproduct of glycolysis.	Pyruvaldehyde	83-86	glyoxalase I	Homo sapiens	12-24
31482070-1	2019	Background: Glyoxalase-I (Glo-I) is essential for detoxification of methylglyoxal (MGO), a byproduct of glycolysis.	Pyruvaldehyde	83-86	glyoxalase I	Homo sapiens	26-31
31426466-10	2019	Since methylglyoxal (MGO) content, a precursor of advanced glycation endproducts (AGE), was augmented in the three tissues in the fructose-fed mothers and has been related to interfere with the functioning of many proteins, the role of MGO in XBP1s migration should not be discarded.	Pyruvaldehyde	21-24	X-box binding protein 1	Rattus norvegicus	243-247
31103701-10	2019	In both animals and cell cultures, methylglyoxal was shown to induce osteoclastogenesis by increased gene expression of osteoclast bone biomarkers CTSK, OSCAR and TRACP5.	Pyruvaldehyde	35-48	osteoclast associated Ig-like receptor	Homo sapiens	153-158
31136758-7	2019	Exposure of MGO resulted in mitochondrial fission and decrease of opa1 and mfn1.	Pyruvaldehyde	12-15	OPA1 mitochondrial dynamin like GTPase	Bos taurus	66-70
31136758-7	2019	Exposure of MGO resulted in mitochondrial fission and decrease of opa1 and mfn1.	Pyruvaldehyde	12-15	mitofusin 1	Bos taurus	75-79
31136758-11	2019	Moreover, overexpression of glyoxalase 1 (GLO1) increased key proteins of mitochondrial fusion, including opa1 and mfn1 in BRECs cultured with MGO.	Pyruvaldehyde	143-146	glyoxalase I	Bos taurus	28-40
31136758-11	2019	Moreover, overexpression of glyoxalase 1 (GLO1) increased key proteins of mitochondrial fusion, including opa1 and mfn1 in BRECs cultured with MGO.	Pyruvaldehyde	143-146	glyoxalase I	Bos taurus	42-46
31136758-12	2019	However, inhibition of GLO1 by siRNA abolished the effect of Tan IIa on induction of mitochondrial fusion in MGO cultured BRECs.	Pyruvaldehyde	109-112	glyoxalase I	Bos taurus	23-27
31136758-0	2019	Tanshinone IIa protects retinal endothelial cells against mitochondrial fission induced by methylglyoxal through glyoxalase 1.	Pyruvaldehyde	91-104	glyoxalase I	Bos taurus	113-125
31136758-5	2019	MGO increased cellular reactive oxygen species formation and cellular nitric oxide (NO) level; enhanced nox1 and iNOS mRNA levels; inhibited prdx1 mRNA level.	Pyruvaldehyde	0-3	NADPH oxidase 1	Bos taurus	104-108
31136758-5	2019	MGO increased cellular reactive oxygen species formation and cellular nitric oxide (NO) level; enhanced nox1 and iNOS mRNA levels; inhibited prdx1 mRNA level.	Pyruvaldehyde	0-3	nitric oxide synthase 2	Bos taurus	113-117
31136758-5	2019	MGO increased cellular reactive oxygen species formation and cellular nitric oxide (NO) level; enhanced nox1 and iNOS mRNA levels; inhibited prdx1 mRNA level.	Pyruvaldehyde	0-3	peroxiredoxin 1	Bos taurus	141-146
31103701-0	2019	Methylglyoxal activates osteoclasts through JNK pathway leading to osteoporosis.	Pyruvaldehyde	0-13	mitogen-activated protein kinase 8	Homo sapiens	44-47
31103701-10	2019	In both animals and cell cultures, methylglyoxal was shown to induce osteoclastogenesis by increased gene expression of osteoclast bone biomarkers CTSK, OSCAR and TRACP5.	Pyruvaldehyde	35-48	cathepsin K	Homo sapiens	147-151
31103701-11	2019	Furthermore, in methylglyoxal-treated macrophages activation of the c-Jun N-terminal kinases signaling pathway was observed, and inhibition of JNK activities resulted in down-regulation of osteoclast biomarkers gene expressions.	Pyruvaldehyde	16-29	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	68-73
31103701-12	2019	Our results therefore suggested that methylglyoxal may contribute to the progression of diabetes-related osteoporosis and imbalanced bone remodeling through JNK pathway in osteoclasts.	Pyruvaldehyde	37-50	mitogen-activated protein kinase 8	Homo sapiens	157-160
30973706-5	2019	Therefore, here we study how nitration and glycation mediated by methylglyoxal affect the redox features of alpha-synuclein.	Pyruvaldehyde	65-78	synuclein alpha	Homo sapiens	108-123
31388341-8	2019	Methylglyoxal administration elevated glyoxalase 1 expression (p &lt; 0.05), involved in methylglyoxal degradation.	Pyruvaldehyde	0-13	glyoxalase 1	Rattus norvegicus	38-50
31388341-8	2019	Methylglyoxal administration elevated glyoxalase 1 expression (p &lt; 0.05), involved in methylglyoxal degradation.	Pyruvaldehyde	89-102	glyoxalase 1	Rattus norvegicus	38-50
30995106-11	2019	Furthermore, siRNA against the KATP channel protein Kir6.1 significantly inhibited endothelial cell function at basal status but rescued impaired endothelial cell function upon MGO exposure.	Pyruvaldehyde	177-180	potassium inwardly rectifying channel subfamily J member 8	Homo sapiens	52-58
30995106-13	2019	MGO exposure enhanced the activation of all three MAPK pathways in H-HAECs, whereas glibenclamide reversed the activation of p-stress-activated protein kinase/JNK induced by MGO.	Pyruvaldehyde	174-177	mitogen-activated protein kinase 8	Homo sapiens	159-162
30995106-14	2019	Glyoxalase-1 (GLO1) is the endogenous MGO-detoxifying enzyme.	Pyruvaldehyde	38-41	glyoxalase I	Homo sapiens	0-12
30995106-14	2019	Glyoxalase-1 (GLO1) is the endogenous MGO-detoxifying enzyme.	Pyruvaldehyde	38-41	glyoxalase I	Homo sapiens	14-18
30995106-15	2019	In healthy mice that received an inhibitor of GLO1, MGO deposition in aortic wall was enhanced and endothelial cell sprouting from isolated aortic segment was significantly inhibited.	Pyruvaldehyde	52-55	glyoxalase 1	Mus musculus	46-50
30995106-16	2019	Our data suggest that MGO triggers endothelial cell dysfunction by activating the JNK/p38 MAPK pathway.	Pyruvaldehyde	22-25	mitogen-activated protein kinase 8	Homo sapiens	82-85
31217350-2	2019	In zebrafish, a transient knockdown of glyoxalase 1, the main MG detoxifying system, led to the elevation of endogenous MG levels and blood vessel alterations.	Pyruvaldehyde	62-64	glyoxalase 1	Danio rerio	39-51
31217350-2	2019	In zebrafish, a transient knockdown of glyoxalase 1, the main MG detoxifying system, led to the elevation of endogenous MG levels and blood vessel alterations.	Pyruvaldehyde	120-122	glyoxalase 1	Danio rerio	39-51
31217350-5	2019	Glo1-/- zebrafish survived until adulthood without growth deficit and showed increased tissue MG concentrations.	Pyruvaldehyde	94-96	glyoxalase 1	Danio rerio	0-4
31059718-9	2019	Strain-dependent differences of the anxiety in mice are probably related to the anxiolytic effects of methylglyoxal, a substrate for Glo1 and Gsr.	Pyruvaldehyde	102-115	glyoxalase 1	Mus musculus	133-137
31059718-9	2019	Strain-dependent differences of the anxiety in mice are probably related to the anxiolytic effects of methylglyoxal, a substrate for Glo1 and Gsr.	Pyruvaldehyde	102-115	gutter shaped root	Mus musculus	142-145
31370192-6	2019	Interestingly, administering LB in MGO-treated cells and mice upregulated the expression of Nrf2 and Glo1, and downregulated the expression of IL-1beta and TNF-alpha.	Pyruvaldehyde	35-38	nuclear factor, erythroid derived 2, like 2	Mus musculus	92-96
31370192-6	2019	Interestingly, administering LB in MGO-treated cells and mice upregulated the expression of Nrf2 and Glo1, and downregulated the expression of IL-1beta and TNF-alpha.	Pyruvaldehyde	35-38	glyoxalase 1	Mus musculus	101-105
31370192-6	2019	Interestingly, administering LB in MGO-treated cells and mice upregulated the expression of Nrf2 and Glo1, and downregulated the expression of IL-1beta and TNF-alpha.	Pyruvaldehyde	35-38	interleukin 1 beta	Mus musculus	143-151
31370192-6	2019	Interestingly, administering LB in MGO-treated cells and mice upregulated the expression of Nrf2 and Glo1, and downregulated the expression of IL-1beta and TNF-alpha.	Pyruvaldehyde	35-38	tumor necrosis factor	Mus musculus	156-165
30807826-9	2019	We conclude that MG and sensitization of a spinal TRPA1-AC1-Epac signaling cascade facilitate PDN in db/db mice.	Pyruvaldehyde	17-19	Rap guanine nucleotide exchange factor (GEF) 3	Mus musculus	60-64
30973706-8	2019	However, only methylglyoxal was able to abolish the ability of alpha-synuclein to inhibit the free radical release.	Pyruvaldehyde	14-27	synuclein alpha	Homo sapiens	63-78
31208152-0	2019	2-Iodo-4"-Methoxychalcone Attenuates Methylglyoxal-Induced Neurotoxicity by Activation of GLP-1 Receptor and Enhancement of Neurotrophic Signal, Antioxidant Defense and Glyoxalase Pathway.	Pyruvaldehyde	37-50	glucagon like peptide 1 receptor	Homo sapiens	90-104
31208152-9	2019	Furthermore, CHA79 attenuated MG-induced reduction of glyoxalase-1 (GLO-1), a vital enzyme on removing AGE precursors.	Pyruvaldehyde	30-32	glyoxalase I	Homo sapiens	54-66
31208152-9	2019	Furthermore, CHA79 attenuated MG-induced reduction of glyoxalase-1 (GLO-1), a vital enzyme on removing AGE precursors.	Pyruvaldehyde	30-32	glyoxalase I	Homo sapiens	68-73
30771486-3	2019	We have investigated the role of the NAD+-dependent Class III deacetylase SIRT1 in the adaptive response to MG in mouse oocytes and ovary.	Pyruvaldehyde	108-110	sirtuin 1	Mus musculus	74-79
31174324-7	2019	Accordingly, MG adduct accumulation in ATC cells in vitro was associated with a marked mesenchymal phenotype and increased migration/invasion, which were both reversed by aminoguanidine (AG)-a scavenger of MG-and resveratrol-an activator of Glyoxalase 1 (Glo1), the key metabolizing enzyme of MG.	Pyruvaldehyde	13-15	glyoxalase I	Homo sapiens	241-253
31174324-7	2019	Accordingly, MG adduct accumulation in ATC cells in vitro was associated with a marked mesenchymal phenotype and increased migration/invasion, which were both reversed by aminoguanidine (AG)-a scavenger of MG-and resveratrol-an activator of Glyoxalase 1 (Glo1), the key metabolizing enzyme of MG.	Pyruvaldehyde	13-15	glyoxalase I	Homo sapiens	255-259
30771486-4	2019	In mouse oocytes, MG induced up-expression of glyoxalase 1 (Glo1) and glyoxalase 2 (Glo2) genes, components of the main MG detoxification system, whereas inhibition of SIRT1 by Ex527 or sirtinol reduced this response.	Pyruvaldehyde	18-20	glyoxalase 1	Mus musculus	46-58
30771486-4	2019	In mouse oocytes, MG induced up-expression of glyoxalase 1 (Glo1) and glyoxalase 2 (Glo2) genes, components of the main MG detoxification system, whereas inhibition of SIRT1 by Ex527 or sirtinol reduced this response.	Pyruvaldehyde	18-20	glyoxalase 1	Mus musculus	60-64
30771486-4	2019	In mouse oocytes, MG induced up-expression of glyoxalase 1 (Glo1) and glyoxalase 2 (Glo2) genes, components of the main MG detoxification system, whereas inhibition of SIRT1 by Ex527 or sirtinol reduced this response.	Pyruvaldehyde	18-20	hydroxyacyl glutathione hydrolase	Mus musculus	84-88
30771486-4	2019	In mouse oocytes, MG induced up-expression of glyoxalase 1 (Glo1) and glyoxalase 2 (Glo2) genes, components of the main MG detoxification system, whereas inhibition of SIRT1 by Ex527 or sirtinol reduced this response.	Pyruvaldehyde	18-20	sirtuin 1	Mus musculus	168-173
30771486-4	2019	In mouse oocytes, MG induced up-expression of glyoxalase 1 (Glo1) and glyoxalase 2 (Glo2) genes, components of the main MG detoxification system, whereas inhibition of SIRT1 by Ex527 or sirtinol reduced this response.	Pyruvaldehyde	120-122	hydroxyacyl glutathione hydrolase	Mus musculus	84-88
30771486-5	2019	In addition, the inhibition of SIRT1 worsened the effects of MG on oocyte maturation rates, while SIRT1 activation by resveratrol counteracted MG insult.	Pyruvaldehyde	61-63	sirtuin 1	Mus musculus	31-36
30885990-3	2019	We hypothesized that the MGO scavenger glyoxalase 1 (GLO1) reverses bone marrow-derived PC (BMPC) dysfunction through augmenting the activity of an important endoplasmic reticulum stress sensor, inositol-requiring enzyme 1alpha (IRE1alpha), resulting in improved diabetic wound healing.	Pyruvaldehyde	25-28	glyoxalase 1	Mus musculus	39-51
30947068-2	2019	It comprises two enzymes; Glyoxalase I (Glo-I) and Glyoxalase II (Glo-II) which perform detoxifying endogenous harmful metabolites, mainly methylglyoxal (MG) into non-toxic bystanders.	Pyruvaldehyde	139-152	glyoxalase I	Homo sapiens	26-38
30947068-2	2019	It comprises two enzymes; Glyoxalase I (Glo-I) and Glyoxalase II (Glo-II) which perform detoxifying endogenous harmful metabolites, mainly methylglyoxal (MG) into non-toxic bystanders.	Pyruvaldehyde	139-152	glyoxalase I	Homo sapiens	40-45
30947068-2	2019	It comprises two enzymes; Glyoxalase I (Glo-I) and Glyoxalase II (Glo-II) which perform detoxifying endogenous harmful metabolites, mainly methylglyoxal (MG) into non-toxic bystanders.	Pyruvaldehyde	139-152	hydroxyacylglutathione hydrolase	Homo sapiens	51-64
30947068-2	2019	It comprises two enzymes; Glyoxalase I (Glo-I) and Glyoxalase II (Glo-II) which perform detoxifying endogenous harmful metabolites, mainly methylglyoxal (MG) into non-toxic bystanders.	Pyruvaldehyde	139-152	hydroxyacylglutathione hydrolase	Homo sapiens	66-72
30947068-2	2019	It comprises two enzymes; Glyoxalase I (Glo-I) and Glyoxalase II (Glo-II) which perform detoxifying endogenous harmful metabolites, mainly methylglyoxal (MG) into non-toxic bystanders.	Pyruvaldehyde	154-156	glyoxalase I	Homo sapiens	26-38
30947068-2	2019	It comprises two enzymes; Glyoxalase I (Glo-I) and Glyoxalase II (Glo-II) which perform detoxifying endogenous harmful metabolites, mainly methylglyoxal (MG) into non-toxic bystanders.	Pyruvaldehyde	154-156	glyoxalase I	Homo sapiens	40-45
30947068-2	2019	It comprises two enzymes; Glyoxalase I (Glo-I) and Glyoxalase II (Glo-II) which perform detoxifying endogenous harmful metabolites, mainly methylglyoxal (MG) into non-toxic bystanders.	Pyruvaldehyde	154-156	hydroxyacylglutathione hydrolase	Homo sapiens	51-64
30947068-2	2019	It comprises two enzymes; Glyoxalase I (Glo-I) and Glyoxalase II (Glo-II) which perform detoxifying endogenous harmful metabolites, mainly methylglyoxal (MG) into non-toxic bystanders.	Pyruvaldehyde	154-156	hydroxyacylglutathione hydrolase	Homo sapiens	66-72
30885990-3	2019	We hypothesized that the MGO scavenger glyoxalase 1 (GLO1) reverses bone marrow-derived PC (BMPC) dysfunction through augmenting the activity of an important endoplasmic reticulum stress sensor, inositol-requiring enzyme 1alpha (IRE1alpha), resulting in improved diabetic wound healing.	Pyruvaldehyde	25-28	glyoxalase 1	Mus musculus	53-57
30885990-3	2019	We hypothesized that the MGO scavenger glyoxalase 1 (GLO1) reverses bone marrow-derived PC (BMPC) dysfunction through augmenting the activity of an important endoplasmic reticulum stress sensor, inositol-requiring enzyme 1alpha (IRE1alpha), resulting in improved diabetic wound healing.	Pyruvaldehyde	25-28	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	229-238
30885990-5	2019	MGO at the concentration of 10 micromol/L induced immediate and severe BMPC dysfunction, including impaired network formation, migration, and proliferation and increased apoptosis, which were rescued by adenovirus-mediated GLO1 overexpression.	Pyruvaldehyde	0-3	glyoxalase 1	Mus musculus	223-227
30885990-6	2019	IRE1alpha expression and activation in BMPCs were significantly attenuated by MGO exposure but rescued by GLO1 overexpression.	Pyruvaldehyde	78-81	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	0-9
30885990-7	2019	MGO can diminish IRE1alpha RNase activity by directly binding to IRE1alpha in vitro.	Pyruvaldehyde	0-3	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	17-26
30885990-7	2019	MGO can diminish IRE1alpha RNase activity by directly binding to IRE1alpha in vitro.	Pyruvaldehyde	0-3	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	65-74
30885990-10	2019	In conclusion, our data suggest that GLO1 rescues BMPC dysfunction and facilitates wound healing in diabetic animals, at least partly through preventing MGO-induced impairment of IRE1alpha expression and activity.	Pyruvaldehyde	153-156	glyoxalase 1	Mus musculus	37-41
30885990-10	2019	In conclusion, our data suggest that GLO1 rescues BMPC dysfunction and facilitates wound healing in diabetic animals, at least partly through preventing MGO-induced impairment of IRE1alpha expression and activity.	Pyruvaldehyde	153-156	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	179-188
31285762-13	2019	injection of MGO or in STZ-induced diabetic mice, which was abolished by MGO scavengers, intrathecal injection of TRPA1 blockers, and in Trpa1-/- mice.	Pyruvaldehyde	13-16	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	114-119
31285762-9	2019	Addition of MGO directly activated transient receptor potential ankyrin 1 (TRPA1) to induce inward currents and calcium influx in dorsal root ganglia (DRG) neurons or in TRPA1-expressing HEK293 cells.	Pyruvaldehyde	12-15	transient receptor potential cation channel subfamily A member 1	Homo sapiens	35-73
31285762-13	2019	injection of MGO or in STZ-induced diabetic mice, which was abolished by MGO scavengers, intrathecal injection of TRPA1 blockers, and in Trpa1-/- mice.	Pyruvaldehyde	13-16	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	137-142
31285762-9	2019	Addition of MGO directly activated transient receptor potential ankyrin 1 (TRPA1) to induce inward currents and calcium influx in dorsal root ganglia (DRG) neurons or in TRPA1-expressing HEK293 cells.	Pyruvaldehyde	12-15	transient receptor potential cation channel subfamily A member 1	Homo sapiens	75-80
31285762-14	2019	Conclusion: This study revealed that Nav1.7 and MGO-mediated activation of TRPA1 play key roles in itch and hypoalgesia in a murine model of type 1 diabetes.	Pyruvaldehyde	48-51	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	75-80
31285762-9	2019	Addition of MGO directly activated transient receptor potential ankyrin 1 (TRPA1) to induce inward currents and calcium influx in dorsal root ganglia (DRG) neurons or in TRPA1-expressing HEK293 cells.	Pyruvaldehyde	12-15	transient receptor potential cation channel subfamily A member 1	Homo sapiens	170-175
31133647-9	2019	MG was increased in high glucose by increased flux of MG formation linked to increased glucose metabolism mediated by proteolytic stabilisation and increase of hexokinase-2 (HK-2); later potentiated by proteolytic down regulation of glyoxalase 1 (Glo1) - the major enzyme of MG metabolism.	Pyruvaldehyde	0-2	hexokinase 2	Homo sapiens	160-172
31133647-9	2019	MG was increased in high glucose by increased flux of MG formation linked to increased glucose metabolism mediated by proteolytic stabilisation and increase of hexokinase-2 (HK-2); later potentiated by proteolytic down regulation of glyoxalase 1 (Glo1) - the major enzyme of MG metabolism.	Pyruvaldehyde	54-56	glyoxalase I	Homo sapiens	247-251
31133647-9	2019	MG was increased in high glucose by increased flux of MG formation linked to increased glucose metabolism mediated by proteolytic stabilisation and increase of hexokinase-2 (HK-2); later potentiated by proteolytic down regulation of glyoxalase 1 (Glo1) - the major enzyme of MG metabolism.	Pyruvaldehyde	0-2	hexokinase 2	Homo sapiens	174-178
31133647-10	2019	Silencing of Glo1, selectively increasing MG, activated the UPR similarly.	Pyruvaldehyde	42-44	glyoxalase I	Homo sapiens	13-17
31133647-9	2019	MG was increased in high glucose by increased flux of MG formation linked to increased glucose metabolism mediated by proteolytic stabilisation and increase of hexokinase-2 (HK-2); later potentiated by proteolytic down regulation of glyoxalase 1 (Glo1) - the major enzyme of MG metabolism.	Pyruvaldehyde	0-2	glyoxalase I	Homo sapiens	233-245
31133647-11	2019	Silencing of HK-2 prevented increased glucose metabolism and MG formation.	Pyruvaldehyde	61-63	hexokinase 2	Homo sapiens	13-17
31133647-9	2019	MG was increased in high glucose by increased flux of MG formation linked to increased glucose metabolism mediated by proteolytic stabilisation and increase of hexokinase-2 (HK-2); later potentiated by proteolytic down regulation of glyoxalase 1 (Glo1) - the major enzyme of MG metabolism.	Pyruvaldehyde	0-2	glyoxalase I	Homo sapiens	247-251
31133647-9	2019	MG was increased in high glucose by increased flux of MG formation linked to increased glucose metabolism mediated by proteolytic stabilisation and increase of hexokinase-2 (HK-2); later potentiated by proteolytic down regulation of glyoxalase 1 (Glo1) - the major enzyme of MG metabolism.	Pyruvaldehyde	54-56	hexokinase 2	Homo sapiens	174-178
31133647-9	2019	MG was increased in high glucose by increased flux of MG formation linked to increased glucose metabolism mediated by proteolytic stabilisation and increase of hexokinase-2 (HK-2); later potentiated by proteolytic down regulation of glyoxalase 1 (Glo1) - the major enzyme of MG metabolism.	Pyruvaldehyde	54-56	glyoxalase I	Homo sapiens	233-245
30625358-4	2019	In the present study, fibrinogen was incubated with varying concentration of MGO for 7 days followed by its biochemical and biophysical analysis.	Pyruvaldehyde	77-80	fibrinogen beta chain	Homo sapiens	22-32
30796974-5	2019	Treatment of cells with Parkinsonian mimetic, 1-methyl-4-phenylpyridinium ion (MPP+); oxidants, such as H2O2 and methylglyoxal (MGO) lead to a dose-dependent decrease in the levels of DJ-1 with a concomitant increase in CML-syn.	Pyruvaldehyde	128-131	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	184-188
30796974-6	2019	Also, MGO induced cytosolic alpha-synuclein aggregates in cells which stained positive with the anti-CML antibody.	Pyruvaldehyde	6-9	synuclein, alpha	Mus musculus	28-43
30796974-7	2019	Further, unilateral stereotaxic administration of MGO into the SNpc of mice induced alpha-synuclein aggregates and CML-syn with a concomitant reduction in the number of TH positive neurons, protein levels of TH and DJ-1 at the site of injection.	Pyruvaldehyde	50-53	synuclein, alpha	Mus musculus	84-99
30796974-7	2019	Further, unilateral stereotaxic administration of MGO into the SNpc of mice induced alpha-synuclein aggregates and CML-syn with a concomitant reduction in the number of TH positive neurons, protein levels of TH and DJ-1 at the site of injection.	Pyruvaldehyde	50-53	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	215-219
30796974-8	2019	Interestingly, overexpression of DJ-1 enhanced the clearance of preformed CML-syn in cells, mitigated MGO induced CML-syn and intracellular alpha-synuclein aggregates.	Pyruvaldehyde	102-105	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	33-37
30796974-8	2019	Interestingly, overexpression of DJ-1 enhanced the clearance of preformed CML-syn in cells, mitigated MGO induced CML-syn and intracellular alpha-synuclein aggregates.	Pyruvaldehyde	102-105	synuclein, alpha	Mus musculus	140-155
30145785-7	2019	EX-4 abrogated the decrease in glutamate uptake and GluN1 content caused by methylglyoxal (MG) in hippocampal slices, in addition to leading to an increase in glutamate uptake in astrocyte culture cells and hippocampal slices under basal conditions.	Pyruvaldehyde	76-89	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	52-57
31143470-9	2019	This study suggests that MG has a potential proangiogenic effect via VEGF signaling in the retina of zebrafish embryos.	Pyruvaldehyde	25-27	vascular endothelial growth factor Aa	Danio rerio	69-73
30639428-4	2019	The resulting product was compared with the alpha-synuclein modified by methylglyoxal (MGO).	Pyruvaldehyde	72-85	synuclein alpha	Homo sapiens	44-59
30639428-4	2019	The resulting product was compared with the alpha-synuclein modified by methylglyoxal (MGO).	Pyruvaldehyde	87-90	synuclein alpha	Homo sapiens	44-59
30639428-9	2019	In the aggregates produced by the modified alpha-synuclein, short fibrils of 65-230 nm or 85-260 nm were detected in the case of the protein treated with MGO and GA-3-P, respectively.	Pyruvaldehyde	154-157	synuclein alpha	Homo sapiens	43-58
30796974-3	2019	Our results demonstrate that DJ-1 has a higher affinity towards the substrate methylglyoxal (MGO) (Km = 900 mM) as compared to its familial mutant, L166P (Km = 1900 mM).	Pyruvaldehyde	78-91	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	29-33
30796974-3	2019	Our results demonstrate that DJ-1 has a higher affinity towards the substrate methylglyoxal (MGO) (Km = 900 mM) as compared to its familial mutant, L166P (Km = 1900 mM).	Pyruvaldehyde	93-96	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	29-33
30796974-5	2019	Treatment of cells with Parkinsonian mimetic, 1-methyl-4-phenylpyridinium ion (MPP+); oxidants, such as H2O2 and methylglyoxal (MGO) lead to a dose-dependent decrease in the levels of DJ-1 with a concomitant increase in CML-syn.	Pyruvaldehyde	113-126	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	184-188
30715843-6	2019	In this study, four physiologically relevant monosaccharides, methylglyoxal, glucose, fructose, and ribose were used to glycate human insulin and two C-terminus truncated insulin analogues.	Pyruvaldehyde	62-75	insulin	Homo sapiens	134-141
31049129-5	2019	We previously showed that methylglyoxal induced a decrease in the antioxidant proteins thioredoxin 1 (Trx1) and glyoxalase 2 (Glo2), which was mediated by AMPK-dependent autophagy.	Pyruvaldehyde	26-39	thioredoxin 1	Mus musculus	87-100
31049129-5	2019	We previously showed that methylglyoxal induced a decrease in the antioxidant proteins thioredoxin 1 (Trx1) and glyoxalase 2 (Glo2), which was mediated by AMPK-dependent autophagy.	Pyruvaldehyde	26-39	thioredoxin 1	Mus musculus	102-106
31049129-5	2019	We previously showed that methylglyoxal induced a decrease in the antioxidant proteins thioredoxin 1 (Trx1) and glyoxalase 2 (Glo2), which was mediated by AMPK-dependent autophagy.	Pyruvaldehyde	26-39	hydroxyacyl glutathione hydrolase	Mus musculus	112-124
31049129-5	2019	We previously showed that methylglyoxal induced a decrease in the antioxidant proteins thioredoxin 1 (Trx1) and glyoxalase 2 (Glo2), which was mediated by AMPK-dependent autophagy.	Pyruvaldehyde	26-39	hydroxyacyl glutathione hydrolase	Mus musculus	126-130
30911085-6	2019	We show that the drug interferes with triosephosphate isomerase (TPI) causing release of methylglyoxal (MG).	Pyruvaldehyde	89-102	triosephosphate isomerase 1	Homo sapiens	65-68
30715843-6	2019	In this study, four physiologically relevant monosaccharides, methylglyoxal, glucose, fructose, and ribose were used to glycate human insulin and two C-terminus truncated insulin analogues.	Pyruvaldehyde	62-75	insulin	Homo sapiens	171-178
30944692-9	2019	In MG-treated HUVECs, glycine restored the function of Glo1, suppressed the AGE/RAGE signaling pathway, and inhibited the generation of reactive oxygen species.	Pyruvaldehyde	3-5	glyoxalase 1	Rattus norvegicus	55-59
30886207-1	2019	The effects of glycation by glyoxal (Gly) and methylglyoxal (MGly) on the early and late conformational alterations in Cytochrome c (Cyt c) were studied.	Pyruvaldehyde	46-59	cytochrome c, somatic	Homo sapiens	119-131
30886207-1	2019	The effects of glycation by glyoxal (Gly) and methylglyoxal (MGly) on the early and late conformational alterations in Cytochrome c (Cyt c) were studied.	Pyruvaldehyde	61-65	cytochrome c, somatic	Homo sapiens	119-131
30886207-1	2019	The effects of glycation by glyoxal (Gly) and methylglyoxal (MGly) on the early and late conformational alterations in Cytochrome c (Cyt c) were studied.	Pyruvaldehyde	61-65	cytochrome c, somatic	Homo sapiens	133-138
30886207-2	2019	Spectroscopic measurements revealed that Cyt c undergo certain conformational alterations and exposure of heme upon overnight incubation with Gly and MGly.	Pyruvaldehyde	150-154	cytochrome c, somatic	Homo sapiens	41-46
30658323-7	2019	Likewise, MG pre-incubation for 6 h increased the angiotensin II-evoked Ca2+ entry in MCECs and muMECs which was abrogated by inhibition of Calcium release activated calcium (CRAC) channels with GSK-7975A, but unaffected by an inhibitor specific to TRPA1 channels.	Pyruvaldehyde	10-12	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	249-254
30668418-14	2019	Moreover, LWDH-WE could attenuate MG-induced atrophy of C2C12 myotubes accompanied with regulating protein synthesis (IGF-1R, Akt, mTOR) and protein degradation (FoxO3a, atrogin-1, MuRF-1) signals.	Pyruvaldehyde	34-36	F-box protein 32	Mus musculus	170-179
30421661-1	2019	BACKGROUND: The enzyme glyoxalase1 (GLO1) is the main opponent in the degradation of the reactive metabolite methylglyoxal (MG), which by glycation of macromolecules is involved in atherogenesis.	Pyruvaldehyde	109-122	glyoxalase I	Homo sapiens	23-34
30421661-1	2019	BACKGROUND: The enzyme glyoxalase1 (GLO1) is the main opponent in the degradation of the reactive metabolite methylglyoxal (MG), which by glycation of macromolecules is involved in atherogenesis.	Pyruvaldehyde	109-122	glyoxalase I	Homo sapiens	36-40
30421661-1	2019	BACKGROUND: The enzyme glyoxalase1 (GLO1) is the main opponent in the degradation of the reactive metabolite methylglyoxal (MG), which by glycation of macromolecules is involved in atherogenesis.	Pyruvaldehyde	124-126	glyoxalase I	Homo sapiens	23-34
30421661-1	2019	BACKGROUND: The enzyme glyoxalase1 (GLO1) is the main opponent in the degradation of the reactive metabolite methylglyoxal (MG), which by glycation of macromolecules is involved in atherogenesis.	Pyruvaldehyde	124-126	glyoxalase I	Homo sapiens	36-40
30628789-3	2019	GLO1 is a Zn2+-dependent enzyme that isomerizes a hemithioacetal, formed from glutathione and methylglyoxal, to a lactic acid thioester.	Pyruvaldehyde	94-107	glyoxalase 1	Mus musculus	0-4
30387069-9	2019	The effects of two putative agonists of GABAA, beta-hydroxybutyrate and methylglyoxal, on S100B secretion were also evaluated.	Pyruvaldehyde	72-85	S100 calcium binding protein B	Homo sapiens	90-95
30756294-8	2019	Therefore, conclusions based on utilization of anti-argpyrimidine antibodies and indicating that HspB1 is the predominant and preferential target of MG modification in the cell require revision.	Pyruvaldehyde	149-151	heat shock protein family B (small) member 1	Homo sapiens	97-102
30781346-2	2019	Methylglyoxal (MG), a glycolytic by-product with cytotoxic and pro-oxidant power, is the major precursor in vivo of advanced glycation end products (AGEs), which are known to exert their detrimental effect via receptor- (e.g., RAGE) or non-receptor-mediated mechanisms in several neurological diseases.	Pyruvaldehyde	0-13	advanced glycosylation end-product specific receptor	Homo sapiens	227-231
30781346-2	2019	Methylglyoxal (MG), a glycolytic by-product with cytotoxic and pro-oxidant power, is the major precursor in vivo of advanced glycation end products (AGEs), which are known to exert their detrimental effect via receptor- (e.g., RAGE) or non-receptor-mediated mechanisms in several neurological diseases.	Pyruvaldehyde	15-17	advanced glycosylation end-product specific receptor	Homo sapiens	227-231
30781346-4	2019	Our results revealed that RTT is linked to an alteration of the GLOs system (specifically, increased GLO2 activity), that ensures unchanged MG-dependent damage levels.	Pyruvaldehyde	140-142	hydroxyacylglutathione hydrolase	Homo sapiens	101-105
30718683-3	2019	Microarray analysis revealed that exposure of HUVECs to high MGO concentrations significantly changes gene expression, characterized by prominent down-regulation of cell cycle associated genes and up-regulation of heme oxygenase-1 (HO-1).	Pyruvaldehyde	61-64	heme oxygenase 1	Homo sapiens	214-230
30718683-5	2019	No significant enrichment of inflammatory pathways was found, yet, MGO did inhibit VCAM-1 expression in Western blot analysis.	Pyruvaldehyde	67-70	vascular cell adhesion molecule 1	Homo sapiens	83-89
30580027-9	2019	Crocin pretreatment also reversed MG-induced changes in mitochondrial mass, mitochondrial membrane potential, mitochondrial superoxide, and glyoxalase I levels.	Pyruvaldehyde	34-36	glyoxalase I	Homo sapiens	140-152
30668418-14	2019	Moreover, LWDH-WE could attenuate MG-induced atrophy of C2C12 myotubes accompanied with regulating protein synthesis (IGF-1R, Akt, mTOR) and protein degradation (FoxO3a, atrogin-1, MuRF-1) signals.	Pyruvaldehyde	34-36	tripartite motif-containing 63	Mus musculus	181-187
29160087-7	2019	Increased formation of MG is linked to increased glyceroneogenesis and hyperglycemia in obesity and diabetes and also down-regulation of glyoxalase 1 (Glo1)-which provides the main enzymatic detoxification of MG.	Pyruvaldehyde	23-25	glyoxalase I	Homo sapiens	137-149
30674353-0	2019	Methylglyoxal, a glycolysis metabolite, triggers metastasis through MEK/ERK/SMAD1 pathway activation in breast cancer.	Pyruvaldehyde	0-13	mitogen-activated protein kinase kinase 7	Homo sapiens	68-71
30674353-0	2019	Methylglyoxal, a glycolysis metabolite, triggers metastasis through MEK/ERK/SMAD1 pathway activation in breast cancer.	Pyruvaldehyde	0-13	mitogen-activated protein kinase 1	Homo sapiens	72-75
30674353-0	2019	Methylglyoxal, a glycolysis metabolite, triggers metastasis through MEK/ERK/SMAD1 pathway activation in breast cancer.	Pyruvaldehyde	0-13	SMAD family member 1	Homo sapiens	76-81
30674353-7	2019	Hyperactivation of MEK/ERK/SMAD1 pathway was evidenced using western blotting upon endogenous MG stress and exogenous MG treatment conditions.	Pyruvaldehyde	94-96	mitogen-activated protein kinase kinase 7	Homo sapiens	19-22
30674353-7	2019	Hyperactivation of MEK/ERK/SMAD1 pathway was evidenced using western blotting upon endogenous MG stress and exogenous MG treatment conditions.	Pyruvaldehyde	94-96	mitogen-activated protein kinase 1	Homo sapiens	23-26
30674353-7	2019	Hyperactivation of MEK/ERK/SMAD1 pathway was evidenced using western blotting upon endogenous MG stress and exogenous MG treatment conditions.	Pyruvaldehyde	94-96	SMAD family member 1	Homo sapiens	27-32
30674353-7	2019	Hyperactivation of MEK/ERK/SMAD1 pathway was evidenced using western blotting upon endogenous MG stress and exogenous MG treatment conditions.	Pyruvaldehyde	118-120	mitogen-activated protein kinase kinase 7	Homo sapiens	19-22
30674353-7	2019	Hyperactivation of MEK/ERK/SMAD1 pathway was evidenced using western blotting upon endogenous MG stress and exogenous MG treatment conditions.	Pyruvaldehyde	118-120	mitogen-activated protein kinase 1	Homo sapiens	23-26
30674353-7	2019	Hyperactivation of MEK/ERK/SMAD1 pathway was evidenced using western blotting upon endogenous MG stress and exogenous MG treatment conditions.	Pyruvaldehyde	118-120	SMAD family member 1	Homo sapiens	27-32
30728759-9	2018	Methylglyoxal, a product of a deviation of glycolysis, and its derivative D-lactate are also released by astrocytes and bind to GABAA receptors and HCAR1, respectively.	Pyruvaldehyde	0-13	hydroxycarboxylic acid receptor 1	Homo sapiens	148-153
29160087-7	2019	Increased formation of MG is linked to increased glyceroneogenesis and hyperglycemia in obesity and diabetes and also down-regulation of glyoxalase 1 (Glo1)-which provides the main enzymatic detoxification of MG.	Pyruvaldehyde	23-25	glyoxalase I	Homo sapiens	151-155
29160087-7	2019	Increased formation of MG is linked to increased glyceroneogenesis and hyperglycemia in obesity and diabetes and also down-regulation of glyoxalase 1 (Glo1)-which provides the main enzymatic detoxification of MG.	Pyruvaldehyde	209-211	glyoxalase I	Homo sapiens	137-149
29160087-7	2019	Increased formation of MG is linked to increased glyceroneogenesis and hyperglycemia in obesity and diabetes and also down-regulation of glyoxalase 1 (Glo1)-which provides the main enzymatic detoxification of MG.	Pyruvaldehyde	209-211	glyoxalase I	Homo sapiens	151-155
30508605-2	2019	In general, MG is metabolized by the glyoxalase 1(GLO1)/GLO2 system and aldose reductase (AR); however, excessive MG can react with proteins and nucleic acids to induce the accumulation of advanced glycation end products (AGEs).	Pyruvaldehyde	12-14	glyoxalase 1	Mus musculus	37-49
30577692-0	2019	Effect of Methylglyoxal-Induced Glycation on the Composition and Structure of beta-Lactoglobulin and alpha-Lactalbumin.	Pyruvaldehyde	10-23	lactalbumin alpha	Homo sapiens	101-118
30577692-5	2019	This study investigated whether and how MGO exposure, with or without concurrent heat exposure, affected the major whey proteins beta-lactoglobulin and alpha-lactalbumin.	Pyruvaldehyde	40-43	lactalbumin alpha	Homo sapiens	152-169
30577692-8	2019	UPLC analysis revealed MGO-dependent consumption of specific amino acids in the order Cys &gt; Arg &gt; Lys &gt; Trp for both proteins, with alpha-lactalbumin affected to a greater extent than beta-lactoglobulin.	Pyruvaldehyde	23-26	lactalbumin alpha	Homo sapiens	141-158
30391748-5	2019	The pathological concentration of MGO (100 muM) was then applied to investigate its effect on inducible nitric oxide synthase (iNOS) expression and NO release on interferon-gamma (IFN-gamma) (100 IU/ml) and lipopolysaccharide (LPS) (100 microg/ml)-stimulated control ASMCs.	Pyruvaldehyde	34-37	nitric oxide synthase 2	Rattus norvegicus	94-125
30391748-5	2019	The pathological concentration of MGO (100 muM) was then applied to investigate its effect on inducible nitric oxide synthase (iNOS) expression and NO release on interferon-gamma (IFN-gamma) (100 IU/ml) and lipopolysaccharide (LPS) (100 microg/ml)-stimulated control ASMCs.	Pyruvaldehyde	34-37	nitric oxide synthase 2	Rattus norvegicus	127-131
30391748-5	2019	The pathological concentration of MGO (100 muM) was then applied to investigate its effect on inducible nitric oxide synthase (iNOS) expression and NO release on interferon-gamma (IFN-gamma) (100 IU/ml) and lipopolysaccharide (LPS) (100 microg/ml)-stimulated control ASMCs.	Pyruvaldehyde	34-37	interferon gamma	Rattus norvegicus	162-178
30391748-5	2019	The pathological concentration of MGO (100 muM) was then applied to investigate its effect on inducible nitric oxide synthase (iNOS) expression and NO release on interferon-gamma (IFN-gamma) (100 IU/ml) and lipopolysaccharide (LPS) (100 microg/ml)-stimulated control ASMCs.	Pyruvaldehyde	34-37	interferon gamma	Rattus norvegicus	180-189
30391748-6	2019	MGO (100 microM) inhibited IFN-gamma and LPS-stimulated iNOS expression through inhibiting Akt phosphorylation and inhibition of iNOS expression was prevented by L-arginine (100 microM) co-treatment.	Pyruvaldehyde	0-3	interferon gamma	Rattus norvegicus	27-36
30391748-6	2019	MGO (100 microM) inhibited IFN-gamma and LPS-stimulated iNOS expression through inhibiting Akt phosphorylation and inhibition of iNOS expression was prevented by L-arginine (100 microM) co-treatment.	Pyruvaldehyde	0-3	nitric oxide synthase 2	Rattus norvegicus	56-60
30391748-6	2019	MGO (100 microM) inhibited IFN-gamma and LPS-stimulated iNOS expression through inhibiting Akt phosphorylation and inhibition of iNOS expression was prevented by L-arginine (100 microM) co-treatment.	Pyruvaldehyde	0-3	AKT serine/threonine kinase 1	Rattus norvegicus	91-94
30391748-6	2019	MGO (100 microM) inhibited IFN-gamma and LPS-stimulated iNOS expression through inhibiting Akt phosphorylation and inhibition of iNOS expression was prevented by L-arginine (100 microM) co-treatment.	Pyruvaldehyde	0-3	nitric oxide synthase 2	Rattus norvegicus	129-133
30342159-0	2019	Methylglyoxal accumulation de-regulates HoxA5 expression, thereby impairing angiogenesis in glyoxalase 1 knock-down mouse aortic endothelial cells.	Pyruvaldehyde	0-13	homeobox A5	Mus musculus	40-45
30342159-0	2019	Methylglyoxal accumulation de-regulates HoxA5 expression, thereby impairing angiogenesis in glyoxalase 1 knock-down mouse aortic endothelial cells.	Pyruvaldehyde	0-13	glyoxalase 1	Mus musculus	92-104
30342159-2	2019	Methylglyoxal (MGO) is a glycolysis byproduct that accumulates in DM and is detoxified by the Glyoxalase 1 (Glo1).	Pyruvaldehyde	0-13	glyoxalase 1	Mus musculus	94-106
30342159-2	2019	Methylglyoxal (MGO) is a glycolysis byproduct that accumulates in DM and is detoxified by the Glyoxalase 1 (Glo1).	Pyruvaldehyde	0-13	glyoxalase 1	Mus musculus	108-112
30342159-2	2019	Methylglyoxal (MGO) is a glycolysis byproduct that accumulates in DM and is detoxified by the Glyoxalase 1 (Glo1).	Pyruvaldehyde	15-18	glyoxalase 1	Mus musculus	94-106
30342159-2	2019	Methylglyoxal (MGO) is a glycolysis byproduct that accumulates in DM and is detoxified by the Glyoxalase 1 (Glo1).	Pyruvaldehyde	15-18	glyoxalase 1	Mus musculus	108-112
30342159-6	2019	Reduction in Glo1 expression led to an accumulation of MGO and MGO-modified proteins and impaired angiogenesis of Glo1KD MAECs.	Pyruvaldehyde	55-58	glyoxalase 1	Mus musculus	13-17
30342159-6	2019	Reduction in Glo1 expression led to an accumulation of MGO and MGO-modified proteins and impaired angiogenesis of Glo1KD MAECs.	Pyruvaldehyde	63-66	glyoxalase 1	Mus musculus	13-17
30342159-11	2019	This study demonstrates, for the first time, that MGO accumulation increases the antiangiogenic factor HoxA5 via NF-kB-p65, thereby impairing the angiogenic ability of endothelial cells.	Pyruvaldehyde	50-53	homeobox A5	Mus musculus	103-108
30342159-11	2019	This study demonstrates, for the first time, that MGO accumulation increases the antiangiogenic factor HoxA5 via NF-kB-p65, thereby impairing the angiogenic ability of endothelial cells.	Pyruvaldehyde	50-53	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	119-122
30391748-7	2019	These findings show for the first time that MGO inhibits IFN-gamma and LPS-stimulated iNOS expression in ASMCs, in addition to inhibiting IFN-gamma and LPS-induced Akt phosphorylation.	Pyruvaldehyde	44-47	interferon gamma	Rattus norvegicus	57-66
30391748-7	2019	These findings show for the first time that MGO inhibits IFN-gamma and LPS-stimulated iNOS expression in ASMCs, in addition to inhibiting IFN-gamma and LPS-induced Akt phosphorylation.	Pyruvaldehyde	44-47	nitric oxide synthase 2	Rattus norvegicus	86-90
30391748-7	2019	These findings show for the first time that MGO inhibits IFN-gamma and LPS-stimulated iNOS expression in ASMCs, in addition to inhibiting IFN-gamma and LPS-induced Akt phosphorylation.	Pyruvaldehyde	44-47	interferon gamma	Rattus norvegicus	138-147
30391748-7	2019	These findings show for the first time that MGO inhibits IFN-gamma and LPS-stimulated iNOS expression in ASMCs, in addition to inhibiting IFN-gamma and LPS-induced Akt phosphorylation.	Pyruvaldehyde	44-47	AKT serine/threonine kinase 1	Rattus norvegicus	164-167
30508605-2	2019	In general, MG is metabolized by the glyoxalase 1(GLO1)/GLO2 system and aldose reductase (AR); however, excessive MG can react with proteins and nucleic acids to induce the accumulation of advanced glycation end products (AGEs).	Pyruvaldehyde	12-14	glyoxalase 1	Mus musculus	50-54
30508605-2	2019	In general, MG is metabolized by the glyoxalase 1(GLO1)/GLO2 system and aldose reductase (AR); however, excessive MG can react with proteins and nucleic acids to induce the accumulation of advanced glycation end products (AGEs).	Pyruvaldehyde	12-14	hydroxyacyl glutathione hydrolase	Mus musculus	56-60
30508605-2	2019	In general, MG is metabolized by the glyoxalase 1(GLO1)/GLO2 system and aldose reductase (AR); however, excessive MG can react with proteins and nucleic acids to induce the accumulation of advanced glycation end products (AGEs).	Pyruvaldehyde	12-14	aldo-keto reductase family 1, member B3 (aldose reductase)	Mus musculus	72-88
30508605-2	2019	In general, MG is metabolized by the glyoxalase 1(GLO1)/GLO2 system and aldose reductase (AR); however, excessive MG can react with proteins and nucleic acids to induce the accumulation of advanced glycation end products (AGEs).	Pyruvaldehyde	12-14	aldo-keto reductase family 1, member B3 (aldose reductase)	Mus musculus	90-92
30508605-7	2019	We also investigated the expression levels of GLO1 and AR, the main metabolizing enzymes of MG, in various brain regions, across age groups.	Pyruvaldehyde	92-94	glyoxalase 1	Mus musculus	46-50
30508605-7	2019	We also investigated the expression levels of GLO1 and AR, the main metabolizing enzymes of MG, in various brain regions, across age groups.	Pyruvaldehyde	92-94	aldo-keto reductase family 1, member B3 (aldose reductase)	Mus musculus	55-57
30508605-10	2019	Moreover, although a significant positive correlation was observed between GLO1 expression and MG concentration in the brains of young mice, no significant correlations were observed in the brains of aged mice.	Pyruvaldehyde	95-97	glyoxalase 1	Mus musculus	75-79
30398646-10	2018	Gene expression of glyoxalase 1 (GLO1), the enzyme involved in the degradation of MGO, was determined by either microarray or quantitative reverse transcriptase-polymerase chain reaction.	Pyruvaldehyde	82-85	glyoxalase I	Homo sapiens	19-31
30943519-11	2019	STAT3 inhibitor reduced the high glucose-induced EMT, via reducing TGF-beta expression and repressing the accumulation of MGO and AGEs.	Pyruvaldehyde	122-125	signal transducer and activator of transcription 3	Homo sapiens	0-5
30306863-2	2019	It is composed of Glyoxalase-I (Glo-I) and Glyoxalase- II which perform an essential metabolic process inside the cell by detoxifying endogenous harmful metabolites, mainly methylglyoxal (MG) into non-toxic D-lactic acid.	Pyruvaldehyde	173-186	glyoxalase I	Homo sapiens	18-30
30306863-2	2019	It is composed of Glyoxalase-I (Glo-I) and Glyoxalase- II which perform an essential metabolic process inside the cell by detoxifying endogenous harmful metabolites, mainly methylglyoxal (MG) into non-toxic D-lactic acid.	Pyruvaldehyde	173-186	glyoxalase I	Homo sapiens	32-37
30306863-2	2019	It is composed of Glyoxalase-I (Glo-I) and Glyoxalase- II which perform an essential metabolic process inside the cell by detoxifying endogenous harmful metabolites, mainly methylglyoxal (MG) into non-toxic D-lactic acid.	Pyruvaldehyde	173-186	hydroxyacylglutathione hydrolase	Homo sapiens	43-57
30306863-2	2019	It is composed of Glyoxalase-I (Glo-I) and Glyoxalase- II which perform an essential metabolic process inside the cell by detoxifying endogenous harmful metabolites, mainly methylglyoxal (MG) into non-toxic D-lactic acid.	Pyruvaldehyde	188-190	glyoxalase I	Homo sapiens	18-30
30306863-2	2019	It is composed of Glyoxalase-I (Glo-I) and Glyoxalase- II which perform an essential metabolic process inside the cell by detoxifying endogenous harmful metabolites, mainly methylglyoxal (MG) into non-toxic D-lactic acid.	Pyruvaldehyde	188-190	glyoxalase I	Homo sapiens	32-37
30306863-2	2019	It is composed of Glyoxalase-I (Glo-I) and Glyoxalase- II which perform an essential metabolic process inside the cell by detoxifying endogenous harmful metabolites, mainly methylglyoxal (MG) into non-toxic D-lactic acid.	Pyruvaldehyde	188-190	hydroxyacylglutathione hydrolase	Homo sapiens	43-57
30693045-2	2018	Chronic hyperglycemia produces advanced glycation end products such as the methylglyoxal (MGO) which interferes with cell functions, insulin signaling, and beta-cell functions.	Pyruvaldehyde	75-88	insulin	Homo sapiens	133-140
30693045-2	2018	Chronic hyperglycemia produces advanced glycation end products such as the methylglyoxal (MGO) which interferes with cell functions, insulin signaling, and beta-cell functions.	Pyruvaldehyde	90-93	insulin	Homo sapiens	133-140
30217477-0	2018	Effects of methylglyoxal on RANKL-induced osteoclast differentiation in RAW264.7 cells.	Pyruvaldehyde	11-24	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	28-33
30217477-3	2018	The objective of this study was to evaluate the effect of MG on RANKL-induced osteoclast differentiation in RAW264.7 cells, a murine macrophage cell line.	Pyruvaldehyde	58-60	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	64-69
30217477-7	2018	MG markedly inhibited RANKL-induced TRAP activity.	Pyruvaldehyde	0-2	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	22-27
30217477-8	2018	MG treatment resulted in a significant decrease in intracellular calcium concentration, mitochondrial mass, mitochondrial membrane potential, and glyoxalase I level during osteoclastogenesis.	Pyruvaldehyde	0-2	glyoxalase 1	Mus musculus	146-158
30217477-12	2018	Our findings indicate that MG inhibits TRAP and glyoxalase I activity and impairs mitochondrial function in osteoclasts.	Pyruvaldehyde	27-29	glyoxalase 1	Mus musculus	48-60
30404736-6	2018	Methylglyoxal significantly increased maximal contraction of the rat aorta to PE, Ang II and VP.	Pyruvaldehyde	0-13	angiotensinogen	Rattus norvegicus	82-88
30280601-0	2018	Anti-C5a complementary peptide mitigates zymosan-induced severe peritonitis with fibrotic encapsulation in rats pretreated with methylglyoxal.	Pyruvaldehyde	128-141	complement C5	Rattus norvegicus	5-8
30398646-10	2018	Gene expression of glyoxalase 1 (GLO1), the enzyme involved in the degradation of MGO, was determined by either microarray or quantitative reverse transcriptase-polymerase chain reaction.	Pyruvaldehyde	82-85	glyoxalase I	Homo sapiens	33-37
30125541-5	2018	Glyoxalase 1 (Glo1) detoxifies methylglyoxal (MG), a highly reactive carbonyl species mainly formed during glycolysis, which is a potent precursor of cytotoxic advanced glycation end products (AGEs).	Pyruvaldehyde	31-44	glyoxalase I	Homo sapiens	14-18
30287091-1	2018	OBJECTIVES: The deficit of Glyoxalase I (Glo1) and the subsequent increase in methylglyoxal (MG) has been reported to be one the five mechanisms by which hyperglycemia causes diabetic late complications.	Pyruvaldehyde	78-91	glyoxalase I	Homo sapiens	27-39
30287091-1	2018	OBJECTIVES: The deficit of Glyoxalase I (Glo1) and the subsequent increase in methylglyoxal (MG) has been reported to be one the five mechanisms by which hyperglycemia causes diabetic late complications.	Pyruvaldehyde	78-91	glyoxalase I	Homo sapiens	41-45
30287091-6	2018	It was subsequently found that the enzymatic efficiency of various oxidoreductases in the liver and kidney towards MG were increased in the Glo1-/- mice.	Pyruvaldehyde	115-117	glyoxalase 1	Mus musculus	140-144
29982163-3	2018	Glycation experiments are carried out using glucose and methylglyoxal to validate the molecular modelling results on the interaction of modified BSA with C3G.	Pyruvaldehyde	56-69	Rap guanine nucleotide exchange factor 1	Homo sapiens	154-157
30125541-5	2018	Glyoxalase 1 (Glo1) detoxifies methylglyoxal (MG), a highly reactive carbonyl species mainly formed during glycolysis, which is a potent precursor of cytotoxic advanced glycation end products (AGEs).	Pyruvaldehyde	31-44	glyoxalase I	Homo sapiens	0-12
30062553-1	2018	Glyoxalase 1 (Glo-1) is an ubiquitous cellular enzyme that participates in the detoxification of methylglyoxal (MG), a cytotoxic byproduct of glycolysis that induces protein modification (advanced glycation end products [AGEs]), oxidative stress, and inflammation.	Pyruvaldehyde	97-110	glyoxalase 1	Rattus norvegicus	0-12
30062553-1	2018	Glyoxalase 1 (Glo-1) is an ubiquitous cellular enzyme that participates in the detoxification of methylglyoxal (MG), a cytotoxic byproduct of glycolysis that induces protein modification (advanced glycation end products [AGEs]), oxidative stress, and inflammation.	Pyruvaldehyde	97-110	glyoxalase 1	Rattus norvegicus	14-19
30062553-1	2018	Glyoxalase 1 (Glo-1) is an ubiquitous cellular enzyme that participates in the detoxification of methylglyoxal (MG), a cytotoxic byproduct of glycolysis that induces protein modification (advanced glycation end products [AGEs]), oxidative stress, and inflammation.	Pyruvaldehyde	112-114	glyoxalase 1	Rattus norvegicus	0-12
30062553-1	2018	Glyoxalase 1 (Glo-1) is an ubiquitous cellular enzyme that participates in the detoxification of methylglyoxal (MG), a cytotoxic byproduct of glycolysis that induces protein modification (advanced glycation end products [AGEs]), oxidative stress, and inflammation.	Pyruvaldehyde	112-114	glyoxalase 1	Rattus norvegicus	14-19
30150385-6	2018	In addition, MGO treatment of cells lacking the major detoxifying enzyme, glyoxalase 1, results in marked disruption of H2B acetylation and ubiquitylation without affecting H2A, H3, and H4 modifications.	Pyruvaldehyde	13-16	H2A clustered histone 18	Homo sapiens	173-188
30279491-0	2018	Hyperglycaemia-induced methylglyoxal accumulation potentiates VEGF resistance of diabetic monocytes through the aberrant activation of tyrosine phosphatase SHP-2/SRC kinase signalling axis.	Pyruvaldehyde	23-36	vascular endothelial growth factor A	Homo sapiens	62-66
30279491-0	2018	Hyperglycaemia-induced methylglyoxal accumulation potentiates VEGF resistance of diabetic monocytes through the aberrant activation of tyrosine phosphatase SHP-2/SRC kinase signalling axis.	Pyruvaldehyde	23-36	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	156-161
30279491-6	2018	Mechanistically, DM conditions or MG exposure resulted in the upregulation of the expression of SHP-2 phosphatase.	Pyruvaldehyde	34-36	protein tyrosine phosphatase, non-receptor type 11	Mus musculus	96-101
30279491-9	2018	We demonstrated that MG-induced molecular changes could be reversed by pharmacological inhibitors of SHP-2 and SRC and by genetic depletion of SHP-2.	Pyruvaldehyde	21-23	protein tyrosine phosphatase, non-receptor type 11	Mus musculus	101-106
30279491-9	2018	We demonstrated that MG-induced molecular changes could be reversed by pharmacological inhibitors of SHP-2 and SRC and by genetic depletion of SHP-2.	Pyruvaldehyde	21-23	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	111-114
30279491-9	2018	We demonstrated that MG-induced molecular changes could be reversed by pharmacological inhibitors of SHP-2 and SRC and by genetic depletion of SHP-2.	Pyruvaldehyde	21-23	protein tyrosine phosphatase, non-receptor type 11	Mus musculus	143-148
30170097-5	2018	Additionally, acridine orange staining and immunoblotting with LC3B antibody indicated the suppression of doxorubicin induced autophagy flux with methylglyoxal co-treatment.	Pyruvaldehyde	146-159	microtubule associated protein 1 light chain 3 beta	Homo sapiens	63-67
30323285-6	2018	Inhibition of PGK1 results in accumulation of the reactive metabolite methylglyoxal, which selectively modifies KEAP1 to form a methylimidazole crosslink between proximal cysteine and arginine residues (MICA).	Pyruvaldehyde	70-83	phosphoglycerate kinase 1	Homo sapiens	14-18
30323285-6	2018	Inhibition of PGK1 results in accumulation of the reactive metabolite methylglyoxal, which selectively modifies KEAP1 to form a methylimidazole crosslink between proximal cysteine and arginine residues (MICA).	Pyruvaldehyde	70-83	kelch like ECH associated protein 1	Homo sapiens	112-117
30323285-6	2018	Inhibition of PGK1 results in accumulation of the reactive metabolite methylglyoxal, which selectively modifies KEAP1 to form a methylimidazole crosslink between proximal cysteine and arginine residues (MICA).	Pyruvaldehyde	70-83	MHC class I polypeptide-related sequence A	Homo sapiens	203-207
30099685-1	2018	Glyoxalase 1 (GLO1) is a ubiquitous cellular enzyme involved in detoxification of methylglyoxal (MGO), a cytotoxic byproduct of glycolysis, whose excess can cause oxidative stress.	Pyruvaldehyde	82-95	glyoxalase I	Homo sapiens	0-12
30099685-1	2018	Glyoxalase 1 (GLO1) is a ubiquitous cellular enzyme involved in detoxification of methylglyoxal (MGO), a cytotoxic byproduct of glycolysis, whose excess can cause oxidative stress.	Pyruvaldehyde	82-95	glyoxalase I	Homo sapiens	14-18
30099685-1	2018	Glyoxalase 1 (GLO1) is a ubiquitous cellular enzyme involved in detoxification of methylglyoxal (MGO), a cytotoxic byproduct of glycolysis, whose excess can cause oxidative stress.	Pyruvaldehyde	97-100	glyoxalase I	Homo sapiens	0-12
30099685-1	2018	Glyoxalase 1 (GLO1) is a ubiquitous cellular enzyme involved in detoxification of methylglyoxal (MGO), a cytotoxic byproduct of glycolysis, whose excess can cause oxidative stress.	Pyruvaldehyde	97-100	glyoxalase I	Homo sapiens	14-18
30150385-7	2018	Using RNA sequencing, we show that MGO is capable of altering gene transcription, most notably in cells lacking GLO1.	Pyruvaldehyde	35-38	glyoxalase I	Homo sapiens	112-116
29902553-8	2018	The formation of specific semialdehydes in HSA after incubation with GO and MGO at pathological concentrations was reported for the first time in this study, and may be used as early and specific biomarkers of the oxidative stress undergone by diabetic patients.	Pyruvaldehyde	76-79	albumin	Homo sapiens	43-46
30015246-2	2018	Interaction of SERCA1 with MGX was investigated by molecular docking and experimentally in a cell-free system.	Pyruvaldehyde	27-30	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 1	Rattus norvegicus	15-21
29802959-4	2018	ApoA-I was chemically glycated by two different glucose metabolites (methylglyoxal and glycolaldehyde).	Pyruvaldehyde	69-82	apolipoprotein A1	Rattus norvegicus	0-6
29802959-9	2018	The stimulatory effects of apoA-I on the in vivo glucose clearance were negatively affected when apoA-I was modified with methylglyoxal, but not with glycolaldehyde.	Pyruvaldehyde	122-135	apolipoprotein A1	Rattus norvegicus	27-33
29802959-9	2018	The stimulatory effects of apoA-I on the in vivo glucose clearance were negatively affected when apoA-I was modified with methylglyoxal, but not with glycolaldehyde.	Pyruvaldehyde	122-135	apolipoprotein A1	Rattus norvegicus	97-103
30015246-3	2018	MGX concentration- and time-dependently decreased SERCA1 activity.	Pyruvaldehyde	0-3	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 1	Rattus norvegicus	50-56
30015246-6	2018	Molecular docking indicated binding of MGX at the cytosolic region of SERCA1, inducing conformational changes in the cytosolic-transmembrane interface.	Pyruvaldehyde	39-42	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 1	Rattus norvegicus	70-76
29775571-0	2018	Effect of methylglyoxal on reactive oxygen species, KI-67, and caspase-3 expression in MCF-7 cells.	Pyruvaldehyde	10-23	caspase 3	Homo sapiens	63-72
29775571-12	2018	The caspase-3 expressions were significantly greater in all groups of MCF-7 cells treated with MG groups compared to the control group (p &lt; .05).	Pyruvaldehyde	95-97	caspase 3	Homo sapiens	4-13
29550330-4	2018	In particular, MG-collagen-induced apoptosis is associated with the activation of the PERK-eIF2alpha pathway and caspase-12.	Pyruvaldehyde	15-17	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	86-90
29603293-4	2018	Treatment of RIN-m5F cells with sciadopitysin prevented MG-induced production of interleukin-1beta, intracellular reactive oxygen species and cardiolipin peroxidation.	Pyruvaldehyde	56-58	interleukin 1 beta	Rattus norvegicus	81-98
29481950-0	2018	Methylglyoxal induced glycation and aggregation of human serum albumin: Biochemical and biophysical approach.	Pyruvaldehyde	0-13	albumin	Homo sapiens	57-70
29481950-3	2018	In our present study, methylglyoxal was investigated for its effect on the structure of human serum albumin (HSA); exploring the formation of AGEs and aggregates of HSA.	Pyruvaldehyde	22-35	albumin	Homo sapiens	94-107
29481950-3	2018	In our present study, methylglyoxal was investigated for its effect on the structure of human serum albumin (HSA); exploring the formation of AGEs and aggregates of HSA.	Pyruvaldehyde	22-35	albumin	Homo sapiens	109-112
29481950-3	2018	In our present study, methylglyoxal was investigated for its effect on the structure of human serum albumin (HSA); exploring the formation of AGEs and aggregates of HSA.	Pyruvaldehyde	22-35	albumin	Homo sapiens	165-168
29792365-5	2018	Piceatannol also increased glyoxalase I activity and glutathione levels in MG-treated cells, which indicates that it enhanced the glyoxalase system and thus cellular protection.	Pyruvaldehyde	75-77	glyoxalase 1	Mus musculus	27-39
29550330-4	2018	In particular, MG-collagen-induced apoptosis is associated with the activation of the PERK-eIF2alpha pathway and caspase-12.	Pyruvaldehyde	15-17	eukaryotic translation initiation factor 2A	Homo sapiens	91-100
29525672-0	2018	Isoferulic acid attenuates methylglyoxal-induced apoptosis in INS-1 rat pancreatic beta-cell through mitochondrial survival pathways and increasing glyoxalase-1 activity.	Pyruvaldehyde	27-40	insulin 1	Rattus norvegicus	62-67
29783710-2	2018	Methylglyoxal is efficiently detoxified by enzyme glyoxalase 1 (GLO1).	Pyruvaldehyde	0-13	glyoxalase I	Homo sapiens	50-62
29783710-2	2018	Methylglyoxal is efficiently detoxified by enzyme glyoxalase 1 (GLO1).	Pyruvaldehyde	0-13	glyoxalase I	Homo sapiens	64-68
29723250-7	2018	SET7/9 expression was elevated in both MGO-injected mice and nonadherent cells isolated from the effluent of PD patients.	Pyruvaldehyde	39-42	SET domain containing (lysine methyltransferase) 7	Mus musculus	0-6
29532486-1	2018	BACKGROUND: Glyoxalase 1 (GLO1) is an enzyme that metabolizes methylglyoxal (MG), which is a competitive partial agonist at GABAA receptors.	Pyruvaldehyde	62-75	glyoxalase 1	Mus musculus	12-24
29532486-1	2018	BACKGROUND: Glyoxalase 1 (GLO1) is an enzyme that metabolizes methylglyoxal (MG), which is a competitive partial agonist at GABAA receptors.	Pyruvaldehyde	62-75	glyoxalase 1	Mus musculus	26-30
29532486-1	2018	BACKGROUND: Glyoxalase 1 (GLO1) is an enzyme that metabolizes methylglyoxal (MG), which is a competitive partial agonist at GABAA receptors.	Pyruvaldehyde	77-79	glyoxalase 1	Mus musculus	12-24
29532486-1	2018	BACKGROUND: Glyoxalase 1 (GLO1) is an enzyme that metabolizes methylglyoxal (MG), which is a competitive partial agonist at GABAA receptors.	Pyruvaldehyde	77-79	glyoxalase 1	Mus musculus	26-30
29532486-2	2018	Inhibition of GLO1 increases concentrations of MG in the brain and decreases binge-like ethanol (EtOH) drinking.	Pyruvaldehyde	47-49	glyoxalase 1	Mus musculus	14-18
29524430-3	2018	MGO is detoxified by glyoxalase 1 (GLO1) system in the cytoplasm.	Pyruvaldehyde	0-3	glyoxalase I	Homo sapiens	21-33
29524430-3	2018	MGO is detoxified by glyoxalase 1 (GLO1) system in the cytoplasm.	Pyruvaldehyde	0-3	glyoxalase I	Homo sapiens	35-39
29525672-0	2018	Isoferulic acid attenuates methylglyoxal-induced apoptosis in INS-1 rat pancreatic beta-cell through mitochondrial survival pathways and increasing glyoxalase-1 activity.	Pyruvaldehyde	27-40	glyoxalase 1	Rattus norvegicus	148-160
29525672-6	2018	The results showed that pretreatment of INS-1 cells with 100 muM IFA for 48 h prevented MG-induced decrease in cell viability and impairment of glucose-stimulated insulin secretion (GSIS).	Pyruvaldehyde	88-90	insulin 1	Rattus norvegicus	40-45
29525672-8	2018	Furthermore, IFA pretreatment reduced MG-induced increase in caspase-3 activity, suggesting a reduction of apoptotic cell death.	Pyruvaldehyde	38-40	caspase 3	Rattus norvegicus	61-70
29525672-9	2018	IFA (50-100 muM) itself markedly increased the activity of glyoxalase 1 (GLO1), a major enzyme for the detoxification of MG.	Pyruvaldehyde	121-123	glyoxalase 1	Rattus norvegicus	59-71
29525672-9	2018	IFA (50-100 muM) itself markedly increased the activity of glyoxalase 1 (GLO1), a major enzyme for the detoxification of MG.	Pyruvaldehyde	121-123	glyoxalase 1	Rattus norvegicus	73-77
29525672-10	2018	The results showed that 100 muM IFA protected MG-induced loss of GLO1 activity in INS-1 cells.	Pyruvaldehyde	46-48	glyoxalase 1	Rattus norvegicus	65-69
29525672-10	2018	The results showed that 100 muM IFA protected MG-induced loss of GLO1 activity in INS-1 cells.	Pyruvaldehyde	46-48	insulin 1	Rattus norvegicus	82-87
29525672-11	2018	These findings suggest that IFA pretreatment attentuates MG-induced dysfunction and apoptosis in INS-1 pancreatic beta-cells through mitochondrial survival pathway and increasing GLO1 activity.	Pyruvaldehyde	57-59	glyoxalase 1	Rattus norvegicus	179-183
29154133-3	2018	In this study, compared with the Cd-stressed seedlings without MG treatment, MG treatment could stimulate the activities of glutathione reductase (GR) and gamma-glutamylcysteine synthetase (gamma-ECS) in Cd-stressed wheat seedlings, which in turn induced an increase of reduced glutathione (GSH).	Pyruvaldehyde	77-79	glutamate--cysteine ligase B, chloroplastic	Triticum aestivum	155-188
29504694-4	2018	Glyoxalase 1 (Glo1) is the detoxification enzyme of methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs).	Pyruvaldehyde	52-65	glyoxalase I	Homo sapiens	0-12
29504694-4	2018	Glyoxalase 1 (Glo1) is the detoxification enzyme of methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs).	Pyruvaldehyde	52-65	glyoxalase I	Homo sapiens	14-18
29504694-4	2018	Glyoxalase 1 (Glo1) is the detoxification enzyme of methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs).	Pyruvaldehyde	67-69	glyoxalase I	Homo sapiens	0-12
29504694-4	2018	Glyoxalase 1 (Glo1) is the detoxification enzyme of methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs).	Pyruvaldehyde	67-69	glyoxalase I	Homo sapiens	14-18
29307109-4	2018	The glyoxalase system member glyoxalase 1 (GLO1) is the principal scavenging enzyme of methylglyoxal (MG), a toxic byproduct of glycolysis.	Pyruvaldehyde	87-100	glyoxalase I	Homo sapiens	29-41
29307109-4	2018	The glyoxalase system member glyoxalase 1 (GLO1) is the principal scavenging enzyme of methylglyoxal (MG), a toxic byproduct of glycolysis.	Pyruvaldehyde	87-100	glyoxalase I	Homo sapiens	43-47
29307109-4	2018	The glyoxalase system member glyoxalase 1 (GLO1) is the principal scavenging enzyme of methylglyoxal (MG), a toxic byproduct of glycolysis.	Pyruvaldehyde	102-104	glyoxalase I	Homo sapiens	29-41
29307109-4	2018	The glyoxalase system member glyoxalase 1 (GLO1) is the principal scavenging enzyme of methylglyoxal (MG), a toxic byproduct of glycolysis.	Pyruvaldehyde	102-104	glyoxalase I	Homo sapiens	43-47
29477239-7	2018	A key precursor of AGEs is the dicarbonyl metabolite MG, which is metabolized by glyoxalase 1 (Glo1) of the cytoplasmic glyoxalase system.	Pyruvaldehyde	53-55	glyoxalase I	Homo sapiens	81-93
29477239-7	2018	A key precursor of AGEs is the dicarbonyl metabolite MG, which is metabolized by glyoxalase 1 (Glo1) of the cytoplasmic glyoxalase system.	Pyruvaldehyde	53-55	glyoxalase I	Homo sapiens	95-99
28506645-11	2018	Tumour stem cells and tumours with high flux of MG formation and Glo1 expression are sensitive to Glo1 inhibitor therapy.	Pyruvaldehyde	48-50	glyoxalase I	Homo sapiens	98-102
29556176-3	2018	However, MG is also a substrate in the generation of advanced glycation end products (AGEs) that function by activating the receptor of AGEs (RAGE).	Pyruvaldehyde	9-11	advanced glycosylation end-product specific receptor	Homo sapiens	142-146
29355739-3	2018	Glyoxalase 1 (Glo1) is the detoxification enzyme of methylglyoxal (MG), a major precursor of advanced glycation end products (AGEs), potent pro-apoptotic agents.	Pyruvaldehyde	52-65	glyoxalase I	Homo sapiens	0-12
29355739-3	2018	Glyoxalase 1 (Glo1) is the detoxification enzyme of methylglyoxal (MG), a major precursor of advanced glycation end products (AGEs), potent pro-apoptotic agents.	Pyruvaldehyde	67-69	glyoxalase I	Homo sapiens	14-18
29355739-3	2018	Glyoxalase 1 (Glo1) is the detoxification enzyme of methylglyoxal (MG), a major precursor of advanced glycation end products (AGEs), potent pro-apoptotic agents.	Pyruvaldehyde	67-69	glyoxalase I	Homo sapiens	0-12
29355739-3	2018	Glyoxalase 1 (Glo1) is the detoxification enzyme of methylglyoxal (MG), a major precursor of advanced glycation end products (AGEs), potent pro-apoptotic agents.	Pyruvaldehyde	52-65	glyoxalase I	Homo sapiens	14-18
29495397-7	2018	However, the EU-treated group showed a significant increase in the protein expression and activity of glyoxalase 1 (Glo1), which detoxifies the AGE precursor, methylglyoxal (MGO).	Pyruvaldehyde	159-172	glyoxalase 1	Mus musculus	102-114
29238976-7	2018	Exposure to reactive aldehydes (3-deoxyglucosone, methylglyoxal, and 4-hydroxynonenal) significantly up-regulated the mRNA expression of AKR1B7 and AKR1B8 in IKARS1 cells, but not in 1970C3 cells.	Pyruvaldehyde	50-63	aldo-keto reductase family 1, member B7	Mus musculus	137-143
29238976-7	2018	Exposure to reactive aldehydes (3-deoxyglucosone, methylglyoxal, and 4-hydroxynonenal) significantly up-regulated the mRNA expression of AKR1B7 and AKR1B8 in IKARS1 cells, but not in 1970C3 cells.	Pyruvaldehyde	50-63	aldo-keto reductase family 1, member B8	Mus musculus	148-154
29373286-10	2018	The RCS metabolite methylglyoxal, which represents a key mediator for the development of diabetic retinopathy, was significantly reduced in plasma and red blood cells (RBCs) of STZ-treated Trpc1/4/5/6-/- mice compared to controls.	Pyruvaldehyde	19-32	transient receptor potential cation channel, subfamily C, member 1	Mus musculus	189-194
29495397-7	2018	However, the EU-treated group showed a significant increase in the protein expression and activity of glyoxalase 1 (Glo1), which detoxifies the AGE precursor, methylglyoxal (MGO).	Pyruvaldehyde	159-172	glyoxalase 1	Mus musculus	116-120
29495397-7	2018	However, the EU-treated group showed a significant increase in the protein expression and activity of glyoxalase 1 (Glo1), which detoxifies the AGE precursor, methylglyoxal (MGO).	Pyruvaldehyde	174-177	glyoxalase 1	Mus musculus	102-114
29495397-7	2018	However, the EU-treated group showed a significant increase in the protein expression and activity of glyoxalase 1 (Glo1), which detoxifies the AGE precursor, methylglyoxal (MGO).	Pyruvaldehyde	174-177	glyoxalase 1	Mus musculus	116-120
29434207-7	2018	Additionally, increased activities of glyoxalases I and II were correlated with reduced levels of methylglyoxal in JA-pretreated alkaline-stressed maize plants.	Pyruvaldehyde	98-111	glyoxylase 1	Zea mays	38-58
29425121-0	2018	miR-214-Dependent Increase of PHLPP2 Levels Mediates the Impairment of Insulin-Stimulated Akt Activation in Mouse Aortic Endothelial Cells Exposed to Methylglyoxal.	Pyruvaldehyde	150-163	thymoma viral proto-oncogene 1	Mus musculus	90-93
29425121-7	2018	This study reveals a 4-fold increase of PHLPP2 in MGO-treated MAECs.	Pyruvaldehyde	50-53	PH domain and leucine rich repeat protein phosphatase 2	Mus musculus	40-46
29425121-0	2018	miR-214-Dependent Increase of PHLPP2 Levels Mediates the Impairment of Insulin-Stimulated Akt Activation in Mouse Aortic Endothelial Cells Exposed to Methylglyoxal.	Pyruvaldehyde	150-163	microRNA 214	Mus musculus	0-7
29425121-0	2018	miR-214-Dependent Increase of PHLPP2 Levels Mediates the Impairment of Insulin-Stimulated Akt Activation in Mouse Aortic Endothelial Cells Exposed to Methylglyoxal.	Pyruvaldehyde	150-163	PH domain and leucine rich repeat protein phosphatase 2	Mus musculus	30-36
29425121-9	2018	Moreover, miR-214 overexpression is able to reduce PHLPP2 levels in MGO-treated MAECs.	Pyruvaldehyde	68-71	microRNA 214	Mus musculus	10-17
29425121-9	2018	Moreover, miR-214 overexpression is able to reduce PHLPP2 levels in MGO-treated MAECs.	Pyruvaldehyde	68-71	PH domain and leucine rich repeat protein phosphatase 2	Mus musculus	51-57
29425121-11	2018	Finally, the inhibition of miR-214 impairs the insulin-dependent Akt activation, while its overexpression rescues the insulin effect on Akt activation in MGO-treated MAECs.	Pyruvaldehyde	154-157	thymoma viral proto-oncogene 1	Mus musculus	136-139
29425121-12	2018	In conclusion, this study shows that PHLPP2 is a target of miR-214 in MAECs, and identifies miR-214 downregulation as a contributing factor to MGO-induced endothelial insulin-resistance.	Pyruvaldehyde	143-146	PH domain and leucine rich repeat protein phosphatase 2	Mus musculus	37-43
29425121-12	2018	In conclusion, this study shows that PHLPP2 is a target of miR-214 in MAECs, and identifies miR-214 downregulation as a contributing factor to MGO-induced endothelial insulin-resistance.	Pyruvaldehyde	143-146	microRNA 214	Mus musculus	92-99
28664581-7	2018	However, the levels of MGO and d-lactate were higher in the livers of CCl4 -treated animals than in untreated animals (MGO: 128.2 +- 18.8 and 248.1 +- 64.9 mug/g protein, p &lt; 0.01; d-lactate: 0.860 +- 0.040 and 1.293 +- 0.078 mumol/g protein, respectively p &lt; 0.01).	Pyruvaldehyde	23-26	C-C motif chemokine ligand 4	Rattus norvegicus	70-74
29422602-3	2018	Rats daily administered 20 mM methylglyoxal intraperitoneally developed significant peritoneal fibrosis after 7 days with increased expression of TGF-beta and V-ATPase, which was reduced by the inhibition of V-ATPase with co-administration of 100 mM bafilomycin A1.	Pyruvaldehyde	30-43	transforming growth factor, beta 1	Rattus norvegicus	146-154
29401462-3	2018	MR1 tetramers, typically stabilized by the adduct of 5-amino-6-D-ribitylaminouracil (5-A-RU) and methylglyoxal (MeG), are important tools for the study of MAIT cells.	Pyruvaldehyde	97-110	major histocompatibility complex, class I-related	Homo sapiens	0-3
28664581-7	2018	However, the levels of MGO and d-lactate were higher in the livers of CCl4 -treated animals than in untreated animals (MGO: 128.2 +- 18.8 and 248.1 +- 64.9 mug/g protein, p &lt; 0.01; d-lactate: 0.860 +- 0.040 and 1.293 +- 0.078 mumol/g protein, respectively p &lt; 0.01).	Pyruvaldehyde	119-122	C-C motif chemokine ligand 4	Rattus norvegicus	70-74
29385039-4	2018	Glyoxalases, consisting of glyoxalase 1 (Glo1) and glyoxalase 2 (Glo2), are enzymes that catalyze the glutathione-dependent metabolism of cytotoxic methylglyoxal (MG), thus protecting against cellular damage and apoptosis.	Pyruvaldehyde	148-161	glyoxalase I	Homo sapiens	41-45
29170092-3	2018	To address this possibility, we investigated major redox-sensitive pathways and enzymatic systems that play critical roles in fundamental cytoprotective mechanisms of adaptive responses to oxidative stress, including the master Nrf2 antioxidant defense pathway and its downstream target Glyoxalase 1 (Glo1), a pivotal stress-responsive defense enzyme involved in cellular protection against glycative and oxidative stress through the metabolism of methylglyoxal (MG).	Pyruvaldehyde	448-461	glyoxalase I	Homo sapiens	287-299
29170092-3	2018	To address this possibility, we investigated major redox-sensitive pathways and enzymatic systems that play critical roles in fundamental cytoprotective mechanisms of adaptive responses to oxidative stress, including the master Nrf2 antioxidant defense pathway and its downstream target Glyoxalase 1 (Glo1), a pivotal stress-responsive defense enzyme involved in cellular protection against glycative and oxidative stress through the metabolism of methylglyoxal (MG).	Pyruvaldehyde	463-465	glyoxalase I	Homo sapiens	287-299
29170092-5	2018	Experimental outcomes showed that KRIT1 loss-of-function induces a redox-sensitive sustained upregulation of Nrf2 and Glo1, and a drop in intracellular levels of MG-modified Hsp70 and Hsp27 proteins, leading to a chronic adaptive redox homeostasis that counteracts intrinsic oxidative stress but increases susceptibility to oxidative DNA damage and apoptosis, sensitizing cells to further oxidative challenges.	Pyruvaldehyde	162-164	KRIT1 ankyrin repeat containing	Homo sapiens	34-39
29170092-5	2018	Experimental outcomes showed that KRIT1 loss-of-function induces a redox-sensitive sustained upregulation of Nrf2 and Glo1, and a drop in intracellular levels of MG-modified Hsp70 and Hsp27 proteins, leading to a chronic adaptive redox homeostasis that counteracts intrinsic oxidative stress but increases susceptibility to oxidative DNA damage and apoptosis, sensitizing cells to further oxidative challenges.	Pyruvaldehyde	162-164	heat shock protein family A (Hsp70) member 4	Homo sapiens	174-179
29385039-4	2018	Glyoxalases, consisting of glyoxalase 1 (Glo1) and glyoxalase 2 (Glo2), are enzymes that catalyze the glutathione-dependent metabolism of cytotoxic methylglyoxal (MG), thus protecting against cellular damage and apoptosis.	Pyruvaldehyde	148-161	hydroxyacylglutathione hydrolase	Homo sapiens	65-69
29385039-4	2018	Glyoxalases, consisting of glyoxalase 1 (Glo1) and glyoxalase 2 (Glo2), are enzymes that catalyze the glutathione-dependent metabolism of cytotoxic methylglyoxal (MG), thus protecting against cellular damage and apoptosis.	Pyruvaldehyde	163-165	glyoxalase I	Homo sapiens	41-45
29385039-4	2018	Glyoxalases, consisting of glyoxalase 1 (Glo1) and glyoxalase 2 (Glo2), are enzymes that catalyze the glutathione-dependent metabolism of cytotoxic methylglyoxal (MG), thus protecting against cellular damage and apoptosis.	Pyruvaldehyde	163-165	hydroxyacylglutathione hydrolase	Homo sapiens	65-69
29386487-0	2018	Methylglyoxal Impairs beta2-Adrenoceptor-Mediated Vasodilatory Mechanisms in Rat Retinal Arterioles.	Pyruvaldehyde	0-13	adrenoceptor beta 2	Rattus norvegicus	22-40
29386487-3	2018	In this study, we examined the effects of methylglyoxal on beta2-adrenoceptor-mediated vasodilatory mechanisms in rat retinal arterioles.	Pyruvaldehyde	42-55	adrenoceptor beta 2	Rattus norvegicus	59-77
29386487-5	2018	Intravitreal injection of methylglyoxal significantly diminished the vasodilation of retinal arterioles induced by the beta2-adrenoceptor agonist salbutamol.	Pyruvaldehyde	26-39	adrenoceptor beta 2	Rattus norvegicus	119-137
29386487-8	2018	Methylglyoxal attenuated retinal vasodilator response to salbutamol under blockade of BKCa channels with iberiotoxin, an inhibitor of the channels.	Pyruvaldehyde	0-13	potassium calcium-activated channel subfamily M alpha 1	Rattus norvegicus	86-90
30179128-5	2018	Under normal conditions, MG is detoxified by the enzyme glyoxalase 1 (Glo1), using reduced glutathione as a co-factor.	Pyruvaldehyde	25-27	glyoxalase I	Homo sapiens	56-68
30179128-5	2018	Under normal conditions, MG is detoxified by the enzyme glyoxalase 1 (Glo1), using reduced glutathione as a co-factor.	Pyruvaldehyde	25-27	glyoxalase I	Homo sapiens	70-74
30179128-10	2018	CONCLUSION: Reducing MG levels directly using scavengers or indirectly via activation of Nrf2/Glo1 may serve as a novel and potent therapeutic strategy to counter the deleterious effects of MG in diabetic complications.	Pyruvaldehyde	21-23	NFE2 like bZIP transcription factor 2	Homo sapiens	89-93
30179128-10	2018	CONCLUSION: Reducing MG levels directly using scavengers or indirectly via activation of Nrf2/Glo1 may serve as a novel and potent therapeutic strategy to counter the deleterious effects of MG in diabetic complications.	Pyruvaldehyde	21-23	glyoxalase I	Homo sapiens	94-98
30179128-10	2018	CONCLUSION: Reducing MG levels directly using scavengers or indirectly via activation of Nrf2/Glo1 may serve as a novel and potent therapeutic strategy to counter the deleterious effects of MG in diabetic complications.	Pyruvaldehyde	190-192	NFE2 like bZIP transcription factor 2	Homo sapiens	89-93
30179128-10	2018	CONCLUSION: Reducing MG levels directly using scavengers or indirectly via activation of Nrf2/Glo1 may serve as a novel and potent therapeutic strategy to counter the deleterious effects of MG in diabetic complications.	Pyruvaldehyde	190-192	glyoxalase I	Homo sapiens	94-98
29151157-2	2018	It contains a furan group at the A-ring of the core isoflavone structure and can inhibit the activity of glyoxalase I, an enzyme that catalyzes the detoxification of methylglyoxal (MG), a by-product of glycolysis.	Pyruvaldehyde	166-179	glyoxalase I	Homo sapiens	105-117
29473788-0	2018	Methylglyoxal induced advanced glycation end products (AGE)/receptor for AGE (RAGE)-mediated angiogenic impairment in bone marrow-derived endothelial progenitor cells.	Pyruvaldehyde	0-13	advanced glycosylation end-product specific receptor	Homo sapiens	78-82
29473788-8	2018	Taken together, data demonstrated that MG induced angiogenic impairment in EPC via alterations in the AGE/RAGE-VEGFR-2 pathway which may be utilized in the development of potential therapeutic and preventive targets for diabetic vascular complications.	Pyruvaldehyde	39-41	advanced glycosylation end-product specific receptor	Homo sapiens	106-110
29473788-8	2018	Taken together, data demonstrated that MG induced angiogenic impairment in EPC via alterations in the AGE/RAGE-VEGFR-2 pathway which may be utilized in the development of potential therapeutic and preventive targets for diabetic vascular complications.	Pyruvaldehyde	39-41	kinase insert domain receptor	Homo sapiens	111-118
29690804-12	2018	Intriguingly, small interfering RNA-transfected knockdown of the migration inhibitory factor gene in methylglyoxal-treated skin keratinocytes increased expression of glyoxalase-I and intraepidermal nerve fibers in comparison with control small interfering RNA-transfected cells, which was decreased by induction of methylglyoxal.	Pyruvaldehyde	101-114	glyoxalase 1	Rattus norvegicus	166-178
29690804-12	2018	Intriguingly, small interfering RNA-transfected knockdown of the migration inhibitory factor gene in methylglyoxal-treated skin keratinocytes increased expression of glyoxalase-I and intraepidermal nerve fibers in comparison with control small interfering RNA-transfected cells, which was decreased by induction of methylglyoxal.	Pyruvaldehyde	315-328	glyoxalase 1	Rattus norvegicus	166-178
28986142-5	2017	Pretreatment with limonene prior to MG exposure reduced MG-induced mitochondrial dysfunction by preventing mitochondrial membrane potential dissipation and adenosine triphosphate loss, and reduced the levels of adenosine monophosphate-activated protein kinase, peroxisome proliferator activated receptor gamma coactivator 1alpha, and nitric oxide.	Pyruvaldehyde	56-58	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	261-328
29038915-4	2017	Mass spectral (MS) analysis of the reactions of Abeta with two representative sugars, ribose-5-phosphate (R5P) and methylglyoxal (MG), revealed Lys-16 and Arg-5 as the primary glycation sites.	Pyruvaldehyde	115-128	amyloid beta precursor protein	Homo sapiens	48-53
30263719-2	2018	Hence, in this work, glyoxalase 1(GLO 1) based, zinc oxide (ZnO) flakes interfaced mediator free electrochemical biosensor was developed to detect MG in grilled chicken.	Pyruvaldehyde	147-149	glyoxalase I	Gallus gallus	34-39
29270106-0	2017	Methylglyoxal Requires AC1 and TRPA1 to Produce Pain and Spinal Neuron Activation.	Pyruvaldehyde	0-13	adenylate cyclase 1	Homo sapiens	23-26
29270106-0	2017	Methylglyoxal Requires AC1 and TRPA1 to Produce Pain and Spinal Neuron Activation.	Pyruvaldehyde	0-13	transient receptor potential cation channel subfamily A member 1	Homo sapiens	31-36
29270106-2	2017	MG increases intracellular calcium in sensory neurons and produces behavioral nociception via the cation channel transient receptor potential ankyrin 1 (TRPA1).	Pyruvaldehyde	0-2	transient receptor potential cation channel subfamily A member 1	Homo sapiens	153-158
29270106-4	2017	Furthermore, it remains unknown whether methylglyoxal is sufficient to activate neurons in the spinal cord dorsal horn, whether this requires TRPA1, and if the calcium-sensitive adenylyl cyclase 1 isoform (AC1) contributes to MG-evoked pain.	Pyruvaldehyde	226-228	adenylate cyclase 1	Homo sapiens	178-196
29270106-4	2017	Furthermore, it remains unknown whether methylglyoxal is sufficient to activate neurons in the spinal cord dorsal horn, whether this requires TRPA1, and if the calcium-sensitive adenylyl cyclase 1 isoform (AC1) contributes to MG-evoked pain.	Pyruvaldehyde	226-228	adenylate cyclase 1	Homo sapiens	206-209
29270106-6	2017	Methylglyoxal produced conditioned place avoidance (CPA) (a measure of affective pain), dose-dependent licking and lifting nociceptive behaviors, hyperalgesia to heat and mechanical stimulation, and p-ERK in the spinal cord dorsal horn.	Pyruvaldehyde	0-13	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	199-204
29270106-7	2017	TRPA1 knockout or intrathecal administration of a TRPA1 antagonist (HC030031) attenuated methylglyoxal-evoked p-ERK, nociception, and hyperalgesia.	Pyruvaldehyde	89-102	transient receptor potential cation channel subfamily A member 1	Homo sapiens	0-5
29270106-7	2017	TRPA1 knockout or intrathecal administration of a TRPA1 antagonist (HC030031) attenuated methylglyoxal-evoked p-ERK, nociception, and hyperalgesia.	Pyruvaldehyde	89-102	transient receptor potential cation channel subfamily A member 1	Homo sapiens	50-55
29270106-7	2017	TRPA1 knockout or intrathecal administration of a TRPA1 antagonist (HC030031) attenuated methylglyoxal-evoked p-ERK, nociception, and hyperalgesia.	Pyruvaldehyde	89-102	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	110-115
29270106-9	2017	These results indicate that intraplantar administration of methylglyoxal recapitulates multiple signs of painful diabetic neuropathy found in animal models of or patients with diabetes, including the activation of spinal nociresponsive neurons and the potential involvement of a TRPA1-AC1 sensitization mechanism.	Pyruvaldehyde	59-72	transient receptor potential cation channel subfamily A member 1	Homo sapiens	279-284
29270106-9	2017	These results indicate that intraplantar administration of methylglyoxal recapitulates multiple signs of painful diabetic neuropathy found in animal models of or patients with diabetes, including the activation of spinal nociresponsive neurons and the potential involvement of a TRPA1-AC1 sensitization mechanism.	Pyruvaldehyde	59-72	adenylate cyclase 1	Homo sapiens	285-288
29270106-10	2017	We conclude that administration of MG is a valuable model for investigating both peripheral and central components of a MG-TRPA1-AC1 pathway that contribute to painful diabetic neuropathy.	Pyruvaldehyde	35-37	transient receptor potential cation channel subfamily A member 1	Homo sapiens	123-128
29270106-10	2017	We conclude that administration of MG is a valuable model for investigating both peripheral and central components of a MG-TRPA1-AC1 pathway that contribute to painful diabetic neuropathy.	Pyruvaldehyde	35-37	adenylate cyclase 1	Homo sapiens	129-132
29195953-2	2017	In this study, the effect of glycation derived from glyoxal (GO), methylglyoxal (MGO) or butanedione (BU) on the in vitro digestibility of beta-casein (beta-CN) and beta-lactoglobulin (beta-Lg) was investigated.	Pyruvaldehyde	66-79	casein beta	Homo sapiens	139-150
29195953-2	2017	In this study, the effect of glycation derived from glyoxal (GO), methylglyoxal (MGO) or butanedione (BU) on the in vitro digestibility of beta-casein (beta-CN) and beta-lactoglobulin (beta-Lg) was investigated.	Pyruvaldehyde	66-79	casein beta	Homo sapiens	152-159
29195953-2	2017	In this study, the effect of glycation derived from glyoxal (GO), methylglyoxal (MGO) or butanedione (BU) on the in vitro digestibility of beta-casein (beta-CN) and beta-lactoglobulin (beta-Lg) was investigated.	Pyruvaldehyde	81-84	casein beta	Homo sapiens	139-150
29195953-2	2017	In this study, the effect of glycation derived from glyoxal (GO), methylglyoxal (MGO) or butanedione (BU) on the in vitro digestibility of beta-casein (beta-CN) and beta-lactoglobulin (beta-Lg) was investigated.	Pyruvaldehyde	81-84	casein beta	Homo sapiens	152-159
29038915-4	2017	Mass spectral (MS) analysis of the reactions of Abeta with two representative sugars, ribose-5-phosphate (R5P) and methylglyoxal (MG), revealed Lys-16 and Arg-5 as the primary glycation sites.	Pyruvaldehyde	130-132	amyloid beta precursor protein	Homo sapiens	48-53
29156655-1	2017	Glyoxalase-I (Glo-I) and glyoxalase-II (Glo-II) comprise the glyoxalase system and are responsible for the detoxification of methylglyoxal (MGO).	Pyruvaldehyde	125-138	glyoxalase I	Homo sapiens	0-12
29156655-1	2017	Glyoxalase-I (Glo-I) and glyoxalase-II (Glo-II) comprise the glyoxalase system and are responsible for the detoxification of methylglyoxal (MGO).	Pyruvaldehyde	125-138	glyoxalase I	Homo sapiens	14-19
29156655-1	2017	Glyoxalase-I (Glo-I) and glyoxalase-II (Glo-II) comprise the glyoxalase system and are responsible for the detoxification of methylglyoxal (MGO).	Pyruvaldehyde	125-138	hydroxyacylglutathione hydrolase	Homo sapiens	25-38
29156655-1	2017	Glyoxalase-I (Glo-I) and glyoxalase-II (Glo-II) comprise the glyoxalase system and are responsible for the detoxification of methylglyoxal (MGO).	Pyruvaldehyde	125-138	hydroxyacylglutathione hydrolase	Homo sapiens	40-46
29156655-1	2017	Glyoxalase-I (Glo-I) and glyoxalase-II (Glo-II) comprise the glyoxalase system and are responsible for the detoxification of methylglyoxal (MGO).	Pyruvaldehyde	140-143	glyoxalase I	Homo sapiens	0-12
29156655-1	2017	Glyoxalase-I (Glo-I) and glyoxalase-II (Glo-II) comprise the glyoxalase system and are responsible for the detoxification of methylglyoxal (MGO).	Pyruvaldehyde	140-143	glyoxalase I	Homo sapiens	14-19
29156655-1	2017	Glyoxalase-I (Glo-I) and glyoxalase-II (Glo-II) comprise the glyoxalase system and are responsible for the detoxification of methylglyoxal (MGO).	Pyruvaldehyde	140-143	hydroxyacylglutathione hydrolase	Homo sapiens	25-38
29156655-1	2017	Glyoxalase-I (Glo-I) and glyoxalase-II (Glo-II) comprise the glyoxalase system and are responsible for the detoxification of methylglyoxal (MGO).	Pyruvaldehyde	140-143	hydroxyacylglutathione hydrolase	Homo sapiens	40-46
29156655-7	2017	Glo-I expression was found to be reduced in early and advanced cirrhosis with a subsequent increase of MGO-levels.	Pyruvaldehyde	103-107	glyoxalase I	Homo sapiens	0-5
28444875-5	2017	In addition, pre-treatment with the ROS scavenger NAC prevented the MGO-induced down-regulation of p65 and c-FLIPL , and the forced expression of c-FLIPL attenuated MGO-mediated apoptosis.	Pyruvaldehyde	165-168	synuclein alpha	Homo sapiens	50-53
31966428-1	2017	Glyoxalase 1 (Glo1) is an enzyme that plays a role to metabolize and inactivate methylglyoxal.	Pyruvaldehyde	80-93	glyoxalase I	Homo sapiens	0-12
31966428-1	2017	Glyoxalase 1 (Glo1) is an enzyme that plays a role to metabolize and inactivate methylglyoxal.	Pyruvaldehyde	80-93	glyoxalase I	Homo sapiens	14-18
28444875-5	2017	In addition, pre-treatment with the ROS scavenger NAC prevented the MGO-induced down-regulation of p65 and c-FLIPL , and the forced expression of c-FLIPL attenuated MGO-mediated apoptosis.	Pyruvaldehyde	165-168	CASP8 and FADD like apoptosis regulator	Homo sapiens	146-153
28444875-0	2017	Methylglyoxal-induced apoptosis is dependent on the suppression of c-FLIPL expression via down-regulation of p65 in endothelial cells.	Pyruvaldehyde	0-13	CASP8 and FADD like apoptosis regulator	Homo sapiens	67-74
28444875-7	2017	Finally, MGO was found to induce apoptosis by down-regulating p65 expression at both the transcriptional and posttranslational levels, and thus, to inhibit c-FLIPL mRNA expression by suppressing NF-kappaB transcriptional activity.	Pyruvaldehyde	9-12	RELA proto-oncogene, NF-kB subunit	Homo sapiens	62-65
28444875-0	2017	Methylglyoxal-induced apoptosis is dependent on the suppression of c-FLIPL expression via down-regulation of p65 in endothelial cells.	Pyruvaldehyde	0-13	RELA proto-oncogene, NF-kB subunit	Homo sapiens	109-112
28444875-4	2017	Treatment with MGO increased ROS levels, followed by dose-dependent down-regulation of c-FLIPL .	Pyruvaldehyde	15-18	CASP8 and FADD like apoptosis regulator	Homo sapiens	87-94
28444875-7	2017	Finally, MGO was found to induce apoptosis by down-regulating p65 expression at both the transcriptional and posttranslational levels, and thus, to inhibit c-FLIPL mRNA expression by suppressing NF-kappaB transcriptional activity.	Pyruvaldehyde	9-12	CASP8 and FADD like apoptosis regulator	Homo sapiens	156-163
28444875-5	2017	In addition, pre-treatment with the ROS scavenger NAC prevented the MGO-induced down-regulation of p65 and c-FLIPL , and the forced expression of c-FLIPL attenuated MGO-mediated apoptosis.	Pyruvaldehyde	68-71	synuclein alpha	Homo sapiens	50-53
28444875-5	2017	In addition, pre-treatment with the ROS scavenger NAC prevented the MGO-induced down-regulation of p65 and c-FLIPL , and the forced expression of c-FLIPL attenuated MGO-mediated apoptosis.	Pyruvaldehyde	68-71	RELA proto-oncogene, NF-kB subunit	Homo sapiens	99-102
28444875-8	2017	Collectively, this study showed that MGO-induced apoptosis is dependent on c-FLIPL down-regulation via ROS-mediated down-regulation of p65 expression in endothelial cells.	Pyruvaldehyde	37-40	CASP8 and FADD like apoptosis regulator	Homo sapiens	75-82
28444875-5	2017	In addition, pre-treatment with the ROS scavenger NAC prevented the MGO-induced down-regulation of p65 and c-FLIPL , and the forced expression of c-FLIPL attenuated MGO-mediated apoptosis.	Pyruvaldehyde	68-71	CASP8 and FADD like apoptosis regulator	Homo sapiens	107-114
28444875-8	2017	Collectively, this study showed that MGO-induced apoptosis is dependent on c-FLIPL down-regulation via ROS-mediated down-regulation of p65 expression in endothelial cells.	Pyruvaldehyde	37-40	RELA proto-oncogene, NF-kB subunit	Homo sapiens	135-138
28926063-8	2017	For the first time, we report that MG induces downregulation of enzymes involved in cholesterol biosynthesis such as acetyl-CoA acetyltransferase, hydroxymethylglutaryl-CoA synthase, farnesyl pyrophosphate synthetase, squalene monooxygenase, and lanosterol synthase.	Pyruvaldehyde	35-37	farnesyl pyrophosphate synthase	Cricetulus griseus	183-216
28926063-8	2017	For the first time, we report that MG induces downregulation of enzymes involved in cholesterol biosynthesis such as acetyl-CoA acetyltransferase, hydroxymethylglutaryl-CoA synthase, farnesyl pyrophosphate synthetase, squalene monooxygenase, and lanosterol synthase.	Pyruvaldehyde	35-37	squalene monooxygenase	Cricetulus griseus	218-240
28698281-6	2017	MiR-27b expression (real-time PCR) in EPCs was decreased after 24 h of exposure to methylglyoxal (MGO) or oxidized low-density lipoprotein but not high glucose, advanced glycation end products, the reactive oxygen species generator LY83583, or H2O2 The increase in BMPC apoptosis in the diabetic mice was rescued following transfection with a miR-27b mimic, and the increased apoptosis induced by MGO was also rescued by the miR-27b mimic.	Pyruvaldehyde	83-96	microRNA 27b	Mus musculus	0-7
28698281-6	2017	MiR-27b expression (real-time PCR) in EPCs was decreased after 24 h of exposure to methylglyoxal (MGO) or oxidized low-density lipoprotein but not high glucose, advanced glycation end products, the reactive oxygen species generator LY83583, or H2O2 The increase in BMPC apoptosis in the diabetic mice was rescued following transfection with a miR-27b mimic, and the increased apoptosis induced by MGO was also rescued by the miR-27b mimic.	Pyruvaldehyde	98-101	microRNA 27b	Mus musculus	0-7
28698281-6	2017	MiR-27b expression (real-time PCR) in EPCs was decreased after 24 h of exposure to methylglyoxal (MGO) or oxidized low-density lipoprotein but not high glucose, advanced glycation end products, the reactive oxygen species generator LY83583, or H2O2 The increase in BMPC apoptosis in the diabetic mice was rescued following transfection with a miR-27b mimic, and the increased apoptosis induced by MGO was also rescued by the miR-27b mimic.	Pyruvaldehyde	397-400	microRNA 27b	Mus musculus	0-7
28729113-0	2017	Activation of RAGE/STAT3 pathway by methylglyoxal contributes to spinal central sensitization and persistent pain induced by bortezomib.	Pyruvaldehyde	36-49	advanced glycosylation end product-specific receptor	Rattus norvegicus	14-18
28263721-0	2017	Hepatoprotective effect of 7-Hydroxycoumarin against Methyl glyoxal toxicity via activation of Nrf2.	Pyruvaldehyde	53-67	NFE2 like bZIP transcription factor 2	Homo sapiens	95-99
28263721-4	2017	Results show that 7-HC pretreatment significantly attenuates MG-induced cytotoxicity, apoptotic changes and ROS accumulation and that this protection is shown to be associated with the induction of the nuclear factor erythroid 2-related factor 2 (NRF2) and its downstream detoxifying enzymes.	Pyruvaldehyde	61-63	NFE2 like bZIP transcription factor 2	Homo sapiens	202-245
28263721-4	2017	Results show that 7-HC pretreatment significantly attenuates MG-induced cytotoxicity, apoptotic changes and ROS accumulation and that this protection is shown to be associated with the induction of the nuclear factor erythroid 2-related factor 2 (NRF2) and its downstream detoxifying enzymes.	Pyruvaldehyde	61-63	NFE2 like bZIP transcription factor 2	Homo sapiens	247-251
28263721-6	2017	In addition, depletion of NRF2 by siRNA significantly reduces the protective effect of 7-HC against MG, suggesting that NRF2 plays an important role in the protective function of 7-HC.	Pyruvaldehyde	100-102	NFE2 like bZIP transcription factor 2	Homo sapiens	26-30
28263721-6	2017	In addition, depletion of NRF2 by siRNA significantly reduces the protective effect of 7-HC against MG, suggesting that NRF2 plays an important role in the protective function of 7-HC.	Pyruvaldehyde	100-102	NFE2 like bZIP transcription factor 2	Homo sapiens	120-124
28263721-7	2017	These findings highlight the potential for the interventional activation of the NRF2 induction via the non-toxic natural phytochemical 7-HC as a novel therapeutic approach towards the detoxification of MG, with the aim of halting the progression of diseases in which MG has been implicated.	Pyruvaldehyde	202-204	NFE2 like bZIP transcription factor 2	Homo sapiens	80-84
28263721-7	2017	These findings highlight the potential for the interventional activation of the NRF2 induction via the non-toxic natural phytochemical 7-HC as a novel therapeutic approach towards the detoxification of MG, with the aim of halting the progression of diseases in which MG has been implicated.	Pyruvaldehyde	267-269	NFE2 like bZIP transcription factor 2	Homo sapiens	80-84
28729113-11	2017	Our results suggest that accumulation of methylglyoxal may activate the RAGE/STAT3 signaling pathway in dorsal horn, and contributes to the spinal central sensitization and persistent pain induced by bortezomib treatment.	Pyruvaldehyde	41-54	advanced glycosylation end product-specific receptor	Rattus norvegicus	72-76
28729113-11	2017	Our results suggest that accumulation of methylglyoxal may activate the RAGE/STAT3 signaling pathway in dorsal horn, and contributes to the spinal central sensitization and persistent pain induced by bortezomib treatment.	Pyruvaldehyde	41-54	signal transducer and activator of transcription 3	Rattus norvegicus	77-82
28729113-0	2017	Activation of RAGE/STAT3 pathway by methylglyoxal contributes to spinal central sensitization and persistent pain induced by bortezomib.	Pyruvaldehyde	36-49	signal transducer and activator of transcription 3	Rattus norvegicus	19-24
28743744-0	2017	Phosphatidylinositol 3,5-bisphosphate is involved in methylglyoxal-induced activation of the Mpk1 mitogen-activated protein kinase cascade in Saccharomyces cerevisiae.	Pyruvaldehyde	53-66	mitogen-activated serine/threonine-protein kinase SLT2	Saccharomyces cerevisiae S288C	93-97
28916747-6	2017	Moreover, upon exogenous MG challenge, glycolytic cells showed elevated amounts of intracellular MG and induced de novo GLO1 detoxifying enzyme and Nrf2 expression.	Pyruvaldehyde	25-27	glyoxalase I	Homo sapiens	120-124
28916747-6	2017	Moreover, upon exogenous MG challenge, glycolytic cells showed elevated amounts of intracellular MG and induced de novo GLO1 detoxifying enzyme and Nrf2 expression.	Pyruvaldehyde	25-27	NFE2 like bZIP transcription factor 2	Homo sapiens	148-152
28478530-0	2017	Methylglyoxal-Induced Protection Response and Toxicity: Role of Glutathione Reductase and Thioredoxin Systems.	Pyruvaldehyde	0-13	glutathione reductase	Mus musculus	64-85
28478530-0	2017	Methylglyoxal-Induced Protection Response and Toxicity: Role of Glutathione Reductase and Thioredoxin Systems.	Pyruvaldehyde	0-13	thioredoxin 1	Mus musculus	90-101
28478530-1	2017	Thioredoxin (Trx) and glyoxalase (Glo) systems have been suggested to be molecular targets of methylglyoxal (MGO).	Pyruvaldehyde	94-107	thioredoxin 1	Mus musculus	0-11
28478530-1	2017	Thioredoxin (Trx) and glyoxalase (Glo) systems have been suggested to be molecular targets of methylglyoxal (MGO).	Pyruvaldehyde	94-107	thioredoxin 1	Mus musculus	13-16
28478530-1	2017	Thioredoxin (Trx) and glyoxalase (Glo) systems have been suggested to be molecular targets of methylglyoxal (MGO).	Pyruvaldehyde	109-112	thioredoxin 1	Mus musculus	0-11
28478530-1	2017	Thioredoxin (Trx) and glyoxalase (Glo) systems have been suggested to be molecular targets of methylglyoxal (MGO).	Pyruvaldehyde	109-112	thioredoxin 1	Mus musculus	13-16
28478530-4	2017	It is shown for the first time that MGO treatment induces an increase in glutathione reductase (GR) protein in hippocampal slices (1 h) and HT22 nerve cells (0.5 and 2.5 h).	Pyruvaldehyde	36-39	glutathione reductase	Mus musculus	73-94
28478530-4	2017	It is shown for the first time that MGO treatment induces an increase in glutathione reductase (GR) protein in hippocampal slices (1 h) and HT22 nerve cells (0.5 and 2.5 h).	Pyruvaldehyde	36-39	glutathione reductase	Mus musculus	96-98
28478530-7	2017	In these cells, GR and TrxR activities were decreased by MGO.	Pyruvaldehyde	57-60	glutathione reductase	Mus musculus	16-18
28478530-7	2017	In these cells, GR and TrxR activities were decreased by MGO.	Pyruvaldehyde	57-60	peroxiredoxin 2	Mus musculus	23-27
28478530-8	2017	This result is in agreement with the idea that MGO can affect the Trx/TrxR reducing system, and now we show that GR and Txnip can also be affected by MGO.	Pyruvaldehyde	47-50	thioredoxin 1	Mus musculus	66-69
28478530-8	2017	This result is in agreement with the idea that MGO can affect the Trx/TrxR reducing system, and now we show that GR and Txnip can also be affected by MGO.	Pyruvaldehyde	47-50	peroxiredoxin 2	Mus musculus	70-74
28478530-8	2017	This result is in agreement with the idea that MGO can affect the Trx/TrxR reducing system, and now we show that GR and Txnip can also be affected by MGO.	Pyruvaldehyde	150-153	thioredoxin 1	Mus musculus	66-69
28478530-8	2017	This result is in agreement with the idea that MGO can affect the Trx/TrxR reducing system, and now we show that GR and Txnip can also be affected by MGO.	Pyruvaldehyde	150-153	peroxiredoxin 2	Mus musculus	70-74
28478530-8	2017	This result is in agreement with the idea that MGO can affect the Trx/TrxR reducing system, and now we show that GR and Txnip can also be affected by MGO.	Pyruvaldehyde	150-153	glutathione reductase	Mus musculus	113-115
28478530-8	2017	This result is in agreement with the idea that MGO can affect the Trx/TrxR reducing system, and now we show that GR and Txnip can also be affected by MGO.	Pyruvaldehyde	150-153	thioredoxin interacting protein	Mus musculus	120-125
28478530-10	2017	In this regard, inhibition of GR and TrxR by 2-AAPA or auranofin, respectively, potentiated MGO toxicity in differentiated SH-SY5Y cells.	Pyruvaldehyde	92-95	peroxiredoxin 2	Mus musculus	37-41
28478530-11	2017	Overall, MGO not only triggers a clear defense response in hippocampal slices and HT22 cells but also impairs the Trx/TrxR and GSH/GR reducing couples in HT22 cells.	Pyruvaldehyde	9-12	thioredoxin 1	Mus musculus	114-117
28478530-11	2017	Overall, MGO not only triggers a clear defense response in hippocampal slices and HT22 cells but also impairs the Trx/TrxR and GSH/GR reducing couples in HT22 cells.	Pyruvaldehyde	9-12	peroxiredoxin 2	Mus musculus	118-122
28478530-11	2017	Overall, MGO not only triggers a clear defense response in hippocampal slices and HT22 cells but also impairs the Trx/TrxR and GSH/GR reducing couples in HT22 cells.	Pyruvaldehyde	9-12	glutathione reductase	Mus musculus	131-133
28478530-12	2017	The increased MGO toxicity caused by inhibition of GR and TrxR with specific inhibitors, or their inhibition by MGO treatment, supports the notion that both reducing systems are relevant molecular targets of MGO.	Pyruvaldehyde	14-17	glutathione reductase	Mus musculus	51-53
28478530-12	2017	The increased MGO toxicity caused by inhibition of GR and TrxR with specific inhibitors, or their inhibition by MGO treatment, supports the notion that both reducing systems are relevant molecular targets of MGO.	Pyruvaldehyde	14-17	peroxiredoxin 2	Mus musculus	58-62
28866888-0	2017	Additive Capacity of [6]-Shogaol and Epicatechin To Trap Methylglyoxal.	Pyruvaldehyde	57-70	acid phosphatase 5, tartrate resistant	Mus musculus	52-56
28866888-3	2017	The present study investigated whether dietary compounds with different structures and active sites have the additive capacity to trap MGO.	Pyruvaldehyde	135-138	acid phosphatase 5, tartrate resistant	Mus musculus	130-134
28743744-3	2017	We previously reported that MG activates the Mpk1 (MAPK) cascade in the yeast Saccharomyces cerevisiae To gain further insights into the cellular functions and responses to MG, we herein screened yeast-deletion mutant collections for susceptibility to MG.	Pyruvaldehyde	28-30	mitogen-activated serine/threonine-protein kinase SLT2	Saccharomyces cerevisiae S288C	45-49
28743744-6	2017	MG activated the Pkc1-Mpk1 MAPK cascade in which a small GTPase Rho1 plays a crucial role, and the MG-induced phosphorylation of Mpk1 was impaired in mutants defective in the PtdIns(3,5)P2 biosynthetic pathway.	Pyruvaldehyde	0-2	protein kinase C	Saccharomyces cerevisiae S288C	17-21
28743744-6	2017	MG activated the Pkc1-Mpk1 MAPK cascade in which a small GTPase Rho1 plays a crucial role, and the MG-induced phosphorylation of Mpk1 was impaired in mutants defective in the PtdIns(3,5)P2 biosynthetic pathway.	Pyruvaldehyde	0-2	mitogen-activated serine/threonine-protein kinase SLT2	Saccharomyces cerevisiae S288C	22-26
28743744-6	2017	MG activated the Pkc1-Mpk1 MAPK cascade in which a small GTPase Rho1 plays a crucial role, and the MG-induced phosphorylation of Mpk1 was impaired in mutants defective in the PtdIns(3,5)P2 biosynthetic pathway.	Pyruvaldehyde	0-2	Rho family GTPase RHO1	Saccharomyces cerevisiae S288C	64-68
28743744-6	2017	MG activated the Pkc1-Mpk1 MAPK cascade in which a small GTPase Rho1 plays a crucial role, and the MG-induced phosphorylation of Mpk1 was impaired in mutants defective in the PtdIns(3,5)P2 biosynthetic pathway.	Pyruvaldehyde	0-2	mitogen-activated serine/threonine-protein kinase SLT2	Saccharomyces cerevisiae S288C	129-133
28743744-8	2017	Our results suggest that PtdIns(3,5)P2 is specifically involved in the MG-induced activation of the Mpk1 MAPK cascade and in the cellular adaptation to MG-induced stress.	Pyruvaldehyde	71-73	mitogen-activated serine/threonine-protein kinase SLT2	Saccharomyces cerevisiae S288C	100-104
28623132-1	2017	Glyoxalase 1 (Glo1) is the first enzyme involved in glutathione-dependent detoxification of methylglyoxal, eventually generating d-lactate by the second enzyme glyoxalase 2 (Glo2).	Pyruvaldehyde	92-105	glyoxalase 1	Mus musculus	0-12
28517972-12	2017	Moreover, use of a triple-helical peptide that reconstitutes the collagen-binding domain for integrins GFOGER reverted the assembly of FN induced by MGO-treated collagen.	Pyruvaldehyde	149-152	fibronectin 1	Homo sapiens	135-137
28780382-9	2017	Mechanistically GO and MGO induce senescence by increasing the ROS production, the expression of p21, the accumulation of AGEs and the arrest of HVECs in the G2 cell cycle phase.	Pyruvaldehyde	23-26	H3 histone pseudogene 16	Homo sapiens	97-100
28722189-7	2017	Methylglyoxal (500 muM for 10 min)-mediated JNK phosphorylation was attenuated in the presence of calcitriol (10 nM).	Pyruvaldehyde	0-13	mitogen-activated protein kinase 8	Homo sapiens	44-47
28623132-1	2017	Glyoxalase 1 (Glo1) is the first enzyme involved in glutathione-dependent detoxification of methylglyoxal, eventually generating d-lactate by the second enzyme glyoxalase 2 (Glo2).	Pyruvaldehyde	92-105	glyoxalase 1	Mus musculus	14-18
28623132-1	2017	Glyoxalase 1 (Glo1) is the first enzyme involved in glutathione-dependent detoxification of methylglyoxal, eventually generating d-lactate by the second enzyme glyoxalase 2 (Glo2).	Pyruvaldehyde	92-105	hydroxyacyl glutathione hydrolase	Mus musculus	174-178
28801605-0	2017	Luteolin, a natural flavonoid, inhibits methylglyoxal induced apoptosis via the mTOR/4E-BP1 signaling pathway.	Pyruvaldehyde	40-53	mechanistic target of rapamycin kinase	Rattus norvegicus	80-84
28801605-0	2017	Luteolin, a natural flavonoid, inhibits methylglyoxal induced apoptosis via the mTOR/4E-BP1 signaling pathway.	Pyruvaldehyde	40-53	eukaryotic translation initiation factor 4E binding protein 1	Rattus norvegicus	85-91
28801605-8	2017	Therefore, these observations unambiguously suggest that the inhibitive effect of Luteolin against MG-induced apoptosis in PC12 cells is associated with inhibition of the mTOR/4E-BP1 signaling pathway.	Pyruvaldehyde	99-101	mechanistic target of rapamycin kinase	Rattus norvegicus	171-175
28801605-8	2017	Therefore, these observations unambiguously suggest that the inhibitive effect of Luteolin against MG-induced apoptosis in PC12 cells is associated with inhibition of the mTOR/4E-BP1 signaling pathway.	Pyruvaldehyde	99-101	eukaryotic translation initiation factor 4E binding protein 1	Rattus norvegicus	176-182
28363601-0	2017	Methylglyoxal-induced AMPK activation leads to autophagic degradation of thioredoxin 1 and glyoxalase 2 in HT22 nerve cells.	Pyruvaldehyde	0-13	thioredoxin 1	Mus musculus	73-86
28941455-2	2017	The primary focus is on the role of the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase in changing the concentration of carbonyl compounds - first and foremost, glyceraldehyde-3-phosphate and methylglyoxal.	Pyruvaldehyde	204-217	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	58-98
28941455-6	2017	Of particular importance during the inhibition of glyceraldehyde-3-phosphate dehydrogenase is an increase in the content of the glycating compound methylglyoxal, which is much more active than reducing sugars (glucose, fructose, and others).	Pyruvaldehyde	147-160	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	50-90
28371750-0	2017	Cysteine persulfides and polysulfides produced by exchange reactions with H2S protect SH-SY5Y cells from methylglyoxal-induced toxicity through Nrf2 activation.	Pyruvaldehyde	105-118	NFE2 like bZIP transcription factor 2	Homo sapiens	144-148
28371750-8	2017	BS-Mix produced with Na2S in cystine-containing medium provided SH-SY5Y cells significant protective effect against MG-induced toxicity.	Pyruvaldehyde	116-118	Mix paired-like homeobox	Homo sapiens	3-6
28371750-12	2017	These results suggested that Na2S protects SH-SY5Y cells from MG cytotoxicity through the activation of Nrf2, mediated by cysteine persulfides and polysulfides that were generated by Na2S addition.	Pyruvaldehyde	62-64	NFE2 like bZIP transcription factor 2	Homo sapiens	104-108
28363601-2	2017	We previously showed that MGO treatment targets the thioredoxin and the glyoxalase systems, leading to a decrease in Trx1 and Glo2 proteins in immortalized mouse hippocampal HT22 nerve cells.	Pyruvaldehyde	26-29	thioredoxin 1	Mus musculus	52-63
28363601-2	2017	We previously showed that MGO treatment targets the thioredoxin and the glyoxalase systems, leading to a decrease in Trx1 and Glo2 proteins in immortalized mouse hippocampal HT22 nerve cells.	Pyruvaldehyde	26-29	thioredoxin 1	Mus musculus	117-121
28363601-2	2017	We previously showed that MGO treatment targets the thioredoxin and the glyoxalase systems, leading to a decrease in Trx1 and Glo2 proteins in immortalized mouse hippocampal HT22 nerve cells.	Pyruvaldehyde	26-29	hydroxyacyl glutathione hydrolase	Mus musculus	126-130
28363601-4	2017	The autophagic markers p62, and the lipidated and active form of LC3, were increased by MGO (0.5mM).	Pyruvaldehyde	88-91	nucleoporin 62	Mus musculus	23-26
28363601-5	2017	Autophagy inhibition with bafilomycin or chloroquine prevented the decrease in Trx1 and Glo2 at 6 and 18h after MGO treatment.	Pyruvaldehyde	112-115	thioredoxin 1	Mus musculus	79-83
28363601-5	2017	Autophagy inhibition with bafilomycin or chloroquine prevented the decrease in Trx1 and Glo2 at 6 and 18h after MGO treatment.	Pyruvaldehyde	112-115	hydroxyacyl glutathione hydrolase	Mus musculus	88-92
28363601-10	2017	To confirm that MGO-mediated Trx1 and Glo2 degradation was AMPK-dependent, AMPK-deficient mouse embryonic fibroblasts (MEFs) were treated with MGO.	Pyruvaldehyde	16-19	thioredoxin 1	Mus musculus	29-33
28363601-10	2017	To confirm that MGO-mediated Trx1 and Glo2 degradation was AMPK-dependent, AMPK-deficient mouse embryonic fibroblasts (MEFs) were treated with MGO.	Pyruvaldehyde	16-19	hydroxyacyl glutathione hydrolase	Mus musculus	38-42
28363601-12	2017	Overall, the data indicate that MGO activates autophagy in an AMPK-dependent manner, and that autophagy was responsible for Trx1 and Glo2 degradation, confirming that Trx1 and Glo2 are molecular targets of MGO.	Pyruvaldehyde	206-209	thioredoxin 1	Mus musculus	167-171
28363601-12	2017	Overall, the data indicate that MGO activates autophagy in an AMPK-dependent manner, and that autophagy was responsible for Trx1 and Glo2 degradation, confirming that Trx1 and Glo2 are molecular targets of MGO.	Pyruvaldehyde	206-209	hydroxyacyl glutathione hydrolase	Mus musculus	176-180
28117932-0	2017	Methylglyoxal induces inhibition of growth, accumulation of anthocyanin, and activation of glyoxalase I and II in Arabidopsis thaliana.	Pyruvaldehyde	0-13	glyoxalase/bleomycin resistance protein/dioxygenase superfamily protein	Arabidopsis thaliana	91-103
28444544-3	2017	However, MG is routinely detoxified through the action of DJ1/PARK7/Hsp31 proteins that are highly conserved across kingdoms and mutations in such genes are associated with neurodegenerative diseases.	Pyruvaldehyde	9-11	glutathione-independent methylglyoxalase	Saccharomyces cerevisiae S288C	68-73
28444544-5	2017	We show that overexpression of yeast Heat shock protein 31 (Hsp31), a DJ-1 homolog with robust MG detoxifying capabilities, confers dual biotic and abiotic stress tolerance in model plant Nicotiana tabacum.	Pyruvaldehyde	95-97	glutathione-independent methylglyoxalase	Saccharomyces cerevisiae S288C	37-58
28444544-5	2017	We show that overexpression of yeast Heat shock protein 31 (Hsp31), a DJ-1 homolog with robust MG detoxifying capabilities, confers dual biotic and abiotic stress tolerance in model plant Nicotiana tabacum.	Pyruvaldehyde	95-97	glutathione-independent methylglyoxalase	Saccharomyces cerevisiae S288C	60-65
28032668-7	2017	Moreover, they measure plasma methylglyoxal (a glycating agent, whose availability is hindered by TKT) without however finding a relation with TKT single-nucleotide polymorphisms.	Pyruvaldehyde	30-43	transketolase	Homo sapiens	98-101
28903386-2	2017	Glyoxalase I (GLOI), which catalyzes MG metabolism, is associated with the progression of human malignancies.	Pyruvaldehyde	37-39	glyoxalase I	Homo sapiens	0-12
28903386-2	2017	Glyoxalase I (GLOI), which catalyzes MG metabolism, is associated with the progression of human malignancies.	Pyruvaldehyde	37-39	glyoxalase I	Homo sapiens	14-18
28341536-0	2017	The role of cPLA2 in Methylglyoxal-induced cell apoptosis of HUVECs.	Pyruvaldehyde	21-34	phospholipase A2 group IVA	Homo sapiens	12-17
28341536-5	2017	Our data revealed that cytosolic phospholipase A2 (cPLA2) played an important role in MGO-induced cell apoptosis.	Pyruvaldehyde	86-89	phospholipase A2 group IVA	Homo sapiens	23-49
28341536-5	2017	Our data revealed that cytosolic phospholipase A2 (cPLA2) played an important role in MGO-induced cell apoptosis.	Pyruvaldehyde	86-89	phospholipase A2 group IVA	Homo sapiens	51-56
28341536-6	2017	It was found that MGO could increase both the activity and expression of cPLA2.	Pyruvaldehyde	18-21	phospholipase A2 group IVA	Homo sapiens	73-78
28341536-7	2017	Inhibition of cPLA2 by Pyrrophenone (PYR) or siRNA significantly attenuated the MGO-induced apoptosis.	Pyruvaldehyde	80-83	phospholipase A2 group IVA	Homo sapiens	14-19
28341536-8	2017	Additionally, MGO time-dependently decreased the phosphorylation of nuclear factor kappaB (NF-kappaB).	Pyruvaldehyde	14-17	nuclear factor kappa B subunit 1	Homo sapiens	91-100
28341536-9	2017	Pretreatment of the cells with NF-kappaB inhibitor, BAY11-7082, further increased MGO-induced apoptosis of HUVECs, indicating that NF-kappaB played a survival role in this MGO-induced apoptosis.	Pyruvaldehyde	82-85	nuclear factor kappa B subunit 1	Homo sapiens	31-40
28341536-9	2017	Pretreatment of the cells with NF-kappaB inhibitor, BAY11-7082, further increased MGO-induced apoptosis of HUVECs, indicating that NF-kappaB played a survival role in this MGO-induced apoptosis.	Pyruvaldehyde	82-85	nuclear factor kappa B subunit 1	Homo sapiens	131-140
28341536-9	2017	Pretreatment of the cells with NF-kappaB inhibitor, BAY11-7082, further increased MGO-induced apoptosis of HUVECs, indicating that NF-kappaB played a survival role in this MGO-induced apoptosis.	Pyruvaldehyde	172-175	nuclear factor kappa B subunit 1	Homo sapiens	31-40
28341536-9	2017	Pretreatment of the cells with NF-kappaB inhibitor, BAY11-7082, further increased MGO-induced apoptosis of HUVECs, indicating that NF-kappaB played a survival role in this MGO-induced apoptosis.	Pyruvaldehyde	172-175	nuclear factor kappa B subunit 1	Homo sapiens	131-140
28341536-10	2017	Furthermore, in the presence of si-cPLA2 or PYR, MGO no longer decreased NF-kappaB phosphorylation.	Pyruvaldehyde	49-52	phospholipase A2 group IVA	Homo sapiens	35-40
28341536-10	2017	Furthermore, in the presence of si-cPLA2 or PYR, MGO no longer decreased NF-kappaB phosphorylation.	Pyruvaldehyde	49-52	nuclear factor kappa B subunit 1	Homo sapiens	73-82
28341536-11	2017	Beyond that, the antioxidant N-acetyl cysteine (NAC) could reverse the changes of both cPLA2 and NF-kappaB caused by MGO.	Pyruvaldehyde	117-120	phospholipase A2 group IVA	Homo sapiens	87-92
28341536-11	2017	Beyond that, the antioxidant N-acetyl cysteine (NAC) could reverse the changes of both cPLA2 and NF-kappaB caused by MGO.	Pyruvaldehyde	117-120	nuclear factor kappa B subunit 1	Homo sapiens	97-106
28341536-12	2017	p38, the upstream of cPLA2, was also significantly phosphorylated by MGO.	Pyruvaldehyde	69-72	mitogen-activated protein kinase 14	Homo sapiens	0-3
28341536-12	2017	p38, the upstream of cPLA2, was also significantly phosphorylated by MGO.	Pyruvaldehyde	69-72	phospholipase A2 group IVA	Homo sapiens	21-26
28490763-6	2017	In turn, hypoxia was only observed when MG was combined (HFDMG group), being associated with impaired activation of the insulin receptor (Tyr1163), glucose intolerance and systemic and muscle insulin resistance.	Pyruvaldehyde	40-42	insulin receptor	Rattus norvegicus	120-136
27425255-5	2017	Non-enzymatic glycation of proteins in a decellularized fibroblast ECM was achieved by incubating the ECM in a solution of methylglyoxal (MGO).	Pyruvaldehyde	123-136	multimerin 1	Homo sapiens	67-70
27425255-5	2017	Non-enzymatic glycation of proteins in a decellularized fibroblast ECM was achieved by incubating the ECM in a solution of methylglyoxal (MGO).	Pyruvaldehyde	123-136	multimerin 1	Homo sapiens	102-105
27425255-5	2017	Non-enzymatic glycation of proteins in a decellularized fibroblast ECM was achieved by incubating the ECM in a solution of methylglyoxal (MGO).	Pyruvaldehyde	138-141	multimerin 1	Homo sapiens	67-70
27425255-5	2017	Non-enzymatic glycation of proteins in a decellularized fibroblast ECM was achieved by incubating the ECM in a solution of methylglyoxal (MGO).	Pyruvaldehyde	138-141	multimerin 1	Homo sapiens	102-105
27425255-6	2017	Mass spectrometry of fibronectin (FN) isolated from the glycated matrix identified twenty-eight previously unidentified MGO-derived AGE modification sites including functional sites such as the RGD integrin-binding sequence.	Pyruvaldehyde	120-123	fibronectin 1	Homo sapiens	21-32
27425255-6	2017	Mass spectrometry of fibronectin (FN) isolated from the glycated matrix identified twenty-eight previously unidentified MGO-derived AGE modification sites including functional sites such as the RGD integrin-binding sequence.	Pyruvaldehyde	120-123	fibronectin 1	Homo sapiens	34-36
28479269-4	2017	Therefore, the main objective of this study was to establish whether MGO leads to the degradation of HIF-1alpha in cardiomyocytes subjected to hypoxia.	Pyruvaldehyde	69-72	hypoxia inducible factor 1, alpha subunit	Mus musculus	101-111
28479269-8	2017	RESULTS: The results obtained indicate that MGO induces time- and dose-dependent degradation of HIF-1alpha accumulated under hypoxia.	Pyruvaldehyde	44-47	hypoxia inducible factor 1, alpha subunit	Mus musculus	96-106
28479269-10	2017	CONCLUSION: Taken together, the results obtained in this study suggest that MGO compromises the ability of cells to adapt to low oxygen tensions, by stimulating the degradation of HIF-1alpha, likely contributing to the development of diabetes-associated cardiac dysfunction.	Pyruvaldehyde	76-79	hypoxia inducible factor 1, alpha subunit	Mus musculus	180-190
28091942-9	2017	Administration of MG led to depletion of antioxidant enzymes, induction of fibrosis (p &lt; 0.001), up-regulated expression of RAGE (3.5 fold), TGF-beta (4.4 fold), SMAD2 (3.7 fold), SMAD3 (6.0 fold), IL-6 (4.3 fold) and TNF-alpha (5.5 fold) in the heart tissues compared to control rats.	Pyruvaldehyde	18-20	advanced glycosylation end product-specific receptor	Rattus norvegicus	127-131
28488455-4	2017	MGO treatment also triggered intracellular advanced glycation end products (AGEs) formation, declined mitochondrial membrane potential (MMP), increased oxidative stress and the expression of ER stress mediators Grp78/Bip and p-PERK; activated mitochondrial apoptotic pathway, which could mimic by Glo1 knockdown.	Pyruvaldehyde	0-3	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	211-216
28488455-4	2017	MGO treatment also triggered intracellular advanced glycation end products (AGEs) formation, declined mitochondrial membrane potential (MMP), increased oxidative stress and the expression of ER stress mediators Grp78/Bip and p-PERK; activated mitochondrial apoptotic pathway, which could mimic by Glo1 knockdown.	Pyruvaldehyde	0-3	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	217-220
28488455-4	2017	MGO treatment also triggered intracellular advanced glycation end products (AGEs) formation, declined mitochondrial membrane potential (MMP), increased oxidative stress and the expression of ER stress mediators Grp78/Bip and p-PERK; activated mitochondrial apoptotic pathway, which could mimic by Glo1 knockdown.	Pyruvaldehyde	0-3	glyoxalase 1	Rattus norvegicus	297-301
28488455-7	2017	MGO treatment down-regulated Ire1alpha, a key ER stress mediator, increased JNK phosphorylation and activated mitochondrial apoptosis; down-regulated Bcl-2 expression which could be attenuated by the JNK inhibitor SP600125 and further inhibited cytochrome c leakage from mitochondria and blocked the conversion of pro caspase 3 into cleaved caspase 3, all these might contribute to the inhibition of INS-1 cell apoptosis.	Pyruvaldehyde	0-3	BCL2, apoptosis regulator	Rattus norvegicus	150-155
28091942-9	2017	Administration of MG led to depletion of antioxidant enzymes, induction of fibrosis (p &lt; 0.001), up-regulated expression of RAGE (3.5 fold), TGF-beta (4.4 fold), SMAD2 (3.7 fold), SMAD3 (6.0 fold), IL-6 (4.3 fold) and TNF-alpha (5.5 fold) in the heart tissues compared to control rats.	Pyruvaldehyde	18-20	transforming growth factor, beta 1	Rattus norvegicus	144-152
28091942-9	2017	Administration of MG led to depletion of antioxidant enzymes, induction of fibrosis (p &lt; 0.001), up-regulated expression of RAGE (3.5 fold), TGF-beta (4.4 fold), SMAD2 (3.7 fold), SMAD3 (6.0 fold), IL-6 (4.3 fold) and TNF-alpha (5.5 fold) in the heart tissues compared to control rats.	Pyruvaldehyde	18-20	SMAD family member 2	Rattus norvegicus	165-170
28091942-9	2017	Administration of MG led to depletion of antioxidant enzymes, induction of fibrosis (p &lt; 0.001), up-regulated expression of RAGE (3.5 fold), TGF-beta (4.4 fold), SMAD2 (3.7 fold), SMAD3 (6.0 fold), IL-6 (4.3 fold) and TNF-alpha (5.5 fold) in the heart tissues compared to control rats.	Pyruvaldehyde	18-20	SMAD family member 3	Rattus norvegicus	183-188
28091942-9	2017	Administration of MG led to depletion of antioxidant enzymes, induction of fibrosis (p &lt; 0.001), up-regulated expression of RAGE (3.5 fold), TGF-beta (4.4 fold), SMAD2 (3.7 fold), SMAD3 (6.0 fold), IL-6 (4.3 fold) and TNF-alpha (5.5 fold) in the heart tissues compared to control rats.	Pyruvaldehyde	18-20	interleukin 6	Rattus norvegicus	201-205
28091942-9	2017	Administration of MG led to depletion of antioxidant enzymes, induction of fibrosis (p &lt; 0.001), up-regulated expression of RAGE (3.5 fold), TGF-beta (4.4 fold), SMAD2 (3.7 fold), SMAD3 (6.0 fold), IL-6 (4.3 fold) and TNF-alpha (5.5 fold) in the heart tissues compared to control rats.	Pyruvaldehyde	18-20	tumor necrosis factor	Rattus norvegicus	221-230
27932057-3	2017	An arginine-rich, fatty acid coupled, cyclic peptide (CycK(Myr)R4E) with high proteolytic stability and prolonged circulation was developed for the scavenging of MG.	Pyruvaldehyde	162-164	cyclin K	Mus musculus	54-58
28461715-4	2017	The glyoxalase pathway (consisting of glyoxalase I and glyoxalase II enzymes) for detoxification of methylglyoxal, a cytotoxic molecule, also requires GSH in the first reaction step.	Pyruvaldehyde	100-113	glyoxalase I	Homo sapiens	38-50
28461715-4	2017	The glyoxalase pathway (consisting of glyoxalase I and glyoxalase II enzymes) for detoxification of methylglyoxal, a cytotoxic molecule, also requires GSH in the first reaction step.	Pyruvaldehyde	100-113	hydroxyacylglutathione hydrolase	Homo sapiens	55-68
27302958-7	2017	Hypericin prevented MGO-induced apoptosis in HUVECs by increasing Bcl-2 expression and decreasing Bax expression.	Pyruvaldehyde	20-23	BCL2 apoptosis regulator	Homo sapiens	66-71
27302958-7	2017	Hypericin prevented MGO-induced apoptosis in HUVECs by increasing Bcl-2 expression and decreasing Bax expression.	Pyruvaldehyde	20-23	BCL2 associated X, apoptosis regulator	Homo sapiens	98-101
28000163-9	2017	Therefore, PB activated the Erk1/2-Nrf2 signaling pathway resulting in mitochondrial protection in SH-SY5Y cells exposed to MG.	Pyruvaldehyde	124-126	mitogen-activated protein kinase 3	Homo sapiens	28-34
28000163-9	2017	Therefore, PB activated the Erk1/2-Nrf2 signaling pathway resulting in mitochondrial protection in SH-SY5Y cells exposed to MG.	Pyruvaldehyde	124-126	NFE2 like bZIP transcription factor 2	Homo sapiens	35-39
27590258-11	2017	Furthermore, PCr also inhibited MGO-induced transcriptional activity of Nuclear factor kappa B (NFkappaB).	Pyruvaldehyde	32-35	nuclear factor kappa B subunit 1	Homo sapiens	72-94
27590258-11	2017	Furthermore, PCr also inhibited MGO-induced transcriptional activity of Nuclear factor kappa B (NFkappaB).	Pyruvaldehyde	32-35	nuclear factor kappa B subunit 1	Homo sapiens	96-104
28358304-2	2017	It comprises two enzymes, glyoxalase I (GLYI) and glyoxalase II (GLYII), which act sequentially to convert MG into d-lactate, thereby helping living systems get rid of this otherwise cytotoxic byproduct of metabolism.	Pyruvaldehyde	107-109	glyoxalase I	Homo sapiens	26-38
28358304-2	2017	It comprises two enzymes, glyoxalase I (GLYI) and glyoxalase II (GLYII), which act sequentially to convert MG into d-lactate, thereby helping living systems get rid of this otherwise cytotoxic byproduct of metabolism.	Pyruvaldehyde	107-109	glyoxalase I	Homo sapiens	40-44
28358304-2	2017	It comprises two enzymes, glyoxalase I (GLYI) and glyoxalase II (GLYII), which act sequentially to convert MG into d-lactate, thereby helping living systems get rid of this otherwise cytotoxic byproduct of metabolism.	Pyruvaldehyde	107-109	hydroxyacylglutathione hydrolase	Homo sapiens	50-63
28358304-2	2017	It comprises two enzymes, glyoxalase I (GLYI) and glyoxalase II (GLYII), which act sequentially to convert MG into d-lactate, thereby helping living systems get rid of this otherwise cytotoxic byproduct of metabolism.	Pyruvaldehyde	107-109	hydroxyacylglutathione hydrolase	Homo sapiens	65-70
28358304-4	2017	Humans and Escherichia coli possess a single copy of GLYI (encoding either the Ni- or Zn-dependent form) and GLYII genes, which through MG detoxification provide protection against various pathological and disease conditions.	Pyruvaldehyde	136-138	glyoxalase I	Homo sapiens	53-57
28358304-4	2017	Humans and Escherichia coli possess a single copy of GLYI (encoding either the Ni- or Zn-dependent form) and GLYII genes, which through MG detoxification provide protection against various pathological and disease conditions.	Pyruvaldehyde	136-138	hydroxyacylglutathione hydrolase	Homo sapiens	109-114
27932057-5	2017	CycK(Myr)R4E therefore presents a promising option for the treatment of pain and other diabetic complications associated with high MG levels.	Pyruvaldehyde	131-133	cyclin K	Mus musculus	0-4
27956549-5	2017	Alternative detoxification of MG in GLO1-/- is achieved by increased catalytic efficiency of aldose reductase toward hemithioacetal (product of glutathione and MG), which is most likely caused by S-nitrosylation of aldose reductase.	Pyruvaldehyde	30-32	glyoxalase I	Homo sapiens	36-40
28169168-1	2017	Human glyoxalase I (GLO I), a rate-limiting enzyme for detoxification of methylglyoxal (MG), a by-product of glycolysis, is known to be a potential therapeutic target for cancer.	Pyruvaldehyde	73-86	glyoxalase I	Homo sapiens	6-18
28169168-1	2017	Human glyoxalase I (GLO I), a rate-limiting enzyme for detoxification of methylglyoxal (MG), a by-product of glycolysis, is known to be a potential therapeutic target for cancer.	Pyruvaldehyde	73-86	glyoxalase I	Homo sapiens	20-25
27956549-5	2017	Alternative detoxification of MG in GLO1-/- is achieved by increased catalytic efficiency of aldose reductase toward hemithioacetal (product of glutathione and MG), which is most likely caused by S-nitrosylation of aldose reductase.	Pyruvaldehyde	30-32	aldo-keto reductase family 1 member B	Homo sapiens	93-109
27956549-5	2017	Alternative detoxification of MG in GLO1-/- is achieved by increased catalytic efficiency of aldose reductase toward hemithioacetal (product of glutathione and MG), which is most likely caused by S-nitrosylation of aldose reductase.	Pyruvaldehyde	30-32	aldo-keto reductase family 1 member B	Homo sapiens	215-231
27956549-5	2017	Alternative detoxification of MG in GLO1-/- is achieved by increased catalytic efficiency of aldose reductase toward hemithioacetal (product of glutathione and MG), which is most likely caused by S-nitrosylation of aldose reductase.	Pyruvaldehyde	160-162	glyoxalase I	Homo sapiens	36-40
27956549-5	2017	Alternative detoxification of MG in GLO1-/- is achieved by increased catalytic efficiency of aldose reductase toward hemithioacetal (product of glutathione and MG), which is most likely caused by S-nitrosylation of aldose reductase.	Pyruvaldehyde	160-162	aldo-keto reductase family 1 member B	Homo sapiens	93-109
27956549-7	2017	Inhibition of aldose reductase in GLO1-/- cells is associated with an increased sensitivity against MG, elevated intracellular MG levels, associated modifications, as well as increased oxidative stress.	Pyruvaldehyde	100-102	aldo-keto reductase family 1 member B	Homo sapiens	14-30
27956549-7	2017	Inhibition of aldose reductase in GLO1-/- cells is associated with an increased sensitivity against MG, elevated intracellular MG levels, associated modifications, as well as increased oxidative stress.	Pyruvaldehyde	100-102	glyoxalase I	Homo sapiens	34-38
27956549-7	2017	Inhibition of aldose reductase in GLO1-/- cells is associated with an increased sensitivity against MG, elevated intracellular MG levels, associated modifications, as well as increased oxidative stress.	Pyruvaldehyde	127-129	aldo-keto reductase family 1 member B	Homo sapiens	14-30
27956549-7	2017	Inhibition of aldose reductase in GLO1-/- cells is associated with an increased sensitivity against MG, elevated intracellular MG levels, associated modifications, as well as increased oxidative stress.	Pyruvaldehyde	127-129	glyoxalase I	Homo sapiens	34-38
28112327-5	2017	MSX (500 mug mL-1) reduced the formation of AGEs by 40% in the bovine serum albumin (BSA)-fructose assay and by 30% in the BSA-methylglyoxal (MGO) assay.	Pyruvaldehyde	127-140	L1 cell adhesion molecule	Mus musculus	13-17
28231326-2	2017	MGO is detoxificated enzymatically by glyoxalase-I (Glo-I).	Pyruvaldehyde	0-3	glyoxalase 1	Rattus norvegicus	38-50
28231326-2	2017	MGO is detoxificated enzymatically by glyoxalase-I (Glo-I).	Pyruvaldehyde	0-3	glyoxalase 1	Rattus norvegicus	52-57
28231326-10	2017	RESULTS: Expression of Glo-I was significantly reduced in cirrhosis in whole liver and primary liver cells accompanied by elevated levels of MGO.	Pyruvaldehyde	141-144	glyoxalase 1	Rattus norvegicus	23-28
28231326-14	2017	CONCLUSIONS: Our results show the importance of Glo-I as major detoxifying enzyme for MGO in cirrhosis.	Pyruvaldehyde	86-89	glyoxalase 1	Rattus norvegicus	48-53
28337257-0	2017	Subcutaneous liraglutide ameliorates methylglyoxal-induced Alzheimer-like tau pathology and cognitive impairment by modulating tau hyperphosphorylation and glycogen synthase kinase-3beta.	Pyruvaldehyde	37-50	glycogen synthase kinase 3 beta	Mus musculus	156-186
28212304-5	2017	MGO and MGO-derived AGEs can further activate inflammatory cells by binding to the receptor for advanced glycation endproducts (RAGE).	Pyruvaldehyde	0-3	advanced glycosylation end-product specific receptor	Homo sapiens	83-126
28212304-5	2017	MGO and MGO-derived AGEs can further activate inflammatory cells by binding to the receptor for advanced glycation endproducts (RAGE).	Pyruvaldehyde	0-3	advanced glycosylation end-product specific receptor	Homo sapiens	128-132
28212304-5	2017	MGO and MGO-derived AGEs can further activate inflammatory cells by binding to the receptor for advanced glycation endproducts (RAGE).	Pyruvaldehyde	8-11	advanced glycosylation end-product specific receptor	Homo sapiens	83-126
28212304-5	2017	MGO and MGO-derived AGEs can further activate inflammatory cells by binding to the receptor for advanced glycation endproducts (RAGE).	Pyruvaldehyde	8-11	advanced glycosylation end-product specific receptor	Homo sapiens	128-132
28073699-7	2017	These results indicated that increase in GSH levels, induced by pre-treatment with carnosic acid, promoted the formation of the GLO1 substrate, hemithioacetal, thereby accelerating MG metabolism via the glyoxalase system and suppressing its toxicity.	Pyruvaldehyde	181-183	glyoxalase I	Homo sapiens	128-132
28073699-8	2017	It was, therefore, determined that promotion of GSH synthesis via the Nrf2/Keap1pathway is important in the MG detoxification mechanism against neuronal MG-induced carbonyl stress, and Nrf2 activators contribute to reduction in the accumulation and toxic expression of carbonyl proteins.	Pyruvaldehyde	108-110	NFE2 like bZIP transcription factor 2	Homo sapiens	70-74
28073699-0	2017	Activation of Nrf2 attenuates carbonyl stress induced by methylglyoxal in human neuroblastoma cells: Increase in GSH levels is a critical event for the detoxification mechanism.	Pyruvaldehyde	57-70	NFE2 like bZIP transcription factor 2	Homo sapiens	14-18
28073699-8	2017	It was, therefore, determined that promotion of GSH synthesis via the Nrf2/Keap1pathway is important in the MG detoxification mechanism against neuronal MG-induced carbonyl stress, and Nrf2 activators contribute to reduction in the accumulation and toxic expression of carbonyl proteins.	Pyruvaldehyde	108-110	kelch like ECH associated protein 1	Homo sapiens	75-80
28073699-2	2017	The involvement of nuclear factor erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1) pathway as a defense response against the formation of MG-modified proteins, which is well-known evidence of carbonyl stress, was also examined.	Pyruvaldehyde	169-171	NFE2 like bZIP transcription factor 2	Homo sapiens	19-62
28073699-2	2017	The involvement of nuclear factor erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1) pathway as a defense response against the formation of MG-modified proteins, which is well-known evidence of carbonyl stress, was also examined.	Pyruvaldehyde	169-171	NFE2 like bZIP transcription factor 2	Homo sapiens	64-68
28073699-8	2017	It was, therefore, determined that promotion of GSH synthesis via the Nrf2/Keap1pathway is important in the MG detoxification mechanism against neuronal MG-induced carbonyl stress, and Nrf2 activators contribute to reduction in the accumulation and toxic expression of carbonyl proteins.	Pyruvaldehyde	153-155	NFE2 like bZIP transcription factor 2	Homo sapiens	70-74
28073699-2	2017	The involvement of nuclear factor erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1) pathway as a defense response against the formation of MG-modified proteins, which is well-known evidence of carbonyl stress, was also examined.	Pyruvaldehyde	169-171	kelch like ECH associated protein 1	Homo sapiens	70-105
29109756-2	2017	Utilizing a condensation reaction between carbonyls and a hydrazine moeity, we demonstrate that the fluorescent probe (Aldehydefluor-1) AF1 reacts with a range of reactive carbonyl species including formaldehyde, acetaldehyde, glyoxylic acid, and methyl glyoxal.	Pyruvaldehyde	247-261	interferon gamma receptor 2	Homo sapiens	136-139
28073699-2	2017	The involvement of nuclear factor erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1) pathway as a defense response against the formation of MG-modified proteins, which is well-known evidence of carbonyl stress, was also examined.	Pyruvaldehyde	169-171	kelch like ECH associated protein 1	Homo sapiens	107-112
28073699-4	2017	This accumulation was suppressed by activation of the Nrf2 pathway prior to MG exposure via pre-treatment with an Nrf2 activator, carnosic acid and CDDO-Im, confirming the involvement of the Nrf2 pathway in MG detoxification.	Pyruvaldehyde	76-78	NFE2 like bZIP transcription factor 2	Homo sapiens	114-118
28073699-4	2017	This accumulation was suppressed by activation of the Nrf2 pathway prior to MG exposure via pre-treatment with an Nrf2 activator, carnosic acid and CDDO-Im, confirming the involvement of the Nrf2 pathway in MG detoxification.	Pyruvaldehyde	76-78	NFE2 like bZIP transcription factor 2	Homo sapiens	114-118
28073699-4	2017	This accumulation was suppressed by activation of the Nrf2 pathway prior to MG exposure via pre-treatment with an Nrf2 activator, carnosic acid and CDDO-Im, confirming the involvement of the Nrf2 pathway in MG detoxification.	Pyruvaldehyde	207-209	NFE2 like bZIP transcription factor 2	Homo sapiens	54-58
28073699-4	2017	This accumulation was suppressed by activation of the Nrf2 pathway prior to MG exposure via pre-treatment with an Nrf2 activator, carnosic acid and CDDO-Im, confirming the involvement of the Nrf2 pathway in MG detoxification.	Pyruvaldehyde	207-209	NFE2 like bZIP transcription factor 2	Homo sapiens	114-118
28073699-4	2017	This accumulation was suppressed by activation of the Nrf2 pathway prior to MG exposure via pre-treatment with an Nrf2 activator, carnosic acid and CDDO-Im, confirming the involvement of the Nrf2 pathway in MG detoxification.	Pyruvaldehyde	207-209	NFE2 like bZIP transcription factor 2	Homo sapiens	114-118
27864140-0	2017	The role of miR-190a in methylglyoxal-induced insulin resistance in endothelial cells.	Pyruvaldehyde	24-37	microRNA 190a	Mus musculus	12-20
27864140-7	2017	MGO reduces the expression of miR-190a both in mouse aortic endothelial cells (MAECs) and in aortae from mice knocked-down for glyoxalase-1.	Pyruvaldehyde	0-3	microRNA 190a	Mus musculus	30-38
27864140-7	2017	MGO reduces the expression of miR-190a both in mouse aortic endothelial cells (MAECs) and in aortae from mice knocked-down for glyoxalase-1.	Pyruvaldehyde	0-3	glyoxalase 1	Mus musculus	127-139
27864140-10	2017	Conversely, ERK1/2 activation is sustained by miR-190a inhibitor and the MGO-induced ERK1/2 hyper-activation is reduced by miR-190a mimic transfection.	Pyruvaldehyde	73-76	mitogen-activated protein kinase 3	Mus musculus	12-18
27864140-10	2017	Conversely, ERK1/2 activation is sustained by miR-190a inhibitor and the MGO-induced ERK1/2 hyper-activation is reduced by miR-190a mimic transfection.	Pyruvaldehyde	73-76	microRNA 190a	Mus musculus	46-54
27864140-10	2017	Conversely, ERK1/2 activation is sustained by miR-190a inhibitor and the MGO-induced ERK1/2 hyper-activation is reduced by miR-190a mimic transfection.	Pyruvaldehyde	73-76	mitogen-activated protein kinase 3	Mus musculus	85-91
27864140-10	2017	Conversely, ERK1/2 activation is sustained by miR-190a inhibitor and the MGO-induced ERK1/2 hyper-activation is reduced by miR-190a mimic transfection.	Pyruvaldehyde	73-76	microRNA 190a	Mus musculus	123-131
27984092-5	2017	These transcription factors mediate the HSP31 promoter responses to oxidative, osmotic and thermal stresses, to potentially toxic products of glycolysis, such as methylglyoxal and acetic acid, and to the diauxic shift.	Pyruvaldehyde	162-175	glutathione-independent methylglyoxalase	Saccharomyces cerevisiae S288C	40-45
27984092-7	2017	Overproduction of Hsp31p and its homologue Hsp32p rescued the sensitivity of glo1Delta cells to methylglyoxal.	Pyruvaldehyde	96-109	glutathione-independent methylglyoxalase	Saccharomyces cerevisiae S288C	18-24
27984092-7	2017	Overproduction of Hsp31p and its homologue Hsp32p rescued the sensitivity of glo1Delta cells to methylglyoxal.	Pyruvaldehyde	96-109	glutathione-independent methylglyoxalase family protein	Saccharomyces cerevisiae S288C	43-49
27984092-11	2017	Alternatively, Hsp31p might be effective under high concentration of exogenous methylglyoxal present in some natural environmental niches populated by budding yeast, when glyoxalase I/II system capacity is saturated.	Pyruvaldehyde	79-92	glutathione-independent methylglyoxalase	Saccharomyces cerevisiae S288C	15-21
27864140-11	2017	Similarly, protein levels of the upstream KRAS are increased by both MGO and miR-190a inhibitor, and these levels are reduced by miR-190a mimic transfection.	Pyruvaldehyde	69-72	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	42-46
27864140-11	2017	Similarly, protein levels of the upstream KRAS are increased by both MGO and miR-190a inhibitor, and these levels are reduced by miR-190a mimic transfection.	Pyruvaldehyde	69-72	microRNA 190a	Mus musculus	129-137
27864140-12	2017	Interestingly, silencing of KRAS is able to rescue the MGO-impaired activation of IRS1/Akt/eNOS pathway in response to insulin.	Pyruvaldehyde	55-58	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	28-32
27864140-12	2017	Interestingly, silencing of KRAS is able to rescue the MGO-impaired activation of IRS1/Akt/eNOS pathway in response to insulin.	Pyruvaldehyde	55-58	insulin receptor substrate 1	Mus musculus	82-86
27864140-12	2017	Interestingly, silencing of KRAS is able to rescue the MGO-impaired activation of IRS1/Akt/eNOS pathway in response to insulin.	Pyruvaldehyde	55-58	thymoma viral proto-oncogene 1	Mus musculus	87-90
27864140-13	2017	In conclusion, miR-190a down-regulation plays a role in MGO-induced endothelial insulin resistance by increasing KRAS.	Pyruvaldehyde	56-59	microRNA 190a	Mus musculus	15-23
27864140-13	2017	In conclusion, miR-190a down-regulation plays a role in MGO-induced endothelial insulin resistance by increasing KRAS.	Pyruvaldehyde	56-59	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	113-117
28007970-2	2017	Fructose-induced up-regulation of aldolase B (AldoB) contributes to increased vascular MG production but the underlying mechanisms are unclear.	Pyruvaldehyde	87-89	aldolase B, fructose-bisphosphate	Mus musculus	34-44
28007970-2	2017	Fructose-induced up-regulation of aldolase B (AldoB) contributes to increased vascular MG production but the underlying mechanisms are unclear.	Pyruvaldehyde	87-89	aldolase B, fructose-bisphosphate	Mus musculus	46-51
28007970-9	2017	The knockdown of AldoB expression prevented fructose-induced MG overproduction and VSMC proliferation.	Pyruvaldehyde	61-63	aldolase B, fructose-bisphosphate	Mus musculus	17-22
27696457-1	2017	BACKGROUND: Glyoxalase 2 (Glo2), together with glyoxalase 1 (Glo1), forms the main scavenging system of methylglyoxal, a potent pro-apoptotic agent mainly generated by glycolysis.	Pyruvaldehyde	104-117	hydroxyacylglutathione hydrolase	Homo sapiens	12-24
27696457-1	2017	BACKGROUND: Glyoxalase 2 (Glo2), together with glyoxalase 1 (Glo1), forms the main scavenging system of methylglyoxal, a potent pro-apoptotic agent mainly generated by glycolysis.	Pyruvaldehyde	104-117	hydroxyacylglutathione hydrolase	Homo sapiens	26-30
27696457-1	2017	BACKGROUND: Glyoxalase 2 (Glo2), together with glyoxalase 1 (Glo1), forms the main scavenging system of methylglyoxal, a potent pro-apoptotic agent mainly generated by glycolysis.	Pyruvaldehyde	104-117	glyoxalase I	Homo sapiens	47-59
27696457-1	2017	BACKGROUND: Glyoxalase 2 (Glo2), together with glyoxalase 1 (Glo1), forms the main scavenging system of methylglyoxal, a potent pro-apoptotic agent mainly generated by glycolysis.	Pyruvaldehyde	104-117	glyoxalase I	Homo sapiens	61-65
28117708-7	2017	Accordingly, GLO1 depletion in CRC cells promoted tumor growth in vivo that was efficiently reversed using carnosine, a potent MG scavenger.	Pyruvaldehyde	127-129	glyoxalase I	Homo sapiens	13-17
28106778-3	2017	Nonetheless, MGO levels are also increased as consequence of the ineffective action of its main detoxification pathway, the glyoxalase system, of which glyoxalase 1 (Glo1) is the rate-limiting enzyme.	Pyruvaldehyde	13-16	glyoxalase I	Homo sapiens	152-164
28106778-3	2017	Nonetheless, MGO levels are also increased as consequence of the ineffective action of its main detoxification pathway, the glyoxalase system, of which glyoxalase 1 (Glo1) is the rate-limiting enzyme.	Pyruvaldehyde	13-16	glyoxalase I	Homo sapiens	166-170
28106778-4	2017	Indeed, a physiological decrease of Glo1 transcription and activity occurs not only in chronic hyperglycaemia but also with ageing, during which MGO accumulation occurs.	Pyruvaldehyde	145-148	glyoxalase I	Homo sapiens	36-40
28106778-7	2017	Because of these considerations, studies have been centered on understanding the molecular basis of endothelial dysfunction in diabetes, unveiling a central role of MGO-Glo1 imbalance in the onset of vascular complications.	Pyruvaldehyde	165-168	glyoxalase I	Homo sapiens	169-173
27903648-2	2017	Methylglyoxal is detoxified by the Glyoxalase system, consisting of two enzymes, Glo1 and Glo2, that act sequentially to convert MG into d-lactate.	Pyruvaldehyde	0-13	Glyoxalase 1	Drosophila melanogaster	81-85
27903648-2	2017	Methylglyoxal is detoxified by the Glyoxalase system, consisting of two enzymes, Glo1 and Glo2, that act sequentially to convert MG into d-lactate.	Pyruvaldehyde	129-131	Glyoxalase 1	Drosophila melanogaster	81-85
28214842-0	2017	Inhibition of Methylglyoxal-Induced AGEs/RAGE Expression Contributes to Dermal Protection by N-Acetyl-L-Cysteine.	Pyruvaldehyde	14-27	long intergenic non-protein coding RNA 914	Homo sapiens	41-45
28214842-10	2017	The in vitro AGEs generation was also able to be enhanced by the exposure of HaCaT cells to MGO, which reduced dose-dependently cellular viability, damaged mitochondrial function, triggered secretion of interleukin (IL)-6 and IL-8, activated NF-kappaB and upregulated MMP-9 expression.	Pyruvaldehyde	92-95	C-X-C motif chemokine ligand 8	Homo sapiens	226-230
28214842-10	2017	The in vitro AGEs generation was also able to be enhanced by the exposure of HaCaT cells to MGO, which reduced dose-dependently cellular viability, damaged mitochondrial function, triggered secretion of interleukin (IL)-6 and IL-8, activated NF-kappaB and upregulated MMP-9 expression.	Pyruvaldehyde	92-95	matrix metallopeptidase 9	Homo sapiens	268-273
28214842-12	2017	Importantly, before the exposure to MGO, the preconditioning with NAC significantly attenuated MGO-induced AGEs generation, improved cellular viability and mitochondrial function, partially reversed the overexpression of proinflammatory factors and MMP-9, as well as the activation of NF-kappaB.	Pyruvaldehyde	95-98	matrix metallopeptidase 9	Homo sapiens	249-254
29181125-6	2017	GLU + MGO significantly increased the levels of AGE and AGE receptor (RAGE) protein expression of nuclear factor kappa-B (NF-kappaB) in the cytosol, but treatment with EGT, HIP, or EGT + HIP significantly attenuated these levels.	Pyruvaldehyde	6-9	advanced glycosylation end product-specific receptor	Rattus norvegicus	70-74
28214842-13	2017	Lastly, NAC blocked MGO-induced RAGE upregulation, and inhibition of RAGE with its neutralizing antibody significantly alleviated MGO-induced NF-kappaB activation, MMP-9 upregulation and inflammatory injury in HaCaT cells.	Pyruvaldehyde	20-23	long intergenic non-protein coding RNA 914	Homo sapiens	32-36
28214842-13	2017	Lastly, NAC blocked MGO-induced RAGE upregulation, and inhibition of RAGE with its neutralizing antibody significantly alleviated MGO-induced NF-kappaB activation, MMP-9 upregulation and inflammatory injury in HaCaT cells.	Pyruvaldehyde	130-133	long intergenic non-protein coding RNA 914	Homo sapiens	69-73
28214842-13	2017	Lastly, NAC blocked MGO-induced RAGE upregulation, and inhibition of RAGE with its neutralizing antibody significantly alleviated MGO-induced NF-kappaB activation, MMP-9 upregulation and inflammatory injury in HaCaT cells.	Pyruvaldehyde	130-133	matrix metallopeptidase 9	Homo sapiens	164-169
28214842-14	2017	CONCLUSION: The present work indicates the administration of NAC can prevent MGO-induced dermal inflammatory injury through inhibition of AGEs/RAGE signal, which may provide a basal support for the treatment of diabetic skin complications with NAC-containing medicines in the future.	Pyruvaldehyde	77-80	long intergenic non-protein coding RNA 914	Homo sapiens	143-147
28582854-0	2017	Activation of Macrophages and Microglia by Interferon-gamma and Lipopolysaccharide Increases Methylglyoxal Production: A New Mechanism in the Development of Vascular Complications and Cognitive Decline in Type 2 Diabetes Mellitus?	Pyruvaldehyde	93-106	interferon gamma	Mus musculus	43-59
28582854-2	2017	It is known that MGO contributes to inflammation as it forms advanced glycation end products (AGEs), which activate macrophages via the receptor RAGE.	Pyruvaldehyde	17-20	MOK protein kinase	Mus musculus	145-149
28582854-5	2017	MGO levels in activated macrophage cells (RAW264.7) peaked at 48 h, increasing 2.86-fold (3.14+-0.4 muM) at 5 U/ml IFN-gamma+5 mug/ml LPS, and 4.74-fold (5.46+-0.30 muM) at 10 U/ml IFN-gamma+10 mug/ml LPS compared to the non-activated controls (1.15+-0.02 muM).	Pyruvaldehyde	0-3	interferon gamma	Mus musculus	115-124
28582854-5	2017	MGO levels in activated macrophage cells (RAW264.7) peaked at 48 h, increasing 2.86-fold (3.14+-0.4 muM) at 5 U/ml IFN-gamma+5 mug/ml LPS, and 4.74-fold (5.46+-0.30 muM) at 10 U/ml IFN-gamma+10 mug/ml LPS compared to the non-activated controls (1.15+-0.02 muM).	Pyruvaldehyde	0-3	interferon gamma	Mus musculus	181-190
29057033-8	2017	PD pretreatment also significantly inhibited MGO-induced ROS production, MMP impairment, mitochondrial morphology changes, and Akt dephosphorylation.	Pyruvaldehyde	45-48	AKT serine/threonine kinase 1	Homo sapiens	127-130
29057033-9	2017	These results and the experiments involving N-acetyl cysteine (antioxidant), Cyclosporin A (mitochondrial protector), and LY294002 (Akt inhibitor) suggest that PD prevents MGO-induced HUVEC apoptosis, at least in part, through inhibiting oxidative stress, maintaining mitochondrial function, and activating Akt pathway.	Pyruvaldehyde	172-175	AKT serine/threonine kinase 1	Homo sapiens	132-135
29057033-9	2017	These results and the experiments involving N-acetyl cysteine (antioxidant), Cyclosporin A (mitochondrial protector), and LY294002 (Akt inhibitor) suggest that PD prevents MGO-induced HUVEC apoptosis, at least in part, through inhibiting oxidative stress, maintaining mitochondrial function, and activating Akt pathway.	Pyruvaldehyde	172-175	AKT serine/threonine kinase 1	Homo sapiens	307-310
27833913-14	2016	In in vitro studies, incubation with methylglyoxal, one of the advanced glycation end products, significantly impaired phosphorylation of Akt and eNOSSer1177 (P &lt; 0.01) and increased the expression of MCP-1, VCAM-1, and ICAM-1 in HUVEC.	Pyruvaldehyde	37-50	thymoma viral proto-oncogene 1	Mus musculus	138-141
28170200-3	2017	The objective of the present study was to detect whether overexpression of methylglyoxal-metabolizing enzyme glyoxalase-1 (GLO1), which reduces ROS in D-ADSCs, can restore their proangiogenic function in a streptozotocin-induced diabetic mice model of CLI.	Pyruvaldehyde	75-88	glyoxalase 1	Mus musculus	109-121
28170200-3	2017	The objective of the present study was to detect whether overexpression of methylglyoxal-metabolizing enzyme glyoxalase-1 (GLO1), which reduces ROS in D-ADSCs, can restore their proangiogenic function in a streptozotocin-induced diabetic mice model of CLI.	Pyruvaldehyde	75-88	glyoxalase 1	Mus musculus	123-127
27999356-3	2016	This is brought about by an increased expression of glyoxalase 1 (GLO1) that is the rate-limiting enzyme of the MGO-detoxifying glyoxalase system.	Pyruvaldehyde	112-115	glyoxalase I	Homo sapiens	52-64
27999356-3	2016	This is brought about by an increased expression of glyoxalase 1 (GLO1) that is the rate-limiting enzyme of the MGO-detoxifying glyoxalase system.	Pyruvaldehyde	112-115	glyoxalase I	Homo sapiens	66-70
26847600-13	2016	Moreover, soluble methylglyoxal induced apoptotic cell death as indicated by DAPI nuclear staining, annexin V and propidium iodide assays.	Pyruvaldehyde	18-31	annexin A5	Homo sapiens	100-109
26847600-17	2016	TIMP-1 is induced in these cells upon direct exposure to methylglyoxal or after culture of gingival fibroblasts over methylglyoxal-treated collagen.	Pyruvaldehyde	57-70	TIMP metallopeptidase inhibitor 1	Homo sapiens	0-6
26847600-17	2016	TIMP-1 is induced in these cells upon direct exposure to methylglyoxal or after culture of gingival fibroblasts over methylglyoxal-treated collagen.	Pyruvaldehyde	117-130	TIMP metallopeptidase inhibitor 1	Homo sapiens	0-6
27898103-2	2016	MG is detoxified by glyoxalase 1 (GLO1) of the cytosolic glyoxalase system.	Pyruvaldehyde	0-2	glyoxalase I	Homo sapiens	20-32
27898103-2	2016	MG is detoxified by glyoxalase 1 (GLO1) of the cytosolic glyoxalase system.	Pyruvaldehyde	0-2	glyoxalase I	Homo sapiens	34-38
27898103-3	2016	The aim was to investigate the effects of MG accumulation by GLO1-knockdown under hyperglycaemic conditions in human aortic endothelial cells (HAECs) hypothesizing that the accumulation of MG accounts for the deleterious effects on vascular function.	Pyruvaldehyde	42-44	glyoxalase I	Homo sapiens	61-65
27898103-3	2016	The aim was to investigate the effects of MG accumulation by GLO1-knockdown under hyperglycaemic conditions in human aortic endothelial cells (HAECs) hypothesizing that the accumulation of MG accounts for the deleterious effects on vascular function.	Pyruvaldehyde	189-191	glyoxalase I	Homo sapiens	61-65
27898103-8	2016	GLO1-knockdown increased MG concentration in cells and culture medium.	Pyruvaldehyde	25-27	glyoxalase I	Homo sapiens	0-4
27898103-13	2016	MG accumulation by GLO1-knockdown provoked collagen expression, endothelial inflammation and dysfunction and apoptosis which might contribute to vascular damage.	Pyruvaldehyde	0-2	glyoxalase I	Homo sapiens	19-23
27221336-3	2016	Pretreatment of MC3T3-E1 osteoblastic cells with luteolin prevented MG-induced cell death and production of tumor necrosis factor-alpha, intracellular reactive oxygen species, mitochondrial superoxide, and cardiolipin peroxidation.	Pyruvaldehyde	68-70	tumor necrosis factor	Mus musculus	108-135
27645922-3	2016	The aim of the study was to investigate the inhibitory effect of cyanidin on methylglyoxal (MG)- and glucose-induced protein glycation in bovine serum albumin (BSA) as well as oxidative DNA damage.	Pyruvaldehyde	77-90	albumin	Homo sapiens	145-158
27645922-3	2016	The aim of the study was to investigate the inhibitory effect of cyanidin on methylglyoxal (MG)- and glucose-induced protein glycation in bovine serum albumin (BSA) as well as oxidative DNA damage.	Pyruvaldehyde	92-94	albumin	Homo sapiens	145-158
27769859-4	2016	Biochemical data showed that 4-PBA significantly inhibited MGO-induced protein cleavages of PARP-1 and caspase-3.	Pyruvaldehyde	59-62	poly(ADP-ribose) polymerase 1	Homo sapiens	92-98
27769859-4	2016	Biochemical data showed that 4-PBA significantly inhibited MGO-induced protein cleavages of PARP-1 and caspase-3.	Pyruvaldehyde	59-62	caspase 3	Homo sapiens	103-112
27769859-5	2016	In addition, it was found that high glucose-induced endothelial apoptosis was enhanced in the presence of GLO1 inhibitor, suggesting the role of endogenous MGO in high glucose-induced endothelial dysfunction.	Pyruvaldehyde	156-159	glyoxalase I	Homo sapiens	106-110
27769859-6	2016	MGO-induced endothelial apoptosis was significantly diminished by the depletion of CHOP with si-RNA against human CHOP, but not by SP600125, a specific inhibitor of JNK.	Pyruvaldehyde	0-3	DNA damage inducible transcript 3	Homo sapiens	83-87
27769859-6	2016	MGO-induced endothelial apoptosis was significantly diminished by the depletion of CHOP with si-RNA against human CHOP, but not by SP600125, a specific inhibitor of JNK.	Pyruvaldehyde	0-3	DNA damage inducible transcript 3	Homo sapiens	114-118
27769859-9	2016	Taken together, these findings indicate that MGO specifically induces endothelial dysfunction in a CHOP-dependent manner, suggesting the therapeutic potential of CHOP inhibition in diabetic cardiovascular complications.	Pyruvaldehyde	45-48	DNA damage inducible transcript 3	Homo sapiens	99-103
27769859-9	2016	Taken together, these findings indicate that MGO specifically induces endothelial dysfunction in a CHOP-dependent manner, suggesting the therapeutic potential of CHOP inhibition in diabetic cardiovascular complications.	Pyruvaldehyde	45-48	DNA damage inducible transcript 3	Homo sapiens	162-166
27671893-6	2016	In further investigation of the consequences of dicarbonyl stress in ESCs, we found that prolonged exposure of mouse ESCs in culture to high concentrations of MG and/or hypoxia led to low-level increase in Glo1 copy number.	Pyruvaldehyde	159-161	glyoxalase 1	Mus musculus	206-210
27833913-14	2016	In in vitro studies, incubation with methylglyoxal, one of the advanced glycation end products, significantly impaired phosphorylation of Akt and eNOSSer1177 (P &lt; 0.01) and increased the expression of MCP-1, VCAM-1, and ICAM-1 in HUVEC.	Pyruvaldehyde	37-50	chemokine (C-C motif) ligand 2	Mus musculus	204-209
27833913-14	2016	In in vitro studies, incubation with methylglyoxal, one of the advanced glycation end products, significantly impaired phosphorylation of Akt and eNOSSer1177 (P &lt; 0.01) and increased the expression of MCP-1, VCAM-1, and ICAM-1 in HUVEC.	Pyruvaldehyde	37-50	vascular cell adhesion molecule 1	Mus musculus	211-217
27833913-14	2016	In in vitro studies, incubation with methylglyoxal, one of the advanced glycation end products, significantly impaired phosphorylation of Akt and eNOSSer1177 (P &lt; 0.01) and increased the expression of MCP-1, VCAM-1, and ICAM-1 in HUVEC.	Pyruvaldehyde	37-50	intercellular adhesion molecule 1	Mus musculus	223-229
27759563-0	2016	Methylglyoxal, a glycolysis side-product, induces Hsp90 glycation and YAP-mediated tumor growth and metastasis.	Pyruvaldehyde	0-13	heat shock protein 90 alpha family class A member 1	Homo sapiens	50-55
27478003-1	2016	OBJECTIVE: Glyoxalase 1 (GLO1) is ubiquitously expressed in the cytosol of the cell and is the major opponent against the reactive metabolite methylglyoxal, which is involved in the development of atherosclerosis.	Pyruvaldehyde	142-155	glyoxalase I	Homo sapiens	11-23
27738195-0	2016	Correction for The glucose metabolite methylglyoxal inhibits expression of the glucose transporter genes by inactivating the cell surface glucose sensors Rgt2 and Snf3 in yeast.	Pyruvaldehyde	38-51	glucose sensor	Saccharomyces cerevisiae S288C	154-158
27738195-0	2016	Correction for The glucose metabolite methylglyoxal inhibits expression of the glucose transporter genes by inactivating the cell surface glucose sensors Rgt2 and Snf3 in yeast.	Pyruvaldehyde	38-51	glucose sensor	Saccharomyces cerevisiae S288C	163-167
27626823-6	2016	In particular, we found that methylglyoxal treatment gave rise to altered expression of a number of kinases in the MAPK pathway and diminished expression of several receptor tyrosine kinases, including epidermal growth factor receptor (EGFR), insulin growth factor 2 receptor (IGF2R), fibroblast growth factor receptor (FGFR), etc.	Pyruvaldehyde	29-42	epidermal growth factor receptor	Homo sapiens	202-234
27626823-6	2016	In particular, we found that methylglyoxal treatment gave rise to altered expression of a number of kinases in the MAPK pathway and diminished expression of several receptor tyrosine kinases, including epidermal growth factor receptor (EGFR), insulin growth factor 2 receptor (IGF2R), fibroblast growth factor receptor (FGFR), etc.	Pyruvaldehyde	29-42	epidermal growth factor receptor	Homo sapiens	236-240
27626823-6	2016	In particular, we found that methylglyoxal treatment gave rise to altered expression of a number of kinases in the MAPK pathway and diminished expression of several receptor tyrosine kinases, including epidermal growth factor receptor (EGFR), insulin growth factor 2 receptor (IGF2R), fibroblast growth factor receptor (FGFR), etc.	Pyruvaldehyde	29-42	insulin like growth factor 2 receptor	Homo sapiens	243-275
27626823-6	2016	In particular, we found that methylglyoxal treatment gave rise to altered expression of a number of kinases in the MAPK pathway and diminished expression of several receptor tyrosine kinases, including epidermal growth factor receptor (EGFR), insulin growth factor 2 receptor (IGF2R), fibroblast growth factor receptor (FGFR), etc.	Pyruvaldehyde	29-42	insulin like growth factor 2 receptor	Homo sapiens	277-282
27759563-0	2016	Methylglyoxal, a glycolysis side-product, induces Hsp90 glycation and YAP-mediated tumor growth and metastasis.	Pyruvaldehyde	0-13	Yes1 associated transcriptional regulator	Homo sapiens	70-73
27759563-6	2016	Elevated MG levels resulted in sustained YAP nuclear localization/activity that could be reverted using Carnosine, a scavenger for MG.	Pyruvaldehyde	9-11	Yes1 associated transcriptional regulator	Homo sapiens	41-44
27759563-6	2016	Elevated MG levels resulted in sustained YAP nuclear localization/activity that could be reverted using Carnosine, a scavenger for MG.	Pyruvaldehyde	131-133	Yes1 associated transcriptional regulator	Homo sapiens	41-44
27759563-7	2016	MG treatment affected Hsp90 chaperone activity and decreased its binding to LATS1, a key kinase of the Hippo pathway.	Pyruvaldehyde	0-2	heat shock protein 90 alpha family class A member 1	Homo sapiens	22-27
27759563-7	2016	MG treatment affected Hsp90 chaperone activity and decreased its binding to LATS1, a key kinase of the Hippo pathway.	Pyruvaldehyde	0-2	large tumor suppressor kinase 1	Homo sapiens	76-81
27478003-1	2016	OBJECTIVE: Glyoxalase 1 (GLO1) is ubiquitously expressed in the cytosol of the cell and is the major opponent against the reactive metabolite methylglyoxal, which is involved in the development of atherosclerosis.	Pyruvaldehyde	142-155	glyoxalase I	Homo sapiens	25-29
27695694-6	2016	To this aim, the glycation kinetics of both native and demetalated SOD have been followed using two different glycating agents, i.e., D-ribose and methylglyoxal.	Pyruvaldehyde	147-160	superoxide dismutase 1	Homo sapiens	67-70
27235733-9	2016	Our biochemical findings support the hypothesis that MG induces persistent alterations in the hippocampus, but not in the cortex, related to glyoxalase 1 activity, AGEs content and glutamate uptake.	Pyruvaldehyde	53-55	glyoxalase 1	Rattus norvegicus	141-153
27506242-7	2016	CYTc loss-of-function mutants, as well as the d-LDH mutants, were more sensitive to d-lactate and MGO, indicating that they function in the same pathway.	Pyruvaldehyde	98-101	Cytochrome c	Arabidopsis thaliana	0-4
27506242-8	2016	In addition, overexpression of d-LDH and CYTc increased tolerance to d-lactate and MGO Together with fine-localization of d-LDH, the functional interaction with CYTc in vivo strongly suggests that d-lactate oxidation takes place in the mitochondrial intermembrane space, delivering electrons to the respiratory chain through CYTc These results provide a comprehensive picture of the organization and function of d-LDH in the plant cell and exemplify how the plant mitochondrial respiratory chain can act as a multifunctional electron sink for reductant from cytosolic pathways.	Pyruvaldehyde	83-86	Cytochrome c	Arabidopsis thaliana	41-45
27506242-8	2016	In addition, overexpression of d-LDH and CYTc increased tolerance to d-lactate and MGO Together with fine-localization of d-LDH, the functional interaction with CYTc in vivo strongly suggests that d-lactate oxidation takes place in the mitochondrial intermembrane space, delivering electrons to the respiratory chain through CYTc These results provide a comprehensive picture of the organization and function of d-LDH in the plant cell and exemplify how the plant mitochondrial respiratory chain can act as a multifunctional electron sink for reductant from cytosolic pathways.	Pyruvaldehyde	83-86	Cytochrome c	Arabidopsis thaliana	161-165
27506242-8	2016	In addition, overexpression of d-LDH and CYTc increased tolerance to d-lactate and MGO Together with fine-localization of d-LDH, the functional interaction with CYTc in vivo strongly suggests that d-lactate oxidation takes place in the mitochondrial intermembrane space, delivering electrons to the respiratory chain through CYTc These results provide a comprehensive picture of the organization and function of d-LDH in the plant cell and exemplify how the plant mitochondrial respiratory chain can act as a multifunctional electron sink for reductant from cytosolic pathways.	Pyruvaldehyde	83-86	Cytochrome c	Arabidopsis thaliana	161-165
27513960-1	2016	Recent studies have reported increases of methylglyoxal (MGO) in peritoneal dialysis patients, and that MGO-mediated inflammation plays an important role in the development of peritoneal fibrosis through production of transforming growth factor-beta1 (TGF-beta1).	Pyruvaldehyde	104-107	transforming growth factor beta 1	Homo sapiens	218-250
27605608-8	2016	Independently of AGER, methylglyoxal reduced the release of endothelial CSF-1 (M-CSF), which stimulates polarization of macrophages to a noninflammatory phenotype in the microenvironment of the ischemic brain.	Pyruvaldehyde	23-36	colony stimulating factor 1	Homo sapiens	72-77
27605608-8	2016	Independently of AGER, methylglyoxal reduced the release of endothelial CSF-1 (M-CSF), which stimulates polarization of macrophages to a noninflammatory phenotype in the microenvironment of the ischemic brain.	Pyruvaldehyde	23-36	colony stimulating factor 1	Homo sapiens	79-84
27455418-0	2016	Methylglyoxal suppresses human colon cancer cell lines and tumor growth in a mouse model by impairing glycolytic metabolism of cancer cells associated with down-regulation of c-Myc expression.	Pyruvaldehyde	0-13	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	175-180
27513960-1	2016	Recent studies have reported increases of methylglyoxal (MGO) in peritoneal dialysis patients, and that MGO-mediated inflammation plays an important role in the development of peritoneal fibrosis through production of transforming growth factor-beta1 (TGF-beta1).	Pyruvaldehyde	104-107	transforming growth factor beta 1	Homo sapiens	252-261
27513960-10	2016	Peritoneal injection of MGO increased plasma levels of glucagon-like peptide-1 (GLP-1) in mice, and a further increase was observed in linagliptin-treated mice.	Pyruvaldehyde	24-27	glucagon	Mus musculus	55-78
27513960-10	2016	Peritoneal injection of MGO increased plasma levels of glucagon-like peptide-1 (GLP-1) in mice, and a further increase was observed in linagliptin-treated mice.	Pyruvaldehyde	24-27	glucagon	Mus musculus	80-85
27513960-12	2016	Moreover, linagliptin reduced the TGF-beta1 concentration in the peritoneal fluid of MGO-treated mice.	Pyruvaldehyde	85-88	transforming growth factor, beta 1	Mus musculus	34-43
27208169-3	2016	We previously discovered that amyloid fibrils from ATTR patients are glycated by methylglyoxal.	Pyruvaldehyde	81-94	transthyretin	Homo sapiens	51-55
27233608-4	2016	We also observed suppression of methylglyoxal (MGO) mediated ROS production and deactivation of PKC-alpha.	Pyruvaldehyde	32-45	protein kinase C alpha	Homo sapiens	96-105
27233608-4	2016	We also observed suppression of methylglyoxal (MGO) mediated ROS production and deactivation of PKC-alpha.	Pyruvaldehyde	47-50	protein kinase C alpha	Homo sapiens	96-105
27233608-6	2016	URM-II-81 also alleviated MGO mediated diminished distal insulin signaling by increasing protein kinase B (PKB) and glycogen synthase kinase 3-beta (GSK-3-beta) phosphorylation.	Pyruvaldehyde	26-29	insulin	Homo sapiens	57-64
27233608-6	2016	URM-II-81 also alleviated MGO mediated diminished distal insulin signaling by increasing protein kinase B (PKB) and glycogen synthase kinase 3-beta (GSK-3-beta) phosphorylation.	Pyruvaldehyde	26-29	glycogen synthase kinase 3 beta	Homo sapiens	116-147
27233608-6	2016	URM-II-81 also alleviated MGO mediated diminished distal insulin signaling by increasing protein kinase B (PKB) and glycogen synthase kinase 3-beta (GSK-3-beta) phosphorylation.	Pyruvaldehyde	26-29	glycogen synthase kinase 3 beta	Homo sapiens	149-159
27779479-0	2016	Pronociceptive effects induced by cutaneous application of a transient receptor potential ankyrin 1 (TRPA1) channel agonist methylglyoxal in diabetic animals: comparison with tunicamycin-induced endoplastic reticulum stress.	Pyruvaldehyde	124-137	transient receptor potential cation channel subfamily A member 1	Homo sapiens	61-99
27779479-0	2016	Pronociceptive effects induced by cutaneous application of a transient receptor potential ankyrin 1 (TRPA1) channel agonist methylglyoxal in diabetic animals: comparison with tunicamycin-induced endoplastic reticulum stress.	Pyruvaldehyde	124-137	transient receptor potential cation channel subfamily A member 1	Homo sapiens	101-106
27779479-2	2016	MG is an established transient receptor potential ankyrin 1 (TRPA1) channel agonist that contributes to TRPA1-mediated diabetic pain hypersensitivity.	Pyruvaldehyde	0-2	transient receptor potential cation channel subfamily A member 1	Homo sapiens	21-59
27779479-2	2016	MG is an established transient receptor potential ankyrin 1 (TRPA1) channel agonist that contributes to TRPA1-mediated diabetic pain hypersensitivity.	Pyruvaldehyde	0-2	transient receptor potential cation channel subfamily A member 1	Homo sapiens	61-66
27779479-2	2016	MG is an established transient receptor potential ankyrin 1 (TRPA1) channel agonist that contributes to TRPA1-mediated diabetic pain hypersensitivity.	Pyruvaldehyde	0-2	transient receptor potential cation channel subfamily A member 1	Homo sapiens	104-109
27208169-7	2016	Here we show the existence of a proteostasis imbalance in ATTR linked to fibrinogen glycation by methylglyoxal.	Pyruvaldehyde	97-110	transthyretin	Homo sapiens	58-62
27208169-7	2016	Here we show the existence of a proteostasis imbalance in ATTR linked to fibrinogen glycation by methylglyoxal.	Pyruvaldehyde	97-110	fibrinogen beta chain	Homo sapiens	73-83
26956489-3	2016	We examined if overexpression of the MG-metabolizing enzyme glyoxalase 1 (GLO1) in macrophages and the vasculature could reduce MG-induced inflammation and prevent ventricular dysfunction in diabetes.	Pyruvaldehyde	37-39	glyoxalase 1	Mus musculus	60-72
27423812-7	2016	Prior application of MG evoked reciprocal suppression of subsequent [Ca(2+)]i responses to allylisothiocyanate, a TRPA1 agonist, and vice versa.	Pyruvaldehyde	21-23	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	114-119
27423812-9	2016	The present results suggest that MG promotes 5-HT secretion through the activation of TRPA1 in RIN-14B cells.	Pyruvaldehyde	33-35	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	86-91
27084712-1	2016	The purpose of the study is to identify the sites of modification when fibronectin reacts with glycolaldehyde or methylglyoxal as a model system for aging of Bruch"s membrane.	Pyruvaldehyde	113-126	fibronectin 1	Homo sapiens	71-82
27061807-1	2016	Human small heat shock protein HspB6 (Hsp20) was modified by metabolic alpha-dicarbonyl compound methylglyoxal (MGO).	Pyruvaldehyde	112-115	heat shock protein family B (small) member 6	Homo sapiens	31-36
27061807-1	2016	Human small heat shock protein HspB6 (Hsp20) was modified by metabolic alpha-dicarbonyl compound methylglyoxal (MGO).	Pyruvaldehyde	112-115	heat shock protein family B (small) member 6	Homo sapiens	38-43
27061807-4	2016	Both mild and extensive MGO modification decreased susceptibility of HspB6 to trypsinolysis and prevented its heat-induced aggregation.	Pyruvaldehyde	24-27	heat shock protein family B (small) member 6	Homo sapiens	69-74
27061807-7	2016	Phosphorylation of HspB6 by cyclic adenosine monophosphate (cAMP)-dependent protein kinase was inhibited after mild modification and completely prevented after extensive modification by MGO.	Pyruvaldehyde	186-189	heat shock protein family B (small) member 6	Homo sapiens	19-24
27061807-8	2016	Chaperone-like activity of HspB6 measured with subfragment 1 of skeletal myosin was enhanced after MGO modifications.	Pyruvaldehyde	99-102	heat shock protein family B (small) member 6	Homo sapiens	27-32
27061807-9	2016	It is concluded that Arg residues located in the N-terminal domain of HspB6 are easily accessible to MGO modification and that even mild modification by MGO affects susceptibility to trypsinolysis, phosphorylation by cAMP-dependent protein kinase, and chaperone-like activity of HspB6.	Pyruvaldehyde	101-104	heat shock protein family B (small) member 6	Homo sapiens	70-75
27061807-9	2016	It is concluded that Arg residues located in the N-terminal domain of HspB6 are easily accessible to MGO modification and that even mild modification by MGO affects susceptibility to trypsinolysis, phosphorylation by cAMP-dependent protein kinase, and chaperone-like activity of HspB6.	Pyruvaldehyde	153-156	heat shock protein family B (small) member 6	Homo sapiens	70-75
27061807-9	2016	It is concluded that Arg residues located in the N-terminal domain of HspB6 are easily accessible to MGO modification and that even mild modification by MGO affects susceptibility to trypsinolysis, phosphorylation by cAMP-dependent protein kinase, and chaperone-like activity of HspB6.	Pyruvaldehyde	153-156	heat shock protein family B (small) member 6	Homo sapiens	279-284
27083140-5	2016	When PGHS-1 was incubated with glycating/acetylating agents (glucose, Glu; 1,6-bisphosphofructose, 1,6-BPF; methylglyoxal, MGO, acetylsalicylic acid, ASA), the enzyme was modified in 13.4 +- 1.6, 5.3 +- 0.5, 10.7 +- 1.2 and 6.4 +- 1.1 mol/mol protein, respectively, and its activity was significantly reduced.	Pyruvaldehyde	108-121	prostaglandin-endoperoxide synthase 1	Homo sapiens	5-11
26930003-2	2016	TRPA1 is activated by several inflammatory mediators including formaldehyde and methylglyoxal that are products of the semicarbazide-sensitive amine-oxidase enzyme (SSAO).	Pyruvaldehyde	80-93	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	0-5
26930003-2	2016	TRPA1 is activated by several inflammatory mediators including formaldehyde and methylglyoxal that are products of the semicarbazide-sensitive amine-oxidase enzyme (SSAO).	Pyruvaldehyde	80-93	amine oxidase, copper containing 3	Rattus norvegicus	119-163
26930003-2	2016	TRPA1 is activated by several inflammatory mediators including formaldehyde and methylglyoxal that are products of the semicarbazide-sensitive amine-oxidase enzyme (SSAO).	Pyruvaldehyde	80-93	amine oxidase, copper containing 3	Rattus norvegicus	165-169
26956489-3	2016	We examined if overexpression of the MG-metabolizing enzyme glyoxalase 1 (GLO1) in macrophages and the vasculature could reduce MG-induced inflammation and prevent ventricular dysfunction in diabetes.	Pyruvaldehyde	128-130	glyoxalase 1	Mus musculus	74-78
26956489-3	2016	We examined if overexpression of the MG-metabolizing enzyme glyoxalase 1 (GLO1) in macrophages and the vasculature could reduce MG-induced inflammation and prevent ventricular dysfunction in diabetes.	Pyruvaldehyde	37-39	glyoxalase 1	Mus musculus	74-78
26956489-3	2016	We examined if overexpression of the MG-metabolizing enzyme glyoxalase 1 (GLO1) in macrophages and the vasculature could reduce MG-induced inflammation and prevent ventricular dysfunction in diabetes.	Pyruvaldehyde	128-130	glyoxalase 1	Mus musculus	60-72
26861824-0	2016	Neo-epitopes on methylglyoxal modified human serum albumin lead to aggressive autoimmune response in diabetes.	Pyruvaldehyde	16-29	albumin	Homo sapiens	51-58
29931846-8	2016	CONCLUSIONS: This study demonstrates that Ex-4 can increase the viabilities of PC12 cells and protect PC12 cells from oxidative stress induced by methylglyoxal, the mechanism may involve in suppressing the activation of protein IkappaB-alpha.	Pyruvaldehyde	146-159	NFKB inhibitor alpha	Rattus norvegicus	228-241
26861824-2	2016	Human serum albumin is prone to glyco-oxidative attack by sugars and methylglyoxal being a strong glycating agent may have severe impact on its structure and consequent role in diabetes.	Pyruvaldehyde	69-82	albumin	Homo sapiens	12-19
26975538-9	2016	CONCLUSION: Endogenously increased methylglyoxal may mediate diabetic neuropathic pain via activation of both TRPA1 and Nav1.8 expressed on primary afferent sensory neurons, and injection of methylglyoxal into the hindpaw may serve as a simple and robust model for testing the anti-diabetic pain drugs.	Pyruvaldehyde	35-48	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	110-115
27083416-1	2016	BACKGROUND: Glyoxalase pathway consists of two enzymes, glyoxalase I (GLYI) and glyoxalase II (GLYII) which detoxifies a highly cytotoxic metabolite methylglyoxal (MG) to its non-toxic form.	Pyruvaldehyde	149-162	lactoylglutathione lyase	Glycine max	56-68
27083416-1	2016	BACKGROUND: Glyoxalase pathway consists of two enzymes, glyoxalase I (GLYI) and glyoxalase II (GLYII) which detoxifies a highly cytotoxic metabolite methylglyoxal (MG) to its non-toxic form.	Pyruvaldehyde	149-162	lactoylglutathione lyase	Glycine max	70-74
27083416-1	2016	BACKGROUND: Glyoxalase pathway consists of two enzymes, glyoxalase I (GLYI) and glyoxalase II (GLYII) which detoxifies a highly cytotoxic metabolite methylglyoxal (MG) to its non-toxic form.	Pyruvaldehyde	164-166	lactoylglutathione lyase	Glycine max	56-68
27083416-1	2016	BACKGROUND: Glyoxalase pathway consists of two enzymes, glyoxalase I (GLYI) and glyoxalase II (GLYII) which detoxifies a highly cytotoxic metabolite methylglyoxal (MG) to its non-toxic form.	Pyruvaldehyde	164-166	lactoylglutathione lyase	Glycine max	70-74
26975538-0	2016	Methylglyoxal mediates streptozotocin-induced diabetic neuropathic pain via activation of the peripheral TRPA1 and Nav1.8 channels.	Pyruvaldehyde	0-13	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	105-110
26975538-0	2016	Methylglyoxal mediates streptozotocin-induced diabetic neuropathic pain via activation of the peripheral TRPA1 and Nav1.8 channels.	Pyruvaldehyde	0-13	sodium voltage-gated channel alpha subunit 10	Rattus norvegicus	115-121
26108947-1	2016	Glyoxalase-I (GLO-I) is a component of the ubiquitous detoxification system involved in the conversion of methylglyoxal (MG) to d-lactate in the glycolytic pathway.	Pyruvaldehyde	106-119	glyoxalase I	Homo sapiens	0-12
26108947-1	2016	Glyoxalase-I (GLO-I) is a component of the ubiquitous detoxification system involved in the conversion of methylglyoxal (MG) to d-lactate in the glycolytic pathway.	Pyruvaldehyde	106-119	glyoxalase I	Homo sapiens	14-19
26975648-5	2016	Furthermore, methylglyoxal induced carbonyl stress promotes the expression of the pro-inflammatory interleukins IL-6 and IL-8.	Pyruvaldehyde	13-26	interleukin 6	Homo sapiens	112-116
26975648-5	2016	Furthermore, methylglyoxal induced carbonyl stress promotes the expression of the pro-inflammatory interleukins IL-6 and IL-8.	Pyruvaldehyde	13-26	C-X-C motif chemokine ligand 8	Homo sapiens	121-125
26690780-10	2016	In addition, the levels of hippocampal BDNF and synaptophysin were significantly lower in the hippocampi of mice treated with MG at 1 %.	Pyruvaldehyde	126-128	brain derived neurotrophic factor	Mus musculus	39-43
26690780-10	2016	In addition, the levels of hippocampal BDNF and synaptophysin were significantly lower in the hippocampi of mice treated with MG at 1 %.	Pyruvaldehyde	126-128	synaptophysin	Mus musculus	48-61
26975538-9	2016	CONCLUSION: Endogenously increased methylglyoxal may mediate diabetic neuropathic pain via activation of both TRPA1 and Nav1.8 expressed on primary afferent sensory neurons, and injection of methylglyoxal into the hindpaw may serve as a simple and robust model for testing the anti-diabetic pain drugs.	Pyruvaldehyde	35-48	sodium voltage-gated channel alpha subunit 10	Rattus norvegicus	120-126
26997114-0	2016	Glucagon-like peptide-1 prevents methylglyoxal-induced apoptosis of beta cells through improving mitochondrial function and suppressing prolonged AMPK activation.	Pyruvaldehyde	33-46	glucagon	Homo sapiens	0-23
26997114-0	2016	Glucagon-like peptide-1 prevents methylglyoxal-induced apoptosis of beta cells through improving mitochondrial function and suppressing prolonged AMPK activation.	Pyruvaldehyde	33-46	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	146-150
26997114-2	2016	The molecular mechanism by which GLP-1 protects MG-induced beta cell apoptosis remains unclear.	Pyruvaldehyde	48-50	glucagon like peptide 1 receptor	Homo sapiens	33-38
26997114-6	2016	MG treatment induced apoptosis of beta cells, impaired mitochondrial function, and prolonged activation of AMP-dependent protein kinase (AMPK).	Pyruvaldehyde	0-2	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	107-135
26997114-6	2016	MG treatment induced apoptosis of beta cells, impaired mitochondrial function, and prolonged activation of AMP-dependent protein kinase (AMPK).	Pyruvaldehyde	0-2	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	137-141
26997114-7	2016	The MG-induced pro-apoptotic effects were abolished by an AMPK inhibitor.	Pyruvaldehyde	4-6	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	58-62
26997114-8	2016	Pretreatment of GLP-1 reversed MG-induced apoptosis, and mitochondrial dysfunction, and suppressed prolonged AMPK activation.	Pyruvaldehyde	31-33	glucagon like peptide 1 receptor	Homo sapiens	16-21
26997114-11	2016	In parallel, GLP-1 also prevents MG-induced beta cell apoptosis through PKA and PI3K-dependent pathway.	Pyruvaldehyde	33-35	glucagon like peptide 1 receptor	Homo sapiens	13-18
26997114-12	2016	In conclusion, these data indicates GLP-1 but not metformin protects MG-induced beta cell apoptosis through improving mitochondrial function, and alleviating the prolonged AMPK activation.	Pyruvaldehyde	69-71	glucagon like peptide 1 receptor	Homo sapiens	36-41
26898122-0	2016	Methylglyoxal activates NF-kappaB nuclear translocation and induces COX-2 expression via a p38-dependent pathway in synovial cells.	Pyruvaldehyde	0-13	nuclear factor kappa B subunit 1	Homo sapiens	24-33
26711908-1	2016	GLO1 (Glyoxalase1) is a ubiquitous cellular enzyme that detoxifies methylglyoxal (MG), which is a byproduct of glycolysis.	Pyruvaldehyde	67-80	glyoxalase 1	Mus musculus	0-4
26711908-1	2016	GLO1 (Glyoxalase1) is a ubiquitous cellular enzyme that detoxifies methylglyoxal (MG), which is a byproduct of glycolysis.	Pyruvaldehyde	67-80	glyoxalase 1	Mus musculus	6-17
26711908-1	2016	GLO1 (Glyoxalase1) is a ubiquitous cellular enzyme that detoxifies methylglyoxal (MG), which is a byproduct of glycolysis.	Pyruvaldehyde	82-84	glyoxalase 1	Mus musculus	0-4
26711908-1	2016	GLO1 (Glyoxalase1) is a ubiquitous cellular enzyme that detoxifies methylglyoxal (MG), which is a byproduct of glycolysis.	Pyruvaldehyde	82-84	glyoxalase 1	Mus musculus	6-17
26711908-2	2016	Previously, we showed that ubiquitous overexpression of Glo1 reduced concentrations of MG and increased anxiety-like behavior, whereas systemic injection of MG reduced anxiety-like behavior.	Pyruvaldehyde	87-89	glyoxalase 1	Mus musculus	56-60
26898122-0	2016	Methylglyoxal activates NF-kappaB nuclear translocation and induces COX-2 expression via a p38-dependent pathway in synovial cells.	Pyruvaldehyde	0-13	prostaglandin-endoperoxide synthase 2	Homo sapiens	68-73
26898122-10	2016	Moreover, MGO induces p38-dependent COX-2 protein expression as well as the phosphorylations of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and Akt/mammalian target of rapamycin (mTOR)/p70S6K; however, inhibition of JNK and Akt/mTOR/p70S6K phosphorylations further activates COX-2 protein expression.	Pyruvaldehyde	10-13	ribosomal protein S6 kinase B1	Homo sapiens	211-217
26898122-10	2016	Moreover, MGO induces p38-dependent COX-2 protein expression as well as the phosphorylations of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and Akt/mammalian target of rapamycin (mTOR)/p70S6K; however, inhibition of JNK and Akt/mTOR/p70S6K phosphorylations further activates COX-2 protein expression.	Pyruvaldehyde	10-13	mitogen-activated protein kinase 8	Homo sapiens	242-245
26898122-0	2016	Methylglyoxal activates NF-kappaB nuclear translocation and induces COX-2 expression via a p38-dependent pathway in synovial cells.	Pyruvaldehyde	0-13	mitogen-activated protein kinase 14	Homo sapiens	91-94
26898122-10	2016	Moreover, MGO induces p38-dependent COX-2 protein expression as well as the phosphorylations of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and Akt/mammalian target of rapamycin (mTOR)/p70S6K; however, inhibition of JNK and Akt/mTOR/p70S6K phosphorylations further activates COX-2 protein expression.	Pyruvaldehyde	10-13	AKT serine/threonine kinase 1	Homo sapiens	250-253
26898122-10	2016	Moreover, MGO induces p38-dependent COX-2 protein expression as well as the phosphorylations of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and Akt/mammalian target of rapamycin (mTOR)/p70S6K; however, inhibition of JNK and Akt/mTOR/p70S6K phosphorylations further activates COX-2 protein expression.	Pyruvaldehyde	10-13	mechanistic target of rapamycin kinase	Homo sapiens	254-258
26898122-10	2016	Moreover, MGO induces p38-dependent COX-2 protein expression as well as the phosphorylations of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and Akt/mammalian target of rapamycin (mTOR)/p70S6K; however, inhibition of JNK and Akt/mTOR/p70S6K phosphorylations further activates COX-2 protein expression.	Pyruvaldehyde	10-13	ribosomal protein S6 kinase B1	Homo sapiens	259-265
26898122-10	2016	Moreover, MGO induces p38-dependent COX-2 protein expression as well as the phosphorylations of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and Akt/mammalian target of rapamycin (mTOR)/p70S6K; however, inhibition of JNK and Akt/mTOR/p70S6K phosphorylations further activates COX-2 protein expression.	Pyruvaldehyde	10-13	prostaglandin-endoperoxide synthase 2	Homo sapiens	301-306
26898122-4	2016	In this study, we investigated the effects of the treatment of different MGO concentrations to rabbit HIG-82 synovial cells on COX-2 expression.	Pyruvaldehyde	73-76	prostaglandin-endoperoxide synthase 2	Homo sapiens	127-132
26898122-5	2016	MAIN METHODS: The MGO induced COX-2 mRNA expression was detected by quantitative polymerase chain reaction.	Pyruvaldehyde	18-21	prostaglandin-endoperoxide synthase 2	Homo sapiens	30-35
26898122-6	2016	The MGO induced COX-2 protein production and its signaling pathways were detected by western blotting.	Pyruvaldehyde	4-7	prostaglandin-endoperoxide synthase 2	Homo sapiens	16-21
26898122-7	2016	The nuclear factor-kappa B (NF-kappaB) nuclear translocation by MGO was examined by immunofluorescence.	Pyruvaldehyde	64-67	nuclear factor kappa B subunit 1	Homo sapiens	4-26
26898122-11	2016	Furthermore, MGO is shown to activate of nuclear factor-kappa B (NF-kappaB) nuclear translocation.	Pyruvaldehyde	13-16	nuclear factor kappa B subunit 1	Homo sapiens	41-63
26898122-7	2016	The nuclear factor-kappa B (NF-kappaB) nuclear translocation by MGO was examined by immunofluorescence.	Pyruvaldehyde	64-67	nuclear factor kappa B subunit 1	Homo sapiens	28-37
26898122-11	2016	Furthermore, MGO is shown to activate of nuclear factor-kappa B (NF-kappaB) nuclear translocation.	Pyruvaldehyde	13-16	nuclear factor kappa B subunit 1	Homo sapiens	65-74
26898122-12	2016	SIGNIFICANCE: Our results suggest that MGO can induce COX-2 expression via a p38-dependent pathway and activate NF-kappaB nuclear translocation in synovial cells.	Pyruvaldehyde	39-42	prostaglandin-endoperoxide synthase 2	Homo sapiens	54-59
26898122-9	2016	Our analysis demonstrates that MGO induced COX-2 mRNA and protein production.	Pyruvaldehyde	31-34	prostaglandin-endoperoxide synthase 2	Homo sapiens	43-48
26898122-12	2016	SIGNIFICANCE: Our results suggest that MGO can induce COX-2 expression via a p38-dependent pathway and activate NF-kappaB nuclear translocation in synovial cells.	Pyruvaldehyde	39-42	mitogen-activated protein kinase 14	Homo sapiens	77-80
26898122-10	2016	Moreover, MGO induces p38-dependent COX-2 protein expression as well as the phosphorylations of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and Akt/mammalian target of rapamycin (mTOR)/p70S6K; however, inhibition of JNK and Akt/mTOR/p70S6K phosphorylations further activates COX-2 protein expression.	Pyruvaldehyde	10-13	mitogen-activated protein kinase 14	Homo sapiens	22-25
26898122-12	2016	SIGNIFICANCE: Our results suggest that MGO can induce COX-2 expression via a p38-dependent pathway and activate NF-kappaB nuclear translocation in synovial cells.	Pyruvaldehyde	39-42	nuclear factor kappa B subunit 1	Homo sapiens	112-121
26898122-10	2016	Moreover, MGO induces p38-dependent COX-2 protein expression as well as the phosphorylations of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and Akt/mammalian target of rapamycin (mTOR)/p70S6K; however, inhibition of JNK and Akt/mTOR/p70S6K phosphorylations further activates COX-2 protein expression.	Pyruvaldehyde	10-13	prostaglandin-endoperoxide synthase 2	Homo sapiens	36-41
26898122-10	2016	Moreover, MGO induces p38-dependent COX-2 protein expression as well as the phosphorylations of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and Akt/mammalian target of rapamycin (mTOR)/p70S6K; however, inhibition of JNK and Akt/mTOR/p70S6K phosphorylations further activates COX-2 protein expression.	Pyruvaldehyde	10-13	mitogen-activated protein kinase 8	Homo sapiens	135-158
26898122-10	2016	Moreover, MGO induces p38-dependent COX-2 protein expression as well as the phosphorylations of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and Akt/mammalian target of rapamycin (mTOR)/p70S6K; however, inhibition of JNK and Akt/mTOR/p70S6K phosphorylations further activates COX-2 protein expression.	Pyruvaldehyde	10-13	mitogen-activated protein kinase 8	Homo sapiens	160-163
26898122-10	2016	Moreover, MGO induces p38-dependent COX-2 protein expression as well as the phosphorylations of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and Akt/mammalian target of rapamycin (mTOR)/p70S6K; however, inhibition of JNK and Akt/mTOR/p70S6K phosphorylations further activates COX-2 protein expression.	Pyruvaldehyde	10-13	AKT serine/threonine kinase 1	Homo sapiens	170-173
26898122-10	2016	Moreover, MGO induces p38-dependent COX-2 protein expression as well as the phosphorylations of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and Akt/mammalian target of rapamycin (mTOR)/p70S6K; however, inhibition of JNK and Akt/mTOR/p70S6K phosphorylations further activates COX-2 protein expression.	Pyruvaldehyde	10-13	mechanistic target of rapamycin kinase	Homo sapiens	174-203
26898122-10	2016	Moreover, MGO induces p38-dependent COX-2 protein expression as well as the phosphorylations of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and Akt/mammalian target of rapamycin (mTOR)/p70S6K; however, inhibition of JNK and Akt/mTOR/p70S6K phosphorylations further activates COX-2 protein expression.	Pyruvaldehyde	10-13	mechanistic target of rapamycin kinase	Homo sapiens	205-209
26554310-0	2016	Methylglyoxal-induced modification causes aggregation of myoglobin.	Pyruvaldehyde	0-13	myoglobin	Homo sapiens	57-66
26764094-0	2016	The glucose metabolite methylglyoxal inhibits expression of the glucose transporter genes by inactivating the cell surface glucose sensors Rgt2 and Snf3 in yeast.	Pyruvaldehyde	23-36	glucose sensor	Saccharomyces cerevisiae S288C	139-143
26764094-0	2016	The glucose metabolite methylglyoxal inhibits expression of the glucose transporter genes by inactivating the cell surface glucose sensors Rgt2 and Snf3 in yeast.	Pyruvaldehyde	23-36	glucose sensor	Saccharomyces cerevisiae S288C	148-152
26764094-8	2016	In addition, the inhibitory effect of MG on the glucose sensors is greatly enhanced in cells lacking Glo1, a key component of the MG detoxification system.	Pyruvaldehyde	38-40	lactoylglutathione lyase GLO1	Saccharomyces cerevisiae S288C	101-105
26764094-8	2016	In addition, the inhibitory effect of MG on the glucose sensors is greatly enhanced in cells lacking Glo1, a key component of the MG detoxification system.	Pyruvaldehyde	130-132	lactoylglutathione lyase GLO1	Saccharomyces cerevisiae S288C	101-105
26911935-3	2016	Previously, we reported that GAPDH purified from a variety of malignant tissues, but not from normal tissues, was strongly inactivated by a normal metabolite, methylglyoxal (MG).	Pyruvaldehyde	159-172	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	29-34
26911935-4	2016	Molecular mechanism behind MG mediated GAPDH inhibition in cancer cells is not well understood.	Pyruvaldehyde	27-29	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	39-44
26911935-8	2016	Mechanism of MG mediated GAPDH inactivation in cancer cells was evaluated by measuring enzyme activity, Circular dichroism (CD) spectroscopy, IP and mass spectrometry analyses.	Pyruvaldehyde	13-15	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	25-30
26911935-13	2016	In presence of 1 mM MG, association of GAPDH with PKM2 or GPI is not perturbed, but the enzymatic activity of GAPDH is reduced to 26.8 +- 5 % in 3MC induced tumor and 57.8 +- 2.3 % in EAC cells.	Pyruvaldehyde	20-22	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	39-44
26911935-13	2016	In presence of 1 mM MG, association of GAPDH with PKM2 or GPI is not perturbed, but the enzymatic activity of GAPDH is reduced to 26.8 +- 5 % in 3MC induced tumor and 57.8 +- 2.3 % in EAC cells.	Pyruvaldehyde	20-22	pyruvate kinase, muscle	Mus musculus	50-54
26911935-13	2016	In presence of 1 mM MG, association of GAPDH with PKM2 or GPI is not perturbed, but the enzymatic activity of GAPDH is reduced to 26.8 +- 5 % in 3MC induced tumor and 57.8 +- 2.3 % in EAC cells.	Pyruvaldehyde	20-22	glucose-6-phosphate isomerase 1	Mus musculus	58-61
26911935-13	2016	In presence of 1 mM MG, association of GAPDH with PKM2 or GPI is not perturbed, but the enzymatic activity of GAPDH is reduced to 26.8 +- 5 % in 3MC induced tumor and 57.8 +- 2.3 % in EAC cells.	Pyruvaldehyde	20-22	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	110-115
26911935-14	2016	Treatment of MG to purified GAPDH complex leads to glycation at R399 residue of PKM2 only, and changes the secondary structure of the protein complex.	Pyruvaldehyde	13-15	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	28-33
26911935-14	2016	Treatment of MG to purified GAPDH complex leads to glycation at R399 residue of PKM2 only, and changes the secondary structure of the protein complex.	Pyruvaldehyde	13-15	pyruvate kinase, muscle	Mus musculus	80-84
26911935-18	2016	Glycation at R399 of PKM2 and changes in the secondary structure of GAPDH complex could be one of the mechanisms by which GAPDH activity is inhibited in tumor cells by MG.	Pyruvaldehyde	168-170	pyruvate kinase, muscle	Mus musculus	21-25
26911935-18	2016	Glycation at R399 of PKM2 and changes in the secondary structure of GAPDH complex could be one of the mechanisms by which GAPDH activity is inhibited in tumor cells by MG.	Pyruvaldehyde	168-170	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	68-73
26911935-18	2016	Glycation at R399 of PKM2 and changes in the secondary structure of GAPDH complex could be one of the mechanisms by which GAPDH activity is inhibited in tumor cells by MG.	Pyruvaldehyde	168-170	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	122-127
26784015-1	2016	Glyoxalase I (Glo1) is the main scavenging enzyme of methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs).	Pyruvaldehyde	53-66	glyoxalase I	Homo sapiens	0-12
26784015-1	2016	Glyoxalase I (Glo1) is the main scavenging enzyme of methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs).	Pyruvaldehyde	53-66	glyoxalase I	Homo sapiens	14-18
26784015-1	2016	Glyoxalase I (Glo1) is the main scavenging enzyme of methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs).	Pyruvaldehyde	68-70	glyoxalase I	Homo sapiens	0-12
26784015-1	2016	Glyoxalase I (Glo1) is the main scavenging enzyme of methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs).	Pyruvaldehyde	68-70	glyoxalase I	Homo sapiens	14-18
26629685-0	2016	Glycolytic metabolite methylglyoxal inhibits cold and menthol activation of the transient receptor potential melastatin type 8 channel.	Pyruvaldehyde	22-35	transient receptor potential cation channel subfamily M member 8	Homo sapiens	80-126
26629685-4	2016	This study assesses effects of MG on TRPM8, an ion channel involved in innocuous cold sensing and cold allodynia and also in cold-mediated analgesia.	Pyruvaldehyde	31-33	transient receptor potential cation channel subfamily M member 8	Homo sapiens	37-42
26629685-5	2016	Acute treatment with MG inhibited the activation of recombinant rat and human transient receptor potential melastatin type 8 (TRPM8) by cold and chemical agonists.	Pyruvaldehyde	21-23	transient receptor potential cation channel subfamily M member 8	Homo sapiens	78-124
26629685-5	2016	Acute treatment with MG inhibited the activation of recombinant rat and human transient receptor potential melastatin type 8 (TRPM8) by cold and chemical agonists.	Pyruvaldehyde	21-23	transient receptor potential cation channel subfamily M member 8	Homo sapiens	126-131
26629685-9	2016	The same prolonged exposure to MG significantly reduced the expression of TRPM8 at the mRNA level.	Pyruvaldehyde	31-33	transient receptor potential cation channel subfamily M member 8	Homo sapiens	74-79
26629685-10	2016	Overall, our data provide evidence for decreased activity and expression level of TRPM8 in the presence of MG, which may be linked to some of the alterations in pain and temperature sensing reported by diabetic patients.	Pyruvaldehyde	107-109	transient receptor potential cation channel subfamily M member 8	Homo sapiens	82-87
26554310-3	2016	We have investigated the in vitro effect of MG (200muM) on the monomeric heme protein myoglobin (Mb) (100muM) in a time-dependent manner (7 to 18days incubation at 25 C).	Pyruvaldehyde	44-46	myoglobin	Homo sapiens	86-95
26616456-4	2016	The aim of this study was to investigate the protective effects of PC on INS-1 rat insulinoma beta-cell against MG-induced cell dysfunction, as well as the underlying mechanisms.	Pyruvaldehyde	112-114	insulin 1	Rattus norvegicus	73-78
26805012-0	2016	Phycocyanin prevents methylglyoxal-induced mitochondrial-dependent apoptosis in INS-1 cells by Nrf2.	Pyruvaldehyde	21-34	insulin 1	Rattus norvegicus	80-85
26805012-0	2016	Phycocyanin prevents methylglyoxal-induced mitochondrial-dependent apoptosis in INS-1 cells by Nrf2.	Pyruvaldehyde	21-34	NFE2 like bZIP transcription factor 2	Rattus norvegicus	95-99
26805012-6	2016	The aim of this study was to determine the protective effect of PC against methylglyoxal (MG)-induced dysfunction in pancreatic beta-cell INS-1 and also the mechanism.	Pyruvaldehyde	75-88	insulin 1	Rattus norvegicus	138-143
26805012-6	2016	The aim of this study was to determine the protective effect of PC against methylglyoxal (MG)-induced dysfunction in pancreatic beta-cell INS-1 and also the mechanism.	Pyruvaldehyde	90-92	insulin 1	Rattus norvegicus	138-143
26347375-0	2016	Methylglyoxal and carboxyethyllysine reduce glutamate uptake and S100B secretion in the hippocampus independently of RAGE activation.	Pyruvaldehyde	0-13	S100 calcium binding protein B	Homo sapiens	65-70
26616456-7	2016	Furthermore, MG induced dephosphorylation of Akt and FoxO1, resulting in nuclear localization and transactivation of FoxO1.	Pyruvaldehyde	13-15	AKT serine/threonine kinase 1	Rattus norvegicus	45-48
26616456-7	2016	Furthermore, MG induced dephosphorylation of Akt and FoxO1, resulting in nuclear localization and transactivation of FoxO1.	Pyruvaldehyde	13-15	forkhead box O1	Rattus norvegicus	53-58
26616456-7	2016	Furthermore, MG induced dephosphorylation of Akt and FoxO1, resulting in nuclear localization and transactivation of FoxO1.	Pyruvaldehyde	13-15	forkhead box O1	Rattus norvegicus	117-122
26670935-0	2016	Glabridin Alleviates the Toxic Effects of Methylglyoxal on Osteoblastic MC3T3-E1 Cells by Increasing Expression of the Glyoxalase System and Nrf2/HO-1 Signaling and Protecting Mitochondrial Function.	Pyruvaldehyde	42-55	nuclear factor, erythroid derived 2, like 2	Mus musculus	141-145
26718010-11	2016	Furthermore, there was a significant reduction in the expression levels of transforming growth factor-beta1 and intercellular adhesion molecule(-1) following treatment with Cur-MGO adducts compared with MGO alone.	Pyruvaldehyde	177-180	transforming growth factor beta 1	Homo sapiens	75-146
26718010-11	2016	Furthermore, there was a significant reduction in the expression levels of transforming growth factor-beta1 and intercellular adhesion molecule(-1) following treatment with Cur-MGO adducts compared with MGO alone.	Pyruvaldehyde	203-206	transforming growth factor beta 1	Homo sapiens	75-146
26660853-1	2016	Methylglyoxal (MGO) is a toxic, dicarbonyl metabolite in all living cells and its detoxification is regulated by glyoxalase I (GLOI).	Pyruvaldehyde	0-13	glyoxalase I	Homo sapiens	113-125
26660853-1	2016	Methylglyoxal (MGO) is a toxic, dicarbonyl metabolite in all living cells and its detoxification is regulated by glyoxalase I (GLOI).	Pyruvaldehyde	0-13	glyoxalase I	Homo sapiens	127-131
26660853-1	2016	Methylglyoxal (MGO) is a toxic, dicarbonyl metabolite in all living cells and its detoxification is regulated by glyoxalase I (GLOI).	Pyruvaldehyde	15-18	glyoxalase I	Homo sapiens	113-125
26660853-1	2016	Methylglyoxal (MGO) is a toxic, dicarbonyl metabolite in all living cells and its detoxification is regulated by glyoxalase I (GLOI).	Pyruvaldehyde	15-18	glyoxalase I	Homo sapiens	127-131
26670935-0	2016	Glabridin Alleviates the Toxic Effects of Methylglyoxal on Osteoblastic MC3T3-E1 Cells by Increasing Expression of the Glyoxalase System and Nrf2/HO-1 Signaling and Protecting Mitochondrial Function.	Pyruvaldehyde	42-55	heme oxygenase 1	Mus musculus	146-150
26670935-5	2016	The soluble form of receptor for advanced glycation end products (sRAGEs)/RAGE ratio increased upon MG treatment, but less so after pretreatment with glabridin, which also increased the level of reduced glutathione and the activities of glyoxalase I and heme oxygenase-1, all of which were reduced by MG.	Pyruvaldehyde	100-102	advanced glycosylation end product-specific receptor	Mus musculus	67-71
26670935-5	2016	The soluble form of receptor for advanced glycation end products (sRAGEs)/RAGE ratio increased upon MG treatment, but less so after pretreatment with glabridin, which also increased the level of reduced glutathione and the activities of glyoxalase I and heme oxygenase-1, all of which were reduced by MG.	Pyruvaldehyde	100-102	glyoxalase 1	Mus musculus	237-270
27150153-1	2016	Human glyoxalase I (hGLO I) is a rate-limiting enzyme in the pathway for detoxification of apoptosis-inducible methylglyoxal (MG), which is the side product of tumor-specific aerobic glycolysis.	Pyruvaldehyde	111-124	glyoxalase I	Homo sapiens	6-18
26965039-0	2016	Methylglyoxal, A Metabolite Increased in Diabetes is Associated with Insulin Resistance, Vascular Dysfunction and Neuropathies.	Pyruvaldehyde	0-13	insulin	Homo sapiens	69-76
26779540-0	2016	Methylglyoxal Impairs Insulin Secretion of Pancreatic beta-Cells through Increased Production of ROS and Mitochondrial Dysfunction Mediated by Upregulation of UCP2 and MAPKs.	Pyruvaldehyde	0-13	uncoupling protein 2 (mitochondrial, proton carrier)	Mus musculus	159-163
26779540-7	2016	Furthermore, the expression of UCP2, JNK, and P38 as well as the phosphorylation JNK and P38 was increased by MG.	Pyruvaldehyde	110-112	uncoupling protein 2 (mitochondrial, proton carrier)	Mus musculus	31-35
26779540-7	2016	Furthermore, the expression of UCP2, JNK, and P38 as well as the phosphorylation JNK and P38 was increased by MG.	Pyruvaldehyde	110-112	mitogen-activated protein kinase 8	Mus musculus	37-40
26779540-7	2016	Furthermore, the expression of UCP2, JNK, and P38 as well as the phosphorylation JNK and P38 was increased by MG.	Pyruvaldehyde	110-112	mitogen-activated protein kinase 14	Mus musculus	46-49
26779540-7	2016	Furthermore, the expression of UCP2, JNK, and P38 as well as the phosphorylation JNK and P38 was increased by MG.	Pyruvaldehyde	110-112	mitogen-activated protein kinase 8	Mus musculus	81-84
26779540-7	2016	Furthermore, the expression of UCP2, JNK, and P38 as well as the phosphorylation JNK and P38 was increased by MG.	Pyruvaldehyde	110-112	mitogen-activated protein kinase 14	Mus musculus	89-92
26788517-2	2016	Glyoxalase-1 is an enzyme detoxifying methylglyoxal (MG).	Pyruvaldehyde	38-51	glyoxalase 1	Mus musculus	0-12
26788517-2	2016	Glyoxalase-1 is an enzyme detoxifying methylglyoxal (MG).	Pyruvaldehyde	53-55	glyoxalase 1	Mus musculus	0-12
26715035-0	2015	Arg354 in the catalytic centre of bovine liver catalase is protected from methylglyoxal-mediated glycation.	Pyruvaldehyde	74-87	catalase	Bos taurus	47-55
26715035-7	2015	RESULTS: Here, bovine liver catalase was incubated with high levels of methylglyoxal to induce its glycation.	Pyruvaldehyde	71-84	catalase	Bos taurus	28-36
27251720-4	2015	Here we show that glyoxalase I (GLO1), an enzyme that is required for the detoxification of methylglyoxal (MG, a cytotoxic by-product of glycolysis), is a stigmatic compatibility factor required for pollination to occur and is targeted by the self-incompatibility system.	Pyruvaldehyde	92-105	putative lactoylglutathione lyase	Brassica napus	18-30
26577515-9	2015	CA prevented MG-dependent neurotoxicity by activating the PI3K/Akt/Nrf2 signaling pathway and the antioxidant enzymes modulated by Nrf2 transcription factor.	Pyruvaldehyde	13-15	AKT serine/threonine kinase 1	Homo sapiens	63-66
26577515-9	2015	CA prevented MG-dependent neurotoxicity by activating the PI3K/Akt/Nrf2 signaling pathway and the antioxidant enzymes modulated by Nrf2 transcription factor.	Pyruvaldehyde	13-15	NFE2 like bZIP transcription factor 2	Homo sapiens	67-71
26577515-9	2015	CA prevented MG-dependent neurotoxicity by activating the PI3K/Akt/Nrf2 signaling pathway and the antioxidant enzymes modulated by Nrf2 transcription factor.	Pyruvaldehyde	13-15	NFE2 like bZIP transcription factor 2	Homo sapiens	131-135
26165190-4	2015	We found that nuclear Nrf2 is induced by MGO treatment in HT22 cells, as corroborated by induction of the Nrf2-controlled target genes and proteins glutamate cysteine ligase and heme oxygenase 1.	Pyruvaldehyde	41-44	nuclear factor, erythroid derived 2, like 2	Mus musculus	22-26
26165190-4	2015	We found that nuclear Nrf2 is induced by MGO treatment in HT22 cells, as corroborated by induction of the Nrf2-controlled target genes and proteins glutamate cysteine ligase and heme oxygenase 1.	Pyruvaldehyde	41-44	nuclear factor, erythroid derived 2, like 2	Mus musculus	106-110
26165190-4	2015	We found that nuclear Nrf2 is induced by MGO treatment in HT22 cells, as corroborated by induction of the Nrf2-controlled target genes and proteins glutamate cysteine ligase and heme oxygenase 1.	Pyruvaldehyde	41-44	heme oxygenase 1	Mus musculus	178-194
26165190-5	2015	Nrf2 knockdown prevented MGO-dependent induction of glutamate cysteine ligase and heme oxygenase 1.	Pyruvaldehyde	25-28	nuclear factor, erythroid derived 2, like 2	Mus musculus	0-4
26165190-5	2015	Nrf2 knockdown prevented MGO-dependent induction of glutamate cysteine ligase and heme oxygenase 1.	Pyruvaldehyde	25-28	heme oxygenase 1	Mus musculus	82-98
26165190-8	2015	The data indicate that MGO can act as both a foe and a friend of the glyoxalase and the Trx/TrxR systems.	Pyruvaldehyde	23-26	thioredoxin 1	Mus musculus	88-91
26165190-9	2015	At low concentrations of MGO (0.3mM), GLO2 is strongly induced, but at high MGO (0.75 mM) concentrations, GLO1 is inhibited and GLO2 is downregulated.	Pyruvaldehyde	25-28	hydroxyacyl glutathione hydrolase	Mus musculus	38-42
26165190-9	2015	At low concentrations of MGO (0.3mM), GLO2 is strongly induced, but at high MGO (0.75 mM) concentrations, GLO1 is inhibited and GLO2 is downregulated.	Pyruvaldehyde	25-28	hydroxyacyl glutathione hydrolase	Mus musculus	128-132
26165190-9	2015	At low concentrations of MGO (0.3mM), GLO2 is strongly induced, but at high MGO (0.75 mM) concentrations, GLO1 is inhibited and GLO2 is downregulated.	Pyruvaldehyde	76-79	glyoxalase 1	Mus musculus	106-110
26165190-9	2015	At low concentrations of MGO (0.3mM), GLO2 is strongly induced, but at high MGO (0.75 mM) concentrations, GLO1 is inhibited and GLO2 is downregulated.	Pyruvaldehyde	76-79	hydroxyacyl glutathione hydrolase	Mus musculus	128-132
26165190-10	2015	The cytosolic Trx/TrxR system is impaired by MGO, where Trx is downregulated yet TrxR is induced, but strong MGO-dependent glycation may explain the loss in TrxR activity.	Pyruvaldehyde	45-48	thioredoxin 1	Mus musculus	14-17
26165190-10	2015	The cytosolic Trx/TrxR system is impaired by MGO, where Trx is downregulated yet TrxR is induced, but strong MGO-dependent glycation may explain the loss in TrxR activity.	Pyruvaldehyde	45-48	thioredoxin 1	Mus musculus	18-21
26165190-10	2015	The cytosolic Trx/TrxR system is impaired by MGO, where Trx is downregulated yet TrxR is induced, but strong MGO-dependent glycation may explain the loss in TrxR activity.	Pyruvaldehyde	109-112	thioredoxin 1	Mus musculus	14-17
26165190-10	2015	The cytosolic Trx/TrxR system is impaired by MGO, where Trx is downregulated yet TrxR is induced, but strong MGO-dependent glycation may explain the loss in TrxR activity.	Pyruvaldehyde	109-112	thioredoxin 1	Mus musculus	18-21
26367488-8	2015	IL-10 also abrogated the extent of MGO-induced bowel adhesions mimicking a cocoon-like mass.	Pyruvaldehyde	35-38	interleukin 10	Rattus norvegicus	0-5
26410776-5	2015	However, methylglyoxal induced significant structural changes in HSA compared with glyoxal and glyceraldehydes.	Pyruvaldehyde	9-22	albumin	Homo sapiens	65-68
26594175-10	2015	We will also discuss more recent findings that the ubiquitination of Nav1.7 by Nedd4-2 and the effect of methylglyoxal on Nav1.8 are also implicated in the development of experimental neuropathic pain.	Pyruvaldehyde	105-118	sodium voltage-gated channel alpha subunit 10	Homo sapiens	122-128
26320622-1	2015	The zinc metalloenzyme glyoxalase I (GlxI) catalyzes the glutathione-dependent inactivation of cytotoxic methylglyoxal.	Pyruvaldehyde	105-118	glyoxalase I	Homo sapiens	23-35
26320622-1	2015	The zinc metalloenzyme glyoxalase I (GlxI) catalyzes the glutathione-dependent inactivation of cytotoxic methylglyoxal.	Pyruvaldehyde	105-118	glyoxalase I	Homo sapiens	37-41
26410776-2	2015	In the current manuscript, effect of glycation in structural changes of human serum albumin (HSA) by the metabolites of glucose such as glyoxal, methylglyoxal and glyceraldehyde was studied using different spectroscopy techniques.	Pyruvaldehyde	145-158	albumin	Homo sapiens	78-91
26410776-2	2015	In the current manuscript, effect of glycation in structural changes of human serum albumin (HSA) by the metabolites of glucose such as glyoxal, methylglyoxal and glyceraldehyde was studied using different spectroscopy techniques.	Pyruvaldehyde	145-158	albumin	Homo sapiens	93-96
26519157-5	2015	MK-I-81 also alleviated MGO mediated diminished distal insulin signaling by increasing protein kinase B and glycogen synthase kinase 3-beta phosphorylation.	Pyruvaldehyde	24-27	glycogen synthase kinase 3 beta	Mus musculus	108-139
26370081-6	2015	Our results show that Hsp31 possesses robust glutathione-independent methylglyoxalase activity and suppresses MG-mediated toxicity and ROS levels as compared with another paralog, Hsp34.	Pyruvaldehyde	110-112	glutathione-independent methylglyoxalase	Saccharomyces cerevisiae S288C	22-27
26519157-9	2015	MK-I-81 also reduced MGO mediated IRS-1, PKC-alpha and RAGE interaction in muscle cells.	Pyruvaldehyde	21-24	insulin receptor substrate 1	Mus musculus	34-39
26519157-9	2015	MK-I-81 also reduced MGO mediated IRS-1, PKC-alpha and RAGE interaction in muscle cells.	Pyruvaldehyde	21-24	protein kinase C, alpha	Mus musculus	41-50
26519157-9	2015	MK-I-81 also reduced MGO mediated IRS-1, PKC-alpha and RAGE interaction in muscle cells.	Pyruvaldehyde	21-24	advanced glycosylation end product-specific receptor	Mus musculus	55-59
26021238-6	2015	Signaling kinetic observation indicated that MGO remarkably triggered phosphorylation of Akt, ERK1/2, p38 MAPK, and JNK1/2.	Pyruvaldehyde	45-48	AKT serine/threonine kinase 1	Homo sapiens	89-92
26251121-11	2015	Autophagy inhibitors bafilomycin A1, AC, 3-MA, and BECN1 siRNA exacerbated MGO-induced HBMEC injury.	Pyruvaldehyde	75-78	beclin 1	Rattus norvegicus	51-56
26290603-4	2015	The present study analyzed whether autoantibodies against MGO-modified epitopes of the low-density lipoprotein apolipoprotein B (apoB) 100 predict cardiovascular events.	Pyruvaldehyde	58-61	apolipoprotein B	Homo sapiens	111-127
26290603-4	2015	The present study analyzed whether autoantibodies against MGO-modified epitopes of the low-density lipoprotein apolipoprotein B (apoB) 100 predict cardiovascular events.	Pyruvaldehyde	58-61	apolipoprotein B	Homo sapiens	129-133
26290603-5	2015	A library consisting of 302 peptides comprising the complete apoB100 molecule was screened to identify peptides targeted by MGO-specific autoantibodies.	Pyruvaldehyde	124-127	apolipoprotein B	Homo sapiens	61-68
26290603-13	2015	These data show that subjects with low levels of IgM recognizing MGO-modified p220 in apoB have an increased risk to develop cardiovascular events and that this association is present in nondiabetic subjects.	Pyruvaldehyde	65-68	apolipoprotein B	Homo sapiens	86-90
26547330-0	2015	[Methylglyoxal inhibits human umbilical vein cell migration in vitro by down-regulating integrinbeta3].	Pyruvaldehyde	1-14	integrin subunit beta 3	Homo sapiens	88-102
26547330-5	2015	Methylglyoxal decreased the expression of integrin beta3 in a time- and concentration-dependent manner (P&lt;0.05).	Pyruvaldehyde	0-13	integrin subunit beta 3	Homo sapiens	42-56
26547330-7	2015	CONCLUSION: Methylglyoxal inhibits HUVEC migration in vitro by down-regulating integrin beta3 expression.	Pyruvaldehyde	12-25	integrin subunit beta 3	Homo sapiens	79-93
26021238-6	2015	Signaling kinetic observation indicated that MGO remarkably triggered phosphorylation of Akt, ERK1/2, p38 MAPK, and JNK1/2.	Pyruvaldehyde	45-48	mitogen-activated protein kinase 3	Homo sapiens	94-100
26021238-6	2015	Signaling kinetic observation indicated that MGO remarkably triggered phosphorylation of Akt, ERK1/2, p38 MAPK, and JNK1/2.	Pyruvaldehyde	45-48	mitogen-activated protein kinase 1	Homo sapiens	102-105
26021238-6	2015	Signaling kinetic observation indicated that MGO remarkably triggered phosphorylation of Akt, ERK1/2, p38 MAPK, and JNK1/2.	Pyruvaldehyde	45-48	mitogen-activated protein kinase 8	Homo sapiens	116-122
26021238-7	2015	Blockade of kinase activity demonstrated that the hyperphosphorylation of Akt, ERK1/2, JNK, and p38 MAPK were all involved in the MGO-enhanced autophagy and growth-arresting effect in ARPE-19 cells.	Pyruvaldehyde	130-133	AKT serine/threonine kinase 1	Homo sapiens	74-77
26021238-7	2015	Blockade of kinase activity demonstrated that the hyperphosphorylation of Akt, ERK1/2, JNK, and p38 MAPK were all involved in the MGO-enhanced autophagy and growth-arresting effect in ARPE-19 cells.	Pyruvaldehyde	130-133	mitogen-activated protein kinase 3	Homo sapiens	79-85
26021238-7	2015	Blockade of kinase activity demonstrated that the hyperphosphorylation of Akt, ERK1/2, JNK, and p38 MAPK were all involved in the MGO-enhanced autophagy and growth-arresting effect in ARPE-19 cells.	Pyruvaldehyde	130-133	mitogen-activated protein kinase 8	Homo sapiens	87-90
26021238-7	2015	Blockade of kinase activity demonstrated that the hyperphosphorylation of Akt, ERK1/2, JNK, and p38 MAPK were all involved in the MGO-enhanced autophagy and growth-arresting effect in ARPE-19 cells.	Pyruvaldehyde	130-133	mitogen-activated protein kinase 1	Homo sapiens	96-99
26021238-7	2015	Blockade of kinase activity demonstrated that the hyperphosphorylation of Akt, ERK1/2, JNK, and p38 MAPK were all involved in the MGO-enhanced autophagy and growth-arresting effect in ARPE-19 cells.	Pyruvaldehyde	130-133	mitogen-activated protein kinase 3	Homo sapiens	100-104
26594764-2	2015	GLO I catalyzes the reaction to transform hemimercaptal, a compound formed from methylglyoxal (MG) and reduced glutathione, into S-D-lactoylglutathione, which is then converted to D-lactic acid by glyoxalase II.	Pyruvaldehyde	80-93	glyoxalase I	Homo sapiens	0-5
26442067-2	2015	Recent studies have shown that Ni may activate an isoform of glyoxalase I, which performs an important step in the degradation of methylglyoxal (MG), a potent cytotoxic compound naturally produced by cellular metabolism.	Pyruvaldehyde	130-143	glyoxalase I	Homo sapiens	61-73
26442067-2	2015	Recent studies have shown that Ni may activate an isoform of glyoxalase I, which performs an important step in the degradation of methylglyoxal (MG), a potent cytotoxic compound naturally produced by cellular metabolism.	Pyruvaldehyde	145-147	glyoxalase I	Homo sapiens	61-73
26121315-3	2015	We investigated whether VEGF receptor-3 (VEGFR-3), the receptor for VEGF-C and -D, might be a new target to improve net ultrafiltration by using adenovirus-expressing soluble VEGFR-3 (Adeno-sVEGFR-3) in rodent models of peritoneal injury induced by methylglyoxal (MGO).	Pyruvaldehyde	249-262	fms related receptor tyrosine kinase 4	Homo sapiens	24-39
26121315-3	2015	We investigated whether VEGF receptor-3 (VEGFR-3), the receptor for VEGF-C and -D, might be a new target to improve net ultrafiltration by using adenovirus-expressing soluble VEGFR-3 (Adeno-sVEGFR-3) in rodent models of peritoneal injury induced by methylglyoxal (MGO).	Pyruvaldehyde	249-262	fms related receptor tyrosine kinase 4	Homo sapiens	41-48
26121315-3	2015	We investigated whether VEGF receptor-3 (VEGFR-3), the receptor for VEGF-C and -D, might be a new target to improve net ultrafiltration by using adenovirus-expressing soluble VEGFR-3 (Adeno-sVEGFR-3) in rodent models of peritoneal injury induced by methylglyoxal (MGO).	Pyruvaldehyde	264-267	fms related receptor tyrosine kinase 4	Homo sapiens	24-39
26121315-3	2015	We investigated whether VEGF receptor-3 (VEGFR-3), the receptor for VEGF-C and -D, might be a new target to improve net ultrafiltration by using adenovirus-expressing soluble VEGFR-3 (Adeno-sVEGFR-3) in rodent models of peritoneal injury induced by methylglyoxal (MGO).	Pyruvaldehyde	264-267	fms related receptor tyrosine kinase 4	Homo sapiens	41-48
26121315-5	2015	In MGO models, VEGF-D was significantly increased in the diaphragm; however, VEGF-C was not significantly upregulated.	Pyruvaldehyde	3-6	vascular endothelial growth factor D	Homo sapiens	15-21
26594764-2	2015	GLO I catalyzes the reaction to transform hemimercaptal, a compound formed from methylglyoxal (MG) and reduced glutathione, into S-D-lactoylglutathione, which is then converted to D-lactic acid by glyoxalase II.	Pyruvaldehyde	80-93	hydroxyacylglutathione hydrolase	Homo sapiens	197-210
26594764-7	2015	Thus, it is suggested that isolupalbigenin inhibits the enzyme GLO I, resulting in MG accumulation in the medium, and leading to cell apoptosis.	Pyruvaldehyde	83-85	glyoxalase I	Homo sapiens	63-68
26027784-4	2015	Intriguingly, the MGO activated unfolded protein response pathway accompanying apoptotic events, such as cleavages of PARP-1 and caspase-3.	Pyruvaldehyde	18-21	poly (ADP-ribose) polymerase 1	Rattus norvegicus	118-124
26244639-0	2015	Modification of beta-Defensin-2 by Dicarbonyls Methylglyoxal and Glyoxal Inhibits Antibacterial and Chemotactic Function In Vitro.	Pyruvaldehyde	47-60	defensin beta 4A	Homo sapiens	16-31
25962521-3	2015	To counteract the deleterious effects of MGO, organisms have an enzymatic glyoxalase defence system in which MGO is converted to D-lactate, with glyoxalase 1 (GLO1) as the key enzyme in this system.	Pyruvaldehyde	41-44	glyoxalase I	Homo sapiens	145-157
25962521-3	2015	To counteract the deleterious effects of MGO, organisms have an enzymatic glyoxalase defence system in which MGO is converted to D-lactate, with glyoxalase 1 (GLO1) as the key enzyme in this system.	Pyruvaldehyde	41-44	glyoxalase I	Homo sapiens	159-163
25962521-3	2015	To counteract the deleterious effects of MGO, organisms have an enzymatic glyoxalase defence system in which MGO is converted to D-lactate, with glyoxalase 1 (GLO1) as the key enzyme in this system.	Pyruvaldehyde	109-112	glyoxalase I	Homo sapiens	159-163
26027784-4	2015	Intriguingly, the MGO activated unfolded protein response pathway accompanying apoptotic events, such as cleavages of PARP-1 and caspase-3.	Pyruvaldehyde	18-21	caspase 3	Rattus norvegicus	129-138
26027784-5	2015	In addition, Western blot analysis revealed that MGO-induced myocyte apoptosis was inhibited by depletion of CHOP with siRNA against Ddit3, the gene name for rat CHOP.	Pyruvaldehyde	49-52	DNA-damage inducible transcript 3	Rattus norvegicus	109-113
26027784-5	2015	In addition, Western blot analysis revealed that MGO-induced myocyte apoptosis was inhibited by depletion of CHOP with siRNA against Ddit3, the gene name for rat CHOP.	Pyruvaldehyde	49-52	DNA-damage inducible transcript 3	Rattus norvegicus	133-138
26027784-5	2015	In addition, Western blot analysis revealed that MGO-induced myocyte apoptosis was inhibited by depletion of CHOP with siRNA against Ddit3, the gene name for rat CHOP.	Pyruvaldehyde	49-52	DNA-damage inducible transcript 3	Rattus norvegicus	162-166
26027784-9	2015	These results showed that CHOP is the key signal for myocyte apoptosis and cardiac dysfunction induced by MGO.	Pyruvaldehyde	106-109	DNA-damage inducible transcript 3	Rattus norvegicus	26-30
26111058-5	2015	Unmodified and MGO-glycated VN were used as substrates for human umbilical vein endothelial cells (HUVECs).	Pyruvaldehyde	15-18	vitronectin	Homo sapiens	28-30
24767709-3	2015	Dicarbonyls, in particular methylglyoxal, participate in the development of atherosclerosis, and their major detoxification route is the enzyme glyoxalase 1 (GLO1), which is known to decrease during aging.	Pyruvaldehyde	27-40	glyoxalase I	Homo sapiens	144-156
24767709-3	2015	Dicarbonyls, in particular methylglyoxal, participate in the development of atherosclerosis, and their major detoxification route is the enzyme glyoxalase 1 (GLO1), which is known to decrease during aging.	Pyruvaldehyde	27-40	glyoxalase I	Homo sapiens	158-162
25867911-10	2015	These results provide the first evidence that hyperglycemia and acute glucose fluctuation promote MG-occludin formation and exacerbate brain microvascular endothelial dysfunction.	Pyruvaldehyde	98-100	occludin	Rattus norvegicus	101-109
26073427-2	2015	This assay could detect MGO at as low as 1 muM by the naked eye and 0.05 muM by UV/vis spectrometry, within the clinical range marking oxidative stress in diabetes, and demonstrated high selectivity over other physiologically relevant ketones and aldehydes.	Pyruvaldehyde	24-27	latexin	Homo sapiens	43-46
26111058-3	2015	To explore whether the glycation of VN affects angiogenic signaling and to understand the molecular mechanisms involved, we synthesized glycated VN by incubating VN with methylglyoxal (MGO) in vitro and identified the formation of glycated VN by an LC-ESI-MS/MS-based method.	Pyruvaldehyde	170-183	vitronectin	Homo sapiens	145-147
26111058-3	2015	To explore whether the glycation of VN affects angiogenic signaling and to understand the molecular mechanisms involved, we synthesized glycated VN by incubating VN with methylglyoxal (MGO) in vitro and identified the formation of glycated VN by an LC-ESI-MS/MS-based method.	Pyruvaldehyde	170-183	vitronectin	Homo sapiens	145-147
26111058-3	2015	To explore whether the glycation of VN affects angiogenic signaling and to understand the molecular mechanisms involved, we synthesized glycated VN by incubating VN with methylglyoxal (MGO) in vitro and identified the formation of glycated VN by an LC-ESI-MS/MS-based method.	Pyruvaldehyde	170-183	vitronectin	Homo sapiens	145-147
25867911-1	2015	We previously demonstrated that in normal glucose (5mM), methylglyoxal (MG, a model of carbonyl stress) induced brain microvascular endothelial cell (IHEC) dysfunction that was associated with occludin glycation and prevented by N-acetylcysteine (NAC).	Pyruvaldehyde	57-70	occludin	Rattus norvegicus	193-201
25867911-1	2015	We previously demonstrated that in normal glucose (5mM), methylglyoxal (MG, a model of carbonyl stress) induced brain microvascular endothelial cell (IHEC) dysfunction that was associated with occludin glycation and prevented by N-acetylcysteine (NAC).	Pyruvaldehyde	72-74	occludin	Rattus norvegicus	193-201
25841781-1	2015	Glyoxalase I (Glo1) is a cellular defense enzyme involved in the detoxification of methylglyoxal (MG), a cytotoxic by-product of glycolysis, and MG-derived advanced glycation end products (AGEs).	Pyruvaldehyde	83-96	glyoxalase I	Homo sapiens	0-12
25841781-1	2015	Glyoxalase I (Glo1) is a cellular defense enzyme involved in the detoxification of methylglyoxal (MG), a cytotoxic by-product of glycolysis, and MG-derived advanced glycation end products (AGEs).	Pyruvaldehyde	83-96	glyoxalase I	Homo sapiens	14-18
26111058-3	2015	To explore whether the glycation of VN affects angiogenic signaling and to understand the molecular mechanisms involved, we synthesized glycated VN by incubating VN with methylglyoxal (MGO) in vitro and identified the formation of glycated VN by an LC-ESI-MS/MS-based method.	Pyruvaldehyde	185-188	vitronectin	Homo sapiens	145-147
26111058-3	2015	To explore whether the glycation of VN affects angiogenic signaling and to understand the molecular mechanisms involved, we synthesized glycated VN by incubating VN with methylglyoxal (MGO) in vitro and identified the formation of glycated VN by an LC-ESI-MS/MS-based method.	Pyruvaldehyde	185-188	vitronectin	Homo sapiens	145-147
26111058-3	2015	To explore whether the glycation of VN affects angiogenic signaling and to understand the molecular mechanisms involved, we synthesized glycated VN by incubating VN with methylglyoxal (MGO) in vitro and identified the formation of glycated VN by an LC-ESI-MS/MS-based method.	Pyruvaldehyde	185-188	vitronectin	Homo sapiens	145-147
25042521-4	2015	In addition, apocynin increased glutathione levels and restored the activity of glyoxalase I inhibited by MG.	Pyruvaldehyde	106-108	glyoxalase 1	Mus musculus	80-92
25451587-0	2015	Nrf2-mediated adaptive response to methyl glyoxal in HepG2 cells involves the induction of AKR7A2.	Pyruvaldehyde	35-49	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
25451587-0	2015	Nrf2-mediated adaptive response to methyl glyoxal in HepG2 cells involves the induction of AKR7A2.	Pyruvaldehyde	35-49	aldo-keto reductase family 7 member A2	Homo sapiens	91-97
25451587-4	2015	We have shown that treating HepG2 cells with sub-lethal concentrations of MG increases the level of NADPH:quinone oxidoreductase (NQO1) mRNA by 4.5-fold, AKR1C3 mRNA by 14-fold and AKR7A2 mRNA by 4-fold.	Pyruvaldehyde	74-76	NAD(P)H quinone dehydrogenase 1	Homo sapiens	130-134
25451587-4	2015	We have shown that treating HepG2 cells with sub-lethal concentrations of MG increases the level of NADPH:quinone oxidoreductase (NQO1) mRNA by 4.5-fold, AKR1C3 mRNA by 14-fold and AKR7A2 mRNA by 4-fold.	Pyruvaldehyde	74-76	aldo-keto reductase family 1 member C3	Homo sapiens	154-160
25451587-4	2015	We have shown that treating HepG2 cells with sub-lethal concentrations of MG increases the level of NADPH:quinone oxidoreductase (NQO1) mRNA by 4.5-fold, AKR1C3 mRNA by 14-fold and AKR7A2 mRNA by 4-fold.	Pyruvaldehyde	74-76	aldo-keto reductase family 7 member A2	Homo sapiens	181-187
25451587-5	2015	Levels of AKR7A2 protein are increased by 2.1- and 1.8-fold following 9h and 24h exposure of cells to 50 muM MG.	Pyruvaldehyde	109-111	aldo-keto reductase family 7 member A2	Homo sapiens	10-16
25451587-6	2015	The role of AKR7A2 in protecting HepG2 cells against MG toxicity was further investigated using specific siRNAs against AKR7A2 and Nrf2.	Pyruvaldehyde	53-55	aldo-keto reductase family 7, member A5 (aflatoxin aldehyde reductase)	Mus musculus	12-18
25451587-7	2015	Knockdown of AKR7A2 in HepG2 shows that AKR7A2 is responsible for up to 50% of the protection against MG toxicity in HepG2 cells.	Pyruvaldehyde	102-104	aldo-keto reductase family 7 member A2	Homo sapiens	13-19
25451587-7	2015	Knockdown of AKR7A2 in HepG2 shows that AKR7A2 is responsible for up to 50% of the protection against MG toxicity in HepG2 cells.	Pyruvaldehyde	102-104	aldo-keto reductase family 7 member A2	Homo sapiens	40-46
25451587-8	2015	We have also shown that MG was able to induce the translocation of the transcription factor Nrf2 to the nucleus.	Pyruvaldehyde	24-26	NFE2 like bZIP transcription factor 2	Homo sapiens	92-96
25451587-10	2015	In conclusion, these findings indicate that protective enzymes are significantly up-regulated in response to low concentrations of MG in HepG2 cells and that AKR7A2 contributes to protection against MG-induced toxicity.	Pyruvaldehyde	199-201	aldo-keto reductase family 7 member A2	Homo sapiens	158-164
25451587-11	2015	Nrf2 is critical in mediating MG induced expression of protective genes.	Pyruvaldehyde	30-32	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
25818485-4	2015	Under physiological circumstances, MGO is detoxified by the glyoxalase system into D-lactate, with glyoxalase I (GLO1) as the key enzyme in the anti-glycation defence.	Pyruvaldehyde	35-38	glyoxalase I	Homo sapiens	99-111
25818485-4	2015	Under physiological circumstances, MGO is detoxified by the glyoxalase system into D-lactate, with glyoxalase I (GLO1) as the key enzyme in the anti-glycation defence.	Pyruvaldehyde	35-38	glyoxalase I	Homo sapiens	113-117
25818485-8	2015	Small bioactive inducers of GLO1 can potentially form the basis for new treatment strategies for age-related disorders in which MGO plays a pivotal role.	Pyruvaldehyde	128-131	glyoxalase I	Homo sapiens	28-32
25687235-7	2015	Rage (-/-) mice showed comparable diabetes but accumulated less MG and this corresponded to enhanced activity of the MG-detoxifying enzyme glyoxalase I in their retina when compared with WT mice.	Pyruvaldehyde	64-66	advanced glycosylation end product-specific receptor	Mus musculus	0-4
25832198-10	2015	delta-Tocopherol prevented MGO-induced apoptosis in HUVECs by increasing Bcl-2 expression and decreasing Bax expression.	Pyruvaldehyde	27-30	BCL2 apoptosis regulator	Homo sapiens	73-78
25832198-10	2015	delta-Tocopherol prevented MGO-induced apoptosis in HUVECs by increasing Bcl-2 expression and decreasing Bax expression.	Pyruvaldehyde	27-30	BCL2 associated X, apoptosis regulator	Homo sapiens	105-108
25855294-5	2015	GLDC inhibition impairs cells with high SHMT2 levels as the excess glycine not metabolized by GLDC can be converted to the toxic molecules aminoacetone and methylglyoxal.	Pyruvaldehyde	156-169	glycine decarboxylase	Homo sapiens	0-4
25855294-5	2015	GLDC inhibition impairs cells with high SHMT2 levels as the excess glycine not metabolized by GLDC can be converted to the toxic molecules aminoacetone and methylglyoxal.	Pyruvaldehyde	156-169	serine hydroxymethyltransferase 2	Homo sapiens	40-45
25884658-5	2015	Treatment with resveratrol markedly improved blood glucose level from the oral glucose tolerance test and promoted nuclear factor erythroid 2-related factor-2 (Nrf2) phosphorylation (p &lt; 0.05) in the pancreas of MG-treated mice.	Pyruvaldehyde	215-217	nuclear factor, erythroid derived 2, like 2	Mus musculus	115-158
25884658-6	2015	However, these effects were abolished by retinoic acid, Nrf2 inhibitor, in resveratrol and retinoic acid-treated and MG-induced mice.	Pyruvaldehyde	117-119	nuclear factor, erythroid derived 2, like 2	Mus musculus	56-60
25042521-6	2015	Apocynin treatment decreased the levels of proinflammatory cytokines such as tumor necrosis factor-alpha and interleukin-6 induced by MG.	Pyruvaldehyde	134-136	tumor necrosis factor	Mus musculus	77-104
25042521-6	2015	Apocynin treatment decreased the levels of proinflammatory cytokines such as tumor necrosis factor-alpha and interleukin-6 induced by MG.	Pyruvaldehyde	134-136	interleukin 6	Mus musculus	109-122
25624345-2	2015	We show here that methylglyoxal activates the Pkc1-Mpk1 mitogen-activated protein (MAP) kinase cascade in a target of rapamycin complex 2 (TORC2)-dependent manner in the budding yeast Saccharomyces cerevisiae.	Pyruvaldehyde	18-31	protein kinase C	Saccharomyces cerevisiae S288C	46-50
25624345-2	2015	We show here that methylglyoxal activates the Pkc1-Mpk1 mitogen-activated protein (MAP) kinase cascade in a target of rapamycin complex 2 (TORC2)-dependent manner in the budding yeast Saccharomyces cerevisiae.	Pyruvaldehyde	18-31	mitogen-activated serine/threonine-protein kinase SLT2	Saccharomyces cerevisiae S288C	51-55
25624345-2	2015	We show here that methylglyoxal activates the Pkc1-Mpk1 mitogen-activated protein (MAP) kinase cascade in a target of rapamycin complex 2 (TORC2)-dependent manner in the budding yeast Saccharomyces cerevisiae.	Pyruvaldehyde	18-31	CREB regulated transcription coactivator 2	Homo sapiens	139-144
25624345-4	2015	Methylglyoxal enhanced the phosphorylation of Pkc1 at Ser(1143), which transmitted the signal to the downstream Mpk1 MAP kinase cascade.	Pyruvaldehyde	0-13	protein kinase C	Saccharomyces cerevisiae S288C	46-50
25624345-4	2015	Methylglyoxal enhanced the phosphorylation of Pkc1 at Ser(1143), which transmitted the signal to the downstream Mpk1 MAP kinase cascade.	Pyruvaldehyde	0-13	mitogen-activated serine/threonine-protein kinase SLT2	Saccharomyces cerevisiae S288C	112-116
25624345-6	2015	Methylglyoxal activated mammalian TORC2 signaling, which, in turn, phosphorylated Akt at Ser(473).	Pyruvaldehyde	0-13	CREB regulated transcription coactivator 2	Homo sapiens	34-39
25624345-7	2015	Our results suggest that methylglyoxal is a conserved initiator of TORC2 signaling among eukaryotes.	Pyruvaldehyde	25-38	CREB regulated transcription coactivator 2	Homo sapiens	67-72
25692475-7	2015	Glyoxalase 1 (Glo1) works to neutralize MG, reducing its deleterious effects.	Pyruvaldehyde	40-42	glyoxalase I	Homo sapiens	0-12
25387474-5	2015	In this study, the role of glyoxalase 1 (Glo1), the major detoxification pathway for dicarbonyl-derived GD such as methylglyoxal (MG) and glyoxal (Gx), was investigated in vivo using heterozygous knock-down mice for Glo1 (Glo1(-/+)).	Pyruvaldehyde	115-128	glyoxalase 1	Mus musculus	27-39
25387474-5	2015	In this study, the role of glyoxalase 1 (Glo1), the major detoxification pathway for dicarbonyl-derived GD such as methylglyoxal (MG) and glyoxal (Gx), was investigated in vivo using heterozygous knock-down mice for Glo1 (Glo1(-/+)).	Pyruvaldehyde	115-128	glyoxalase 1	Mus musculus	41-45
25387474-5	2015	In this study, the role of glyoxalase 1 (Glo1), the major detoxification pathway for dicarbonyl-derived GD such as methylglyoxal (MG) and glyoxal (Gx), was investigated in vivo using heterozygous knock-down mice for Glo1 (Glo1(-/+)).	Pyruvaldehyde	130-132	glyoxalase 1	Mus musculus	27-39
25387474-5	2015	In this study, the role of glyoxalase 1 (Glo1), the major detoxification pathway for dicarbonyl-derived GD such as methylglyoxal (MG) and glyoxal (Gx), was investigated in vivo using heterozygous knock-down mice for Glo1 (Glo1(-/+)).	Pyruvaldehyde	130-132	glyoxalase 1	Mus musculus	41-45
25655840-0	2015	Creatine is a scavenger for methylglyoxal under physiological conditions via formation of N-(4-methyl-5-oxo-1-imidazolin-2-yl)sarcosine (MG-HCr).	Pyruvaldehyde	28-41	coiled-coil alpha-helical rod protein 1	Homo sapiens	140-143
25692475-7	2015	Glyoxalase 1 (Glo1) works to neutralize MG, reducing its deleterious effects.	Pyruvaldehyde	40-42	glyoxalase I	Homo sapiens	14-18
25932127-9	2015	On the molecular level, tanshinone IIA administration altered the expression of apoptosis-related proteins such as p53, Bax, Bcl-2 and cyto C. In addition, MGO treatment remarkably increased the phosphorylation of MAPK family including p38, JNK and ERK.	Pyruvaldehyde	156-159	tumor protein p53	Homo sapiens	115-118
25932127-9	2015	On the molecular level, tanshinone IIA administration altered the expression of apoptosis-related proteins such as p53, Bax, Bcl-2 and cyto C. In addition, MGO treatment remarkably increased the phosphorylation of MAPK family including p38, JNK and ERK.	Pyruvaldehyde	156-159	BCL2 associated X, apoptosis regulator	Homo sapiens	120-123
25932127-9	2015	On the molecular level, tanshinone IIA administration altered the expression of apoptosis-related proteins such as p53, Bax, Bcl-2 and cyto C. In addition, MGO treatment remarkably increased the phosphorylation of MAPK family including p38, JNK and ERK.	Pyruvaldehyde	156-159	BCL2 apoptosis regulator	Homo sapiens	125-130
25932127-9	2015	On the molecular level, tanshinone IIA administration altered the expression of apoptosis-related proteins such as p53, Bax, Bcl-2 and cyto C. In addition, MGO treatment remarkably increased the phosphorylation of MAPK family including p38, JNK and ERK.	Pyruvaldehyde	156-159	mitogen-activated protein kinase 1	Homo sapiens	214-218
25932127-9	2015	On the molecular level, tanshinone IIA administration altered the expression of apoptosis-related proteins such as p53, Bax, Bcl-2 and cyto C. In addition, MGO treatment remarkably increased the phosphorylation of MAPK family including p38, JNK and ERK.	Pyruvaldehyde	156-159	mitogen-activated protein kinase 14	Homo sapiens	236-239
25932127-9	2015	On the molecular level, tanshinone IIA administration altered the expression of apoptosis-related proteins such as p53, Bax, Bcl-2 and cyto C. In addition, MGO treatment remarkably increased the phosphorylation of MAPK family including p38, JNK and ERK.	Pyruvaldehyde	156-159	mitogen-activated protein kinase 8	Homo sapiens	241-244
25932127-9	2015	On the molecular level, tanshinone IIA administration altered the expression of apoptosis-related proteins such as p53, Bax, Bcl-2 and cyto C. In addition, MGO treatment remarkably increased the phosphorylation of MAPK family including p38, JNK and ERK.	Pyruvaldehyde	156-159	mitogen-activated protein kinase 1	Homo sapiens	249-252
25932127-11	2015	These data indicated that tanshinone IIA could protect against MGO-induced cell injury through inhibiting MAPK activation in HBMEC.	Pyruvaldehyde	63-66	mitogen-activated protein kinase 1	Homo sapiens	106-110
25671364-2	2015	MG can be metabolized by phase-II enzymes in liver through the positive regulation of nuclear factor-erythroid 2-related factor 2 (Nrf2).	Pyruvaldehyde	0-2	NFE2 like bZIP transcription factor 2	Rattus norvegicus	86-129
25671364-2	2015	MG can be metabolized by phase-II enzymes in liver through the positive regulation of nuclear factor-erythroid 2-related factor 2 (Nrf2).	Pyruvaldehyde	0-2	NFE2 like bZIP transcription factor 2	Rattus norvegicus	131-135
25671364-6	2015	Our results suggested that SP activated Nrf2 by Ser40 phosphorylation, resulting in the metabolism of MG into d-lactic acid and the inhibition of AGEs generation, which reduced the accumulation of AGEs in the livers of MG-induced rats.	Pyruvaldehyde	102-104	NFE2 like bZIP transcription factor 2	Rattus norvegicus	40-44
25581570-12	2015	Furthermore, AGE- or MGO-induced increased expression of VEGF and MCP-1 was significantly reduced in the presence of NAC or SB203580.	Pyruvaldehyde	21-24	vascular endothelial growth factor A	Homo sapiens	57-61
25671364-6	2015	Our results suggested that SP activated Nrf2 by Ser40 phosphorylation, resulting in the metabolism of MG into d-lactic acid and the inhibition of AGEs generation, which reduced the accumulation of AGEs in the livers of MG-induced rats.	Pyruvaldehyde	219-221	NFE2 like bZIP transcription factor 2	Rattus norvegicus	40-44
25539570-6	2015	Using this method, a model protein bovine serum albumin was investigated over 3 days of incubation with the glycation agent methylglyoxal in the absence or presence of the glycation inhibitor aminoguanidine (pimagedine).	Pyruvaldehyde	124-137	albumin	Homo sapiens	42-55
25581570-9	2015	The mRNA and protein expression of cytokines including vascular endothelial growth factor (VEGF) and monocyte chemotactic protein-1 (MCP-1) was significantly increased after treatment with MGO and AGE-HSA.	Pyruvaldehyde	189-192	vascular endothelial growth factor A	Homo sapiens	55-89
25581570-12	2015	Furthermore, AGE- or MGO-induced increased expression of VEGF and MCP-1 was significantly reduced in the presence of NAC or SB203580.	Pyruvaldehyde	21-24	C-C motif chemokine ligand 2	Homo sapiens	66-71
25581570-9	2015	The mRNA and protein expression of cytokines including vascular endothelial growth factor (VEGF) and monocyte chemotactic protein-1 (MCP-1) was significantly increased after treatment with MGO and AGE-HSA.	Pyruvaldehyde	189-192	vascular endothelial growth factor A	Homo sapiens	91-95
25581570-9	2015	The mRNA and protein expression of cytokines including vascular endothelial growth factor (VEGF) and monocyte chemotactic protein-1 (MCP-1) was significantly increased after treatment with MGO and AGE-HSA.	Pyruvaldehyde	189-192	C-C motif chemokine ligand 2	Homo sapiens	101-131
25581570-9	2015	The mRNA and protein expression of cytokines including vascular endothelial growth factor (VEGF) and monocyte chemotactic protein-1 (MCP-1) was significantly increased after treatment with MGO and AGE-HSA.	Pyruvaldehyde	189-192	C-C motif chemokine ligand 2	Homo sapiens	133-138
25581570-11	2015	Western blot showed that MGO and AGE increased the phosphorylation levels of p38 MAPK, which was significantly attenuated after treatment of NAC or p38 MAPK inhibitor SB203580.	Pyruvaldehyde	25-28	mitogen-activated protein kinase 14	Homo sapiens	77-80
25581570-13	2015	CONCLUSIONS: Together, this study suggested that AGE or MGO promoted VEGF and MCP-1 expression through activation of p38 MAPK signaling.	Pyruvaldehyde	56-59	vascular endothelial growth factor A	Homo sapiens	69-73
25581570-11	2015	Western blot showed that MGO and AGE increased the phosphorylation levels of p38 MAPK, which was significantly attenuated after treatment of NAC or p38 MAPK inhibitor SB203580.	Pyruvaldehyde	25-28	mitogen-activated protein kinase 14	Homo sapiens	148-151
25581570-13	2015	CONCLUSIONS: Together, this study suggested that AGE or MGO promoted VEGF and MCP-1 expression through activation of p38 MAPK signaling.	Pyruvaldehyde	56-59	C-C motif chemokine ligand 2	Homo sapiens	78-83
25581570-13	2015	CONCLUSIONS: Together, this study suggested that AGE or MGO promoted VEGF and MCP-1 expression through activation of p38 MAPK signaling.	Pyruvaldehyde	56-59	mitogen-activated protein kinase 14	Homo sapiens	117-120
26770971-4	2015	In the MGO-treated rats, tenascin-C (TN-C) levels in the peritoneal effluents were remarkably high and a cluster of TN-C-positive mesothelial cells with epithelial-to-mesenchymal transition- (EMT-) like change excessively proliferated at the peritoneal surface, but not in the FA-treated rats.	Pyruvaldehyde	7-10	tenascin C	Rattus norvegicus	25-35
25184957-8	2015	Finally, the GLO1 regulation of SCC-13 cells might be relevant to methylglyoxal-induced p53 translocation.	Pyruvaldehyde	66-79	glyoxalase I	Homo sapiens	13-17
25184957-8	2015	Finally, the GLO1 regulation of SCC-13 cells might be relevant to methylglyoxal-induced p53 translocation.	Pyruvaldehyde	66-79	serpin family B member 3	Homo sapiens	32-35
25184957-8	2015	Finally, the GLO1 regulation of SCC-13 cells might be relevant to methylglyoxal-induced p53 translocation.	Pyruvaldehyde	66-79	tumor protein p53	Homo sapiens	88-91
26027252-6	2015	The model of cellular metabolism is proposed where methyl glyoxal plays a key role in development of resistance to insulin, hyperglycemia, hypokalemia and hypertension.	Pyruvaldehyde	51-65	insulin	Homo sapiens	115-122
25416785-0	2015	Parkinsonism-associated protein DJ-1/Park7 is a major protein deglycase that repairs methylglyoxal- and glyoxal-glycated cysteine, arginine, and lysine residues.	Pyruvaldehyde	85-98	Parkinsonism associated deglycase	Homo sapiens	32-36
25416785-0	2015	Parkinsonism-associated protein DJ-1/Park7 is a major protein deglycase that repairs methylglyoxal- and glyoxal-glycated cysteine, arginine, and lysine residues.	Pyruvaldehyde	85-98	Parkinsonism associated deglycase	Homo sapiens	37-42
25354529-0	2015	The SUR2B subunit of rat vascular KATP channel is targeted by miR-9a-3p induced by prolonged exposure to methylglyoxal.	Pyruvaldehyde	105-118	microRNA 9-3	Rattus norvegicus	62-71
25354529-8	2015	Of them, miR-9a-3p, increased its expression level by ~240% when the cultured smooth muscle cell line was exposed to micromolar concentrations of MGO.	Pyruvaldehyde	146-149	microRNA 9-3	Rattus norvegicus	9-18
25354529-10	2015	Antisense nucleotides of miR-9a-3p alleviated the effects of MGO.	Pyruvaldehyde	61-64	microRNA 9-3	Rattus norvegicus	25-34
25354529-13	2015	Our functional assays showed that K(ATP) currents were impaired by miR-9a-3p induced with MGO treatment.	Pyruvaldehyde	90-93	microRNA 9-3	Rattus norvegicus	67-75
25354529-14	2015	These results suggest that MGO exposure raises the expression of miR-9a-3p, which subsequently downregulates the SUR2B mRNA, compromising K(ATP) channel function in vascular smooth muscle.	Pyruvaldehyde	27-30	microRNA 9-3	Rattus norvegicus	65-74
26770971-4	2015	In the MGO-treated rats, tenascin-C (TN-C) levels in the peritoneal effluents were remarkably high and a cluster of TN-C-positive mesothelial cells with epithelial-to-mesenchymal transition- (EMT-) like change excessively proliferated at the peritoneal surface, but not in the FA-treated rats.	Pyruvaldehyde	7-10	tenascin C	Rattus norvegicus	37-41
26770971-4	2015	In the MGO-treated rats, tenascin-C (TN-C) levels in the peritoneal effluents were remarkably high and a cluster of TN-C-positive mesothelial cells with epithelial-to-mesenchymal transition- (EMT-) like change excessively proliferated at the peritoneal surface, but not in the FA-treated rats.	Pyruvaldehyde	7-10	tenascin C	Rattus norvegicus	116-120
26770971-5	2015	Effluent matrix metalloproteinase-2 (MMP-2) levels increased in both the MGO- and FA-treated rats.	Pyruvaldehyde	73-76	matrix metallopeptidase 2	Rattus norvegicus	9-35
26770971-5	2015	Effluent matrix metalloproteinase-2 (MMP-2) levels increased in both the MGO- and FA-treated rats.	Pyruvaldehyde	73-76	matrix metallopeptidase 2	Rattus norvegicus	37-42
25243815-4	2014	In vivo, CE administration for 16 wk significantly ameliorated renal dysfunction in type 2 diabetic db/db mice, partially due to MG trapping, which in turn inhibited AGEs formation and lowered proinflammatory cytokines, including tumor necrosis factor alpha and IL-1beta.	Pyruvaldehyde	129-131	tumor necrosis factor	Mus musculus	230-257
25283443-2	2014	Here, we obtained crystals of Arabidopsis thaliana DJ-1d (atDJ-1d) and Homo sapiens DJ-1 (hDJ-1) covalently bound to glyoxylate, an analog of methylglyoxal, forming a hemithioacetal that presumably mimics an intermediate structure in catalysis of methylglyoxal to lactate.	Pyruvaldehyde	142-155	Class I glutamine amidotransferase-like superfamily protein	Arabidopsis thaliana	51-56
25283443-2	2014	Here, we obtained crystals of Arabidopsis thaliana DJ-1d (atDJ-1d) and Homo sapiens DJ-1 (hDJ-1) covalently bound to glyoxylate, an analog of methylglyoxal, forming a hemithioacetal that presumably mimics an intermediate structure in catalysis of methylglyoxal to lactate.	Pyruvaldehyde	142-155	Parkinsonism associated deglycase	Homo sapiens	51-55
25283443-2	2014	Here, we obtained crystals of Arabidopsis thaliana DJ-1d (atDJ-1d) and Homo sapiens DJ-1 (hDJ-1) covalently bound to glyoxylate, an analog of methylglyoxal, forming a hemithioacetal that presumably mimics an intermediate structure in catalysis of methylglyoxal to lactate.	Pyruvaldehyde	142-155	Parkinsonism associated deglycase	Homo sapiens	90-95
25283443-2	2014	Here, we obtained crystals of Arabidopsis thaliana DJ-1d (atDJ-1d) and Homo sapiens DJ-1 (hDJ-1) covalently bound to glyoxylate, an analog of methylglyoxal, forming a hemithioacetal that presumably mimics an intermediate structure in catalysis of methylglyoxal to lactate.	Pyruvaldehyde	247-260	Class I glutamine amidotransferase-like superfamily protein	Arabidopsis thaliana	51-56
25283443-2	2014	Here, we obtained crystals of Arabidopsis thaliana DJ-1d (atDJ-1d) and Homo sapiens DJ-1 (hDJ-1) covalently bound to glyoxylate, an analog of methylglyoxal, forming a hemithioacetal that presumably mimics an intermediate structure in catalysis of methylglyoxal to lactate.	Pyruvaldehyde	247-260	Class I glutamine amidotransferase-like superfamily protein	Arabidopsis thaliana	58-65
25283443-2	2014	Here, we obtained crystals of Arabidopsis thaliana DJ-1d (atDJ-1d) and Homo sapiens DJ-1 (hDJ-1) covalently bound to glyoxylate, an analog of methylglyoxal, forming a hemithioacetal that presumably mimics an intermediate structure in catalysis of methylglyoxal to lactate.	Pyruvaldehyde	247-260	Parkinsonism associated deglycase	Homo sapiens	51-55
25283443-2	2014	Here, we obtained crystals of Arabidopsis thaliana DJ-1d (atDJ-1d) and Homo sapiens DJ-1 (hDJ-1) covalently bound to glyoxylate, an analog of methylglyoxal, forming a hemithioacetal that presumably mimics an intermediate structure in catalysis of methylglyoxal to lactate.	Pyruvaldehyde	247-260	Parkinsonism associated deglycase	Homo sapiens	90-95
26064894-0	2015	Methylglyoxal Induced Basophilic Spindle Cells with Podoplanin at the Surface of Peritoneum in Rat Peritoneal Dialysis Model.	Pyruvaldehyde	0-13	podoplanin	Rattus norvegicus	52-62
26064894-6	2015	In rats treated with MGO, peritoneal fibrous thickening with the appearance of basophilic spindle cells with podoplanin, cytokeratin, and alpha-smooth muscle actin at the surface of the peritoneum was observed.	Pyruvaldehyde	21-24	podoplanin	Rattus norvegicus	109-119
26064894-6	2015	In rats treated with MGO, peritoneal fibrous thickening with the appearance of basophilic spindle cells with podoplanin, cytokeratin, and alpha-smooth muscle actin at the surface of the peritoneum was observed.	Pyruvaldehyde	21-24	actin gamma 2, smooth muscle	Rattus norvegicus	138-163
24671236-5	2015	Humans developed effective mechanism of the MG metabolism involving two enzymes glyoxalase 1 (GLO1) and hydroxyacylglutathione hydrolase (HAGH).	Pyruvaldehyde	44-46	glyoxalase I	Homo sapiens	80-92
24671236-5	2015	Humans developed effective mechanism of the MG metabolism involving two enzymes glyoxalase 1 (GLO1) and hydroxyacylglutathione hydrolase (HAGH).	Pyruvaldehyde	44-46	glyoxalase I	Homo sapiens	94-98
24671236-5	2015	Humans developed effective mechanism of the MG metabolism involving two enzymes glyoxalase 1 (GLO1) and hydroxyacylglutathione hydrolase (HAGH).	Pyruvaldehyde	44-46	hydroxyacylglutathione hydrolase	Homo sapiens	104-136
24671236-5	2015	Humans developed effective mechanism of the MG metabolism involving two enzymes glyoxalase 1 (GLO1) and hydroxyacylglutathione hydrolase (HAGH).	Pyruvaldehyde	44-46	hydroxyacylglutathione hydrolase	Homo sapiens	138-142
25243815-4	2014	In vivo, CE administration for 16 wk significantly ameliorated renal dysfunction in type 2 diabetic db/db mice, partially due to MG trapping, which in turn inhibited AGEs formation and lowered proinflammatory cytokines, including tumor necrosis factor alpha and IL-1beta.	Pyruvaldehyde	129-131	interleukin 1 beta	Mus musculus	262-270
25426955-1	2014	This study examined the effect of methylglyoxal (MGO)-derived nonenzymatic posttranslational modifications (nePTMs) on the binding affinity of S100A12 to its natural receptor for advanced glycation end-products (RAGE).	Pyruvaldehyde	34-47	long intergenic non-protein coding RNA 914	Homo sapiens	212-216
25307422-3	2014	MGO has been shown to inhibit ATIII activity in vitro, however the mechanism of inhibition is incompletely understood.	Pyruvaldehyde	0-3	serpin family C member 1	Homo sapiens	30-35
25307422-4	2014	As such, we designed this study to investigate the kinetics and mechanism of MGO-mediated ATIII inhibition.	Pyruvaldehyde	77-80	serpin family C member 1	Homo sapiens	90-95
25307422-5	2014	METHODS: MGO-mediated ATIII inhibition was confirmed using inverse experiments detecting activity of the ATIII targets thrombin and factor Xa.	Pyruvaldehyde	9-12	serpin family C member 1	Homo sapiens	22-27
25307422-5	2014	METHODS: MGO-mediated ATIII inhibition was confirmed using inverse experiments detecting activity of the ATIII targets thrombin and factor Xa.	Pyruvaldehyde	9-12	serpin family C member 1	Homo sapiens	105-110
25307422-5	2014	METHODS: MGO-mediated ATIII inhibition was confirmed using inverse experiments detecting activity of the ATIII targets thrombin and factor Xa.	Pyruvaldehyde	9-12	coagulation factor II, thrombin	Homo sapiens	119-127
25307422-5	2014	METHODS: MGO-mediated ATIII inhibition was confirmed using inverse experiments detecting activity of the ATIII targets thrombin and factor Xa.	Pyruvaldehyde	9-12	coagulation factor X	Homo sapiens	132-141
25307422-6	2014	Fluorogenic assays were performed in both PBS and plasma after incubation of ATIII with MGO, at molar ratios comparable to those observed in the plasma of diabetic patients.	Pyruvaldehyde	88-91	serpin family C member 1	Homo sapiens	77-82
25307422-7	2014	LC-coupled tandem mass spectrometry was utilized to investigate the exact mechanism of MGO-mediated ATIII inhibition.	Pyruvaldehyde	87-90	serpin family C member 1	Homo sapiens	100-105
25307422-8	2014	RESULTS AND CONCLUSIONS: MGO concentration-dependently attenuated inhibition of thrombin and factor Xa by ATIII in PBS-based assays, both in the presence and absence of heparin.	Pyruvaldehyde	25-28	coagulation factor II, thrombin	Homo sapiens	80-88
25307422-8	2014	RESULTS AND CONCLUSIONS: MGO concentration-dependently attenuated inhibition of thrombin and factor Xa by ATIII in PBS-based assays, both in the presence and absence of heparin.	Pyruvaldehyde	25-28	coagulation factor X	Homo sapiens	93-102
25307422-8	2014	RESULTS AND CONCLUSIONS: MGO concentration-dependently attenuated inhibition of thrombin and factor Xa by ATIII in PBS-based assays, both in the presence and absence of heparin.	Pyruvaldehyde	25-28	serpin family C member 1	Homo sapiens	106-111
25307422-9	2014	In addition, MGO concentration-dependently inhibited ATIII activity in a plasma-based system, to the level of plasma completely deficient in ATIII, again both in the presence and absence of heparin.	Pyruvaldehyde	13-16	serpin family C member 1	Homo sapiens	53-58
25307422-9	2014	In addition, MGO concentration-dependently inhibited ATIII activity in a plasma-based system, to the level of plasma completely deficient in ATIII, again both in the presence and absence of heparin.	Pyruvaldehyde	13-16	serpin family C member 1	Homo sapiens	141-146
25307422-10	2014	Results from LC-MS/MS experiments revealed that MGO covalently adducts the active site Arg 393 of ATIII through two distinct glyoxalation mechanisms.	Pyruvaldehyde	48-51	serpin family C member 1	Homo sapiens	98-103
25307422-11	2014	We posit that active site adduction is the mechanism of MGO-mediated inhibition of ATIII, and thus contributes to the underlying pathophysiology of the diabetic hypercoagulable state and complications thereof.	Pyruvaldehyde	56-59	serpin family C member 1	Homo sapiens	83-88
25426955-1	2014	This study examined the effect of methylglyoxal (MGO)-derived nonenzymatic posttranslational modifications (nePTMs) on the binding affinity of S100A12 to its natural receptor for advanced glycation end-products (RAGE).	Pyruvaldehyde	49-52	long intergenic non-protein coding RNA 914	Homo sapiens	212-216
25426955-2	2014	Binding of MGO-modified S100A12 to RAGE decreased significantly with increasing MGO concentration and incubation time.	Pyruvaldehyde	11-14	long intergenic non-protein coding RNA 914	Homo sapiens	35-39
25426955-2	2014	Binding of MGO-modified S100A12 to RAGE decreased significantly with increasing MGO concentration and incubation time.	Pyruvaldehyde	80-83	long intergenic non-protein coding RNA 914	Homo sapiens	35-39
25426955-7	2014	Thus, nePTMs at R21 seem to be the major cause of MGO-induced impairment of S100A12 oligomerization and RAGE binding.	Pyruvaldehyde	50-53	long intergenic non-protein coding RNA 914	Homo sapiens	104-108
25274329-7	2014	The results showed that MGO induced an increase in TH and DAT expressions in SH-SY5Y neuroblastoma cells, while the levels of dopamine, DOPAC, and endogenous neurotoxin salsolinol also increased.	Pyruvaldehyde	24-27	solute carrier family 6 member 3	Homo sapiens	58-61
25172898-8	2014	Ruthenium red (RR), a general cation channel blocker, and HC030031, a selective transient receptor potential ankyrin 1 (TRPA1) antagonist, inhibited MG-induced Ca(2+) entry.	Pyruvaldehyde	149-151	transient receptor potential cation channel subfamily A member 1	Homo sapiens	80-118
25172898-16	2014	The present results suggest that methylglyoxal activates TRPA1 and promotes cell cycle progression and differentiation in human cardiac fibroblasts.	Pyruvaldehyde	33-46	transient receptor potential cation channel subfamily A member 1	Homo sapiens	57-62
25172898-17	2014	MG might participate the development of pathophysiological conditions including diabetic cardiomyopathy via activation of TRPA1.	Pyruvaldehyde	0-2	transient receptor potential cation channel subfamily A member 1	Homo sapiens	122-127
25172898-8	2014	Ruthenium red (RR), a general cation channel blocker, and HC030031, a selective transient receptor potential ankyrin 1 (TRPA1) antagonist, inhibited MG-induced Ca(2+) entry.	Pyruvaldehyde	149-151	transient receptor potential cation channel subfamily A member 1	Homo sapiens	120-125
25172898-11	2014	The use of small interfering RNA to knock down TRPA1 reduced the MG-induced Ca(2+) entry as well as TRPA1 mRNA expression.	Pyruvaldehyde	65-67	transient receptor potential cation channel subfamily A member 1	Homo sapiens	47-52
25446614-11	2014	From the tested 11 compounds only all-trans-retinoic acid, an antioxidant and antiglycation agent, U0126, a MAP/ERK kinase inhibitor and aminoguanidine attenuated methylglyoxal-induced damage in hCMEC/D3 cells.	Pyruvaldehyde	163-176	mitogen-activated protein kinase 1	Homo sapiens	112-115
25003317-0	2014	Regulation of methylglyoxal-elicited leukocyte recruitment by endothelial SGK1/GSK3 signaling.	Pyruvaldehyde	14-27	serum/glucocorticoid regulated kinase 1	Mus musculus	74-78
25003317-0	2014	Regulation of methylglyoxal-elicited leukocyte recruitment by endothelial SGK1/GSK3 signaling.	Pyruvaldehyde	14-27	glycogen synthase kinase 3 beta	Mus musculus	79-83
25003317-4	2014	Using intravital microscopy of mouse cremasteric microvasculature, we demonstrate that GSK3 inhibitors lithium and SB216763 mitigate MG-elicited leukocyte recruitment and microvascular hyperpermeability.	Pyruvaldehyde	133-135	glycogen synthase kinase 3 beta	Mus musculus	87-91
25003317-6	2014	At later time points (&gt;=1h), MG induces GSK3 deactivation which is dissipated by siRNA silencing of SGK.	Pyruvaldehyde	32-34	glycogen synthase kinase 3 beta	Mus musculus	43-47
25003317-6	2014	At later time points (&gt;=1h), MG induces GSK3 deactivation which is dissipated by siRNA silencing of SGK.	Pyruvaldehyde	32-34	serum/glucocorticoid regulated kinase 1	Mus musculus	103-106
25003317-7	2014	MG treatment potentiates endothelial SGK1 mRNA, total SGK1, phospho-SGK1 and phospho-NDRG1.	Pyruvaldehyde	0-2	serum/glucocorticoid regulated kinase 1	Mus musculus	37-41
25003317-7	2014	MG treatment potentiates endothelial SGK1 mRNA, total SGK1, phospho-SGK1 and phospho-NDRG1.	Pyruvaldehyde	0-2	serum/glucocorticoid regulated kinase 1	Mus musculus	54-58
25003317-7	2014	MG treatment potentiates endothelial SGK1 mRNA, total SGK1, phospho-SGK1 and phospho-NDRG1.	Pyruvaldehyde	0-2	serum/glucocorticoid regulated kinase 1	Mus musculus	54-58
25003317-7	2014	MG treatment potentiates endothelial SGK1 mRNA, total SGK1, phospho-SGK1 and phospho-NDRG1.	Pyruvaldehyde	0-2	N-myc downstream regulated gene 1	Mus musculus	85-90
24812427-2	2014	In this article, we demonstrate that increasing plasma MG to levels observed in diabetic mice either using an exogenous source (1% in drinking water) or generated following inhibition, its primary clearance enzyme, glyoxalase-1 (with 50 mg/kg IP bromobenzyl-glutathione cyclopentyl diester every second day), was able to increase vascular adhesion and augment atherogenesis in euglycemic apolipoprotein E knockout mice to a similar magnitude as that observed in hyperglycemic mice with diabetes.	Pyruvaldehyde	55-57	glyoxalase 1	Mus musculus	215-227
24812427-2	2014	In this article, we demonstrate that increasing plasma MG to levels observed in diabetic mice either using an exogenous source (1% in drinking water) or generated following inhibition, its primary clearance enzyme, glyoxalase-1 (with 50 mg/kg IP bromobenzyl-glutathione cyclopentyl diester every second day), was able to increase vascular adhesion and augment atherogenesis in euglycemic apolipoprotein E knockout mice to a similar magnitude as that observed in hyperglycemic mice with diabetes.	Pyruvaldehyde	55-57	apolipoprotein E	Mus musculus	388-404
24812427-3	2014	The effects of MG appear partly mediated by activation of the receptor for advanced glycation end products (RAGE), as deletion of RAGE was able to reduce inflammation and atherogenesis associated with MG exposure.	Pyruvaldehyde	15-17	advanced glycosylation end product-specific receptor	Mus musculus	62-106
24812427-3	2014	The effects of MG appear partly mediated by activation of the receptor for advanced glycation end products (RAGE), as deletion of RAGE was able to reduce inflammation and atherogenesis associated with MG exposure.	Pyruvaldehyde	15-17	advanced glycosylation end product-specific receptor	Mus musculus	108-112
24812427-3	2014	The effects of MG appear partly mediated by activation of the receptor for advanced glycation end products (RAGE), as deletion of RAGE was able to reduce inflammation and atherogenesis associated with MG exposure.	Pyruvaldehyde	15-17	advanced glycosylation end product-specific receptor	Mus musculus	130-134
24812427-3	2014	The effects of MG appear partly mediated by activation of the receptor for advanced glycation end products (RAGE), as deletion of RAGE was able to reduce inflammation and atherogenesis associated with MG exposure.	Pyruvaldehyde	201-203	advanced glycosylation end product-specific receptor	Mus musculus	62-106
25151220-0	2014	Resveratrol attenuates methylglyoxal-induced mitochondrial dysfunction and apoptosis by Sestrin2 induction.	Pyruvaldehyde	23-36	sestrin 2	Homo sapiens	88-96
24812427-3	2014	The effects of MG appear partly mediated by activation of the receptor for advanced glycation end products (RAGE), as deletion of RAGE was able to reduce inflammation and atherogenesis associated with MG exposure.	Pyruvaldehyde	201-203	advanced glycosylation end product-specific receptor	Mus musculus	108-112
24812427-3	2014	The effects of MG appear partly mediated by activation of the receptor for advanced glycation end products (RAGE), as deletion of RAGE was able to reduce inflammation and atherogenesis associated with MG exposure.	Pyruvaldehyde	201-203	advanced glycosylation end product-specific receptor	Mus musculus	130-134
25151220-8	2014	Resveratrol treatment inhibited SESN2 depletion elicited by methylglyoxal.	Pyruvaldehyde	60-73	sestrin 2	Homo sapiens	32-37
25151220-9	2014	SESN2 overexpression repressed methylglyoxal-induced mitochondrial dysfunction and apoptosis.	Pyruvaldehyde	31-44	sestrin 2	Homo sapiens	0-5
25151220-11	2014	Furthermore, siRNA knockdown of SESN2 reduced the ability of resveratrol to prevent methylglyoxal-induced mitochondrial permeability transition.	Pyruvaldehyde	84-97	sestrin 2	Homo sapiens	32-37
25151220-12	2014	In addition, when mice were exposed to methylglyoxal after infection of Ad-SESN2, the plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and GSH depletion by methylglyoxal in liver was reduced in Ad-SESN2 infected mice.	Pyruvaldehyde	39-52	sestrin 2	Mus musculus	75-80
25151220-12	2014	In addition, when mice were exposed to methylglyoxal after infection of Ad-SESN2, the plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and GSH depletion by methylglyoxal in liver was reduced in Ad-SESN2 infected mice.	Pyruvaldehyde	39-52	glutamic pyruvic transaminase, soluble	Mus musculus	103-127
25151220-12	2014	In addition, when mice were exposed to methylglyoxal after infection of Ad-SESN2, the plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and GSH depletion by methylglyoxal in liver was reduced in Ad-SESN2 infected mice.	Pyruvaldehyde	39-52	glutamic pyruvic transaminase, soluble	Mus musculus	129-132
25151220-12	2014	In addition, when mice were exposed to methylglyoxal after infection of Ad-SESN2, the plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and GSH depletion by methylglyoxal in liver was reduced in Ad-SESN2 infected mice.	Pyruvaldehyde	39-52	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	138-164
25151220-12	2014	In addition, when mice were exposed to methylglyoxal after infection of Ad-SESN2, the plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and GSH depletion by methylglyoxal in liver was reduced in Ad-SESN2 infected mice.	Pyruvaldehyde	39-52	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	166-169
25151220-12	2014	In addition, when mice were exposed to methylglyoxal after infection of Ad-SESN2, the plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and GSH depletion by methylglyoxal in liver was reduced in Ad-SESN2 infected mice.	Pyruvaldehyde	39-52	sestrin 2	Mus musculus	233-238
25151220-13	2014	Our results demonstrated that resveratrol is capable of protecting cells from methylglyoxal-induced mitochondrial dysfunction and oxidative stress via SESN2 induction.	Pyruvaldehyde	78-91	sestrin 2	Homo sapiens	151-156
25033248-6	2014	Profiling of the advanced glycation end products formed during the incubation of RNase A with methylglyoxal revealed predominant formation of the arginine modifications imidazolinone, CEA/dihydroxyimidazoline, and tetrahydropyrimidine at Arg10, Arg33, Arg39, and Arg85.	Pyruvaldehyde	94-107	ribonuclease A family member 1, pancreatic	Homo sapiens	81-88
24974304-4	2014	In this study, we aimed at investigating whether glucose and major AGE precursor methylglyoxal induce increased CD74 expression in the retina.	Pyruvaldehyde	81-94	CD74 molecule	Rattus norvegicus	112-116
24974304-10	2014	Methylglyoxal induced an 9.4-fold increase of CD74-positive cells in the superficial vascular layer and elevated gene expression of CD74 in the mouse retina 2.8-fold.	Pyruvaldehyde	0-13	CD74 antigen (invariant polypeptide of major histocompatibility complex, class II antigen-associated)	Mus musculus	46-50
24974304-10	2014	Methylglyoxal induced an 9.4-fold increase of CD74-positive cells in the superficial vascular layer and elevated gene expression of CD74 in the mouse retina 2.8-fold.	Pyruvaldehyde	0-13	CD74 antigen (invariant polypeptide of major histocompatibility complex, class II antigen-associated)	Mus musculus	132-136
25107330-2	2014	We studied the activity of renal semicarbazide-sensitive amine oxidase (SSAO), a key enzyme involved in MGO generation, in AA-treated mice, and investigated nephroprotective effects produced by metformin, a MGO scavenger.	Pyruvaldehyde	104-107	amine oxidase, copper containing 3	Mus musculus	33-70
25107330-2	2014	We studied the activity of renal semicarbazide-sensitive amine oxidase (SSAO), a key enzyme involved in MGO generation, in AA-treated mice, and investigated nephroprotective effects produced by metformin, a MGO scavenger.	Pyruvaldehyde	104-107	amine oxidase, copper containing 3	Mus musculus	72-76
25107330-8	2014	SIGNIFICANCE: This study is the first to show elevated renal SSAO activity in AA-treated mice, which could be involved in MGO accumulation.	Pyruvaldehyde	122-125	amine oxidase, copper containing 3	Mus musculus	61-65
25107330-11	2014	SSAO is a key enzyme involved in MGO generation, and consequently, inhibition of renal SSAO activity is worth investigating in AA nephrotoxicity and other renal pathologies further.	Pyruvaldehyde	33-36	amine oxidase, copper containing 3	Mus musculus	0-4
25102327-0	2014	Methylglyoxal reduces mitochondrial potential and activates Bax and caspase-3 in neurons: Implications for Alzheimer"s disease.	Pyruvaldehyde	0-13	BCL2 associated X, apoptosis regulator	Homo sapiens	60-63
25102327-0	2014	Methylglyoxal reduces mitochondrial potential and activates Bax and caspase-3 in neurons: Implications for Alzheimer"s disease.	Pyruvaldehyde	0-13	caspase 3	Homo sapiens	68-77
25102327-4	2014	Methylglyoxal (MG) is a by-product of TPI activity whose production is triggered when TPI is nitrotyrosinated.	Pyruvaldehyde	0-13	triosephosphate isomerase 1	Homo sapiens	38-41
25102327-4	2014	Methylglyoxal (MG) is a by-product of TPI activity whose production is triggered when TPI is nitrotyrosinated.	Pyruvaldehyde	0-13	triosephosphate isomerase 1	Homo sapiens	86-89
25102327-4	2014	Methylglyoxal (MG) is a by-product of TPI activity whose production is triggered when TPI is nitrotyrosinated.	Pyruvaldehyde	15-17	triosephosphate isomerase 1	Homo sapiens	38-41
25102327-4	2014	Methylglyoxal (MG) is a by-product of TPI activity whose production is triggered when TPI is nitrotyrosinated.	Pyruvaldehyde	15-17	triosephosphate isomerase 1	Homo sapiens	86-89
25451453-0	2014	Dihydromyricetin ameliorates the oxidative stress response induced by methylglyoxal via the AMPK/GLUT4 signaling pathway in PC12 cells.	Pyruvaldehyde	70-83	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	92-96
25451453-0	2014	Dihydromyricetin ameliorates the oxidative stress response induced by methylglyoxal via the AMPK/GLUT4 signaling pathway in PC12 cells.	Pyruvaldehyde	70-83	solute carrier family 2 member 4	Rattus norvegicus	97-102
25451453-11	2014	We found that DMY protected PC12 cells against MG-induced apoptosis and glycometabolic disorders, at least in part by restraining the hyperactivation of p-AMPK activity and normalizing the translocation of GLUT4 from the intracellular compartment, resulting in a balance in glucose uptake.	Pyruvaldehyde	47-49	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	155-159
25451453-11	2014	We found that DMY protected PC12 cells against MG-induced apoptosis and glycometabolic disorders, at least in part by restraining the hyperactivation of p-AMPK activity and normalizing the translocation of GLUT4 from the intracellular compartment, resulting in a balance in glucose uptake.	Pyruvaldehyde	47-49	solute carrier family 2 member 4	Rattus norvegicus	206-211
25270604-0	2014	Endothelial Na+/H+ exchanger NHE1 participates in redox-sensitive leukocyte recruitment triggered by methylglyoxal.	Pyruvaldehyde	101-114	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	29-33
25270604-11	2014	RESULTS: MG treatment significantly upregulated NHE1 mRNA and dose-dependently increased total- and phospho-NHE1.	Pyruvaldehyde	9-11	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	48-52
25270604-11	2014	RESULTS: MG treatment significantly upregulated NHE1 mRNA and dose-dependently increased total- and phospho-NHE1.	Pyruvaldehyde	9-11	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	108-112
25270604-15	2014	CONCLUSION: MG elicits SGK1-dependent activation of endothelial Na+/H+ exchanger NHE1 which participates in MG-induced ROS production, upregulation of endothelial ICAM-1, leukocyte recruitment and microvascular hyperpermeability.	Pyruvaldehyde	12-14	serum/glucocorticoid regulated kinase 1	Mus musculus	23-27
25270604-15	2014	CONCLUSION: MG elicits SGK1-dependent activation of endothelial Na+/H+ exchanger NHE1 which participates in MG-induced ROS production, upregulation of endothelial ICAM-1, leukocyte recruitment and microvascular hyperpermeability.	Pyruvaldehyde	12-14	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	81-85
25270604-15	2014	CONCLUSION: MG elicits SGK1-dependent activation of endothelial Na+/H+ exchanger NHE1 which participates in MG-induced ROS production, upregulation of endothelial ICAM-1, leukocyte recruitment and microvascular hyperpermeability.	Pyruvaldehyde	12-14	intercellular adhesion molecule 1	Mus musculus	163-169
25270604-16	2014	Pharmacological inhibition of NHE1 attenuates the proinflammatory effects of excessive MG and may, thus, be beneficial in diabetes-associated inflammation.	Pyruvaldehyde	87-89	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	30-34
25177914-9	2014	HDL2 and HDL3 were modified by methylglyoxal to similar extents in vitro.	Pyruvaldehyde	31-44	junctophilin 3	Homo sapiens	0-4
25177914-9	2014	HDL2 and HDL3 were modified by methylglyoxal to similar extents in vitro.	Pyruvaldehyde	31-44	HDL3	Homo sapiens	9-13
25343013-9	2014	Furthermore, acute treatment of mice with methylglyoxal increased the plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), indicating liver toxicity.	Pyruvaldehyde	42-55	glutamic pyruvic transaminase, soluble	Mus musculus	87-111
25343013-9	2014	Furthermore, acute treatment of mice with methylglyoxal increased the plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), indicating liver toxicity.	Pyruvaldehyde	42-55	glutamic pyruvic transaminase, soluble	Mus musculus	113-116
25343013-9	2014	Furthermore, acute treatment of mice with methylglyoxal increased the plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), indicating liver toxicity.	Pyruvaldehyde	42-55	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	122-148
25343013-9	2014	Furthermore, acute treatment of mice with methylglyoxal increased the plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), indicating liver toxicity.	Pyruvaldehyde	42-55	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	150-153
25033248-6	2014	Profiling of the advanced glycation end products formed during the incubation of RNase A with methylglyoxal revealed predominant formation of the arginine modifications imidazolinone, CEA/dihydroxyimidazoline, and tetrahydropyrimidine at Arg10, Arg33, Arg39, and Arg85.	Pyruvaldehyde	94-107	CEA cell adhesion molecule 3	Homo sapiens	184-187
24510749-7	2014	Additionally, myricitrin was capable of inhibiting AGEs formation, blocking RAGE expression, and inhibiting NF-kappaB activation and translocation triggered by MGO in SH-SY5Y cells.	Pyruvaldehyde	160-163	nuclear factor kappa B subunit 1	Homo sapiens	108-117
24933520-4	2014	Incubation of SOD with glucose, methylglyoxal (MG) or both at 37C resulted in progressive hyperchromicity at 280nm, intrinsic fluorescence quenching at 310nm, decrease in negative ellipticity at 208nm, AGE-specific fluorescence enhancement in the wavelength range 400-480nm and Thioflavin T (ThT) fluorescence enhancement at 480nm (fibrillar state enhancement).	Pyruvaldehyde	32-45	superoxide dismutase 1	Homo sapiens	14-17
24510749-8	2014	Our results suggest that myricitrin alleviates MGO-induced mitochondrial dysfunction, and the possible mechanism is through modulating the AGEs/RAGE/NF-kappaB pathway.	Pyruvaldehyde	47-50	long intergenic non-protein coding RNA 914	Homo sapiens	144-148
24510749-8	2014	Our results suggest that myricitrin alleviates MGO-induced mitochondrial dysfunction, and the possible mechanism is through modulating the AGEs/RAGE/NF-kappaB pathway.	Pyruvaldehyde	47-50	nuclear factor kappa B subunit 1	Homo sapiens	149-158
25036934-2	2014	In the present study, while MG treatment of mouse bone marrow stroma-derived ST2 cells rapidly suppressed the expression of osteotrophic Wnt-targeted genes, including that of osteoprotegerin (OPG, a decoy receptor of the receptor activator of NF-kappaB ligand (RANKL)), it significantly enhanced that of secreted Frizzled-related protein 4 (sFRP-4, a soluble inhibitor of Wnts).	Pyruvaldehyde	28-30	tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin)	Mus musculus	175-190
24978626-7	2014	Using breast cancer cell lines, we substantiated these clinical observations by showing that, in contrast to triple positive, triple negative cells induced Glo-1 expression and activity in response to MG treatment.	Pyruvaldehyde	201-203	glyoxalase I	Homo sapiens	156-161
24752777-6	2014	The PPARgamma agonist activity had been investigated and its exerted benefits are inhibition of inflammation in methylglyoxal (MG)-treated rats, prevention of pancreas impairment causing advanced glycation endproducts (AGEs), promotion of insulin expression in vivo and in vitro, and attenuated carboxymethyllysine (CML)-induced hepatic stellate cell (HSC) activation in the past several years.	Pyruvaldehyde	112-125	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	4-13
24752777-6	2014	The PPARgamma agonist activity had been investigated and its exerted benefits are inhibition of inflammation in methylglyoxal (MG)-treated rats, prevention of pancreas impairment causing advanced glycation endproducts (AGEs), promotion of insulin expression in vivo and in vitro, and attenuated carboxymethyllysine (CML)-induced hepatic stellate cell (HSC) activation in the past several years.	Pyruvaldehyde	127-129	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	4-13
24789098-4	2014	Pretreatment of MC3T3-E1 cells with liquiritigenin prevented the MG-induced cell death and production of protein adduct, intracellular reactive oxygen species, mitochondrial superoxide, cardiolipin peroxidation, and TNF-alpha in osteoblastic MC3T3-E1 cells.	Pyruvaldehyde	65-67	tumor necrosis factor	Mus musculus	216-225
24789098-5	2014	In addition, liquiritigenin increased the activity of glyoxalase I inhibited by MG.	Pyruvaldehyde	80-82	glyoxalase 1	Mus musculus	54-66
25036934-2	2014	In the present study, while MG treatment of mouse bone marrow stroma-derived ST2 cells rapidly suppressed the expression of osteotrophic Wnt-targeted genes, including that of osteoprotegerin (OPG, a decoy receptor of the receptor activator of NF-kappaB ligand (RANKL)), it significantly enhanced that of secreted Frizzled-related protein 4 (sFRP-4, a soluble inhibitor of Wnts).	Pyruvaldehyde	28-30	tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin)	Mus musculus	192-195
25036934-2	2014	In the present study, while MG treatment of mouse bone marrow stroma-derived ST2 cells rapidly suppressed the expression of osteotrophic Wnt-targeted genes, including that of osteoprotegerin (OPG, a decoy receptor of the receptor activator of NF-kappaB ligand (RANKL)), it significantly enhanced that of secreted Frizzled-related protein 4 (sFRP-4, a soluble inhibitor of Wnts).	Pyruvaldehyde	28-30	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	221-259
25036934-2	2014	In the present study, while MG treatment of mouse bone marrow stroma-derived ST2 cells rapidly suppressed the expression of osteotrophic Wnt-targeted genes, including that of osteoprotegerin (OPG, a decoy receptor of the receptor activator of NF-kappaB ligand (RANKL)), it significantly enhanced that of secreted Frizzled-related protein 4 (sFRP-4, a soluble inhibitor of Wnts).	Pyruvaldehyde	28-30	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	261-266
25036934-2	2014	In the present study, while MG treatment of mouse bone marrow stroma-derived ST2 cells rapidly suppressed the expression of osteotrophic Wnt-targeted genes, including that of osteoprotegerin (OPG, a decoy receptor of the receptor activator of NF-kappaB ligand (RANKL)), it significantly enhanced that of secreted Frizzled-related protein 4 (sFRP-4, a soluble inhibitor of Wnts).	Pyruvaldehyde	28-30	secreted frizzled-related protein 4	Mus musculus	304-339
25036934-2	2014	In the present study, while MG treatment of mouse bone marrow stroma-derived ST2 cells rapidly suppressed the expression of osteotrophic Wnt-targeted genes, including that of osteoprotegerin (OPG, a decoy receptor of the receptor activator of NF-kappaB ligand (RANKL)), it significantly enhanced that of secreted Frizzled-related protein 4 (sFRP-4, a soluble inhibitor of Wnts).	Pyruvaldehyde	28-30	secreted frizzled-related protein 4	Mus musculus	341-347
25036934-6	2014	These in vitro data suggest that MG-derived oxidative stress (not CpG demethylation) epigenetically and rapidly derepress sFRP-4 gene expression.	Pyruvaldehyde	33-35	secreted frizzled-related protein 4	Mus musculus	122-128
24918814-1	2014	BACKGROUND: Glyoxalase I (GI) is a cellular defence enzyme involved in the detoxification of methylglyoxal (MG), a cytotoxic byproduct of glycolysis, and MG-derived advanced glycation end products (AGEs).	Pyruvaldehyde	93-106	glyoxalase I	Homo sapiens	12-24
24759959-5	2014	The glyoxalase-1 inhibitor S-p-bromobenzylglutathione-cyclopentyl-diester (SpBrBzGSHCp2) was used to increase the endogenous levels of MGO.	Pyruvaldehyde	135-138	glyoxalase 1	Mus musculus	4-16
24856185-3	2014	Studies have shown that inhibitors of glyoxalase I (GLO1), the first enzyme of this pathway, have chemotherapeutic effects both in vitro and in vivo, presumably by increasing intracellular MG concentrations leading to apoptosis and cell death.	Pyruvaldehyde	189-191	glyoxalase I	Homo sapiens	38-50
24856185-3	2014	Studies have shown that inhibitors of glyoxalase I (GLO1), the first enzyme of this pathway, have chemotherapeutic effects both in vitro and in vivo, presumably by increasing intracellular MG concentrations leading to apoptosis and cell death.	Pyruvaldehyde	189-191	glyoxalase I	Homo sapiens	52-56
24759959-10	2014	In MGO- and SpBrBzGSHCp2-exposed cells, inhibition of ERK1/2 decreased IRS1 phosphorylation on S616 and rescued insulin-dependent Akt activation and NO generation, indicating that MGO inhibition of the IRS1/Akt/eNOS pathway is mediated, at least in part, by ERK1/2.	Pyruvaldehyde	3-6	mitogen-activated protein kinase 3	Mus musculus	54-60
24759959-10	2014	In MGO- and SpBrBzGSHCp2-exposed cells, inhibition of ERK1/2 decreased IRS1 phosphorylation on S616 and rescued insulin-dependent Akt activation and NO generation, indicating that MGO inhibition of the IRS1/Akt/eNOS pathway is mediated, at least in part, by ERK1/2.	Pyruvaldehyde	3-6	insulin receptor substrate 1	Mus musculus	71-75
24759959-10	2014	In MGO- and SpBrBzGSHCp2-exposed cells, inhibition of ERK1/2 decreased IRS1 phosphorylation on S616 and rescued insulin-dependent Akt activation and NO generation, indicating that MGO inhibition of the IRS1/Akt/eNOS pathway is mediated, at least in part, by ERK1/2.	Pyruvaldehyde	3-6	thymoma viral proto-oncogene 1	Mus musculus	130-133
24918814-1	2014	BACKGROUND: Glyoxalase I (GI) is a cellular defence enzyme involved in the detoxification of methylglyoxal (MG), a cytotoxic byproduct of glycolysis, and MG-derived advanced glycation end products (AGEs).	Pyruvaldehyde	93-106	glyoxalase I	Homo sapiens	26-28
24759959-8	2014	RESULTS: MGO prevented the insulin-dependent activation of the IRS1/protein kinase Akt/endothelial nitric oxide synthase (eNOS) pathway, thereby blunting nitric oxide (NO) production, while extracellular signal-regulated kinase (ERK1/2) activation and endothelin-1 (ET-1) release were increased by MGO in MAECs.	Pyruvaldehyde	9-12	insulin receptor substrate 1	Mus musculus	63-67
24759959-8	2014	RESULTS: MGO prevented the insulin-dependent activation of the IRS1/protein kinase Akt/endothelial nitric oxide synthase (eNOS) pathway, thereby blunting nitric oxide (NO) production, while extracellular signal-regulated kinase (ERK1/2) activation and endothelin-1 (ET-1) release were increased by MGO in MAECs.	Pyruvaldehyde	9-12	thymoma viral proto-oncogene 1	Mus musculus	83-86
24759959-8	2014	RESULTS: MGO prevented the insulin-dependent activation of the IRS1/protein kinase Akt/endothelial nitric oxide synthase (eNOS) pathway, thereby blunting nitric oxide (NO) production, while extracellular signal-regulated kinase (ERK1/2) activation and endothelin-1 (ET-1) release were increased by MGO in MAECs.	Pyruvaldehyde	9-12	nitric oxide synthase 3, endothelial cell	Mus musculus	87-120
24759959-10	2014	In MGO- and SpBrBzGSHCp2-exposed cells, inhibition of ERK1/2 decreased IRS1 phosphorylation on S616 and rescued insulin-dependent Akt activation and NO generation, indicating that MGO inhibition of the IRS1/Akt/eNOS pathway is mediated, at least in part, by ERK1/2.	Pyruvaldehyde	180-183	mitogen-activated protein kinase 3	Mus musculus	54-60
24759959-10	2014	In MGO- and SpBrBzGSHCp2-exposed cells, inhibition of ERK1/2 decreased IRS1 phosphorylation on S616 and rescued insulin-dependent Akt activation and NO generation, indicating that MGO inhibition of the IRS1/Akt/eNOS pathway is mediated, at least in part, by ERK1/2.	Pyruvaldehyde	180-183	insulin receptor substrate 1	Mus musculus	71-75
24759959-8	2014	RESULTS: MGO prevented the insulin-dependent activation of the IRS1/protein kinase Akt/endothelial nitric oxide synthase (eNOS) pathway, thereby blunting nitric oxide (NO) production, while extracellular signal-regulated kinase (ERK1/2) activation and endothelin-1 (ET-1) release were increased by MGO in MAECs.	Pyruvaldehyde	9-12	nitric oxide synthase 3, endothelial cell	Mus musculus	122-126
24759959-10	2014	In MGO- and SpBrBzGSHCp2-exposed cells, inhibition of ERK1/2 decreased IRS1 phosphorylation on S616 and rescued insulin-dependent Akt activation and NO generation, indicating that MGO inhibition of the IRS1/Akt/eNOS pathway is mediated, at least in part, by ERK1/2.	Pyruvaldehyde	180-183	thymoma viral proto-oncogene 1	Mus musculus	130-133
24759959-10	2014	In MGO- and SpBrBzGSHCp2-exposed cells, inhibition of ERK1/2 decreased IRS1 phosphorylation on S616 and rescued insulin-dependent Akt activation and NO generation, indicating that MGO inhibition of the IRS1/Akt/eNOS pathway is mediated, at least in part, by ERK1/2.	Pyruvaldehyde	180-183	insulin receptor substrate 1	Mus musculus	202-206
24759959-8	2014	RESULTS: MGO prevented the insulin-dependent activation of the IRS1/protein kinase Akt/endothelial nitric oxide synthase (eNOS) pathway, thereby blunting nitric oxide (NO) production, while extracellular signal-regulated kinase (ERK1/2) activation and endothelin-1 (ET-1) release were increased by MGO in MAECs.	Pyruvaldehyde	9-12	mitogen-activated protein kinase 3	Mus musculus	229-235
24759959-10	2014	In MGO- and SpBrBzGSHCp2-exposed cells, inhibition of ERK1/2 decreased IRS1 phosphorylation on S616 and rescued insulin-dependent Akt activation and NO generation, indicating that MGO inhibition of the IRS1/Akt/eNOS pathway is mediated, at least in part, by ERK1/2.	Pyruvaldehyde	180-183	thymoma viral proto-oncogene 1	Mus musculus	207-210
24759959-8	2014	RESULTS: MGO prevented the insulin-dependent activation of the IRS1/protein kinase Akt/endothelial nitric oxide synthase (eNOS) pathway, thereby blunting nitric oxide (NO) production, while extracellular signal-regulated kinase (ERK1/2) activation and endothelin-1 (ET-1) release were increased by MGO in MAECs.	Pyruvaldehyde	9-12	endothelin 1	Mus musculus	252-264
24759959-10	2014	In MGO- and SpBrBzGSHCp2-exposed cells, inhibition of ERK1/2 decreased IRS1 phosphorylation on S616 and rescued insulin-dependent Akt activation and NO generation, indicating that MGO inhibition of the IRS1/Akt/eNOS pathway is mediated, at least in part, by ERK1/2.	Pyruvaldehyde	180-183	nitric oxide synthase 3, endothelial cell	Mus musculus	211-215
24759959-10	2014	In MGO- and SpBrBzGSHCp2-exposed cells, inhibition of ERK1/2 decreased IRS1 phosphorylation on S616 and rescued insulin-dependent Akt activation and NO generation, indicating that MGO inhibition of the IRS1/Akt/eNOS pathway is mediated, at least in part, by ERK1/2.	Pyruvaldehyde	180-183	mitogen-activated protein kinase 3	Mus musculus	258-264
24920125-2	2014	Glyoxal and MG are detoxified by the sequential activities of glyoxalase 1 (GLO1) and glyoxalase 2.	Pyruvaldehyde	12-14	glyoxalase 1	Mus musculus	62-74
24759959-12	2014	CONCLUSIONS/INTERPRETATION: MGO impairs the action of insulin on the endothelium both in vitro and in vivo, at least in part through an ERK1/2-mediated mechanism.	Pyruvaldehyde	28-31	mitogen-activated protein kinase 3	Mus musculus	136-142
24746615-0	2014	Methylglyoxal induces endoplasmic reticulum stress and DNA demethylation in the Keap1 promoter of human lens epithelial cells and age-related cataracts.	Pyruvaldehyde	0-13	kelch like ECH associated protein 1	Homo sapiens	80-85
24746615-4	2014	Here, we report the methylglyoxal-mediated sequential events responsible for Keap1 promoter DNA demethylation in human lens epithelial cells, because Keap1 is a negative regulatory protein that regulates the Nrf2 antioxidant protein.	Pyruvaldehyde	20-33	kelch like ECH associated protein 1	Homo sapiens	77-82
24746615-4	2014	Here, we report the methylglyoxal-mediated sequential events responsible for Keap1 promoter DNA demethylation in human lens epithelial cells, because Keap1 is a negative regulatory protein that regulates the Nrf2 antioxidant protein.	Pyruvaldehyde	20-33	kelch like ECH associated protein 1	Homo sapiens	150-155
24746615-4	2014	Here, we report the methylglyoxal-mediated sequential events responsible for Keap1 promoter DNA demethylation in human lens epithelial cells, because Keap1 is a negative regulatory protein that regulates the Nrf2 antioxidant protein.	Pyruvaldehyde	20-33	NFE2 like bZIP transcription factor 2	Homo sapiens	208-212
24920125-2	2014	Glyoxal and MG are detoxified by the sequential activities of glyoxalase 1 (GLO1) and glyoxalase 2.	Pyruvaldehyde	12-14	glyoxalase 1	Mus musculus	76-80
24612481-3	2014	Here, to investigate how vascular glycation affects age-related endothelial function, we employed rats systemically overexpressing glyoxalase I (GLO1), which detoxifies methylglyoxal (MG), a representative precursor of glycation.	Pyruvaldehyde	169-182	glyoxalase 1	Rattus norvegicus	131-143
24612481-3	2014	Here, to investigate how vascular glycation affects age-related endothelial function, we employed rats systemically overexpressing glyoxalase I (GLO1), which detoxifies methylglyoxal (MG), a representative precursor of glycation.	Pyruvaldehyde	169-182	glyoxalase 1	Rattus norvegicus	145-149
24612481-9	2014	In vitro, MG increased phosphorylation of eNOS (Thr495) in primary human aortic endothelial cells (HAECs), and overexpression of GLO1 decreased glycative stress and phosphorylation of eNOS (Thr495).	Pyruvaldehyde	10-12	glyoxalase I	Homo sapiens	129-133
24898602-0	2014	MiR-30b is involved in methylglyoxal-induced epithelial-mesenchymal transition of peritoneal mesothelial cells in rats.	Pyruvaldehyde	23-36	microRNA 30b	Rattus norvegicus	0-7
24898602-5	2014	We assessed whether miR-30b has a possible role in MGO-induced EMT of PMCs in rats.	Pyruvaldehyde	51-54	microRNA 30b	Rattus norvegicus	20-27
24898602-13	2014	Our results revealed that miR-30b is involved in MGO-induced EMT of PMCs in rats.	Pyruvaldehyde	49-52	microRNA 30b	Rattus norvegicus	26-33
24695216-7	2014	The MAIT antigens formed by the reactions between 5-A-RU and glyoxal/methylglyoxal were simple adducts, 5-(2-oxoethylideneamino)-6-D-ribitylaminouracil (5-OE-RU) and 5-(2-oxopropylideneamino)-6-D-ribitylaminouracil (5-OP-RU), respectively, which bound to MR1 as shown by crystal structures of MAIT TCR ternary complexes.	Pyruvaldehyde	69-82	major histocompatibility complex, class I-related	Homo sapiens	255-258
24824951-4	2014	Here we show that binding of methylglyoxal-modified albumin to RAGE results in signal transduction.	Pyruvaldehyde	29-42	advanced glycosylation end-product specific receptor	Homo sapiens	63-67
24631568-4	2014	Furthermore, we found that venlafaxine inhibits MGO-induced phosphorylation of JNK.	Pyruvaldehyde	48-51	mitogen-activated protein kinase 8	Homo sapiens	79-82
24631568-6	2014	These findings suggest that venlafaxine protects MGO-induced HBMEC injury through PI3K/AKT and JNK pathway as the potential underlying mechanisms of HBMEC injury in diabetes.	Pyruvaldehyde	49-52	AKT serine/threonine kinase 1	Homo sapiens	87-90
24631568-6	2014	These findings suggest that venlafaxine protects MGO-induced HBMEC injury through PI3K/AKT and JNK pathway as the potential underlying mechanisms of HBMEC injury in diabetes.	Pyruvaldehyde	49-52	mitogen-activated protein kinase 8	Homo sapiens	95-98
24966916-8	2014	In addition, Glo1 knocking-down with shRNA interfering caused cellular accumulation of methylglyoxal, a Glo1 cytotoxic substrate.	Pyruvaldehyde	87-100	glyoxalase I	Homo sapiens	13-17
24747646-0	2014	Kinetics of glycoxidation of bovine serum albumin by methylglyoxal and glyoxal and its prevention by various compounds.	Pyruvaldehyde	53-66	albumin	Homo sapiens	36-49
24747646-1	2014	The aim of this study was to compare several methods for measurement of bovine serum albumin (BSA) modification by glycoxidation with reactive dicarbonyl compounds (methylglyoxal--MGO and glyoxal--GO), for studies of the kinetics of this process and to compare the effects of 19 selected compounds on BSA glycation by the aldehydes.	Pyruvaldehyde	165-178	albumin	Homo sapiens	79-92
24615331-8	2014	LR-90 dose-dependently prevented MGO-associated HUVEC cytotoxicity and apoptotic biochemical changes such as loss of MMP, increased Bax/Bcl-2 protein ratio, mitochondrial cytochrome c release and activation of caspase-3 and 9.	Pyruvaldehyde	33-36	caspase 3	Homo sapiens	210-225
24710646-3	2014	The reduction in MG was paralleled by a significant increase in the activity of Glyoxalase 1 (Glo1), the major route of MG detoxification, in peripheral blood mononuclear cells and red blood cells.	Pyruvaldehyde	17-19	glyoxalase I	Homo sapiens	80-92
24710646-3	2014	The reduction in MG was paralleled by a significant increase in the activity of Glyoxalase 1 (Glo1), the major route of MG detoxification, in peripheral blood mononuclear cells and red blood cells.	Pyruvaldehyde	17-19	glyoxalase I	Homo sapiens	94-98
24710646-3	2014	The reduction in MG was paralleled by a significant increase in the activity of Glyoxalase 1 (Glo1), the major route of MG detoxification, in peripheral blood mononuclear cells and red blood cells.	Pyruvaldehyde	120-122	glyoxalase I	Homo sapiens	80-92
24710646-3	2014	The reduction in MG was paralleled by a significant increase in the activity of Glyoxalase 1 (Glo1), the major route of MG detoxification, in peripheral blood mononuclear cells and red blood cells.	Pyruvaldehyde	120-122	glyoxalase I	Homo sapiens	94-98
24707974-0	2014	Actinidia callosa peel (kiwi fruit) ethanol extracts protected neural cells apoptosis induced by methylglyoxal through Nrf2 activation.	Pyruvaldehyde	97-110	nuclear factor, erythroid derived 2, like 2	Mus musculus	119-123
24707974-4	2014	OBJECTIVE: This study investigated the protective effects of A. callosa (kiwi fruits) peel ethanol extracts (ACE) on MG-induced Neuro-2A cell apoptosis.	Pyruvaldehyde	117-119	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	109-112
24707974-6	2014	ACE and AITC elevated Bcl2 and inhibited Bax expressions in MG-induced Neuro-2A cells.	Pyruvaldehyde	60-62	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	0-3
24707974-6	2014	ACE and AITC elevated Bcl2 and inhibited Bax expressions in MG-induced Neuro-2A cells.	Pyruvaldehyde	60-62	BCL2-associated X protein	Mus musculus	41-44
24707974-7	2014	ACE elevated Nrf2 transcriptional activity and nuclear translocation in MG-induced Neuro-2A cells.	Pyruvaldehyde	72-74	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	0-3
24707974-7	2014	ACE elevated Nrf2 transcriptional activity and nuclear translocation in MG-induced Neuro-2A cells.	Pyruvaldehyde	72-74	nuclear factor, erythroid derived 2, like 2	Mus musculus	13-17
24707974-8	2014	Nrf2 down-stream molecules including HO-1 and GCL were elevated by ACE or AITC treatment in MG-induced Neuro-2A cells.	Pyruvaldehyde	92-94	nuclear factor, erythroid derived 2, like 2	Mus musculus	0-4
24707974-8	2014	Nrf2 down-stream molecules including HO-1 and GCL were elevated by ACE or AITC treatment in MG-induced Neuro-2A cells.	Pyruvaldehyde	92-94	germ cell-less, spermatogenesis associated 1	Mus musculus	46-49
24707974-8	2014	Nrf2 down-stream molecules including HO-1 and GCL were elevated by ACE or AITC treatment in MG-induced Neuro-2A cells.	Pyruvaldehyde	92-94	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	67-70
24707974-9	2014	The protective effects of ACE on MG-induced Neuro-2A apoptosis were attenuated while Nrf2 knockdown.	Pyruvaldehyde	33-35	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	26-29
24707974-10	2014	DISCUSSION AND CONCLUSION: We established the first evidence that ACE might contribute to the prevention of the development of diabetic neuropathy by blocking the MG-mediated intracellular glycation system.	Pyruvaldehyde	163-165	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	66-69
24966916-8	2014	In addition, Glo1 knocking-down with shRNA interfering caused cellular accumulation of methylglyoxal, a Glo1 cytotoxic substrate.	Pyruvaldehyde	87-100	glyoxalase I	Homo sapiens	104-108
24646255-14	2014	Glyoxalase I metabolizes &gt;99% methylglyoxal and thereby protects the proteome and genome.	Pyruvaldehyde	33-46	glyoxalase I	Homo sapiens	0-12
24646257-5	2014	Recently it has been shown that the endogenous reactive metabolite MG (methylglyoxal), elevated as a consequence of reduced Glo1 (glyoxalase I), can contribute to the gain of function via post-translational modification of neuronal ion channels involved in chemosensing and action potential generation in nociceptive nerve endings.	Pyruvaldehyde	67-69	glyoxalase I	Homo sapiens	124-128
24646257-5	2014	Recently it has been shown that the endogenous reactive metabolite MG (methylglyoxal), elevated as a consequence of reduced Glo1 (glyoxalase I), can contribute to the gain of function via post-translational modification of neuronal ion channels involved in chemosensing and action potential generation in nociceptive nerve endings.	Pyruvaldehyde	67-69	glyoxalase I	Homo sapiens	130-142
24646257-5	2014	Recently it has been shown that the endogenous reactive metabolite MG (methylglyoxal), elevated as a consequence of reduced Glo1 (glyoxalase I), can contribute to the gain of function via post-translational modification of neuronal ion channels involved in chemosensing and action potential generation in nociceptive nerve endings.	Pyruvaldehyde	71-84	glyoxalase I	Homo sapiens	124-128
24646257-5	2014	Recently it has been shown that the endogenous reactive metabolite MG (methylglyoxal), elevated as a consequence of reduced Glo1 (glyoxalase I), can contribute to the gain of function via post-translational modification of neuronal ion channels involved in chemosensing and action potential generation in nociceptive nerve endings.	Pyruvaldehyde	71-84	glyoxalase I	Homo sapiens	130-142
24646258-6	2014	MG can be detoxified by Glo1 (glyoxalase I), thereby preventing the accumulation of MG and MG-derived AGEs.	Pyruvaldehyde	0-2	glyoxalase I	Homo sapiens	24-28
24646258-6	2014	MG can be detoxified by Glo1 (glyoxalase I), thereby preventing the accumulation of MG and MG-derived AGEs.	Pyruvaldehyde	0-2	glyoxalase I	Homo sapiens	30-42
24646261-4	2014	These effects are likely to be mediated through the regulation of MG (methylglyoxal) by Glo1, as MG acts as a competitive partial agonist at GABA(A) (gamma-aminobutyric acid A) receptors.	Pyruvaldehyde	66-68	glyoxalase I	Homo sapiens	88-92
24646261-6	2014	In the present article, we evaluate the therapeutic potential of indirectly modulating MG concentrations through Glo1 inhibitors for the treatment of neuropsychiatric disorders.	Pyruvaldehyde	87-89	glyoxalase I	Homo sapiens	113-117
24646266-1	2014	Glyoxalase I catalyses the isomerization of the hemithioacetal formed non-enzymatically from methylglyoxal and glutathione to S-D-lactoylglutathione.	Pyruvaldehyde	93-106	glyoxalase I	Homo sapiens	0-12
24412154-0	2014	Protective effect of thymoquinone on glucose or methylglyoxal-induced glycation of superoxide dismutase.	Pyruvaldehyde	48-61	superoxide dismutase 1	Homo sapiens	83-103
24574346-5	2014	The consequences of in vitro glycation by methylglyoxal on the electrostatic properties of apoC1 and on its inhibitory effect on CETP activity were studied.	Pyruvaldehyde	42-55	apolipoprotein C1	Homo sapiens	91-96
24412154-5	2014	Therefore, the glycation of SOD by glucose or methylglyoxal (MG) and its protection by TQ has been investigated.	Pyruvaldehyde	46-59	superoxide dismutase 1	Homo sapiens	28-31
24436324-9	2014	Methylglyoxal level and protein and mRNA for angiotensin, AT1 receptor, adrenergic alpha1D receptor, and renin were significantly increased in the aorta and/or kidney of methylglyoxal-treated rats, a novel finding.	Pyruvaldehyde	170-183	renin	Rattus norvegicus	105-110
24446986-1	2014	Conversion of dihydroxyacteone (DHA) to methylglyoxal (MGO) has been shown to be the key mechanism for the growth in "apparent" C-4 sugar content in nonperoxide activity (NPA) manuka honey.	Pyruvaldehyde	40-53	complement C4A (Rodgers blood group)	Homo sapiens	128-131
24446986-1	2014	Conversion of dihydroxyacteone (DHA) to methylglyoxal (MGO) has been shown to be the key mechanism for the growth in "apparent" C-4 sugar content in nonperoxide activity (NPA) manuka honey.	Pyruvaldehyde	55-58	complement C4A (Rodgers blood group)	Homo sapiens	128-131
24436324-0	2014	Methylglyoxal, a reactive glucose metabolite, increases renin angiotensin aldosterone and blood pressure in male Sprague-Dawley rats.	Pyruvaldehyde	0-13	renin	Rattus norvegicus	56-61
24436324-8	2014	RESULTS: Methylglyoxal-treated rats developed a significant increase in blood pressure and plasma levels of aldosterone, renin, angiotensin, and catecholamines.	Pyruvaldehyde	9-22	renin	Rattus norvegicus	121-126
24436324-12	2014	Silencing of mRNA for RAGE prevented the increase in NF-kB induced by methylglyoxal.	Pyruvaldehyde	70-83	advanced glycosylation end product-specific receptor	Rattus norvegicus	22-26
24436324-12	2014	Silencing of mRNA for RAGE prevented the increase in NF-kB induced by methylglyoxal.	Pyruvaldehyde	70-83	nuclear factor kappa B subunit 1	Rattus norvegicus	53-58
24436324-14	2014	CONCLUSIONS: Methylglyoxal activates NF-kappaB through RAGE and thereby increases renin-angiotensin levels, a novel finding, and a probable mechanism of increase in blood pressure.	Pyruvaldehyde	13-26	advanced glycosylation end product-specific receptor	Rattus norvegicus	55-59
24436324-14	2014	CONCLUSIONS: Methylglyoxal activates NF-kappaB through RAGE and thereby increases renin-angiotensin levels, a novel finding, and a probable mechanism of increase in blood pressure.	Pyruvaldehyde	13-26	renin	Rattus norvegicus	82-87
24360750-5	2014	The aim of the study was to investigate the effect of in vitro MG-induced glycation on human high density lipoprotein (HDL) and on the activity of the enzyme paraoxonase-1 (PON1).	Pyruvaldehyde	63-65	paraoxonase 1	Homo sapiens	173-177
24360750-12	2014	Therefore, modifications of apoprotein composition and the decrease of paraoxonase-1 activity in MG-treated HDL could affect the protective effect exerted by HDL against oxidative damage and could contribute to complications in patients affected by diseases associated with aging and oxidative stress.	Pyruvaldehyde	97-99	paraoxonase 1	Homo sapiens	71-84
24158671-1	2014	Glyoxalase 1 (Glo1), belonging to the glyoxalase system, participates in the detoxification of methylglyoxal (MG), a byproduct of glycolysis.	Pyruvaldehyde	95-108	glyoxalase I	Homo sapiens	0-12
24158671-1	2014	Glyoxalase 1 (Glo1), belonging to the glyoxalase system, participates in the detoxification of methylglyoxal (MG), a byproduct of glycolysis.	Pyruvaldehyde	95-108	glyoxalase I	Homo sapiens	14-18
24158671-1	2014	Glyoxalase 1 (Glo1), belonging to the glyoxalase system, participates in the detoxification of methylglyoxal (MG), a byproduct of glycolysis.	Pyruvaldehyde	110-112	glyoxalase I	Homo sapiens	0-12
24158671-1	2014	Glyoxalase 1 (Glo1), belonging to the glyoxalase system, participates in the detoxification of methylglyoxal (MG), a byproduct of glycolysis.	Pyruvaldehyde	110-112	glyoxalase I	Homo sapiens	14-18
24252591-2	2014	MG is associated with neurodegeneration, including oxidative stress and impaired glucose metabolism, and is efficiently metabolized to S-D-lactoylglutathione by glyoxalase (GLO).	Pyruvaldehyde	0-2	hydroxyacylglutathione hydrolase	Homo sapiens	173-176
24259499-2	2014	This study assessed whether overexpressing the MG-metabolizing enzyme glyoxalase-1 (GLO1) in only bone marrow cells (BMCs) could restore neovascularization in ischaemic tissue of streptozotocin-induced diabetic mice.	Pyruvaldehyde	47-49	glyoxalase 1	Mus musculus	70-82
24259499-2	2014	This study assessed whether overexpressing the MG-metabolizing enzyme glyoxalase-1 (GLO1) in only bone marrow cells (BMCs) could restore neovascularization in ischaemic tissue of streptozotocin-induced diabetic mice.	Pyruvaldehyde	47-49	glyoxalase 1	Mus musculus	84-88
24259499-13	2014	CONCLUSION: This study demonstrates that protection from MG uniquely in BM is sufficient to restore BMC function and neovascularization of ischaemic tissue in diabetes and identifies GLO1 as a potential therapeutic target.	Pyruvaldehyde	57-59	glyoxalase 1	Mus musculus	183-187
24164256-9	2014	Furthermore, the results demonstrated that methylglyoxal induced protein adduct formation, inactivation of glyoxalase I, and activation of glyoxalase II.	Pyruvaldehyde	43-56	glyoxalase 1	Mus musculus	107-119
24164256-9	2014	Furthermore, the results demonstrated that methylglyoxal induced protein adduct formation, inactivation of glyoxalase I, and activation of glyoxalase II.	Pyruvaldehyde	43-56	hydroxyacyl glutathione hydrolase	Mus musculus	139-152
24252591-5	2014	Purified Tat-GLO protein efficiently transduced into HT-22 neuronal cells and protected cells against MG- and H2O2-induced cell death, DNA fragmentation, and activation of caspase-3 and mitogen-activated protein kinase.	Pyruvaldehyde	102-104	tyrosine aminotransferase	Homo sapiens	9-12
24252591-5	2014	Purified Tat-GLO protein efficiently transduced into HT-22 neuronal cells and protected cells against MG- and H2O2-induced cell death, DNA fragmentation, and activation of caspase-3 and mitogen-activated protein kinase.	Pyruvaldehyde	102-104	hydroxyacylglutathione hydrolase	Homo sapiens	13-16
24252591-6	2014	In addition, transduced Tat-GLO protein increased D-lactate in MG- and H2O2-treated cells whereas glycation end products (AGE) and MG levels were significantly reduced in the same cells.	Pyruvaldehyde	63-65	tyrosine aminotransferase	Homo sapiens	24-27
24252591-6	2014	In addition, transduced Tat-GLO protein increased D-lactate in MG- and H2O2-treated cells whereas glycation end products (AGE) and MG levels were significantly reduced in the same cells.	Pyruvaldehyde	63-65	hydroxyacylglutathione hydrolase	Homo sapiens	28-31
24252591-6	2014	In addition, transduced Tat-GLO protein increased D-lactate in MG- and H2O2-treated cells whereas glycation end products (AGE) and MG levels were significantly reduced in the same cells.	Pyruvaldehyde	131-133	tyrosine aminotransferase	Homo sapiens	24-27
24252591-6	2014	In addition, transduced Tat-GLO protein increased D-lactate in MG- and H2O2-treated cells whereas glycation end products (AGE) and MG levels were significantly reduced in the same cells.	Pyruvaldehyde	131-133	hydroxyacylglutathione hydrolase	Homo sapiens	28-31
24252591-9	2014	Those results demonstrate that transduced Tat-GLO protein protects neuronal cells by inhibiting MG- and H2O2-mediated cytotoxicity in vitro and in vivo.	Pyruvaldehyde	96-98	tyrosine aminotransferase	Homo sapiens	42-45
24252591-9	2014	Those results demonstrate that transduced Tat-GLO protein protects neuronal cells by inhibiting MG- and H2O2-mediated cytotoxicity in vitro and in vivo.	Pyruvaldehyde	96-98	hydroxyacylglutathione hydrolase	Homo sapiens	46-49
24122011-10	2014	MGO (0.1-10 mmol/L) dose-dependently activated Kir6.1/SUR2B channels with an EC50 of 1.7 mmol/L.	Pyruvaldehyde	0-3	potassium inwardly rectifying channel subfamily J member 8	Homo sapiens	47-53
24108388-0	2014	Methylglyoxal impairs GLUT4 trafficking and leads to increased glucose uptake in L6 myoblasts.	Pyruvaldehyde	0-13	solute carrier family 2 member 4	Rattus norvegicus	22-27
24108388-7	2014	A decreased expression of Akt1 but not Akt2 and concomitantly increased apoptosis were detected following MG treatment.	Pyruvaldehyde	106-108	AKT serine/threonine kinase 1	Rattus norvegicus	26-30
24108388-8	2014	To exclude that oxidative stress caused by MG treatment leads to increased GLUT4 translocation, effects of pretreatment with 2 antioxidants were investigated.	Pyruvaldehyde	43-45	solute carrier family 2 member 4	Rattus norvegicus	75-80
24108388-9	2014	The antioxidant and MG scavenger NAC prevented the MG-induced GLUT4 translocation.	Pyruvaldehyde	20-22	solute carrier family 2 member 4	Rattus norvegicus	62-67
24192110-0	2014	Methylglyoxal may affect hydrogen peroxide accumulation in manuka honey through the inhibition of glucose oxidase.	Pyruvaldehyde	0-13	hydroxyacid oxidase 1	Homo sapiens	98-113
24192110-5	2014	In vitro crosslinking of the enzyme glucose oxidase (GOX) after incubation with MGO was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis.	Pyruvaldehyde	80-83	hydroxyacid oxidase 1	Homo sapiens	36-51
24192110-5	2014	In vitro crosslinking of the enzyme glucose oxidase (GOX) after incubation with MGO was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis.	Pyruvaldehyde	80-83	hydroxyacid oxidase 1	Homo sapiens	53-56
24494193-6	2014	In cultured HeLa cells, methylglyoxal challenge causes increase in intracellular levels of reactive oxygen species (ROS) and calcium leading to TG2 activation and subsequent transamidation and activation of GlxI.	Pyruvaldehyde	24-37	transglutaminase 2	Homo sapiens	144-147
24494193-7	2014	The inhibition of TG2 significantly weakens the cell resistance to the methylglyoxal challenge.	Pyruvaldehyde	71-84	transglutaminase 2	Homo sapiens	18-21
24494193-9	2014	Exposure to methylglyoxal elicits a negative feedback loop entailing ROS, calcium, TG2 and GlxI, thus leading to attenuation of the increase in the methylglyoxal level.	Pyruvaldehyde	12-25	transglutaminase 2	Homo sapiens	83-86
24494193-9	2014	Exposure to methylglyoxal elicits a negative feedback loop entailing ROS, calcium, TG2 and GlxI, thus leading to attenuation of the increase in the methylglyoxal level.	Pyruvaldehyde	148-161	transglutaminase 2	Homo sapiens	83-86
24192110-9	2014	In addition, MGO-treated GOX formed high molecular weight adducts with increasing time of incubation accompanied by loss of its enzymatic activity.	Pyruvaldehyde	13-16	hydroxyacid oxidase 1	Homo sapiens	25-28
24192110-10	2014	High levels of MGO in manuka honey, by modifying the enzyme GOX, might be responsible for suppressing H2O2 generation.	Pyruvaldehyde	15-18	hydroxyacid oxidase 1	Homo sapiens	60-63
24122011-11	2014	The activation of Kir6.1/SUR2B channels by MGO was reversible upon washout, and could be inhibited completely by glibenclamide.	Pyruvaldehyde	43-46	potassium inwardly rectifying channel subfamily J member 8	Homo sapiens	18-24
24122011-13	2014	Single channel recordings showed that MGO (3 mmol/L) markedly increased the open probability of Kir6.1/SUR2B channels, leaving the channel conductance unaltered.	Pyruvaldehyde	38-41	potassium inwardly rectifying channel subfamily J member 8	Homo sapiens	96-102
25358632-8	2014	Treatment with MGO significantly augmented the proliferation of mesenchymal-like mesothelial cells, accumulation of AGE, de novo expression of alphaSMA and RAGE and gene expression of type I collagen, TGF-beta1, Snail and MMP-2, whereas both MGO and RF alone had, at most, marginal effects on the changes in these biological parameters.	Pyruvaldehyde	15-18	actin gamma 2, smooth muscle	Rattus norvegicus	143-151
25358632-8	2014	Treatment with MGO significantly augmented the proliferation of mesenchymal-like mesothelial cells, accumulation of AGE, de novo expression of alphaSMA and RAGE and gene expression of type I collagen, TGF-beta1, Snail and MMP-2, whereas both MGO and RF alone had, at most, marginal effects on the changes in these biological parameters.	Pyruvaldehyde	15-18	transforming growth factor, beta 1	Rattus norvegicus	201-210
25358632-8	2014	Treatment with MGO significantly augmented the proliferation of mesenchymal-like mesothelial cells, accumulation of AGE, de novo expression of alphaSMA and RAGE and gene expression of type I collagen, TGF-beta1, Snail and MMP-2, whereas both MGO and RF alone had, at most, marginal effects on the changes in these biological parameters.	Pyruvaldehyde	15-18	matrix metallopeptidase 2	Rattus norvegicus	222-227
24062246-3	2014	Overexpression of the enzyme glyoxalase 1 (Glo1), which prevents posttranslational modification of proteins by the glycolysis-derived alpha-oxoaldehyde, methylglyoxal (MG), prevents hyperglycemia-induced oxidative stress in cultured cells and model organisms.	Pyruvaldehyde	153-166	glyoxalase 1	Mus musculus	29-41
24002659-2	2014	Glyoxalase I (GI) metabolizes methylglyoxal (MG) and MG-derived advanced glycation end products (AGEs) known to cause apoptosis.	Pyruvaldehyde	30-43	glyoxalase I	Homo sapiens	0-12
24002659-2	2014	Glyoxalase I (GI) metabolizes methylglyoxal (MG) and MG-derived advanced glycation end products (AGEs) known to cause apoptosis.	Pyruvaldehyde	30-43	glyoxalase I	Homo sapiens	14-16
24002659-2	2014	Glyoxalase I (GI) metabolizes methylglyoxal (MG) and MG-derived advanced glycation end products (AGEs) known to cause apoptosis.	Pyruvaldehyde	45-47	glyoxalase I	Homo sapiens	0-12
24002659-2	2014	Glyoxalase I (GI) metabolizes methylglyoxal (MG) and MG-derived advanced glycation end products (AGEs) known to cause apoptosis.	Pyruvaldehyde	45-47	glyoxalase I	Homo sapiens	14-16
24002659-2	2014	Glyoxalase I (GI) metabolizes methylglyoxal (MG) and MG-derived advanced glycation end products (AGEs) known to cause apoptosis.	Pyruvaldehyde	53-55	glyoxalase I	Homo sapiens	0-12
24002659-2	2014	Glyoxalase I (GI) metabolizes methylglyoxal (MG) and MG-derived advanced glycation end products (AGEs) known to cause apoptosis.	Pyruvaldehyde	53-55	glyoxalase I	Homo sapiens	14-16
24102997-4	2014	Among endogenous TRPA1 agonists that have been shown to play a role in the pathogenesis of pain and inflammatory conditions are, for example, methylglyoxal, 4-hydroxynonenal, 12-lipoxygenase-derived hepoxilin A3, 5,6-epoxyeicosatrienoic acid and reactive oxygen species, while mustard oil and cinnamaldehyde are most commonly used exogenous TRPA1 agonists in experimental studies.	Pyruvaldehyde	142-155	transient receptor potential cation channel subfamily A member 1	Homo sapiens	17-22
24102997-4	2014	Among endogenous TRPA1 agonists that have been shown to play a role in the pathogenesis of pain and inflammatory conditions are, for example, methylglyoxal, 4-hydroxynonenal, 12-lipoxygenase-derived hepoxilin A3, 5,6-epoxyeicosatrienoic acid and reactive oxygen species, while mustard oil and cinnamaldehyde are most commonly used exogenous TRPA1 agonists in experimental studies.	Pyruvaldehyde	142-155	transient receptor potential cation channel subfamily A member 1	Homo sapiens	341-346
24062246-3	2014	Overexpression of the enzyme glyoxalase 1 (Glo1), which prevents posttranslational modification of proteins by the glycolysis-derived alpha-oxoaldehyde, methylglyoxal (MG), prevents hyperglycemia-induced oxidative stress in cultured cells and model organisms.	Pyruvaldehyde	153-166	glyoxalase 1	Mus musculus	43-47
24062246-3	2014	Overexpression of the enzyme glyoxalase 1 (Glo1), which prevents posttranslational modification of proteins by the glycolysis-derived alpha-oxoaldehyde, methylglyoxal (MG), prevents hyperglycemia-induced oxidative stress in cultured cells and model organisms.	Pyruvaldehyde	168-170	glyoxalase 1	Mus musculus	29-41
24062246-3	2014	Overexpression of the enzyme glyoxalase 1 (Glo1), which prevents posttranslational modification of proteins by the glycolysis-derived alpha-oxoaldehyde, methylglyoxal (MG), prevents hyperglycemia-induced oxidative stress in cultured cells and model organisms.	Pyruvaldehyde	168-170	glyoxalase 1	Mus musculus	43-47
24062246-4	2014	In this study, we show that in nondiabetic mice, knockdown of Glo1 increases to diabetic levels both MG modification of glomerular proteins and oxidative stress, causing alterations in kidney morphology indistinguishable from those caused by diabetes.	Pyruvaldehyde	101-103	glyoxalase 1	Mus musculus	62-66
24162587-2	2014	In this study we used a rat model of diabetes, in which rats transgenically overexpressed the MGO-detoxifying enzyme glyoxalase-I (GLO-I), to determine the impact of intracellular glycation on vascular function and the development of early renal changes in diabetes.	Pyruvaldehyde	94-97	glyoxalase 1	Rattus norvegicus	117-129
24062246-5	2014	We also show that in diabetic mice, Glo1 overexpression completely prevents diabetes-induced increases in MG modification of glomerular proteins, increased oxidative stress, and the development of diabetic kidney pathology, despite unchanged levels of diabetic hyperglycemia.	Pyruvaldehyde	106-108	glyoxalase 1	Mus musculus	36-40
24162587-2	2014	In this study we used a rat model of diabetes, in which rats transgenically overexpressed the MGO-detoxifying enzyme glyoxalase-I (GLO-I), to determine the impact of intracellular glycation on vascular function and the development of early renal changes in diabetes.	Pyruvaldehyde	94-97	glyoxalase 1	Rattus norvegicus	131-136
24614897-0	2014	Methylglyoxal produced by amyloid-beta peptide-induced nitrotyrosination of triosephosphate isomerase triggers neuronal death in Alzheimer"s disease.	Pyruvaldehyde	0-13	triosephosphate isomerase 1	Homo sapiens	76-101
24614897-5	2014	We found an increased production of methylglyoxal (MG), a toxic byproduct of the inefficient nitro-TPI function.	Pyruvaldehyde	36-49	triosephosphate isomerase 1	Homo sapiens	99-102
24614897-5	2014	We found an increased production of methylglyoxal (MG), a toxic byproduct of the inefficient nitro-TPI function.	Pyruvaldehyde	51-53	triosephosphate isomerase 1	Homo sapiens	99-102
24614897-8	2014	Neuroblastoma cells transfected with the double mutant TPI consistently triggered MG production and a decrease in cell viability due to apoptotic mechanisms.	Pyruvaldehyde	82-84	triosephosphate isomerase 1	Homo sapiens	55-58
24614897-9	2014	Our data show for the first time that MG is playing a key role in the neuronal death induced by Abeta oligomers.	Pyruvaldehyde	38-40	amyloid beta precursor protein	Homo sapiens	96-101
25342507-2	2014	The expression of GLO1 was up-regulated in tumor tissues with high metabolic rate, whereas inhibition of GLO1 expression led to the accumulation of glyoxal and methylglyoxal, significantly inducing cell damage or apoptosis.	Pyruvaldehyde	160-173	glyoxalase I	Homo sapiens	105-109
24349480-8	2013	Sulforaphane was able to counteract methylglyoxal-induced apoptosis, ROS production, and glycative stress, likely through glyoxalase 1 up-regulation.	Pyruvaldehyde	36-49	glyoxalase 1	Rattus norvegicus	122-134
24144633-0	2013	Uncoupling of eNOS contributes to redox-sensitive leukocyte recruitment and microvascular leakage elicited by methylglyoxal.	Pyruvaldehyde	110-123	nitric oxide synthase 3, endothelial cell	Mus musculus	14-18
24144633-7	2013	In these tissues and cultured murine and human primary endothelial cells, MG increased eNOS monomerization and decreased BH4/total biopterin ratio, effects that were significantly mitigated by supplementation of BH4 or its precursor sepiapterin but not by L-NAME or tetrahydroneopterin, indicative of MG-triggered eNOS uncoupling.	Pyruvaldehyde	74-76	nitric oxide synthase 3	Homo sapiens	87-91
24144633-7	2013	In these tissues and cultured murine and human primary endothelial cells, MG increased eNOS monomerization and decreased BH4/total biopterin ratio, effects that were significantly mitigated by supplementation of BH4 or its precursor sepiapterin but not by L-NAME or tetrahydroneopterin, indicative of MG-triggered eNOS uncoupling.	Pyruvaldehyde	74-76	nitric oxide synthase 3	Homo sapiens	314-318
24144633-10	2013	Together, our study uncovers eNOS uncoupling as a pivotal mechanism in MG-induced oxidative stress, microvascular hyperpermeability and leukocyte recruitment in vivo.	Pyruvaldehyde	71-73	nitric oxide synthase 3, endothelial cell	Mus musculus	29-33
24060484-6	2013	GSH biosynthesis is heavily dependent upon the antioxidant response element-nuclear respiratory factor pathway (ARE-Nrf) and pharmacological and dietary intervention studies have demonstrated that activation of the ARE-Nrf pathway increases intracellular GSH and glyoxalase enzymes and reduces MGO levels.	Pyruvaldehyde	294-297	NFKB repressing factor	Homo sapiens	116-119
23845007-4	2013	Irrigation decrease during 1 hour leaded to increased activation of ERK1/2 and degradation of Ikappa-Balpha and Perilipin A in methylglyoxal-treated normal Wistar rats.	Pyruvaldehyde	127-140	mitogen activated protein kinase 3	Rattus norvegicus	68-74
23845007-4	2013	Irrigation decrease during 1 hour leaded to increased activation of ERK1/2 and degradation of Ikappa-Balpha and Perilipin A in methylglyoxal-treated normal Wistar rats.	Pyruvaldehyde	127-140	NFKB inhibitor alpha	Rattus norvegicus	94-107
23845007-6	2013	However, methylglyoxal-treated rats had higher free fatty acids and triglycerides levels and decreased adiponectinemia, consequent to decreased PPARgamma levels in partially irrigated adipose tissue.	Pyruvaldehyde	9-22	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	144-153
23841818-8	2013	During ischemia, MG caused an impairment of survival pathways and Bcl-2/Bax ratio, a marker of apoptosis.	Pyruvaldehyde	17-19	BCL2 apoptosis regulator	Homo sapiens	66-71
23841818-8	2013	During ischemia, MG caused an impairment of survival pathways and Bcl-2/Bax ratio, a marker of apoptosis.	Pyruvaldehyde	17-19	BCL2 associated X, apoptosis regulator	Homo sapiens	72-75
23782902-4	2013	Nonetheless, effects of vaspin on MGO-induced apoptosis of vascular EC remain to be determined.	Pyruvaldehyde	34-37	serpin family A member 12	Homo sapiens	24-30
23782902-5	2013	We investigated the effects of vaspin on MGO-induced apoptosis of human umbilical vein ECs (HUVECs).	Pyruvaldehyde	41-44	serpin family A member 12	Homo sapiens	31-37
23782902-12	2013	RESULTS: Vaspin significantly inhibited MGO-induced HUVEC death.	Pyruvaldehyde	40-43	serpin family A member 12	Homo sapiens	9-15
23782902-13	2013	Vaspin significantly attenuated MGO-increased TUNEL-positive ECs.	Pyruvaldehyde	32-35	serpin family A member 12	Homo sapiens	0-6
23782902-14	2013	Moreover, vaspin significantly inhibited MGO-induced caspase-3 cleavage.	Pyruvaldehyde	41-44	serpin family A member 12	Homo sapiens	10-16
23782902-14	2013	Moreover, vaspin significantly inhibited MGO-induced caspase-3 cleavage.	Pyruvaldehyde	41-44	caspase 3	Homo sapiens	53-62
23782902-15	2013	Vaspin significantly inhibited MGO-induced ROS generation as well as NOX activation.	Pyruvaldehyde	31-34	serpin family A member 12	Homo sapiens	0-6
23782902-16	2013	CONCLUSIONS: The present results for the first time demonstrate that vaspin inhibits MGO-induced EC apoptosis by preventing caspase-3 activation via the inhibition of NOX-derived ROS generation.	Pyruvaldehyde	85-88	serpin family A member 12	Homo sapiens	69-75
23782902-16	2013	CONCLUSIONS: The present results for the first time demonstrate that vaspin inhibits MGO-induced EC apoptosis by preventing caspase-3 activation via the inhibition of NOX-derived ROS generation.	Pyruvaldehyde	85-88	caspase 3	Homo sapiens	124-133
24220130-2	2013	The first enzyme of this pathway, glyoxalase I (GlxI), uses methylglyoxal as a substrate and requires either Ni(II)/Co(II) or Zn(II) for activity.	Pyruvaldehyde	60-73	glyoxalase I	Homo sapiens	34-46
24071451-4	2013	METHODS: The in vitro effects of methylglyoxal and 3-deoxyglucosone were studied by investigating migration, invasion, and adhesion of Huh-7, HepG2, and Hep3B cells.	Pyruvaldehyde	33-46	MIR7-3 host gene	Homo sapiens	135-140
24060484-0	2013	A proposed mechanism for exercise attenuated methylglyoxal accumulation: activation of the ARE-Nrf pathway and increased glutathione biosynthesis.	Pyruvaldehyde	45-58	NFKB repressing factor	Homo sapiens	95-98
24060484-6	2013	GSH biosynthesis is heavily dependent upon the antioxidant response element-nuclear respiratory factor pathway (ARE-Nrf) and pharmacological and dietary intervention studies have demonstrated that activation of the ARE-Nrf pathway increases intracellular GSH and glyoxalase enzymes and reduces MGO levels.	Pyruvaldehyde	294-297	NFKB repressing factor	Homo sapiens	219-222
24167592-11	2013	Our results show that TRPA1 is the principal target for MG in sensory neurons but not in pancreatic beta-cells and that activation of TRPA1 by MG produces a painful neuropathy with the behavioral hallmarks of diabetic neuropathy.	Pyruvaldehyde	56-58	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	22-27
23954466-0	2013	A novel natural Nrf2 activator with PPARgamma-agonist (monascin) attenuates the toxicity of methylglyoxal and hyperglycemia.	Pyruvaldehyde	92-105	NFE2 like bZIP transcription factor 2	Rattus norvegicus	16-20
23954466-0	2013	A novel natural Nrf2 activator with PPARgamma-agonist (monascin) attenuates the toxicity of methylglyoxal and hyperglycemia.	Pyruvaldehyde	92-105	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	36-45
23954466-6	2013	Monascin was able to elevate glyoxalase-1 expression via activation of hepatic Nrf2, hence, resulting in MG metabolism to d-lactic acid and protected from AGEs production in MG-treated rats.	Pyruvaldehyde	105-107	glyoxalase 1	Rattus norvegicus	29-41
23954466-6	2013	Monascin was able to elevate glyoxalase-1 expression via activation of hepatic Nrf2, hence, resulting in MG metabolism to d-lactic acid and protected from AGEs production in MG-treated rats.	Pyruvaldehyde	105-107	NFE2 like bZIP transcription factor 2	Rattus norvegicus	79-83
23954466-6	2013	Monascin was able to elevate glyoxalase-1 expression via activation of hepatic Nrf2, hence, resulting in MG metabolism to d-lactic acid and protected from AGEs production in MG-treated rats.	Pyruvaldehyde	174-176	glyoxalase 1	Rattus norvegicus	29-41
23954466-6	2013	Monascin was able to elevate glyoxalase-1 expression via activation of hepatic Nrf2, hence, resulting in MG metabolism to d-lactic acid and protected from AGEs production in MG-treated rats.	Pyruvaldehyde	174-176	NFE2 like bZIP transcription factor 2	Rattus norvegicus	79-83
24167592-0	2013	Methylglyoxal evokes pain by stimulating TRPA1.	Pyruvaldehyde	0-13	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	41-46
24167592-11	2013	Our results show that TRPA1 is the principal target for MG in sensory neurons but not in pancreatic beta-cells and that activation of TRPA1 by MG produces a painful neuropathy with the behavioral hallmarks of diabetic neuropathy.	Pyruvaldehyde	143-145	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	134-139
24098758-0	2013	Edaravone protected human brain microvascular endothelial cells from methylglyoxal-induced injury by inhibiting AGEs/RAGE/oxidative stress.	Pyruvaldehyde	69-82	long intergenic non-protein coding RNA 914	Homo sapiens	117-121
24167592-3	2013	Here we show that MG stimulates heterologously expressed TRPA1 in CHO cells and natively expressed TRPA1 in MDCK cells and DRG neurons.	Pyruvaldehyde	18-20	LOW QUALITY PROTEIN: transient receptor potential cation channel subfamily A member 1	Cricetulus griseus	57-62
24167592-3	2013	Here we show that MG stimulates heterologously expressed TRPA1 in CHO cells and natively expressed TRPA1 in MDCK cells and DRG neurons.	Pyruvaldehyde	18-20	LOW QUALITY PROTEIN: transient receptor potential cation channel subfamily A member 1	Cricetulus griseus	99-104
24167592-5	2013	Consistent with a direct, intracellular action, we show that methylglyoxal is significantly more potent as a TRPA1 agonist when applied to the intracellular face of excised membrane patches than to intact cells.	Pyruvaldehyde	61-74	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	109-114
24167592-7	2013	Furthermore, persistently increased MG levels achieved by two weeks pharmacological inhibition of glyoxalase-1 (GLO-1), the rate-limiting enzyme responsible for detoxification of MG, evokes a progressive and marked thermal (cold and heat) and mechanical hypersensitivity in wildtype but not in Trpa1(-/-) mice.	Pyruvaldehyde	36-38	glyoxalase 1	Mus musculus	98-110
24167592-7	2013	Furthermore, persistently increased MG levels achieved by two weeks pharmacological inhibition of glyoxalase-1 (GLO-1), the rate-limiting enzyme responsible for detoxification of MG, evokes a progressive and marked thermal (cold and heat) and mechanical hypersensitivity in wildtype but not in Trpa1(-/-) mice.	Pyruvaldehyde	36-38	glyoxalase 1	Mus musculus	112-117
24167592-7	2013	Furthermore, persistently increased MG levels achieved by two weeks pharmacological inhibition of glyoxalase-1 (GLO-1), the rate-limiting enzyme responsible for detoxification of MG, evokes a progressive and marked thermal (cold and heat) and mechanical hypersensitivity in wildtype but not in Trpa1(-/-) mice.	Pyruvaldehyde	36-38	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	294-299
24167592-7	2013	Furthermore, persistently increased MG levels achieved by two weeks pharmacological inhibition of glyoxalase-1 (GLO-1), the rate-limiting enzyme responsible for detoxification of MG, evokes a progressive and marked thermal (cold and heat) and mechanical hypersensitivity in wildtype but not in Trpa1(-/-) mice.	Pyruvaldehyde	179-181	glyoxalase 1	Mus musculus	98-110
24167592-7	2013	Furthermore, persistently increased MG levels achieved by two weeks pharmacological inhibition of glyoxalase-1 (GLO-1), the rate-limiting enzyme responsible for detoxification of MG, evokes a progressive and marked thermal (cold and heat) and mechanical hypersensitivity in wildtype but not in Trpa1(-/-) mice.	Pyruvaldehyde	179-181	glyoxalase 1	Mus musculus	112-117
23747692-5	2013	We identified AKR1A1 and confirmed AKR1B1 as the most potent PGFS expressing characteristic inhibition patterns in presence of methylglyoxal, ponalrestat and glucose.	Pyruvaldehyde	127-140	aldo-keto reductase family 1 member B	Homo sapiens	35-41
23747692-5	2013	We identified AKR1A1 and confirmed AKR1B1 as the most potent PGFS expressing characteristic inhibition patterns in presence of methylglyoxal, ponalrestat and glucose.	Pyruvaldehyde	127-140	aldo-keto reductase family 1 member C3	Homo sapiens	61-65
24098758-9	2013	What"s more, treatment of MGO enhanced AGEs accumulation, RAGE expression and ROS release in the cultured HBMEC, which were inhibited by 100 micromol/l edaravone.	Pyruvaldehyde	26-29	long intergenic non-protein coding RNA 914	Homo sapiens	58-62
23579026-0	2013	Methylglyoxal-induced modification of arginine residues decreases the activity of NADPH-generating enzymes.	Pyruvaldehyde	0-13	2,4-dienoyl-CoA reductase 1	Homo sapiens	82-87
24058557-0	2013	Methylglyoxal induces platelet hyperaggregation and reduces thrombus stability by activating PKC and inhibiting PI3K/Akt pathway.	Pyruvaldehyde	0-13	AKT serine/threonine kinase 1	Homo sapiens	117-120
23378107-6	2013	Pharmacological inhibition of Erk, has totally attenuated MGO-induced ROS production and cytotoxicity, suggesting that MEK/Erk pathway could be upstream of ROS generation and cell survival.	Pyruvaldehyde	58-61	Eph receptor B1	Rattus norvegicus	30-33
23378107-6	2013	Pharmacological inhibition of Erk, has totally attenuated MGO-induced ROS production and cytotoxicity, suggesting that MEK/Erk pathway could be upstream of ROS generation and cell survival.	Pyruvaldehyde	58-61	Eph receptor B1	Rattus norvegicus	123-126
23378107-8	2013	We can propose that Erk, p38MAPK and JNK are involved in the cytotoxicity induced by MGO through different signaling pathways.	Pyruvaldehyde	85-88	Eph receptor B1	Rattus norvegicus	20-23
23378107-8	2013	We can propose that Erk, p38MAPK and JNK are involved in the cytotoxicity induced by MGO through different signaling pathways.	Pyruvaldehyde	85-88	mitogen-activated protein kinase 8	Rattus norvegicus	37-40
23579026-5	2013	In this study, the activities of isolated G6PD, IDH, and ME were inhibited by MGO (0-2.5mM, 2-3h, 37 C), in a dose- and time-dependent manner, with G6PD and IDH more sensitive to modification than ME.	Pyruvaldehyde	78-81	glucose-6-phosphate dehydrogenase	Homo sapiens	42-46
23579026-5	2013	In this study, the activities of isolated G6PD, IDH, and ME were inhibited by MGO (0-2.5mM, 2-3h, 37 C), in a dose- and time-dependent manner, with G6PD and IDH more sensitive to modification than ME.	Pyruvaldehyde	78-81	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	48-51
24050620-0	2013	Methylglyoxal modulates endothelial nitric oxide synthase-associated functions in EA.hy926 endothelial cells.	Pyruvaldehyde	0-13	nitric oxide synthase 3	Homo sapiens	24-57
23966111-2	2013	Methylglyoxal is successively catabolized to D-lactate by glyoxalase-1 and glyoxalase-2.	Pyruvaldehyde	0-13	glyoxalase 1	Rattus norvegicus	58-70
21793156-7	2013	Further investigation of these processes revealed that MG directly promotes reactive oxygen species (ROS) generation, loss of mitochondrial membrane potential (MMP), and activation of caspase-3, whereas resveratrol effectively blocks MG-induced ROS production and the accompanying apoptotic biochemical changes.	Pyruvaldehyde	55-57	caspase 3	Mus musculus	184-193
23579026-5	2013	In this study, the activities of isolated G6PD, IDH, and ME were inhibited by MGO (0-2.5mM, 2-3h, 37 C), in a dose- and time-dependent manner, with G6PD and IDH more sensitive to modification than ME.	Pyruvaldehyde	78-81	glucose-6-phosphate dehydrogenase	Homo sapiens	148-152
23579026-3	2013	Arg residues are particularly susceptible to MGO glycation and are essential for binding NADP(+) in several enzymes that generate NADPH, a coenzyme for many critical metabolic and antioxidant enzymes.	Pyruvaldehyde	45-48	2,4-dienoyl-CoA reductase 1	Homo sapiens	130-135
23579026-5	2013	In this study, the activities of isolated G6PD, IDH, and ME were inhibited by MGO (0-2.5mM, 2-3h, 37 C), in a dose- and time-dependent manner, with G6PD and IDH more sensitive to modification than ME.	Pyruvaldehyde	78-81	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	157-160
23579026-7	2013	Incubation with radiolabeled MGO (0-500microM, 0-3h, 37 C) demonstrated dose- and time-dependent adduction to G6PD and IDH.	Pyruvaldehyde	29-32	glucose-6-phosphate dehydrogenase	Homo sapiens	110-114
23434766-8	2013	Furthermore, DMA increased hepatic glyoxalase mRNA and glutathione mediated by Nrf2 activation to metabolize MG into d-lactic acid, thereby reducing serum and hepatic AGE levels and suppressing inflammatory factor generation in MG-treated mice.	Pyruvaldehyde	109-111	nuclear factor, erythroid derived 2, like 2	Mus musculus	79-83
23579026-7	2013	Incubation with radiolabeled MGO (0-500microM, 0-3h, 37 C) demonstrated dose- and time-dependent adduction to G6PD and IDH.	Pyruvaldehyde	29-32	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	119-122
23731245-0	2013	Monascin and AITC attenuate methylglyoxal-induced PPARgamma phosphorylation and degradation through inhibition of the oxidative stress/PKC pathway depending on Nrf2 activation.	Pyruvaldehyde	28-41	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	50-59
29913916-2	2013	Here we review recent experimental evidence supporting the hypothesis that activation of the TRPA1 channel by reactive compounds generated in diabetes mellitus, such as 4-hydroxynonenal and methylglyoxal, exerts an important role in the pathophysiology of peripheral diabetic neuropathy (PDN).	Pyruvaldehyde	190-203	transient receptor potential cation channel subfamily A member 1	Homo sapiens	93-98
29913916-6	2013	Results In vitro studies indicate that under physiological concentration of Ca2+, methylglyoxal and 4-hydroxynonenal produce sustained activation of the TRPA1 channel and sustained inflow of calcium.	Pyruvaldehyde	82-95	transient receptor potential cation channel subfamily A member 1	Homo sapiens	153-158
23731245-0	2013	Monascin and AITC attenuate methylglyoxal-induced PPARgamma phosphorylation and degradation through inhibition of the oxidative stress/PKC pathway depending on Nrf2 activation.	Pyruvaldehyde	28-41	NFE2 like bZIP transcription factor 2	Rattus norvegicus	160-164
23731245-7	2013	The in vitro and in vivo results indicated that MG leads to marked PPARgamma phosphorylation (serine 82); this effect led to reduction in pancreatic and duodenal homeobox-1 (PDX-1), glucokinase (GCK), and insulin expression.	Pyruvaldehyde	48-50	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	67-76
23731245-7	2013	The in vitro and in vivo results indicated that MG leads to marked PPARgamma phosphorylation (serine 82); this effect led to reduction in pancreatic and duodenal homeobox-1 (PDX-1), glucokinase (GCK), and insulin expression.	Pyruvaldehyde	48-50	pancreatic and duodenal homeobox 1	Rattus norvegicus	174-179
23731245-7	2013	The in vitro and in vivo results indicated that MG leads to marked PPARgamma phosphorylation (serine 82); this effect led to reduction in pancreatic and duodenal homeobox-1 (PDX-1), glucokinase (GCK), and insulin expression.	Pyruvaldehyde	48-50	glucokinase	Rattus norvegicus	182-193
23731245-7	2013	The in vitro and in vivo results indicated that MG leads to marked PPARgamma phosphorylation (serine 82); this effect led to reduction in pancreatic and duodenal homeobox-1 (PDX-1), glucokinase (GCK), and insulin expression.	Pyruvaldehyde	48-50	glucokinase	Rattus norvegicus	195-198
23731245-11	2013	This study examined whether MG caused impairment of PDX-1, GCK, and insulin through PPARgamma phosphorylation and degradation.	Pyruvaldehyde	28-30	pancreatic and duodenal homeobox 1	Rattus norvegicus	52-57
23731245-11	2013	This study examined whether MG caused impairment of PDX-1, GCK, and insulin through PPARgamma phosphorylation and degradation.	Pyruvaldehyde	28-30	glucokinase	Rattus norvegicus	59-62
23731245-11	2013	This study examined whether MG caused impairment of PDX-1, GCK, and insulin through PPARgamma phosphorylation and degradation.	Pyruvaldehyde	28-30	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	84-93
23731245-12	2013	MG and AGE accumulation improved on Nrf2 activation, thereby protecting against pancreas damage.	Pyruvaldehyde	0-2	NFE2 like bZIP transcription factor 2	Rattus norvegicus	36-40
23717693-4	2013	Glyoxalase 1 (GLO1), in combination with glyoxalase 2 and the co-factor glutathione constitute the glyoxalase system, which is responsible for the detoxification of MG.	Pyruvaldehyde	165-167	glyoxalase I	Homo sapiens	0-12
22678928-4	2013	The increased synthesis of aldose reductase in transgenic plants correlated with reduced methylglyoxal and malondialdehyde accumulation and an elevated level of sorbitol under stress conditions.	Pyruvaldehyde	89-102	aldose reductase	Nicotiana tabacum	27-43
23411197-4	2013	Moreover, all diotides (100 muM) showed protective effects against methylglyoxal-induced human umbilical vein endothelial cell death.	Pyruvaldehyde	67-80	latexin	Homo sapiens	28-31
23741493-3	2013	Glycation of lipid-free apoA-I by methylglyoxal and glycolaldehyde resulted in Arg, Lys and Trp loss, advanced glycation end-product formation and protein cross-linking.	Pyruvaldehyde	34-47	apolipoprotein A1	Homo sapiens	24-30
23741493-4	2013	The association of apoA-I glycated by glucose, methylglyoxal or glycolaldehyde with phospholipid multilamellar vesicles was impaired in a glycating agent dose-dependent manner, with exposure of apoA-I to both 30 mM glucose (42% decrease in kslow) and 3 mM glycolaldehyde (50% decrease in kfast, 60% decrease in kslow) resulting is significantly reduced affinity.	Pyruvaldehyde	47-60	apolipoprotein A1	Homo sapiens	19-25
23741493-4	2013	The association of apoA-I glycated by glucose, methylglyoxal or glycolaldehyde with phospholipid multilamellar vesicles was impaired in a glycating agent dose-dependent manner, with exposure of apoA-I to both 30 mM glucose (42% decrease in kslow) and 3 mM glycolaldehyde (50% decrease in kfast, 60% decrease in kslow) resulting is significantly reduced affinity.	Pyruvaldehyde	47-60	apolipoprotein A1	Homo sapiens	194-200
23717693-4	2013	Glyoxalase 1 (GLO1), in combination with glyoxalase 2 and the co-factor glutathione constitute the glyoxalase system, which is responsible for the detoxification of MG.	Pyruvaldehyde	165-167	glyoxalase I	Homo sapiens	14-18
23717693-5	2013	A GLO1 specific knock down results in accumulation of MG in targeted cells.	Pyruvaldehyde	54-56	glyoxalase I	Homo sapiens	2-6
23717693-6	2013	The aim of this study was to investigate the effect of intracellularly accumulated MG on insulin signaling and on the translocation of the glucose transporter 4 (GLUT4).	Pyruvaldehyde	83-85	solute carrier family 2 member 4	Homo sapiens	139-160
23717693-6	2013	The aim of this study was to investigate the effect of intracellularly accumulated MG on insulin signaling and on the translocation of the glucose transporter 4 (GLUT4).	Pyruvaldehyde	83-85	solute carrier family 2 member 4	Homo sapiens	162-167
23717693-10	2013	The antioxidant and MG scavenger NAC prevented the MG-induced GLUT4 translocation.	Pyruvaldehyde	20-22	synuclein alpha	Homo sapiens	33-36
23717693-10	2013	The antioxidant and MG scavenger NAC prevented the MG-induced GLUT4 translocation.	Pyruvaldehyde	20-22	solute carrier family 2 member 4	Homo sapiens	62-67
23454834-2	2013	Carbonyl stress is represented by methylglyoxal (MGO) and its downstream advanced glycation end products, such as N(e)-(carboxyethyl)lysine (CEL).	Pyruvaldehyde	34-47	carboxyl ester lipase	Rattus norvegicus	141-144
23126339-9	2013	CONCLUSION AND IMPLICATIONS: Insulin enhanced MG overproduction in insulin-sensitive adipocytes by up-regulating aldolase A, a mechanism that could be involved in the development of insulin resistance and obesity.	Pyruvaldehyde	46-48	insulin	Homo sapiens	29-36
23454834-2	2013	Carbonyl stress is represented by methylglyoxal (MGO) and its downstream advanced glycation end products, such as N(e)-(carboxyethyl)lysine (CEL).	Pyruvaldehyde	49-52	carboxyl ester lipase	Rattus norvegicus	141-144
23126339-9	2013	CONCLUSION AND IMPLICATIONS: Insulin enhanced MG overproduction in insulin-sensitive adipocytes by up-regulating aldolase A, a mechanism that could be involved in the development of insulin resistance and obesity.	Pyruvaldehyde	46-48	insulin	Homo sapiens	67-74
23126339-9	2013	CONCLUSION AND IMPLICATIONS: Insulin enhanced MG overproduction in insulin-sensitive adipocytes by up-regulating aldolase A, a mechanism that could be involved in the development of insulin resistance and obesity.	Pyruvaldehyde	46-48	insulin	Homo sapiens	182-189
23409935-7	2013	Here, we investigated the role of MG and its catabolic enzyme, glyoxalase 1 (GLO1), in seizures.	Pyruvaldehyde	34-36	glyoxalase 1	Mus musculus	63-75
23409935-7	2013	Here, we investigated the role of MG and its catabolic enzyme, glyoxalase 1 (GLO1), in seizures.	Pyruvaldehyde	34-36	glyoxalase 1	Mus musculus	77-81
23409935-14	2013	GLO1 inhibition, which increases MG concentration in vivo, also attenuated seizures.	Pyruvaldehyde	33-35	glyoxalase 1	Mus musculus	0-4
23409935-16	2013	Tg mice overexpressing Glo1 displayed reduced MG concentration in the brain and increased seizure severity.	Pyruvaldehyde	46-48	glyoxalase 1	Mus musculus	23-27
23409935-20	2013	Finally, Glo1 may contribute to the genetic architecture of epilepsy, as Glo1 expression regulates both MG concentration and seizure severity.	Pyruvaldehyde	104-106	glyoxalase 1	Mus musculus	9-13
23409935-20	2013	Finally, Glo1 may contribute to the genetic architecture of epilepsy, as Glo1 expression regulates both MG concentration and seizure severity.	Pyruvaldehyde	104-106	glyoxalase 1	Mus musculus	73-77
23201419-1	2013	The glyoxalase system and its main enzyme, glyoxalase 1 (GLO1), protect cells from advanced glycation end products (AGEs), such as methylglyoxal (MG) and other reactive dicarbonyls, the formation of which is increased in diabetes patients as a result of excessive glycolysis.	Pyruvaldehyde	131-144	glyoxalase I	Homo sapiens	43-55
23643164-1	2013	OBJECTIVE: To study the roles and interrelationship of transcriptional co-activator p300 and protein kinase Cbeta2(PKCbeta2) in the production of reactive oxygen species (ROS) and the expression of fibronectin in human mesangial cells (HMCs) under the stimulation of high glucose and methylglyoxal-derived advanced glycation end products (AGEs).	Pyruvaldehyde	284-297	E1A binding protein p300	Homo sapiens	84-88
23643164-1	2013	OBJECTIVE: To study the roles and interrelationship of transcriptional co-activator p300 and protein kinase Cbeta2(PKCbeta2) in the production of reactive oxygen species (ROS) and the expression of fibronectin in human mesangial cells (HMCs) under the stimulation of high glucose and methylglyoxal-derived advanced glycation end products (AGEs).	Pyruvaldehyde	284-297	fibronectin 1	Homo sapiens	198-209
23504526-0	2013	In vitro study on structural alteration of myoglobin by methylglyoxal.	Pyruvaldehyde	56-69	myoglobin	Homo sapiens	43-52
23504526-3	2013	Although myoglobin (Mb) is known to react with sugars to form AGEs, its interaction with MG is not known.	Pyruvaldehyde	89-91	myoglobin	Homo sapiens	9-18
23333621-3	2013	In this study we examined whether, and through which molecular mechanism, methylglyoxal affects the growth of poorly aggressive LNCaP and invasive PC3 human prostate cancer cells, where its role has not been exhaustively investigated yet.	Pyruvaldehyde	74-87	chromobox 8	Homo sapiens	147-150
23201419-1	2013	The glyoxalase system and its main enzyme, glyoxalase 1 (GLO1), protect cells from advanced glycation end products (AGEs), such as methylglyoxal (MG) and other reactive dicarbonyls, the formation of which is increased in diabetes patients as a result of excessive glycolysis.	Pyruvaldehyde	131-144	glyoxalase I	Homo sapiens	57-61
23201419-1	2013	The glyoxalase system and its main enzyme, glyoxalase 1 (GLO1), protect cells from advanced glycation end products (AGEs), such as methylglyoxal (MG) and other reactive dicarbonyls, the formation of which is increased in diabetes patients as a result of excessive glycolysis.	Pyruvaldehyde	146-148	glyoxalase I	Homo sapiens	43-55
23201419-1	2013	The glyoxalase system and its main enzyme, glyoxalase 1 (GLO1), protect cells from advanced glycation end products (AGEs), such as methylglyoxal (MG) and other reactive dicarbonyls, the formation of which is increased in diabetes patients as a result of excessive glycolysis.	Pyruvaldehyde	146-148	glyoxalase I	Homo sapiens	57-61
23201419-2	2013	MG is partly responsible for harmful protein alterations in living cells, notably in neurons, leading to their dysfunction, and recent studies have shown a negative correlation between GLO1 expression and tissue damage.	Pyruvaldehyde	0-2	glyoxalase I	Homo sapiens	185-189
23331247-5	2013	Inhibitions of RAGE and p47phox by monascin were confirmed by peripheral blood mononuclear cells (PBMCs) of MG-induced rats.	Pyruvaldehyde	108-110	advanced glycosylation end product-specific receptor	Rattus norvegicus	15-19
23331247-8	2013	Suppressions of AGEs, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-beta) in serum of MG-induced rats were attenuated in the monascin administration group treated with retinoic acid (RA).	Pyruvaldehyde	107-109	interleukin 1 beta	Rattus norvegicus	67-84
23108103-2	2013	Here, we test the hypothesis that MG induces occludin glycation and disrupts IHEC barrier function, which is prevented by GSH-dependent MG metabolism.	Pyruvaldehyde	34-36	occludin	Rattus norvegicus	45-53
24096666-6	2013	Both AKR4C10 and AKR4C11 reduced methylglyoxal.	Pyruvaldehyde	33-46	NAD(P)-linked oxidoreductase superfamily protein	Arabidopsis thaliana	5-12
24096666-6	2013	Both AKR4C10 and AKR4C11 reduced methylglyoxal.	Pyruvaldehyde	33-46	NAD(P)-linked oxidoreductase superfamily protein	Arabidopsis thaliana	17-24
23018793-7	2013	Consistently, MGO inhibited ACh (3 microM)-induced phosphorylation of vasodilator stimulated phosphoprotein (an indicator of cyclic GMP production).	Pyruvaldehyde	14-17	vasodilator-stimulated phosphoprotein	Rattus norvegicus	70-107
23108103-5	2013	Moreover, immunofluorescence staining showed that MG disrupted the architectural organization of ZO-1.	Pyruvaldehyde	50-52	tight junction protein 1	Rattus norvegicus	97-101
23108103-8	2013	BSO treatment attenuated D-lactate production, consistent with a role for GSH in glyoxalase I-catalyzed MG elimination.	Pyruvaldehyde	104-106	glyoxalase 1	Rattus norvegicus	81-93
23108103-13	2013	These results provide novel evidence that reactive carbonyl species can mediate occludin glycation in cerebral microvessels and in microvascular endothelial cells that contribute to barrier dysfunction, a process that was prevented by GSH through enhanced MG catabolism.	Pyruvaldehyde	256-258	occludin	Rattus norvegicus	80-88
23022408-0	2012	Ankaflavin: a natural novel PPARgamma agonist upregulates Nrf2 to attenuate methylglyoxal-induced diabetes in vivo.	Pyruvaldehyde	76-89	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	28-37
23797271-1	2013	Methylglyoxal (MG), the major dicarbonyl substrate of the enzyme glyoxalase 1 (GLO1), is a reactive metabolite formed via glycolytic flux.	Pyruvaldehyde	0-13	glyoxalase 1	Mus musculus	65-77
23797271-1	2013	Methylglyoxal (MG), the major dicarbonyl substrate of the enzyme glyoxalase 1 (GLO1), is a reactive metabolite formed via glycolytic flux.	Pyruvaldehyde	0-13	glyoxalase 1	Mus musculus	79-83
23797271-1	2013	Methylglyoxal (MG), the major dicarbonyl substrate of the enzyme glyoxalase 1 (GLO1), is a reactive metabolite formed via glycolytic flux.	Pyruvaldehyde	15-17	glyoxalase 1	Mus musculus	65-77
23797271-1	2013	Methylglyoxal (MG), the major dicarbonyl substrate of the enzyme glyoxalase 1 (GLO1), is a reactive metabolite formed via glycolytic flux.	Pyruvaldehyde	15-17	glyoxalase 1	Mus musculus	79-83
23797271-2	2013	Decreased GLO1 activity in situ has been shown to result in an accumulation of MG and increased formation of advanced glycation endproducts, both of which can accumulate during physiological aging and at an accelerated rate in diabetes and other chronic degenerative diseases.	Pyruvaldehyde	79-81	glyoxalase 1	Mus musculus	10-14
23662713-2	2013	It was shown in system modeling that Maillard reaction interaction of L-lysine (L-lys) with methylglyoxal (MG) led to the formation of compounds reducing methemoglobin (metHb).	Pyruvaldehyde	92-105	hemoglobin subunit gamma 2	Homo sapiens	154-167
23662713-2	2013	It was shown in system modeling that Maillard reaction interaction of L-lysine (L-lys) with methylglyoxal (MG) led to the formation of compounds reducing methemoglobin (metHb).	Pyruvaldehyde	92-105	hemoglobin subunit gamma 2	Homo sapiens	169-174
23662713-2	2013	It was shown in system modeling that Maillard reaction interaction of L-lysine (L-lys) with methylglyoxal (MG) led to the formation of compounds reducing methemoglobin (metHb).	Pyruvaldehyde	107-109	hemoglobin subunit gamma 2	Homo sapiens	154-167
23662713-2	2013	It was shown in system modeling that Maillard reaction interaction of L-lysine (L-lys) with methylglyoxal (MG) led to the formation of compounds reducing methemoglobin (metHb).	Pyruvaldehyde	107-109	hemoglobin subunit gamma 2	Homo sapiens	169-174
24327825-7	2013	Furthermore, Stevia extracts were able to revert the effect of the reduction of glucose uptake caused by methylglyoxal, an inhibitor of the insulin receptor/PI3K/Akt pathway.	Pyruvaldehyde	105-118	insulin	Homo sapiens	140-147
24327825-7	2013	Furthermore, Stevia extracts were able to revert the effect of the reduction of glucose uptake caused by methylglyoxal, an inhibitor of the insulin receptor/PI3K/Akt pathway.	Pyruvaldehyde	105-118	AKT serine/threonine kinase 1	Homo sapiens	162-165
22653787-1	2013	BACKGROUND: Glyoxalase I (GLOI) detoxifies reactive dicarbonyls, as methylglyoxal (MG) that, directly or through the formation of MG-derived adducts, is a growth inhibitor and apoptosis inducer.	Pyruvaldehyde	68-81	glyoxalase I	Homo sapiens	12-24
22653787-1	2013	BACKGROUND: Glyoxalase I (GLOI) detoxifies reactive dicarbonyls, as methylglyoxal (MG) that, directly or through the formation of MG-derived adducts, is a growth inhibitor and apoptosis inducer.	Pyruvaldehyde	68-81	glyoxalase I	Homo sapiens	26-30
22653787-1	2013	BACKGROUND: Glyoxalase I (GLOI) detoxifies reactive dicarbonyls, as methylglyoxal (MG) that, directly or through the formation of MG-derived adducts, is a growth inhibitor and apoptosis inducer.	Pyruvaldehyde	83-85	glyoxalase I	Homo sapiens	12-24
22653787-1	2013	BACKGROUND: Glyoxalase I (GLOI) detoxifies reactive dicarbonyls, as methylglyoxal (MG) that, directly or through the formation of MG-derived adducts, is a growth inhibitor and apoptosis inducer.	Pyruvaldehyde	83-85	glyoxalase I	Homo sapiens	26-30
23022408-0	2012	Ankaflavin: a natural novel PPARgamma agonist upregulates Nrf2 to attenuate methylglyoxal-induced diabetes in vivo.	Pyruvaldehyde	76-89	NFE2 like bZIP transcription factor 2	Rattus norvegicus	58-62
23022408-15	2012	Taken together, the results of our mechanistic study of MG-induced rats suggest that the protective effects of AK against diabetes are mediated by the upregulation of the signaling pathway of Nrf2, which enhances antioxidant activity and serves as a PPARgamma agonist to enhance insulin sensitivity.	Pyruvaldehyde	56-58	NFE2 like bZIP transcription factor 2	Rattus norvegicus	192-196
23022408-15	2012	Taken together, the results of our mechanistic study of MG-induced rats suggest that the protective effects of AK against diabetes are mediated by the upregulation of the signaling pathway of Nrf2, which enhances antioxidant activity and serves as a PPARgamma agonist to enhance insulin sensitivity.	Pyruvaldehyde	56-58	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	250-259
23181072-1	2012	Glyoxalase 1 (GLO1) is a ubiquitous cellular enzyme that participates in the detoxification of methylglyoxal (MG), a cytotoxic byproduct of glycolysis that induces protein modification (advanced glycation end-products, AGEs), oxidative stress, and apoptosis.	Pyruvaldehyde	95-108	glyoxalase I	Homo sapiens	0-12
22798221-0	2012	Methylglyoxal induces tau hyperphosphorylation via promoting AGEs formation.	Pyruvaldehyde	0-13	microtubule associated protein tau	Homo sapiens	22-25
22798221-2	2012	While the level of methylglyoxal (MG) is significantly increased in the AD brains, the role of MG in tau phosphorylation is still not reported.	Pyruvaldehyde	95-97	microtubule associated protein tau	Homo sapiens	101-104
22798221-6	2012	Simultaneous inhibition of GSK-3beta or p38 attenuated the MG-induced tau hyperphosphorylation.	Pyruvaldehyde	59-61	glycogen synthase kinase 3 alpha	Homo sapiens	27-36
22798221-6	2012	Simultaneous inhibition of GSK-3beta or p38 attenuated the MG-induced tau hyperphosphorylation.	Pyruvaldehyde	59-61	mitogen-activated protein kinase 1	Homo sapiens	40-43
22798221-6	2012	Simultaneous inhibition of GSK-3beta or p38 attenuated the MG-induced tau hyperphosphorylation.	Pyruvaldehyde	59-61	microtubule associated protein tau	Homo sapiens	70-73
22798221-7	2012	Aminoguanidine, a blocker of AGEs formation, could effectively reverse the MG-induced tau hyperphosphorylation.	Pyruvaldehyde	75-77	microtubule associated protein tau	Homo sapiens	86-89
22798221-8	2012	These data suggest that MG induces AD-like tau hyperphosphorylation through AGEs formation involving RAGE up-regulation and GSK-3beta activation and p38 activation is also partially involved in MG-induced tau hyperphosphorylation.	Pyruvaldehyde	24-26	microtubule associated protein tau	Homo sapiens	43-46
22798221-8	2012	These data suggest that MG induces AD-like tau hyperphosphorylation through AGEs formation involving RAGE up-regulation and GSK-3beta activation and p38 activation is also partially involved in MG-induced tau hyperphosphorylation.	Pyruvaldehyde	24-26	glycogen synthase kinase 3 alpha	Homo sapiens	124-133
22798221-8	2012	These data suggest that MG induces AD-like tau hyperphosphorylation through AGEs formation involving RAGE up-regulation and GSK-3beta activation and p38 activation is also partially involved in MG-induced tau hyperphosphorylation.	Pyruvaldehyde	24-26	microtubule associated protein tau	Homo sapiens	205-208
23181072-1	2012	Glyoxalase 1 (GLO1) is a ubiquitous cellular enzyme that participates in the detoxification of methylglyoxal (MG), a cytotoxic byproduct of glycolysis that induces protein modification (advanced glycation end-products, AGEs), oxidative stress, and apoptosis.	Pyruvaldehyde	95-108	glyoxalase I	Homo sapiens	14-18
22972803-4	2012	Here we show that the vascular Kir6.1/SUR2B isoform of ATP-sensitive K(+) (K(ATP)) channels is likely to be disrupted with an exposure to submillimolar MGO.	Pyruvaldehyde	152-155	potassium inwardly rectifying channel subfamily J member 8	Homo sapiens	31-37
22972803-4	2012	Here we show that the vascular Kir6.1/SUR2B isoform of ATP-sensitive K(+) (K(ATP)) channels is likely to be disrupted with an exposure to submillimolar MGO.	Pyruvaldehyde	152-155	ATPase phospholipid transporting 8A2	Homo sapiens	55-58
22972803-4	2012	Here we show that the vascular Kir6.1/SUR2B isoform of ATP-sensitive K(+) (K(ATP)) channels is likely to be disrupted with an exposure to submillimolar MGO.	Pyruvaldehyde	152-155	ATPase phospholipid transporting 8A2	Homo sapiens	77-80
22972803-5	2012	Up to 90% of the Kir6.1/SUR2B currents were suppressed by 1 mM MGO with a time constant of ~2 h. Consistently, MGO treatment caused a vast reduction of both Kir6.1 and SUR2B mRNAs endogenously expressed in the A10 vascular smooth muscle cells.	Pyruvaldehyde	63-66	potassium inwardly rectifying channel subfamily J member 8	Homo sapiens	17-23
22972803-5	2012	Up to 90% of the Kir6.1/SUR2B currents were suppressed by 1 mM MGO with a time constant of ~2 h. Consistently, MGO treatment caused a vast reduction of both Kir6.1 and SUR2B mRNAs endogenously expressed in the A10 vascular smooth muscle cells.	Pyruvaldehyde	63-66	potassium inwardly rectifying channel subfamily J member 8	Homo sapiens	157-163
22972803-5	2012	Up to 90% of the Kir6.1/SUR2B currents were suppressed by 1 mM MGO with a time constant of ~2 h. Consistently, MGO treatment caused a vast reduction of both Kir6.1 and SUR2B mRNAs endogenously expressed in the A10 vascular smooth muscle cells.	Pyruvaldehyde	111-114	potassium inwardly rectifying channel subfamily J member 8	Homo sapiens	17-23
22972803-5	2012	Up to 90% of the Kir6.1/SUR2B currents were suppressed by 1 mM MGO with a time constant of ~2 h. Consistently, MGO treatment caused a vast reduction of both Kir6.1 and SUR2B mRNAs endogenously expressed in the A10 vascular smooth muscle cells.	Pyruvaldehyde	111-114	potassium inwardly rectifying channel subfamily J member 8	Homo sapiens	157-163
22972803-6	2012	In the presence of the transcriptional inhibitor actinomycin-D, MGO remained to lower the Kir6.1 and SUR2B mRNAs to the same degree as MGO alone, suggesting that the MGO effect is likely to compromise the mRNA stability.	Pyruvaldehyde	64-67	potassium inwardly rectifying channel subfamily J member 8	Homo sapiens	90-96
22972803-10	2012	These results therefore suggest that acting on the 3"-UTR of Kir6.1 and the coding region of SUR2B, MGO causes instability of Kir6.1 and SUR2B mRNAs, disruption of vascular K(ATP) channels, and impairment of arterial function.	Pyruvaldehyde	100-103	potassium inwardly rectifying channel subfamily J member 8	Homo sapiens	61-67
22972803-10	2012	These results therefore suggest that acting on the 3"-UTR of Kir6.1 and the coding region of SUR2B, MGO causes instability of Kir6.1 and SUR2B mRNAs, disruption of vascular K(ATP) channels, and impairment of arterial function.	Pyruvaldehyde	100-103	potassium inwardly rectifying channel subfamily J member 8	Homo sapiens	126-132
22972803-10	2012	These results therefore suggest that acting on the 3"-UTR of Kir6.1 and the coding region of SUR2B, MGO causes instability of Kir6.1 and SUR2B mRNAs, disruption of vascular K(ATP) channels, and impairment of arterial function.	Pyruvaldehyde	100-103	ATPase phospholipid transporting 8A2	Homo sapiens	164-179
22784708-4	2012	We show for the first time that methylglyoxal treatment or the silencing of GLO1 enhances sensitivity to the promising anticancer agent TRAIL in malignant tumor cells.	Pyruvaldehyde	32-45	TNF superfamily member 10	Homo sapiens	136-141
22869616-3	2012	METHODS AND RESULTS: By microarray, we found that methylglyoxal-treated collagen selectively enhanced alpha11 integrin expression in human cardiac fibroblasts, while levels of other collagen-binding integrins (alpha1, alpha2, and alpha10) were unchanged.	Pyruvaldehyde	50-63	adrenoceptor alpha 1D	Homo sapiens	210-237
22869616-6	2012	Knock-down of alpha11 integrin and TGF-beta receptors with small-interfering RNA blocked the increased expression of TGF-beta2, alpha-smooth muscle actin (alpha-SMA), and alpha11 integrin that were induced in cells plated on methylglyoxal-treated collagen.	Pyruvaldehyde	225-238	transforming growth factor, beta 1	Rattus norvegicus	35-43
22869616-6	2012	Knock-down of alpha11 integrin and TGF-beta receptors with small-interfering RNA blocked the increased expression of TGF-beta2, alpha-smooth muscle actin (alpha-SMA), and alpha11 integrin that were induced in cells plated on methylglyoxal-treated collagen.	Pyruvaldehyde	225-238	transforming growth factor, beta 2	Rattus norvegicus	117-126
22869616-6	2012	Knock-down of alpha11 integrin and TGF-beta receptors with small-interfering RNA blocked the increased expression of TGF-beta2, alpha-smooth muscle actin (alpha-SMA), and alpha11 integrin that were induced in cells plated on methylglyoxal-treated collagen.	Pyruvaldehyde	225-238	actin gamma 2, smooth muscle	Rattus norvegicus	155-164
22784708-5	2012	Methylglyoxal suppressed the expression of antiapoptotic factors, X-linked inhibitor of apoptosis protein (XIAP), survivin, cIAP1, Bcl-2, and Bcl-xL, without affecting TRAIL receptors, DR4 and DR5.	Pyruvaldehyde	0-13	X-linked inhibitor of apoptosis	Homo sapiens	66-105
22784708-5	2012	Methylglyoxal suppressed the expression of antiapoptotic factors, X-linked inhibitor of apoptosis protein (XIAP), survivin, cIAP1, Bcl-2, and Bcl-xL, without affecting TRAIL receptors, DR4 and DR5.	Pyruvaldehyde	0-13	X-linked inhibitor of apoptosis	Homo sapiens	107-111
22784708-5	2012	Methylglyoxal suppressed the expression of antiapoptotic factors, X-linked inhibitor of apoptosis protein (XIAP), survivin, cIAP1, Bcl-2, and Bcl-xL, without affecting TRAIL receptors, DR4 and DR5.	Pyruvaldehyde	0-13	baculoviral IAP repeat containing 2	Homo sapiens	124-129
22784708-5	2012	Methylglyoxal suppressed the expression of antiapoptotic factors, X-linked inhibitor of apoptosis protein (XIAP), survivin, cIAP1, Bcl-2, and Bcl-xL, without affecting TRAIL receptors, DR4 and DR5.	Pyruvaldehyde	0-13	BCL2 apoptosis regulator	Homo sapiens	131-136
22784708-5	2012	Methylglyoxal suppressed the expression of antiapoptotic factors, X-linked inhibitor of apoptosis protein (XIAP), survivin, cIAP1, Bcl-2, and Bcl-xL, without affecting TRAIL receptors, DR4 and DR5.	Pyruvaldehyde	0-13	BCL2 like 1	Homo sapiens	142-148
22784708-5	2012	Methylglyoxal suppressed the expression of antiapoptotic factors, X-linked inhibitor of apoptosis protein (XIAP), survivin, cIAP1, Bcl-2, and Bcl-xL, without affecting TRAIL receptors, DR4 and DR5.	Pyruvaldehyde	0-13	major histocompatibility complex, class II, DR beta 4	Homo sapiens	185-188
22784708-5	2012	Methylglyoxal suppressed the expression of antiapoptotic factors, X-linked inhibitor of apoptosis protein (XIAP), survivin, cIAP1, Bcl-2, and Bcl-xL, without affecting TRAIL receptors, DR4 and DR5.	Pyruvaldehyde	0-13	TNF receptor superfamily member 10b	Homo sapiens	193-196
22917016-4	2012	The aim of this study was to evaluate resveratrol activation of nuclear factor erythroid 2-related factor 2 (Nrf2) to attenuate MG-induced insulin resistance in Hep G2 cells.	Pyruvaldehyde	128-130	NFE2 like bZIP transcription factor 2	Homo sapiens	109-113
22917016-4	2012	The aim of this study was to evaluate resveratrol activation of nuclear factor erythroid 2-related factor 2 (Nrf2) to attenuate MG-induced insulin resistance in Hep G2 cells.	Pyruvaldehyde	128-130	insulin	Homo sapiens	139-146
22917016-0	2012	Resveratrol upregulates Nrf2 expression to attenuate methylglyoxal-induced insulin resistance in Hep G2 cells.	Pyruvaldehyde	53-66	NFE2 like bZIP transcription factor 2	Homo sapiens	24-28
22917016-7	2012	Moreover, resveratrol significantly elevated glucose uptake and protected against MG-induced insulin resistance in Hep G2 cells.	Pyruvaldehyde	82-84	insulin	Homo sapiens	93-100
22917016-0	2012	Resveratrol upregulates Nrf2 expression to attenuate methylglyoxal-induced insulin resistance in Hep G2 cells.	Pyruvaldehyde	53-66	insulin	Homo sapiens	75-82
22917016-2	2012	Methylglyoxal (MG), a highly reactive dicarbonyl metabolite generated during glucose metabolism, has also been confirmed to cause pancreatic injury and induce inflammation, thereby resulting in insulin resistance.	Pyruvaldehyde	0-13	insulin	Homo sapiens	194-201
22917016-2	2012	Methylglyoxal (MG), a highly reactive dicarbonyl metabolite generated during glucose metabolism, has also been confirmed to cause pancreatic injury and induce inflammation, thereby resulting in insulin resistance.	Pyruvaldehyde	15-17	insulin	Homo sapiens	194-201
22516056-4	2012	In this study, we examined the effects of MG on Trx in human aortic endothelial cells (HAECs).	Pyruvaldehyde	42-44	thioredoxin	Homo sapiens	48-51
22917016-4	2012	The aim of this study was to evaluate resveratrol activation of nuclear factor erythroid 2-related factor 2 (Nrf2) to attenuate MG-induced insulin resistance in Hep G2 cells.	Pyruvaldehyde	128-130	NFE2 like bZIP transcription factor 2	Homo sapiens	64-107
22627382-7	2012	Oxidation and glycation levels were found to be enhanced in albumin purified from diabetic patients or glycated with glucose or methylglyoxal, after determination of their ketoamine, free thiol, amino group and carbonyl contents.	Pyruvaldehyde	128-141	albumin	Homo sapiens	60-67
22516056-6	2012	Flow cytometric analyses with annexin-V/propidium iodide double staining revealed that cells incubated with MG displayed features characteristic of apoptosis.	Pyruvaldehyde	108-110	annexin A5	Homo sapiens	30-39
22676051-6	2012	Moreover, the aba2-2 mutation impaired MG-induced RD29B and RAB18 gene expression.	Pyruvaldehyde	39-41	CAP160 protein	Arabidopsis thaliana	50-55
22681228-0	2012	The role of endothelial cell adhesion molecules P-selectin, E-selectin and intercellular adhesion molecule-1 in leucocyte recruitment induced by exogenous methylglyoxal.	Pyruvaldehyde	155-168	selectin, platelet	Mus musculus	48-58
22676051-6	2012	Moreover, the aba2-2 mutation impaired MG-induced RD29B and RAB18 gene expression.	Pyruvaldehyde	39-41	RAB GTPASE HOMOLOG B18	Arabidopsis thaliana	60-65
22580513-3	2012	The "gold standard" method for the determination of MG concentration in the millimolar range is an enzyme-catalyzed endpoint assay based on the glyoxalase I catalyzed formation of S-lactoylglutathione.	Pyruvaldehyde	52-54	glyoxalase I	Homo sapiens	144-156
22750288-7	2012	These data suggest a possible link between the cognitive dysfunction associated with diabetes mellitus and the neurotoxicity of MG, which may alter the expression levels of cleaved Caspase-3, Bcl-2 and Bax in the hippocampus.	Pyruvaldehyde	128-130	BCL2, apoptosis regulator	Rattus norvegicus	192-197
22750288-7	2012	These data suggest a possible link between the cognitive dysfunction associated with diabetes mellitus and the neurotoxicity of MG, which may alter the expression levels of cleaved Caspase-3, Bcl-2 and Bax in the hippocampus.	Pyruvaldehyde	128-130	BCL2 associated X, apoptosis regulator	Rattus norvegicus	202-205
22740698-0	2012	Methylglyoxal activates nociceptors through transient receptor potential channel A1 (TRPA1): a possible mechanism of metabolic neuropathies.	Pyruvaldehyde	0-13	transient receptor potential cation channel subfamily A member 1	Homo sapiens	44-83
22740698-0	2012	Methylglyoxal activates nociceptors through transient receptor potential channel A1 (TRPA1): a possible mechanism of metabolic neuropathies.	Pyruvaldehyde	0-13	transient receptor potential cation channel subfamily A member 1	Homo sapiens	85-90
22740698-4	2012	We demonstrate that extracellularly applied MG accesses specific intracellular binding sites of TRPA1, activating inward currents and calcium influx in transfected cells and sensory neurons, slowing conduction velocity in unmyelinated peripheral nerve fibers, and stimulating release of proinflammatory neuropeptides from and action potential firing in cutaneous nociceptors.	Pyruvaldehyde	44-46	transient receptor potential cation channel subfamily A member 1	Homo sapiens	96-101
22740698-5	2012	Using a model peptide of the N terminus of human TRPA1, we demonstrate the formation of disulfide bonds based on MG-induced modification of cysteines as a novel mechanism.	Pyruvaldehyde	113-115	transient receptor potential cation channel subfamily A member 1	Homo sapiens	49-54
22614840-7	2012	One protein was identified as glyoxalase             1 (GLO1), an enzyme involved in detoxification of methylglyoxal, a cytotoxic product             of glycolysis.	Pyruvaldehyde	103-116	glyoxalase I	Homo sapiens	56-60
22693349-9	2012	Moreover, p66(Shc) activation accounted for the persistent elevation of the advanced glycated end product precursor methylglyoxal.	Pyruvaldehyde	116-129	DNA polymerase delta 3, accessory subunit	Homo sapiens	10-13
22693349-9	2012	Moreover, p66(Shc) activation accounted for the persistent elevation of the advanced glycated end product precursor methylglyoxal.	Pyruvaldehyde	116-129	SHC adaptor protein 1	Homo sapiens	14-17
22696433-9	2012	The present study suggests that inhibition of APX is in part due to the modification of amino acids by MG.	Pyruvaldehyde	103-105	L-ascorbate peroxidase 2, cytosolic	Nicotiana tabacum	46-49
22366273-3	2012	The primary aim of the study was to evaluate the content of defensin1 in honeys of different botanical origins and to investigate a presumed effect of reactive MGO on defensin1 and a dominant protein of honey MRJP1 in manuka honey.	Pyruvaldehyde	160-163	defensin-1	Apis mellifera	167-176
22437147-0	2012	Methylglyoxal-induced stomatal closure accompanied by peroxidase-mediated ROS production in Arabidopsis.	Pyruvaldehyde	0-13	peroxidase	Arabidopsis thaliana	54-64
22437147-5	2012	The MG-induced stomatal closure and ROS production were completely inhibited by a peroxidase inhibitor, salicylhydroxamic acid (SHAM), but were not affected by an NAD(P)H oxidase mutation, atrbohD atrbohF.	Pyruvaldehyde	4-6	peroxidase	Arabidopsis thaliana	82-92
22366273-7	2012	We further showed that (i) the treatment of purified defensin1 in solution containing high amount of MGO caused a time-dependent loss of its antibacterial activity and (ii) increasing MGO concentrations in a non-manuka honey were connected with a gradual increase in the molecular weight of MRJP1.	Pyruvaldehyde	101-104	defensin-1	Apis mellifera	53-62
22366273-7	2012	We further showed that (i) the treatment of purified defensin1 in solution containing high amount of MGO caused a time-dependent loss of its antibacterial activity and (ii) increasing MGO concentrations in a non-manuka honey were connected with a gradual increase in the molecular weight of MRJP1.	Pyruvaldehyde	101-104	major royal jelly protein 1	Apis mellifera	291-296
22366273-7	2012	We further showed that (i) the treatment of purified defensin1 in solution containing high amount of MGO caused a time-dependent loss of its antibacterial activity and (ii) increasing MGO concentrations in a non-manuka honey were connected with a gradual increase in the molecular weight of MRJP1.	Pyruvaldehyde	184-187	defensin-1	Apis mellifera	53-62
22366273-7	2012	We further showed that (i) the treatment of purified defensin1 in solution containing high amount of MGO caused a time-dependent loss of its antibacterial activity and (ii) increasing MGO concentrations in a non-manuka honey were connected with a gradual increase in the molecular weight of MRJP1.	Pyruvaldehyde	184-187	major royal jelly protein 1	Apis mellifera	291-296
22366273-8	2012	Obtained results demonstrate that MGO abrogates the antibacterial activity of defensin1 and modifies MRJP1 in manuka honey.	Pyruvaldehyde	34-37	defensin-1	Apis mellifera	78-87
22366273-8	2012	Obtained results demonstrate that MGO abrogates the antibacterial activity of defensin1 and modifies MRJP1 in manuka honey.	Pyruvaldehyde	34-37	major royal jelly protein 1	Apis mellifera	101-106
22366273-9	2012	We assume that MGO could also have negative effects on the structure and function of other proteins/peptides in manuka honey, including glucose oxidase, generating hydrogen peroxide.	Pyruvaldehyde	15-18	glucose oxidase	Apis mellifera	136-151
22249316-8	2012	In addition, MGO-injected retinas demonstrated increases of both activity and expression of MMP-2 and MMP-9, and the degradation of occludin was found in the MGO-injected retinas.	Pyruvaldehyde	13-16	matrix metallopeptidase 2	Rattus norvegicus	92-97
22585572-0	2012	Glyoxalase 1 increases anxiety by reducing GABAA receptor agonist methylglyoxal.	Pyruvaldehyde	66-79	glyoxalase 1	Mus musculus	0-12
22585572-2	2012	Here, we demonstrate that GLO1 increases anxiety by reducing levels of methylglyoxal (MG), a GABAA receptor agonist.	Pyruvaldehyde	71-84	glyoxalase 1	Mus musculus	26-30
22585572-3	2012	Mice overexpressing Glo1 on a Tg bacterial artificial chromosome displayed increased anxiety-like behavior and reduced brain MG concentrations.	Pyruvaldehyde	125-127	glyoxalase 1	Mus musculus	20-24
22585572-6	2012	These data indicate that GLO1 increases anxiety by reducing levels of MG, thereby decreasing GABAA receptor activation.	Pyruvaldehyde	70-72	glyoxalase 1	Mus musculus	25-29
22581285-4	2012	In mice, treatment with methylglyoxal reduces nerve conduction velocity, facilitates neurosecretion of calcitonin gene-related peptide, increases cyclooxygenase-2 (COX-2) expression and evokes thermal and mechanical hyperalgesia.	Pyruvaldehyde	24-37	prostaglandin-endoperoxide synthase 2	Mus musculus	146-162
22581285-4	2012	In mice, treatment with methylglyoxal reduces nerve conduction velocity, facilitates neurosecretion of calcitonin gene-related peptide, increases cyclooxygenase-2 (COX-2) expression and evokes thermal and mechanical hyperalgesia.	Pyruvaldehyde	24-37	prostaglandin-endoperoxide synthase 2	Mus musculus	164-169
22249316-4	2012	Herein, we hypothesize that increased levels of MGO disrupt the tight junction protein known as occludin protein by matrix metalloproteinases (MMPs), leading to breakage of the BRB.	Pyruvaldehyde	48-51	occludin	Rattus norvegicus	96-104
22249316-8	2012	In addition, MGO-injected retinas demonstrated increases of both activity and expression of MMP-2 and MMP-9, and the degradation of occludin was found in the MGO-injected retinas.	Pyruvaldehyde	13-16	matrix metallopeptidase 9	Rattus norvegicus	102-107
22249316-8	2012	In addition, MGO-injected retinas demonstrated increases of both activity and expression of MMP-2 and MMP-9, and the degradation of occludin was found in the MGO-injected retinas.	Pyruvaldehyde	158-161	occludin	Rattus norvegicus	132-140
22249316-4	2012	Herein, we hypothesize that increased levels of MGO disrupt the tight junction protein known as occludin protein by matrix metalloproteinases (MMPs), leading to breakage of the BRB.	Pyruvaldehyde	48-51	matrix metallopeptidase 2	Rattus norvegicus	143-147
22249316-9	2012	CONCLUSIONS: The results suggest that the activation of MMPs by elevated levels of MGO in the retina may facilitate an increase in vascular permeability by a mechanism involving proteolytic degradation of occludin.	Pyruvaldehyde	83-86	matrix metallopeptidase 2	Rattus norvegicus	56-60
22249316-9	2012	CONCLUSIONS: The results suggest that the activation of MMPs by elevated levels of MGO in the retina may facilitate an increase in vascular permeability by a mechanism involving proteolytic degradation of occludin.	Pyruvaldehyde	83-86	occludin	Rattus norvegicus	205-213
22188542-3	2012	MG-mediated damage is countered by glutathione-dependent metabolism by Glo1 (glyoxalase 1).	Pyruvaldehyde	0-2	glyoxalase I	Homo sapiens	71-75
22755300-1	2012	OBJECTIVES: To determine the serum levels of methylglyoxal (MG) and carbonic anhydrase (CA) activity in known cases of type-II diabetes mellitus with insulin resistance and to compare them with age-sex matched healthy controls.	Pyruvaldehyde	45-58	insulin	Homo sapiens	150-157
22755300-1	2012	OBJECTIVES: To determine the serum levels of methylglyoxal (MG) and carbonic anhydrase (CA) activity in known cases of type-II diabetes mellitus with insulin resistance and to compare them with age-sex matched healthy controls.	Pyruvaldehyde	60-62	insulin	Homo sapiens	150-157
22755300-10	2012	CONCLUSION: Insulin resistance is accompanied by increased activity of carbonic anhydrase which is significantly related to increasing methylglyoxal levels.	Pyruvaldehyde	135-148	insulin	Homo sapiens	12-19
22472358-5	2012	Methylglyoxal has a toxic effect on insulin secretion from pancreatic beta-cells, and on modifications of proteins and nucleic acids.	Pyruvaldehyde	0-13	insulin	Homo sapiens	36-43
22188542-3	2012	MG-mediated damage is countered by glutathione-dependent metabolism by Glo1 (glyoxalase 1).	Pyruvaldehyde	0-2	glyoxalase I	Homo sapiens	77-89
22188542-4	2012	It is not known, however, whether Glo1 has stress-responsive up-regulation to counter periods of high MG concentration or dicarbonyl stress.	Pyruvaldehyde	102-104	glyoxalase I	Homo sapiens	34-38
22188542-8	2012	Increased expression of Glo1 decreased cellular and extracellular concentrations of MG, MG-derived protein adducts, mutagenesis and cell detachment.	Pyruvaldehyde	84-86	glyoxalase I	Homo sapiens	24-28
22143324-2	2012	Normally, MG is detoxified by the glyoxalase (GLO) enzyme system (including component enzymes GLO1 and GLO2).	Pyruvaldehyde	10-12	glyoxalase 1	Rattus norvegicus	94-98
22325990-6	2012	GSH also modulates the activity of glyoxalase 1 (Glo-1), the rate-limiting enzyme for the removal of reactive dicarbonyls such as methylglyoxal (MG).	Pyruvaldehyde	130-143	glyoxalase I	Homo sapiens	35-47
22325990-6	2012	GSH also modulates the activity of glyoxalase 1 (Glo-1), the rate-limiting enzyme for the removal of reactive dicarbonyls such as methylglyoxal (MG).	Pyruvaldehyde	130-143	glyoxalase I	Homo sapiens	49-54
22143324-2	2012	Normally, MG is detoxified by the glyoxalase (GLO) enzyme system (including component enzymes GLO1 and GLO2).	Pyruvaldehyde	10-12	hydroxyacyl glutathione hydrolase	Rattus norvegicus	103-107
22133672-5	2012	In vitro calcium imaging and patch clamp were used to assess whether endogenous TRPA1 agonists (4-hydroxynonenal and methylglyoxal) generated in DM induce sustained activation of the TRPA1 channel.	Pyruvaldehyde	117-130	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	80-85
22036650-6	2012	GLO-1-MCs had lower intracellular levels of MG accumulation, 8-hydroxy-deoxyguanosine (an oxidative DNA damage marker), 4-hydroxyl-2-nonenal (a lipid peroxidation product), and nitrosylated protein (a marker of oxidative-nitrosative stress) compared to control cells.	Pyruvaldehyde	44-46	glyoxalase 1	Mus musculus	0-5
22036650-9	2012	These results suggest that GLO-1 plays a role in high glucose-mediated signaling by reducing MG accumulation and oxidative stress in diabetes mellitus.	Pyruvaldehyde	93-95	glyoxalase 1	Mus musculus	27-32
22101032-9	2012	In the submesothelial compact zone of the MGO+saline-treated mice, CD31-positive vessels and vascular endothelial growth factor-positive cells were significantly increased, as were inflammation, F4/80-positive macrophages, and monocyte chemotactic protein-1.	Pyruvaldehyde	42-45	platelet/endothelial cell adhesion molecule 1	Mus musculus	67-71
22101032-9	2012	In the submesothelial compact zone of the MGO+saline-treated mice, CD31-positive vessels and vascular endothelial growth factor-positive cells were significantly increased, as were inflammation, F4/80-positive macrophages, and monocyte chemotactic protein-1.	Pyruvaldehyde	42-45	chemokine (C-C motif) ligand 2	Mus musculus	227-257
22101032-10	2012	Moreover, 8-hydroxydeoxyguanosine, a marker of reactive oxygen species, and NF-kappaB, determined by Southwestern histochemistry, in the submesothelial compact zone were also increased in MGO+saline-treated mice.	Pyruvaldehyde	188-191	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	76-85
22094464-4	2012	Here, we show that methylglyoxal inhibits the activity of mammalian glucose transporters using recombinant Saccharomyces cerevisiae cells genetically lacking all hexose transporters but carrying cDNA for human GLUT1 or rat GLUT4.	Pyruvaldehyde	19-32	solute carrier family 2 member 1	Homo sapiens	210-215
22094464-4	2012	Here, we show that methylglyoxal inhibits the activity of mammalian glucose transporters using recombinant Saccharomyces cerevisiae cells genetically lacking all hexose transporters but carrying cDNA for human GLUT1 or rat GLUT4.	Pyruvaldehyde	19-32	solute carrier family 2 member 4	Rattus norvegicus	223-228
21668821-0	2012	High levels of IgM against methylglyoxal-modified apolipoprotein B100 are associated with less coronary artery calcification in patients with type 2 diabetes.	Pyruvaldehyde	27-40	apolipoprotein B	Homo sapiens	50-69
21668821-3	2012	The aim of this study was to determine whether antibodies against apolipoprotein B100 modified by methylglyoxal (MGO-apoB100) are associated with coronary atherosclerosis in patients with type 2 diabetes.	Pyruvaldehyde	98-111	apolipoprotein B	Homo sapiens	66-85
21668821-3	2012	The aim of this study was to determine whether antibodies against apolipoprotein B100 modified by methylglyoxal (MGO-apoB100) are associated with coronary atherosclerosis in patients with type 2 diabetes.	Pyruvaldehyde	98-111	apolipoprotein B	Homo sapiens	117-124
22971844-10	2012	The present results demonstrate that MGO accumulation in mesenteric artery may mediate development of hypertension in SHR at least in part via increased ROS-mediated impairment of endothelium-dependent relaxation and AT2R-mediated increased Ang II contraction.	Pyruvaldehyde	37-40	angiotensin II receptor, type 2	Rattus norvegicus	217-221
23047102-4	2012	Other terpene hydroperoxides, as well as T4-H, showed significant cleaving activities, and all these hydroperoxides protected RNase A from the lowering of enzyme activity induced by MGO.	Pyruvaldehyde	182-185	ribonuclease A family member 1, pancreatic	Homo sapiens	126-133
22406446-9	2012	However, the metabolite methylglyoxal modified Arg5 in the Abeta sequence.	Pyruvaldehyde	24-37	amyloid beta precursor protein	Homo sapiens	59-64
22863862-0	2012	Methylglyoxal activates the human transient receptor potential ankyrin 1 channel.	Pyruvaldehyde	0-13	transient receptor potential cation channel subfamily A member 1	Homo sapiens	34-72
22863862-3	2012	In the present study, we investigated the effect of MG on transient receptor potential ankyrin 1 (TRPA1) activation in human TRPA1-expressing HEK293 cells.	Pyruvaldehyde	52-54	transient receptor potential cation channel subfamily A member 1	Homo sapiens	58-96
22863862-3	2012	In the present study, we investigated the effect of MG on transient receptor potential ankyrin 1 (TRPA1) activation in human TRPA1-expressing HEK293 cells.	Pyruvaldehyde	52-54	transient receptor potential cation channel subfamily A member 1	Homo sapiens	98-103
22863862-6	2012	Interestingly, the time course in the intracellular Ca(2+) concentration ([Ca(2+)](i)) in human TRPA1-expressing HEK293 showed considerable differences in response to MG and cinnamaldehyde.	Pyruvaldehyde	167-169	transient receptor potential cation channel subfamily A member 1	Homo sapiens	96-101
22863862-8	2012	These results may provide insight into the TRPA1-mediated effects of MG on diabetic neuropathy.	Pyruvaldehyde	69-71	transient receptor potential cation channel subfamily A member 1	Homo sapiens	43-48
21884795-10	2012	MGO significantly increased expression of a homolog of gp91(phox), NOX1 but not gp91(phox) as determined by Western blotting.	Pyruvaldehyde	0-3	NADPH oxidase 1	Rattus norvegicus	67-71
21884795-11	2012	An NF-kappaB inhibitor, pyrrolidine dithiocarbamate prevented the MGO-induced NOX1 expression.	Pyruvaldehyde	66-69	NADPH oxidase 1	Rattus norvegicus	78-82
21884795-13	2012	Present results indicate that long-term MGO treatment has an inhibitory effect on contractility of isolated blood vessel, which is likely mediated via increased NOX1-derived superoxide production and subsequent apoptosis.	Pyruvaldehyde	40-43	NADPH oxidase 1	Rattus norvegicus	161-165
22133672-5	2012	In vitro calcium imaging and patch clamp were used to assess whether endogenous TRPA1 agonists (4-hydroxynonenal and methylglyoxal) generated in DM induce sustained activation of the TRPA1 channel.	Pyruvaldehyde	117-130	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	183-188
22133672-8	2012	Moreover, in vitro calcium imaging and patch clamp results indicated that reactive compounds generated in DM (4-hydroxynonenal and methylglyoxal) produced sustained activations of the TRPA1 channel, a prerequisite for adverse long-term effects.	Pyruvaldehyde	131-144	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	184-189
22911800-2	2012	High glucose (25 mM) incubation up-regulated mRNA levels of aldose reductase (an enzyme converting glucose to fructose) and aldolase B (a key enzyme that catalyzes MG formation from fructose) and enhanced MG formation in human umbilical vein endothelial cells (HUVECs) and HUVEC-derived EA.	Pyruvaldehyde	164-166	aldo-keto reductase family 1 member B	Homo sapiens	60-76
23226259-8	2012	Axl and Gas6 protein were also increased in cells cultured in high glucose (30 mM) or methylglyoxal (200 microM).	Pyruvaldehyde	86-99	AXL receptor tyrosine kinase	Mus musculus	0-3
23226259-8	2012	Axl and Gas6 protein were also increased in cells cultured in high glucose (30 mM) or methylglyoxal (200 microM).	Pyruvaldehyde	86-99	growth arrest specific 6	Mus musculus	8-12
22911800-6	2012	In addition, inhibition of cytochrome P450 2E1 or semicarbazide-sensitive amine oxidase which produces MG during the metabolism of lipid and proteins, respectively, did not alter MG production.	Pyruvaldehyde	103-105	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	27-46
22911800-7	2012	Both high glucose (25 mM) and MG (30, 100 microM) increased the formation of N(epsilon)-carboxyethyl-lysine (CEL, a MG-induced AGE), oxidative stress (determined by the generation of oxidized DCF, H(2)O(2), protein carbonyls and 8-oxo-dG), O-GlcNAc modification (product of the hexosamine pathway), membrane protein kinase C activity and nuclear translocation of NF-kappaB in EA.	Pyruvaldehyde	30-32	nuclear factor kappa B subunit 1	Homo sapiens	363-372
22606274-8	2012	The effects of MG were efficiently reversed by advanced glycation end product (AGE) breaker alagebrium and Akt inhibitor SH-6.	Pyruvaldehyde	15-17	thymoma viral proto-oncogene 1	Mus musculus	107-110
23056421-5	2012	Incubation with MGO reduced VEGFR2 protein, but not mRNA, levels in a time and dose dependent manner.	Pyruvaldehyde	16-19	kinase insert domain protein receptor	Mus musculus	28-34
23056421-7	2012	Overexpression of Glyoxalase 1, the enzyme that detoxifies MGO, reduced the MGO-protein adducts and prevented VEGFR2 reduction.	Pyruvaldehyde	59-62	glyoxalase 1	Mus musculus	18-30
23056421-7	2012	Overexpression of Glyoxalase 1, the enzyme that detoxifies MGO, reduced the MGO-protein adducts and prevented VEGFR2 reduction.	Pyruvaldehyde	59-62	kinase insert domain protein receptor	Mus musculus	110-116
23056421-7	2012	Overexpression of Glyoxalase 1, the enzyme that detoxifies MGO, reduced the MGO-protein adducts and prevented VEGFR2 reduction.	Pyruvaldehyde	76-79	glyoxalase 1	Mus musculus	18-30
23056421-11	2012	MGO increased endothelial LC3B and Beclin-1, markers of autophagy, which were accompanied by an increase of both autophagic flux (LC3 punctae) and co-immunoprecipitation of VEGFR2 with LC3.	Pyruvaldehyde	0-3	microtubule-associated protein 1 light chain 3 beta	Mus musculus	26-30
23056421-11	2012	MGO increased endothelial LC3B and Beclin-1, markers of autophagy, which were accompanied by an increase of both autophagic flux (LC3 punctae) and co-immunoprecipitation of VEGFR2 with LC3.	Pyruvaldehyde	0-3	beclin 1, autophagy related	Mus musculus	35-43
23056421-11	2012	MGO increased endothelial LC3B and Beclin-1, markers of autophagy, which were accompanied by an increase of both autophagic flux (LC3 punctae) and co-immunoprecipitation of VEGFR2 with LC3.	Pyruvaldehyde	0-3	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	26-29
23056421-11	2012	MGO increased endothelial LC3B and Beclin-1, markers of autophagy, which were accompanied by an increase of both autophagic flux (LC3 punctae) and co-immunoprecipitation of VEGFR2 with LC3.	Pyruvaldehyde	0-3	kinase insert domain protein receptor	Mus musculus	173-179
23056421-11	2012	MGO increased endothelial LC3B and Beclin-1, markers of autophagy, which were accompanied by an increase of both autophagic flux (LC3 punctae) and co-immunoprecipitation of VEGFR2 with LC3.	Pyruvaldehyde	0-3	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	130-133
23056421-15	2012	Taken together, MGO reduces endothelial angiogenesis through RAGE-mediated, ONOO(-)dependent and autophagy-induced VEGFR2 degradation, which may represent a new mechanism for diabetic angiogenesis impairment.	Pyruvaldehyde	16-19	advanced glycosylation end product-specific receptor	Mus musculus	61-65
23056421-15	2012	Taken together, MGO reduces endothelial angiogenesis through RAGE-mediated, ONOO(-)dependent and autophagy-induced VEGFR2 degradation, which may represent a new mechanism for diabetic angiogenesis impairment.	Pyruvaldehyde	16-19	kinase insert domain protein receptor	Mus musculus	115-121
22701540-9	2012	Activation of TRPA1 by allyl isothiocyanate (AITC), hydrogen peroxide (H2O2), 4-hydroxynonenal (4-HNE), and cyclopentenone prostaglandins (PGJ2) and a novel agonist methylglyoxal (MG) induces membrane current, depolarization, and Ca2+ influx leading to generation of action potentials in a pancreatic beta cell line and primary cultured pancreatic beta cells.	Pyruvaldehyde	165-178	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	14-19
22701540-9	2012	Activation of TRPA1 by allyl isothiocyanate (AITC), hydrogen peroxide (H2O2), 4-hydroxynonenal (4-HNE), and cyclopentenone prostaglandins (PGJ2) and a novel agonist methylglyoxal (MG) induces membrane current, depolarization, and Ca2+ influx leading to generation of action potentials in a pancreatic beta cell line and primary cultured pancreatic beta cells.	Pyruvaldehyde	180-182	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	14-19
22606274-9	2012	In summary, our study revealed a previously unrecognized effect of MG in stimulating adipogenesis by up-regulation of Akt signaling pathway and this mechanism might offer a new approach to explain the development of obesity.	Pyruvaldehyde	67-69	thymoma viral proto-oncogene 1	Mus musculus	118-121
23204821-4	2011	Insulin resistance is a common feature of hypertension in both humans and animal models affecting glucose and lipid metabolism producing excess aldehydes including methylglyoxal.	Pyruvaldehyde	164-177	insulin	Homo sapiens	0-7
21890532-9	2011	The excess formation of MG in under these conditions was eliminated by knock-down of aldolase B, but not by knock-down of aldolase A or inhibition of SSAO or CYP 2E1.	Pyruvaldehyde	24-26	aldolase, fructose-bisphosphate B	Rattus norvegicus	85-95
23091854-9	2012	There was a positive correlation between CRP and MG levels (r = 0.45; p = 0.01).	Pyruvaldehyde	49-51	C-reactive protein	Homo sapiens	41-44
21165710-3	2011	We investigated the effect of 13 micronutrients on MGO-mediated in vitro glycation of bovine serum albumin (BSA), as formation of AGEs and protein carbonyls.	Pyruvaldehyde	51-54	albumin	Homo sapiens	93-106
21844128-8	2011	By western blotting and mass spectrometry fibrin(ogen), the cytoskeleton-associated protein moesin and the nuclear proteins lamin A and C were identified as putative main targets for MGO-derived modification.	Pyruvaldehyde	183-186	moesin	Homo sapiens	92-98
21820503-6	2011	In addition, the hepatic activity of the AGE precursor detoxifying enzyme glyoxalase-I was significantly decreased in 8 wk old UCP2-/- animals and concomitantly caused 2-fold higher levels of methylglyoxal-modified AGE in these animals.	Pyruvaldehyde	192-205	glyoxalase 1	Mus musculus	74-86
21738003-1	2011	BACKGROUND: Glyoxalase I (GLO1), which is the major enzyme that catalyzes the metabolism of methylglyoxal (MG), may play an important role in the pathogenesis of diabetic microvascular complications.	Pyruvaldehyde	92-105	glyoxalase I	Homo sapiens	12-24
21738003-1	2011	BACKGROUND: Glyoxalase I (GLO1), which is the major enzyme that catalyzes the metabolism of methylglyoxal (MG), may play an important role in the pathogenesis of diabetic microvascular complications.	Pyruvaldehyde	92-105	glyoxalase I	Homo sapiens	26-30
21738003-1	2011	BACKGROUND: Glyoxalase I (GLO1), which is the major enzyme that catalyzes the metabolism of methylglyoxal (MG), may play an important role in the pathogenesis of diabetic microvascular complications.	Pyruvaldehyde	107-109	glyoxalase I	Homo sapiens	12-24
21738003-1	2011	BACKGROUND: Glyoxalase I (GLO1), which is the major enzyme that catalyzes the metabolism of methylglyoxal (MG), may play an important role in the pathogenesis of diabetic microvascular complications.	Pyruvaldehyde	107-109	glyoxalase I	Homo sapiens	26-30
21861178-6	2011	RESULTS: Non-cytotoxic MGO concentrations inhibited insulin-induced IRS tyrosine phosphorylation and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB) pathway activation independently from reactive oxygen species (ROS) production.	Pyruvaldehyde	23-26	phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit gamma	Rattus norvegicus	101-130
21861178-9	2011	Further, the insulin- and glucose-induced expression of Ins1, Gck and Pdx1 mRNA was abolished by MGO.	Pyruvaldehyde	97-100	insulin 1	Rattus norvegicus	56-60
21861178-9	2011	Further, the insulin- and glucose-induced expression of Ins1, Gck and Pdx1 mRNA was abolished by MGO.	Pyruvaldehyde	97-100	glucokinase	Rattus norvegicus	62-65
21861178-9	2011	Further, the insulin- and glucose-induced expression of Ins1, Gck and Pdx1 mRNA was abolished by MGO.	Pyruvaldehyde	97-100	pancreatic and duodenal homeobox 1	Rattus norvegicus	70-74
21819598-4	2011	In the present work, methylglyoxal was investigated for their effects on the structure, stability and fibril formation of insulin.	Pyruvaldehyde	21-34	insulin	Homo sapiens	122-129
21651995-2	2011	It is suggested here that excessive or continuous glycolysis increases TPI deamidation and thereby lowers TPI activity and causes accumulation of its substrate, DHAP, which in turn decomposes into methylglyoxal (MG), a well-recognised reactive bicarbonyl whose actions in cells and tissues, as well as at the whole organism level, mimic much age-relate dysfunction.	Pyruvaldehyde	212-214	triosephosphate isomerase 1	Homo sapiens	71-74
21652700-9	2011	Besides HG, exposure of cells to oxidants H(2)O(2) and methylglyoxal up-regulated MIOX expression and its phosphorylation and activity, whereas antioxidants N-acetylcysteine, beta-naphthoflavone, and tertiary butyl hydroquinone reduced MIOX expression.	Pyruvaldehyde	55-68	inositol oxygenase	Sus scrofa	82-86
21652700-9	2011	Besides HG, exposure of cells to oxidants H(2)O(2) and methylglyoxal up-regulated MIOX expression and its phosphorylation and activity, whereas antioxidants N-acetylcysteine, beta-naphthoflavone, and tertiary butyl hydroquinone reduced MIOX expression.	Pyruvaldehyde	55-68	inositol oxygenase	Sus scrofa	236-240
21819598-5	2011	RESULTS: Methylglyoxal was found to induce the formation of insulin native-like aggregates and reduce protein fibrillation by blocking the formation of the seeding nuclei.	Pyruvaldehyde	9-22	insulin	Homo sapiens	60-67
21669529-1	2011	The human glyoxalase I (hGLO I), which is a rate-limiting enzyme in the pathway for detoxification of apoptosis-inducible methylglyoxal (MG), has been expected as an attractive target for the development of new anti-cancer drugs.	Pyruvaldehyde	122-135	glyoxalase I	Homo sapiens	10-22
21491613-9	2011	Direct HPLC measurements of the glyoxalase I substrate, methylglyoxal (MG), show an increase in MG in these cells.	Pyruvaldehyde	56-69	glyoxalase I	Homo sapiens	32-44
21491613-12	2011	We suggest that accumulation of MG results in the formation of AGEs, which induce expression of the RAGE that during crucial neuronal development may be a factor in the pathology of autism.	Pyruvaldehyde	32-34	long intergenic non-protein coding RNA 914	Homo sapiens	100-104
21334317-6	2011	This could be attributed to the rapid hepatocyte metabolism of MGO with glyoxalase I, the predominant detoxification enzyme for MGO.	Pyruvaldehyde	63-66	glyoxalase I	Homo sapiens	72-84
21497196-0	2011	Heat-shock protein 27 (Hsp27) as a target of methylglyoxal in gastrointestinal cancer.	Pyruvaldehyde	45-58	heat shock protein family B (small) member 1	Homo sapiens	0-21
21497196-0	2011	Heat-shock protein 27 (Hsp27) as a target of methylglyoxal in gastrointestinal cancer.	Pyruvaldehyde	45-58	heat shock protein family B (small) member 1	Homo sapiens	23-28
21497196-6	2011	However, methylglyoxal-modified heat-shock protein 25/heat-shock protein 27 was not detected in non cancerous cell lines or in normal subject.	Pyruvaldehyde	9-22	heat shock protein family B (small) member 1	Homo sapiens	54-75
21593200-7	2011	RESULTS: Renal Klotho mRNA and protein were significantly decreased in db/db mice, and a similar decline was observed in the primary cultures of mouse tubule epithelial cells treated with methylglyoxal-modified albumin.	Pyruvaldehyde	188-201	klotho	Mus musculus	15-21
21497196-8	2011	The transfer of methylglyoxal-modified heat-shock protein 27 into rat intestinal epithelial cell line RIE was even more effective in preventing apoptotic cell death than that of native control heat-shock protein 27.	Pyruvaldehyde	16-29	heat shock protein family B (small) member 1	Homo sapiens	39-60
21497196-8	2011	The transfer of methylglyoxal-modified heat-shock protein 27 into rat intestinal epithelial cell line RIE was even more effective in preventing apoptotic cell death than that of native control heat-shock protein 27.	Pyruvaldehyde	16-29	heat shock protein family B (small) member 1	Homo sapiens	193-214
21334317-6	2011	This could be attributed to the rapid hepatocyte metabolism of MGO with glyoxalase I, the predominant detoxification enzyme for MGO.	Pyruvaldehyde	128-131	glyoxalase I	Homo sapiens	72-84
20711648-5	2011	GLO1 induction is a known protective cellular response to glucose stress, representing efforts to decrease toxic levels of methylglyoxal (MG), glyoxal and advanced glycation endproducts (AGEs).	Pyruvaldehyde	123-136	glyoxalase 1	Mus musculus	0-4
21310260-7	2011	The physiological significance of GLO1 expression in response to osmotic stress is to combat the increase in the levels of methylglyoxal in cells during the production of glycerol as a compatible osmolyte.	Pyruvaldehyde	123-136	lactoylglutathione lyase GLO1	Saccharomyces cerevisiae S288C	34-38
21310260-9	2011	Yap1 is crucial for oxidative stress response, although methylglyoxal per se does not enhance the intracellular oxidation level in yeast, but it directly modifies cysteine residues of Yap1 that are critical for the nucleocytoplasmic localization of this b-ZIP transcription factor.	Pyruvaldehyde	56-69	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	184-188
21310260-10	2011	Consequently, glyoxalase I can be defined as a negative regulator of Yap1 through modulating the intracellular methylglyoxal level.	Pyruvaldehyde	111-124	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	69-73
21321187-0	2011	Modification of Akt1 by methylglyoxal promotes the proliferation of vascular smooth muscle cells.	Pyruvaldehyde	24-37	AKT serine/threonine kinase 1	Homo sapiens	16-20
21321187-6	2011	Akt1 phosphorylation and activity were also increased by MG treatment (&lt;50 muM) in cultured vascular smooth muscle cells (VSMCs).	Pyruvaldehyde	57-59	AKT serine/threonine kinase 1	Homo sapiens	0-4
21321187-8	2011	These effects of MG were significantly inhibited by silencing Akt1 or by an Akt inhibitor.	Pyruvaldehyde	17-19	AKT serine/threonine kinase 1	Homo sapiens	62-66
21321187-8	2011	These effects of MG were significantly inhibited by silencing Akt1 or by an Akt inhibitor.	Pyruvaldehyde	17-19	AKT serine/threonine kinase 1	Homo sapiens	62-65
21321187-9	2011	Overexpression of Akt1 Cys(77)Ser mutant in HEK-293 cells increased cell proliferation and DNA synthesis, concurrent with an increase in Akt1 activity, which could not be further augmented by MG treatment.	Pyruvaldehyde	192-194	AKT serine/threonine kinase 1	Homo sapiens	18-22
21321187-10	2011	It is concluded that MG-induced VSMC proliferation is mediated by the activation of Akt1 via the modification of Akt1 at Cys(77).	Pyruvaldehyde	21-23	AKT serine/threonine kinase 1	Homo sapiens	84-88
21321187-10	2011	It is concluded that MG-induced VSMC proliferation is mediated by the activation of Akt1 via the modification of Akt1 at Cys(77).	Pyruvaldehyde	21-23	AKT serine/threonine kinase 1	Homo sapiens	113-117
21300842-9	2011	Preincubating with the RCS, methylglyoxal (MGO) likewise reduced SERCA2a activity.	Pyruvaldehyde	28-41	ATPase, Ca++ transporting, cardiac muscle, slow twitch 2	Mus musculus	65-72
21300842-9	2011	Preincubating with the RCS, methylglyoxal (MGO) likewise reduced SERCA2a activity.	Pyruvaldehyde	43-46	ATPase, Ca++ transporting, cardiac muscle, slow twitch 2	Mus musculus	65-72
21056979-7	2011	In diabetic GLO-I rats, glyoxal and MGO composite scores were significantly decreased by 81%, and plasma AGEs and oxidative stress markers scores were significantly decreased by ~50%.	Pyruvaldehyde	36-39	glyoxalase 1	Rattus norvegicus	12-17
22216325-15	2011	In conclusion, overproduction of MG in CSE(-/-) mice is due to a H(2)S-mediated down-regulation of the PGC-1alpha-FBPase pathway, further suggesting the important role of H(2)S in the regulation of glucose metabolism and MG generation.	Pyruvaldehyde	33-35	PPARG coactivator 1 alpha	Homo sapiens	103-113
21124777-6	2010	Moreover, we identified CHIP (Carboxy terminus of Hsp70-Interacting Protein) as the E3 ligase that ubiquitinated HIF-1alpha in the presence of MGO.	Pyruvaldehyde	143-146	hypoxia inducible factor 1 subunit alpha	Homo sapiens	113-123
20825408-11	2010	CONCLUSIONS AND IMPLICATIONS: Our results show for the first time that MG reduced serine-1177 phosphorylation, activity of eNOS and NO production.	Pyruvaldehyde	71-73	nitric oxide synthase 3	Rattus norvegicus	123-127
21124777-0	2010	The chaperone-dependent ubiquitin ligase CHIP targets HIF-1alpha for degradation in the presence of methylglyoxal.	Pyruvaldehyde	100-113	hypoxia inducible factor 1 subunit alpha	Homo sapiens	54-64
21738623-2	2011	We have identified a rare flavone, fisetin, which increases the level and activity of glyoxalase 1, the enzyme required for the removal of MG, as well as the synthesis of its essential co-factor, glutathione.	Pyruvaldehyde	139-141	glyoxalase 1	Mus musculus	86-98
20852029-4	2010	We hypothesized that, in retina, angiotensin II (Ang II) downregulates GLO-I, which leads to an increase in methylglyoxal-AGE formation.	Pyruvaldehyde	108-121	angiotensinogen	Rattus norvegicus	33-47
20852029-4	2010	We hypothesized that, in retina, angiotensin II (Ang II) downregulates GLO-I, which leads to an increase in methylglyoxal-AGE formation.	Pyruvaldehyde	108-121	angiotensinogen	Rattus norvegicus	49-55
20852029-4	2010	We hypothesized that, in retina, angiotensin II (Ang II) downregulates GLO-I, which leads to an increase in methylglyoxal-AGE formation.	Pyruvaldehyde	108-121	glyoxalase 1	Rattus norvegicus	71-76
21124777-4	2010	In this work, we identified a new molecular mechanism whereby methylglyoxal (MGO), which accumulates in high-glucose conditions, led to a rapid proteasome-dependent degradation of HIF-1alpha under hypoxia.	Pyruvaldehyde	62-75	hypoxia inducible factor 1 subunit alpha	Homo sapiens	180-190
21124777-7	2010	Consistently, silencing of endogenous CHIP and overexpression of glyoxalase I both stabilized HIF-1alpha under hypoxia in the presence of MGO.	Pyruvaldehyde	138-141	glyoxalase I	Homo sapiens	65-77
21124777-4	2010	In this work, we identified a new molecular mechanism whereby methylglyoxal (MGO), which accumulates in high-glucose conditions, led to a rapid proteasome-dependent degradation of HIF-1alpha under hypoxia.	Pyruvaldehyde	77-80	hypoxia inducible factor 1 subunit alpha	Homo sapiens	180-190
21124777-5	2010	Significantly, MGO-induced degradation of HIF-1alpha did not require the recruitment of the ubiquitin ligase pVHL nor did it require hydroxylation of the proline residues P402/P564 of HIF-1alpha.	Pyruvaldehyde	15-18	hypoxia inducible factor 1 subunit alpha	Homo sapiens	42-52
21124777-9	2010	Moreover, MGO-induced destabilization of HIF-1alpha led to a dramatic decrease in HIF-1 transcriptional activity.	Pyruvaldehyde	10-13	hypoxia inducible factor 1 subunit alpha	Homo sapiens	41-51
21124777-5	2010	Significantly, MGO-induced degradation of HIF-1alpha did not require the recruitment of the ubiquitin ligase pVHL nor did it require hydroxylation of the proline residues P402/P564 of HIF-1alpha.	Pyruvaldehyde	15-18	hypoxia inducible factor 1 subunit alpha	Homo sapiens	184-194
21124777-9	2010	Moreover, MGO-induced destabilization of HIF-1alpha led to a dramatic decrease in HIF-1 transcriptional activity.	Pyruvaldehyde	10-13	hypoxia inducible factor 1 subunit alpha	Homo sapiens	41-46
21124777-10	2010	Altogether, data is consistent with a new pathway for degradation of HIF-1alpha in response to intracellular accumulation of MGO.	Pyruvaldehyde	125-128	hypoxia inducible factor 1 subunit alpha	Homo sapiens	69-79
21124777-6	2010	Moreover, we identified CHIP (Carboxy terminus of Hsp70-Interacting Protein) as the E3 ligase that ubiquitinated HIF-1alpha in the presence of MGO.	Pyruvaldehyde	143-146	STIP1 homology and U-box containing protein 1	Homo sapiens	30-75
20621070-7	2010	We demonstrated apoptosis, nuclear factor-kappaB (NF-kappaB) activation and inducible nitric oxide synthase (iNOS) induction in cultured pericytes treated with MGO and MGO-injected retinal vessels.	Pyruvaldehyde	160-163	nitric oxide synthase 2	Rattus norvegicus	109-113
20647007-0	2010	Influence of the microenvironment of thiol groups in low molecular mass thiols and serum albumin on the reaction with methylglyoxal.	Pyruvaldehyde	118-131	albumin	Homo sapiens	83-96
20609361-7	2010	In addition, tenuigenin inhibited activation of caspase-3 and reversed down-regulation of the ratio of Bcl-2/Bax, both of which were induced by methylglyoxal stimulation.	Pyruvaldehyde	144-157	BCL2 apoptosis regulator	Homo sapiens	103-108
20609361-7	2010	In addition, tenuigenin inhibited activation of caspase-3 and reversed down-regulation of the ratio of Bcl-2/Bax, both of which were induced by methylglyoxal stimulation.	Pyruvaldehyde	144-157	BCL2 associated X, apoptosis regulator	Homo sapiens	109-112
20609361-8	2010	The results suggest that tenuigenin displays antiapoptotic and antioxidative activity in hippocampal neurons due to scavenging of intracellular reactive oxygen species, regulating Bcl-2 family and suppressing caspase-3 activity induced by methylglyoxal, which might explain at least in part the beneficial effects of tenuigenin against degenerative disorders involving diabetic cognitive impairment.	Pyruvaldehyde	239-252	caspase 3	Homo sapiens	209-218
20621070-0	2010	Cytotoxic role of methylglyoxal in rat retinal pericytes: Involvement of a nuclear factor-kappaB and inducible nitric oxide synthase pathway.	Pyruvaldehyde	18-31	nitric oxide synthase 2	Rattus norvegicus	101-132
20621070-7	2010	We demonstrated apoptosis, nuclear factor-kappaB (NF-kappaB) activation and inducible nitric oxide synthase (iNOS) induction in cultured pericytes treated with MGO and MGO-injected retinal vessels.	Pyruvaldehyde	160-163	nitric oxide synthase 2	Rattus norvegicus	76-107
20621070-7	2010	We demonstrated apoptosis, nuclear factor-kappaB (NF-kappaB) activation and inducible nitric oxide synthase (iNOS) induction in cultured pericytes treated with MGO and MGO-injected retinal vessels.	Pyruvaldehyde	168-171	nitric oxide synthase 2	Rattus norvegicus	76-107
20621070-7	2010	We demonstrated apoptosis, nuclear factor-kappaB (NF-kappaB) activation and inducible nitric oxide synthase (iNOS) induction in cultured pericytes treated with MGO and MGO-injected retinal vessels.	Pyruvaldehyde	168-171	nitric oxide synthase 2	Rattus norvegicus	109-113
20621070-8	2010	In MGO-treated pericytes, TUNEL-positive nuclei were markedly increased, and NF-kappaB was translocalized into the nuclei of pericytes, which paralleled the expression of iNOS.	Pyruvaldehyde	3-6	nitric oxide synthase 2	Rattus norvegicus	171-175
20621070-9	2010	The treatment of pyrrolidine dithiocarbamate (an NF-kappaB inhibitor) or l-N6-(1-iminoethyl)-lysine (an iNOS inhibitor) prevented apoptosis of MGO-treated pericytes.	Pyruvaldehyde	143-146	nitric oxide synthase 2	Rattus norvegicus	104-108
20621070-10	2010	In addition, in intravitreally MGO-injected rat eyes, TUNEL and caspase-3-positive pericytes were significantly increased, and activated NF-kappaB and iNOS were highly expressed.	Pyruvaldehyde	31-34	caspase 3	Rattus norvegicus	64-73
20621070-10	2010	In addition, in intravitreally MGO-injected rat eyes, TUNEL and caspase-3-positive pericytes were significantly increased, and activated NF-kappaB and iNOS were highly expressed.	Pyruvaldehyde	31-34	nitric oxide synthase 2	Rattus norvegicus	151-155
20621070-11	2010	These results suggest that the increased expression of NF-kappaB and iNOS caused by MGO is involved in rat retinal pericyte apoptosis.	Pyruvaldehyde	84-87	nitric oxide synthase 2	Rattus norvegicus	69-73
20885985-7	2010	Data further shows that MGO decreases the levels of the molecular chaperones Hsc70 and Hsp90 and leads to accumulation of CHIP-, Hsp40- and ubiquitin-containing aggregates.	Pyruvaldehyde	24-27	heat shock protein family A (Hsp70) member 8	Homo sapiens	77-82
20801663-1	2010	Glyoxalase I (GLO I) is the rate-limiting enzyme for detoxification of methylglyoxal (MG), a side-product of glycolysis, which is able to induce apoptosis.	Pyruvaldehyde	71-84	glyoxalase I	Homo sapiens	0-12
20801663-1	2010	Glyoxalase I (GLO I) is the rate-limiting enzyme for detoxification of methylglyoxal (MG), a side-product of glycolysis, which is able to induce apoptosis.	Pyruvaldehyde	71-84	glyoxalase I	Homo sapiens	14-19
20801663-1	2010	Glyoxalase I (GLO I) is the rate-limiting enzyme for detoxification of methylglyoxal (MG), a side-product of glycolysis, which is able to induce apoptosis.	Pyruvaldehyde	86-88	glyoxalase I	Homo sapiens	0-12
20801663-1	2010	Glyoxalase I (GLO I) is the rate-limiting enzyme for detoxification of methylglyoxal (MG), a side-product of glycolysis, which is able to induce apoptosis.	Pyruvaldehyde	86-88	glyoxalase I	Homo sapiens	14-19
20397192-3	2010	Hence, we investigated the impact of mitogen-activated protein kinases (MAPK) and nuclear factor kappa B (NF-kappaB) on IL-8 production by human intestinal cells (Caco-2 and HT-29) after stimulation by MG and GL.	Pyruvaldehyde	202-204	C-X-C motif chemokine ligand 8	Homo sapiens	120-124
20397192-5	2010	MAPK p38 and extracellular signal-regulated kinase (ERK) were phosphorylated in these cells after having been stimulated by MG and GL.	Pyruvaldehyde	124-126	mitogen-activated protein kinase 1	Homo sapiens	5-8
20397192-5	2010	MAPK p38 and extracellular signal-regulated kinase (ERK) were phosphorylated in these cells after having been stimulated by MG and GL.	Pyruvaldehyde	124-126	mitogen-activated protein kinase 1	Homo sapiens	13-50
20397192-5	2010	MAPK p38 and extracellular signal-regulated kinase (ERK) were phosphorylated in these cells after having been stimulated by MG and GL.	Pyruvaldehyde	124-126	mitogen-activated protein kinase 1	Homo sapiens	52-55
20397192-7	2010	The most important mechanism by which MG and GL induced IL-8 secretion was the generation of superoxide anions which was confirmed by the inhibition of the cytosolic NADPH oxidase with diphenyl iodonium (DPI) or by application of superoxide dismutase (SOD).	Pyruvaldehyde	38-40	C-X-C motif chemokine ligand 8	Homo sapiens	56-60
20397192-7	2010	The most important mechanism by which MG and GL induced IL-8 secretion was the generation of superoxide anions which was confirmed by the inhibition of the cytosolic NADPH oxidase with diphenyl iodonium (DPI) or by application of superoxide dismutase (SOD).	Pyruvaldehyde	38-40	superoxide dismutase 1	Homo sapiens	230-250
20397192-7	2010	The most important mechanism by which MG and GL induced IL-8 secretion was the generation of superoxide anions which was confirmed by the inhibition of the cytosolic NADPH oxidase with diphenyl iodonium (DPI) or by application of superoxide dismutase (SOD).	Pyruvaldehyde	38-40	superoxide dismutase 1	Homo sapiens	252-255
20885985-7	2010	Data further shows that MGO decreases the levels of the molecular chaperones Hsc70 and Hsp90 and leads to accumulation of CHIP-, Hsp40- and ubiquitin-containing aggregates.	Pyruvaldehyde	24-27	heat shock protein 90 alpha family class A member 1	Homo sapiens	87-92
20885985-7	2010	Data further shows that MGO decreases the levels of the molecular chaperones Hsc70 and Hsp90 and leads to accumulation of CHIP-, Hsp40- and ubiquitin-containing aggregates.	Pyruvaldehyde	24-27	DnaJ heat shock protein family (Hsp40) member B1 pseudogene 1	Homo sapiens	129-134
20885985-10	2010	Interestingly, data further shows that MGO-induced stress induces the activation of heat shock factor-1 (Hsf-1), the main transcription factor involved in the regulation of the expression of heat shock proteins (HSPs) and cell response to stress.	Pyruvaldehyde	39-42	heat shock transcription factor 1	Homo sapiens	84-103
20885985-10	2010	Interestingly, data further shows that MGO-induced stress induces the activation of heat shock factor-1 (Hsf-1), the main transcription factor involved in the regulation of the expression of heat shock proteins (HSPs) and cell response to stress.	Pyruvaldehyde	39-42	heat shock transcription factor 1	Homo sapiens	105-110
20885985-12	2010	However, these MGO-induced changes appear to elicit a response from the Hsf-1 system, which is crucial to help cells to cope with cellular stress and to re-establish homeostasis.	Pyruvaldehyde	15-18	heat shock transcription factor 1	Homo sapiens	72-77
20371360-5	2010	Isoflurane promoted MG-induced modification of GAPDH as evidenced by an increase in fluorescent glycation products, a change in chromatographic elution patterns and a loss of enzyme activity.	Pyruvaldehyde	20-22	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	47-52
20562294-0	2010	Methylglyoxal-induced imbalance in the ratio of vascular endothelial growth factor to angiopoietin 2 secreted by retinal pigment epithelial cells leads to endothelial dysfunction.	Pyruvaldehyde	0-13	vascular endothelial growth factor A	Homo sapiens	48-82
20562294-0	2010	Methylglyoxal-induced imbalance in the ratio of vascular endothelial growth factor to angiopoietin 2 secreted by retinal pigment epithelial cells leads to endothelial dysfunction.	Pyruvaldehyde	0-13	angiopoietin 2	Homo sapiens	86-100
20562294-3	2010	In this study, we hypothesize that increased levels of MGO disrupt the ratio of vascular endothelial growth factor (VEGF) to angiopoietin 2 (Ang 2) secreted by retinal pigment epithelial (RPE) cells, which provides a key destabilizing signal that leads to apoptosis and decreased proliferation of retinal endothelial cells.	Pyruvaldehyde	55-58	vascular endothelial growth factor A	Homo sapiens	80-114
20562294-3	2010	In this study, we hypothesize that increased levels of MGO disrupt the ratio of vascular endothelial growth factor (VEGF) to angiopoietin 2 (Ang 2) secreted by retinal pigment epithelial (RPE) cells, which provides a key destabilizing signal that leads to apoptosis and decreased proliferation of retinal endothelial cells.	Pyruvaldehyde	55-58	vascular endothelial growth factor A	Homo sapiens	116-120
20562294-3	2010	In this study, we hypothesize that increased levels of MGO disrupt the ratio of vascular endothelial growth factor (VEGF) to angiopoietin 2 (Ang 2) secreted by retinal pigment epithelial (RPE) cells, which provides a key destabilizing signal that leads to apoptosis and decreased proliferation of retinal endothelial cells.	Pyruvaldehyde	55-58	angiopoietin 2	Homo sapiens	125-139
20562294-3	2010	In this study, we hypothesize that increased levels of MGO disrupt the ratio of vascular endothelial growth factor (VEGF) to angiopoietin 2 (Ang 2) secreted by retinal pigment epithelial (RPE) cells, which provides a key destabilizing signal that leads to apoptosis and decreased proliferation of retinal endothelial cells.	Pyruvaldehyde	55-58	angiopoietin 2	Homo sapiens	141-146
20562294-4	2010	Indeed, we show that MGO increases the levels of Ang 2 and dramatically decreases the levels of VEGF secreted by RPE cells in response to hypoxia.	Pyruvaldehyde	21-24	angiopoietin 2	Homo sapiens	49-54
20562294-4	2010	Indeed, we show that MGO increases the levels of Ang 2 and dramatically decreases the levels of VEGF secreted by RPE cells in response to hypoxia.	Pyruvaldehyde	21-24	vascular endothelial growth factor A	Homo sapiens	96-100
20562294-6	2010	Data further show that MGO-induced imbalance in the VEGF/Ang II ratio significantly changes the levels of BAX and Bcl-2 in endothelial cells.	Pyruvaldehyde	23-26	vascular endothelial growth factor A	Homo sapiens	52-56
20562294-6	2010	Data further show that MGO-induced imbalance in the VEGF/Ang II ratio significantly changes the levels of BAX and Bcl-2 in endothelial cells.	Pyruvaldehyde	23-26	BCL2 associated X, apoptosis regulator	Homo sapiens	106-109
20562294-6	2010	Data further show that MGO-induced imbalance in the VEGF/Ang II ratio significantly changes the levels of BAX and Bcl-2 in endothelial cells.	Pyruvaldehyde	23-26	BCL2 apoptosis regulator	Homo sapiens	114-119
20562294-8	2010	Data obtained in cell culture systems are consistent with observations in retinas of diabetic animals, where increased availability of MGO is associated with changes in distribution and levels of HIF-1alpha, VEGF and Ang 2 and increased microvascular permeability.	Pyruvaldehyde	135-138	hypoxia inducible factor 1 subunit alpha	Homo sapiens	196-206
20562294-8	2010	Data obtained in cell culture systems are consistent with observations in retinas of diabetic animals, where increased availability of MGO is associated with changes in distribution and levels of HIF-1alpha, VEGF and Ang 2 and increased microvascular permeability.	Pyruvaldehyde	135-138	vascular endothelial growth factor A	Homo sapiens	208-212
20562294-8	2010	Data obtained in cell culture systems are consistent with observations in retinas of diabetic animals, where increased availability of MGO is associated with changes in distribution and levels of HIF-1alpha, VEGF and Ang 2 and increased microvascular permeability.	Pyruvaldehyde	135-138	angiopoietin 2	Homo sapiens	217-222
20562294-9	2010	In conclusion, the MGO-induced imbalance in the VEGF/Ang 2 ratio secreted by retinal epithelial cells activates apoptosis and decreases proliferation of retinal endothelial cells, which are likely to contribute to endothelial dysfunction in diabetic retinopathy.	Pyruvaldehyde	19-22	vascular endothelial growth factor A	Homo sapiens	48-52
20562294-9	2010	In conclusion, the MGO-induced imbalance in the VEGF/Ang 2 ratio secreted by retinal epithelial cells activates apoptosis and decreases proliferation of retinal endothelial cells, which are likely to contribute to endothelial dysfunction in diabetic retinopathy.	Pyruvaldehyde	19-22	angiopoietin 2	Homo sapiens	53-58
20371360-4	2010	We hypothesized that inhaled anesthetics may play a role in protein glycation and examined the effects of isoflurane on MG-induced modification of glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	Pyruvaldehyde	120-122	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	147-187
20371360-4	2010	We hypothesized that inhaled anesthetics may play a role in protein glycation and examined the effects of isoflurane on MG-induced modification of glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	Pyruvaldehyde	120-122	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	189-194
20460580-0	2010	Methylglyoxal increases cardiomyocyte ischemia-reperfusion injury via glycative inhibition of thioredoxin activity.	Pyruvaldehyde	0-13	thioredoxin	Homo sapiens	94-105
20460580-3	2010	Thioredoxin (Trx), a cytoprotective molecule with antiapoptotic function, has been demonstrated to be vulnerable to glycative inhibition, but whether Trx is glycatively inhibited by MG, thus contributing to increased cardiac injury, has never been investigated.	Pyruvaldehyde	182-184	thioredoxin	Homo sapiens	0-11
20460580-3	2010	Thioredoxin (Trx), a cytoprotective molecule with antiapoptotic function, has been demonstrated to be vulnerable to glycative inhibition, but whether Trx is glycatively inhibited by MG, thus contributing to increased cardiac injury, has never been investigated.	Pyruvaldehyde	182-184	thioredoxin	Homo sapiens	150-153
20460580-7	2010	Prior to SI-R, Trx activity was reduced in MG-treated cells, but Trx expression was increased moderately.	Pyruvaldehyde	43-45	thioredoxin	Homo sapiens	15-18
20460580-12	2010	We demonstrated for the first time that methylglyoxal sensitized cultured cardiomyocytes to SI-R injury by posttranslational modification of Trx via glycation.	Pyruvaldehyde	40-53	thioredoxin	Homo sapiens	141-144
20423729-7	2010	In shear-force detachment assays, cells on MGO-treated collagen were less adherent than untreated collagen, and the formation of high affinity, beta1 integrin-dependent adhesions was inhibited.	Pyruvaldehyde	43-46	integrin subunit beta 1	Homo sapiens	144-158
20423729-8	2010	MGO-collagen-induced expression of SMA was dependent on TGF-beta but not on Rho kinase.	Pyruvaldehyde	0-3	survival of motor neuron 1, telomeric	Homo sapiens	35-38
20423729-8	2010	MGO-collagen-induced expression of SMA was dependent on TGF-beta but not on Rho kinase.	Pyruvaldehyde	0-3	transforming growth factor beta 1	Homo sapiens	56-64
20371360-7	2010	Our working model involves the binding of isoflurane to GAPDH, increasing the susceptibility to MG-induced modification of residues involved in oligomerization.	Pyruvaldehyde	96-98	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	56-61
20387042-2	2010	Gly I detoxifies methylglyoxal (MG), a cytotoxic byproduct of glycolysis, to S-lactoylglutathione (SLG) where it uses one molecule of reduced glutathione.	Pyruvaldehyde	17-30	glyoxalase I	Homo sapiens	0-5
20345757-5	2010	Accordingly, repeated intracerebroventricular injections of MG mediated anxiolysis in inbred high anxiety-related behavior and outbred CD1 mice.	Pyruvaldehyde	60-62	CD1 antigen complex	Mus musculus	135-138
20345757-8	2010	Moreover, MG treatment increased expression of GLO1 only in CD1 mice that did not have extra copies of GLO1.	Pyruvaldehyde	10-12	glyoxalase 1	Mus musculus	47-51
20345757-8	2010	Moreover, MG treatment increased expression of GLO1 only in CD1 mice that did not have extra copies of GLO1.	Pyruvaldehyde	10-12	CD1 antigen complex	Mus musculus	60-63
20077113-0	2010	Methylglyoxal activates Gcn2 to phosphorylate eIF2alpha independently of the TOR pathway in Saccharomyces cerevisiae.	Pyruvaldehyde	0-13	serine/threonine-protein kinase GCN2	Saccharomyces cerevisiae S288C	24-28
20077113-2	2010	Previously, we have reported that methylglyoxal attenuates the rate of overall protein synthesis in Saccharomyces cerevisiae through phosphorylation of the alpha subunit of translation initiation factor 2 (eIF2alpha) in a Gcn2-dependent manner.	Pyruvaldehyde	34-47	serine/threonine-protein kinase GCN2	Saccharomyces cerevisiae S288C	222-226
20071071-1	2010	Glyoxalase I (GLOI) is a key metalloenzyme in glycolytic pathway by detoxifying reactive alpha-ketoaldehydes such as methylglyoxal.	Pyruvaldehyde	117-130	glyoxalase I	Homo sapiens	0-12
20071071-1	2010	Glyoxalase I (GLOI) is a key metalloenzyme in glycolytic pathway by detoxifying reactive alpha-ketoaldehydes such as methylglyoxal.	Pyruvaldehyde	117-130	glyoxalase I	Homo sapiens	14-18
20737676-7	2010	At the same time, the cytosol, intercellular environment, and plasma shows the elevated levels of methylglyoxal and D-lactate that it is converted to by the action of glyoxalases I and II.	Pyruvaldehyde	98-111	glyoxalase I	Homo sapiens	167-187
20204770-6	2010	Of note, rats over expressing human glyoxalase I showed amelioration of I/R-induced histological and functional damages and it was associated with a decrease in MG level in the lesion resulting in reduction of oxidative stress and tubular cell apoptosis.	Pyruvaldehyde	161-163	glyoxalase I	Homo sapiens	36-48
20204770-7	2010	In conclusion, glyoxalase I has renoprotective effects in renal hypoxia such as I/R injury via a reduction in cytotoxic MG level in tubular cells.	Pyruvaldehyde	120-122	glyoxalase I	Homo sapiens	15-27
19913507-6	2010	In MGO-treated HLE-B3 cells, the accumulation of argpyrimidine was markedly increased, and caspase-3 and 8-hydroxydeoxyguanosine (8-OHdG) were highly expressed, which paralleled apoptotic cell death.	Pyruvaldehyde	3-6	caspase 3	Homo sapiens	91-100
20410585-6	2010	Flow cytometric analyses with annexin V and propidium iodide double staining revealed that BAECs exposed to MG after BSO pretreatment displayed features characteristic of apoptosis.	Pyruvaldehyde	108-110	annexin A5	Homo sapiens	30-39
20410585-7	2010	Caspase-3 activation induced by MG was increased by BSO.	Pyruvaldehyde	32-34	caspase 3	Homo sapiens	0-9
20385072-4	2010	Our results showed that the biochemical activity of glyoxalase 1, the main component of the MG scavenging system, is significantly decreased in ovaries from reproductively-aged mice in comparison with the young group.	Pyruvaldehyde	92-94	glyoxalase 1	Mus musculus	52-64
19538479-6	2010	We show that the immunomodulatory component of this RM was MG itself, with MG alone causing equivalent block of CD83 and loss of primary stimulation.	Pyruvaldehyde	75-77	CD83 molecule	Homo sapiens	112-116
19803740-5	2010	The expression level and activity of H(2)S-producing enzyme, cystathionine gamma-lyase (CSE), were significantly decreased by MG treatment.	Pyruvaldehyde	126-128	cystathionine gamma-lyase	Rattus norvegicus	61-86
19803740-5	2010	The expression level and activity of H(2)S-producing enzyme, cystathionine gamma-lyase (CSE), were significantly decreased by MG treatment.	Pyruvaldehyde	126-128	cystathionine gamma-lyase	Rattus norvegicus	88-91
20016290-4	2010	HIF-1 dysfunction is the end result of reactive oxygen species-induced modification of its coactivator p300 by the glycolytic metabolite methylglyoxal.	Pyruvaldehyde	137-150	E1A binding protein p300	Mus musculus	103-107
21076237-0	2010	Methylglyoxal augments angiotensin II-induced contraction in rat isolated carotid artery.	Pyruvaldehyde	0-13	angiotensinogen	Rattus norvegicus	23-37
21076237-10	2010	Gp91ds-tat or an Ang II type 1-receptor (AT1R) blocker, losartan (10 microM), prevented the MGO-mediated increased ROS production.	Pyruvaldehyde	92-95	angiotensin II receptor, type 1a	Rattus norvegicus	17-39
21076237-10	2010	Gp91ds-tat or an Ang II type 1-receptor (AT1R) blocker, losartan (10 microM), prevented the MGO-mediated increased ROS production.	Pyruvaldehyde	92-95	angiotensin II receptor, type 1a	Rattus norvegicus	41-45
21076237-11	2010	The present study revealed that MGO augments Ang II-induced contraction by increasing AT1R-mediated NADPH oxidase-derived superoxide and hydrogen peroxide production in endothelium of rat carotid artery.	Pyruvaldehyde	32-35	angiotensin II receptor, type 1a	Rattus norvegicus	86-90
20387042-2	2010	Gly I detoxifies methylglyoxal (MG), a cytotoxic byproduct of glycolysis, to S-lactoylglutathione (SLG) where it uses one molecule of reduced glutathione.	Pyruvaldehyde	32-34	glyoxalase I	Homo sapiens	0-5
21341469-7	2010	Cytosol, intercellular medium, plasma show elevated levels of MG and D-lactate, to which it converts under the action of glyoxalases I and II.	Pyruvaldehyde	62-64	glyoxalase I	Homo sapiens	121-141
19720799-6	2009	Glycation of laminin and fibronectin by methylglyoxal and glucose increased glycation adduct residue contents with methylglyoxal-derived hydroimidazolone and N(epsilon)-fructosyl-lysine, respectively, of greatest quantitative importance.	Pyruvaldehyde	40-53	fibronectin 1	Rattus norvegicus	25-36
19238574-1	2009	Glyoxalase I (GLOI) is the first enzyme of the glyoxalase system that catalyzes the metabolism of reactive dicarbonyls, such as methylglyoxal (MGO).	Pyruvaldehyde	128-141	glyoxalase I	Homo sapiens	0-12
19238574-1	2009	Glyoxalase I (GLOI) is the first enzyme of the glyoxalase system that catalyzes the metabolism of reactive dicarbonyls, such as methylglyoxal (MGO).	Pyruvaldehyde	128-141	glyoxalase I	Homo sapiens	14-18
19238574-1	2009	Glyoxalase I (GLOI) is the first enzyme of the glyoxalase system that catalyzes the metabolism of reactive dicarbonyls, such as methylglyoxal (MGO).	Pyruvaldehyde	143-146	glyoxalase I	Homo sapiens	0-12
19238574-1	2009	Glyoxalase I (GLOI) is the first enzyme of the glyoxalase system that catalyzes the metabolism of reactive dicarbonyls, such as methylglyoxal (MGO).	Pyruvaldehyde	143-146	glyoxalase I	Homo sapiens	14-18
19966511-10	2009	Taken together, these findings suggest that MG causes dysfunction of the Trx system, including Trx and Trx reductase, in BAECs.	Pyruvaldehyde	44-46	thioredoxin	Bos taurus	95-98
20025505-1	2009	Glyoxalase I (GLO1) is a key enzyme that plays a role in the detoxification of methylglyoxal (MG), a toxic cellular metabolite produced during glycolysis.	Pyruvaldehyde	79-92	glyoxalase 1	Mus musculus	0-12
20025505-1	2009	Glyoxalase I (GLO1) is a key enzyme that plays a role in the detoxification of methylglyoxal (MG), a toxic cellular metabolite produced during glycolysis.	Pyruvaldehyde	79-92	glyoxalase 1	Mus musculus	14-18
20025505-1	2009	Glyoxalase I (GLO1) is a key enzyme that plays a role in the detoxification of methylglyoxal (MG), a toxic cellular metabolite produced during glycolysis.	Pyruvaldehyde	94-96	glyoxalase 1	Mus musculus	0-12
20025505-1	2009	Glyoxalase I (GLO1) is a key enzyme that plays a role in the detoxification of methylglyoxal (MG), a toxic cellular metabolite produced during glycolysis.	Pyruvaldehyde	94-96	glyoxalase 1	Mus musculus	14-18
19966511-3	2009	We examined the effects of MG on thioredoxin (Trx) and glutaredoxin (Grx) systems, two thiol-disulfide oxidoreductase systems that protect against oxidative damage of proteins, in bovine aortic endothelial cells (BAECs).	Pyruvaldehyde	27-29	thioredoxin	Bos taurus	33-44
19966511-5	2009	Western blot analysis demonstrated that Trx protein level decreased when BAECs were exposed to 5 mM MG.	Pyruvaldehyde	100-102	thioredoxin	Bos taurus	40-43
19643547-0	2009	"Blinding" of AMP-dependent kinase by methylglyoxal: a mechanism that allows perpetuation of hepatic insulin resistance?	Pyruvaldehyde	38-51	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	14-34
19966511-7	2009	Moreover, peroxiredoxin, which is dependent on Trx and Trx reductase to maintain its reduced state, was oxidized by 5 mM MG.	Pyruvaldehyde	121-123	thioredoxin	Bos taurus	47-50
19966511-7	2009	Moreover, peroxiredoxin, which is dependent on Trx and Trx reductase to maintain its reduced state, was oxidized by 5 mM MG.	Pyruvaldehyde	121-123	thioredoxin	Bos taurus	55-58
19966511-10	2009	Taken together, these findings suggest that MG causes dysfunction of the Trx system, including Trx and Trx reductase, in BAECs.	Pyruvaldehyde	44-46	thioredoxin	Bos taurus	73-76
19966511-10	2009	Taken together, these findings suggest that MG causes dysfunction of the Trx system, including Trx and Trx reductase, in BAECs.	Pyruvaldehyde	44-46	thioredoxin	Bos taurus	95-98
19643547-4	2009	MG accumulates in hyperglycemia, insulin resistance, diabetes and when there is excess flux of reactive oxygen species coming from the mitochondria.	Pyruvaldehyde	0-2	insulin	Homo sapiens	33-40
19643547-5	2009	We hypothesize that excess MG in the above-mentioned conditions blocks the sensing of AMP by AMPK, thereby favoring gluconeogenesis (thus hepatic glucose output and hyperglycemia) and lipogenesis (hepatic steatosis and high VLDL), hallmarks of insulin resistance and diabetes.	Pyruvaldehyde	27-29	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	93-97
19687346-4	2009	Methylglyoxal (MG) that plays a role in the vascular complications of diabetes mellitus and the development of hypertension can be one potential factor that can affect LOX-1 and arginase through its ability to induce oxidative stress in vascular cells.	Pyruvaldehyde	0-13	oxidized low density lipoprotein receptor 1	Homo sapiens	168-173
19651811-8	2009	Acetol formation in methylglyoxal-treated HUVECs was prevented by the aldose reductase inhibitor sorbinil.	Pyruvaldehyde	20-33	aldo-keto reductase family 1, member B3 (aldose reductase)	Mus musculus	70-86
19675139-6	2009	Overexpression of the methylglyoxal-detoxifying enzyme glyoxalase-1 attenuated the life-shortening effect of glucose by reducing AGE accumulation (by 65%) and ROS formation (by 50%) and restored mean (16.5 + or - 0.6 to 20.6 + or - 0.4 days) and maximum life span (23.2 + or - 0.4 to 27.7 + or - 2.3 days).	Pyruvaldehyde	22-35	Glyoxalase 1	Caenorhabditis elegans	55-67
19449196-0	2009	Glycation of aspartate aminotransferase by methylglyoxal, effect of hydroxycitric and uric acid.	Pyruvaldehyde	43-56	solute carrier family 17 member 5	Homo sapiens	13-39
19449196-5	2009	Hydroxycitric acid, at all tested concentrations, reduced AST activity decrease and formation of fluorescent AGEs during incubation of the enzyme with methylglyoxal at 37 degrees C. This compound also prevented formation of high-molecular weight protein cross-links and changes in molecular charge of AST caused by glycation.	Pyruvaldehyde	151-164	solute carrier family 17 member 5	Homo sapiens	301-304
20137606-8	2009	MG increased the cellular levels of BDNF but decreased the TrkB mRNA and protein expression significantly.	Pyruvaldehyde	0-2	brain-derived neurotrophic factor	Rattus norvegicus	36-40
20137606-8	2009	MG increased the cellular levels of BDNF but decreased the TrkB mRNA and protein expression significantly.	Pyruvaldehyde	0-2	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	59-63
20137606-9	2009	However, NAC significantly decreased the BDNF and increased the TrkB mRNA and protein expression in rat hippocampal neuron after MG induction.	Pyruvaldehyde	129-131	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	64-68
20137606-11	2009	CONCLUSION: MG-induced neurotoxicity in hippocampal neurons is mediated by oxidative stress and it can impair the BDNF/TrkB signal pathway.	Pyruvaldehyde	12-14	brain-derived neurotrophic factor	Rattus norvegicus	114-118
20137606-11	2009	CONCLUSION: MG-induced neurotoxicity in hippocampal neurons is mediated by oxidative stress and it can impair the BDNF/TrkB signal pathway.	Pyruvaldehyde	12-14	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	119-123
19687346-10	2009	In conclusion, MG-induced LOX-1 expression is mediated via arginase upregulation likely because of uncoupling of NO synthase, which may have implications in preeclampsia.	Pyruvaldehyde	15-17	oxidized low density lipoprotein receptor 1	Homo sapiens	26-31
19687346-4	2009	Methylglyoxal (MG) that plays a role in the vascular complications of diabetes mellitus and the development of hypertension can be one potential factor that can affect LOX-1 and arginase through its ability to induce oxidative stress in vascular cells.	Pyruvaldehyde	15-17	oxidized low density lipoprotein receptor 1	Homo sapiens	168-173
19687346-5	2009	MG also reacts with lysine residues in proteins to generate advanced glycation end product, N(epsilon)-carboxy ethyl lysine, which also serves as a marker of MG. We hypothesized that markers of MG formation will be increased in the vasculature of preeclamptic women and that exogenous MG will induce oxidative stress by the upregulation of LOX-1 via arginase.	Pyruvaldehyde	0-2	oxidized low density lipoprotein receptor 1	Homo sapiens	340-345
19687346-5	2009	MG also reacts with lysine residues in proteins to generate advanced glycation end product, N(epsilon)-carboxy ethyl lysine, which also serves as a marker of MG. We hypothesized that markers of MG formation will be increased in the vasculature of preeclamptic women and that exogenous MG will induce oxidative stress by the upregulation of LOX-1 via arginase.	Pyruvaldehyde	158-160	oxidized low density lipoprotein receptor 1	Homo sapiens	340-345
19687346-7	2009	Moreover, glyoxalase I and II, enzymes that detoxify MG, and glutathione reductase, which generates reduced glutathione, a cofactor for glyoxalase, are also reduced in preeclampsia.	Pyruvaldehyde	53-55	glyoxalase I	Homo sapiens	10-29
19573895-5	2009	We incubated in vitro plasma and purified antithrombin and human hepatoma cells (HepG2) with methyl-glyoxal and glucose.	Pyruvaldehyde	93-107	serpin family C member 1	Homo sapiens	42-54
19463904-0	2009	Glucagon-like peptide-1 (GLP-1) protects against methylglyoxal-induced PC12 cell apoptosis through the PI3K/Akt/mTOR/GCLc/redox signaling pathway.	Pyruvaldehyde	49-62	glucagon	Rattus norvegicus	0-23
19463904-0	2009	Glucagon-like peptide-1 (GLP-1) protects against methylglyoxal-induced PC12 cell apoptosis through the PI3K/Akt/mTOR/GCLc/redox signaling pathway.	Pyruvaldehyde	49-62	glucagon	Rattus norvegicus	25-30
19463904-0	2009	Glucagon-like peptide-1 (GLP-1) protects against methylglyoxal-induced PC12 cell apoptosis through the PI3K/Akt/mTOR/GCLc/redox signaling pathway.	Pyruvaldehyde	49-62	AKT serine/threonine kinase 1	Rattus norvegicus	108-111
19463904-0	2009	Glucagon-like peptide-1 (GLP-1) protects against methylglyoxal-induced PC12 cell apoptosis through the PI3K/Akt/mTOR/GCLc/redox signaling pathway.	Pyruvaldehyde	49-62	mechanistic target of rapamycin kinase	Rattus norvegicus	112-116
19463904-0	2009	Glucagon-like peptide-1 (GLP-1) protects against methylglyoxal-induced PC12 cell apoptosis through the PI3K/Akt/mTOR/GCLc/redox signaling pathway.	Pyruvaldehyde	49-62	glutamate-cysteine ligase, catalytic subunit	Rattus norvegicus	117-121
19463904-9	2009	GLP-1 protected against this MG-induced apoptosis, which corresponded to the phosphorylation of PI3K, Akt, and mTOR, as well as the upregulation of GCLc and the restoration of the redox imbalance.	Pyruvaldehyde	29-31	glucagon	Rattus norvegicus	0-5
19463904-9	2009	GLP-1 protected against this MG-induced apoptosis, which corresponded to the phosphorylation of PI3K, Akt, and mTOR, as well as the upregulation of GCLc and the restoration of the redox imbalance.	Pyruvaldehyde	29-31	AKT serine/threonine kinase 1	Rattus norvegicus	102-105
19463904-9	2009	GLP-1 protected against this MG-induced apoptosis, which corresponded to the phosphorylation of PI3K, Akt, and mTOR, as well as the upregulation of GCLc and the restoration of the redox imbalance.	Pyruvaldehyde	29-31	mechanistic target of rapamycin kinase	Rattus norvegicus	111-115
19463904-9	2009	GLP-1 protected against this MG-induced apoptosis, which corresponded to the phosphorylation of PI3K, Akt, and mTOR, as well as the upregulation of GCLc and the restoration of the redox imbalance.	Pyruvaldehyde	29-31	glutamate-cysteine ligase, catalytic subunit	Rattus norvegicus	148-152
19463904-10	2009	Inhibitors of PI3K (LY294002), Akt (Akt-I), and mTOR (rapamycin) reduced the GLP-1-induced GCLc upregulation and its protection against MG-induced PC12 apoptosis.	Pyruvaldehyde	136-138	AKT serine/threonine kinase 1	Rattus norvegicus	31-34
19463904-10	2009	Inhibitors of PI3K (LY294002), Akt (Akt-I), and mTOR (rapamycin) reduced the GLP-1-induced GCLc upregulation and its protection against MG-induced PC12 apoptosis.	Pyruvaldehyde	136-138	AKT serine/threonine kinase 1	Rattus norvegicus	36-41
19463904-10	2009	Inhibitors of PI3K (LY294002), Akt (Akt-I), and mTOR (rapamycin) reduced the GLP-1-induced GCLc upregulation and its protection against MG-induced PC12 apoptosis.	Pyruvaldehyde	136-138	mechanistic target of rapamycin kinase	Rattus norvegicus	48-52
19463904-10	2009	Inhibitors of PI3K (LY294002), Akt (Akt-I), and mTOR (rapamycin) reduced the GLP-1-induced GCLc upregulation and its protection against MG-induced PC12 apoptosis.	Pyruvaldehyde	136-138	glucagon	Rattus norvegicus	77-82
19463904-10	2009	Inhibitors of PI3K (LY294002), Akt (Akt-I), and mTOR (rapamycin) reduced the GLP-1-induced GCLc upregulation and its protection against MG-induced PC12 apoptosis.	Pyruvaldehyde	136-138	glutamate-cysteine ligase, catalytic subunit	Rattus norvegicus	91-95
19428325-6	2009	The activity of MnSOD was decreased by MG treatment.	Pyruvaldehyde	39-41	superoxide dismutase 2	Homo sapiens	16-21
19481094-10	2009	One millimolar glucose or 1 mM methylglyoxal raised ATP in the DeltaatpD knockout cells to that of the wild type and restored Ca(2+) efflux.	Pyruvaldehyde	31-44	ATPase	Escherichia coli	52-55
19199007-1	2009	Glyoxalase I (GLO1), together with glyoxalase II and the co-factor GSH, comprise the glyoxalase system, which is responsible for the detoxification of the cytotoxic glycolytic-derived metabolite methylglyoxal (MG).	Pyruvaldehyde	195-208	glyoxalase I	Homo sapiens	0-12
19375802-6	2009	Present study indicated that methylglyoxal stimulates iNOS activation by p38 MAPK-NF-kappa beta dependent pathway and ROS production by ERK and JNK activation in sarcoma-180 tumor bearing mice.	Pyruvaldehyde	29-42	mitogen-activated protein kinase 1	Mus musculus	136-139
19375802-6	2009	Present study indicated that methylglyoxal stimulates iNOS activation by p38 MAPK-NF-kappa beta dependent pathway and ROS production by ERK and JNK activation in sarcoma-180 tumor bearing mice.	Pyruvaldehyde	29-42	mitogen-activated protein kinase 8	Mus musculus	144-147
19375802-9	2009	Hence, concluded that methylglyoxal augmented the IL-6 and IL-1 beta, expression of TLR 4 and TLR 9 and produced MAPKs, important regulators of ROIs and RNIs.	Pyruvaldehyde	22-35	interleukin 6	Mus musculus	50-54
19375802-9	2009	Hence, concluded that methylglyoxal augmented the IL-6 and IL-1 beta, expression of TLR 4 and TLR 9 and produced MAPKs, important regulators of ROIs and RNIs.	Pyruvaldehyde	22-35	interleukin 1 beta	Mus musculus	59-68
19375802-9	2009	Hence, concluded that methylglyoxal augmented the IL-6 and IL-1 beta, expression of TLR 4 and TLR 9 and produced MAPKs, important regulators of ROIs and RNIs.	Pyruvaldehyde	22-35	toll-like receptor 4	Mus musculus	84-89
19375802-9	2009	Hence, concluded that methylglyoxal augmented the IL-6 and IL-1 beta, expression of TLR 4 and TLR 9 and produced MAPKs, important regulators of ROIs and RNIs.	Pyruvaldehyde	22-35	toll-like receptor 9	Mus musculus	94-99
19199007-1	2009	Glyoxalase I (GLO1), together with glyoxalase II and the co-factor GSH, comprise the glyoxalase system, which is responsible for the detoxification of the cytotoxic glycolytic-derived metabolite methylglyoxal (MG).	Pyruvaldehyde	195-208	glyoxalase I	Homo sapiens	14-18
19199007-1	2009	Glyoxalase I (GLO1), together with glyoxalase II and the co-factor GSH, comprise the glyoxalase system, which is responsible for the detoxification of the cytotoxic glycolytic-derived metabolite methylglyoxal (MG).	Pyruvaldehyde	195-208	hydroxyacylglutathione hydrolase	Homo sapiens	35-48
18758988-3	2009	A treatment of cells with 1.0 mM GO or 400 microM MGO leads to the appearance of senescent phenotype within 3 days, as judged by the following criteria: morphological phenotype, irreversible growth arrest and G2 arrest, increased senescence-associated beta-galactosidase (SABG) activity, increased H2O2 level, increased Nxi-(carboxymethyl)-lysine (CML) protein level, and altered activities of superoxide dismutase and catalase antioxidant enzymes.	Pyruvaldehyde	50-53	catalase	Homo sapiens	419-427
19211689-3	2009	MG is efficiently metabolized by the glyoxalase system, namely, glyoxalase I.	Pyruvaldehyde	0-2	glyoxalase 1	Rattus norvegicus	64-76
19211689-9	2009	In conclusion, glyoxalase I exerts renoprotective effects in renal I/R injury via a reduction in MG accumulation in tubular cells.	Pyruvaldehyde	97-99	glyoxalase 1	Rattus norvegicus	15-27
19103312-3	2009	In this study, two dicarbonyl compounds, methylglyoxal (MGO) and glyoxal (GO), were investigated for their effects on the structural and fibril-forming properties of alphaSyn.	Pyruvaldehyde	41-54	synuclein alpha	Homo sapiens	166-174
18830874-1	2009	Methylglyoxal (MG) was studied as an inhibitor and effective glycating factor of human muscle-specific enolase.	Pyruvaldehyde	0-13	enolase 3	Homo sapiens	87-110
18830874-1	2009	Methylglyoxal (MG) was studied as an inhibitor and effective glycating factor of human muscle-specific enolase.	Pyruvaldehyde	15-17	enolase 3	Homo sapiens	87-110
19468318-4	2009	Concentrations of 5 microM MG and 15 mM glucose significantly increased cytoplasmic free calcium and nitric oxide (NO) levels, loss of mitochondrial membrane potential (MMP), activation of caspases-9 and -3, and cell death.	Pyruvaldehyde	27-29	caspase 9	Homo sapiens	189-206
19103312-3	2009	In this study, two dicarbonyl compounds, methylglyoxal (MGO) and glyoxal (GO), were investigated for their effects on the structural and fibril-forming properties of alphaSyn.	Pyruvaldehyde	56-59	synuclein alpha	Homo sapiens	166-174
19014907-7	2009	These findings suggest that GLO1, which is dominantly expressed in the embryonic VZ, reduces the intracellular level of MG and suppresses the formation of argpyrimidine in neural stem and progenitor cells.	Pyruvaldehyde	120-122	glyoxalase I	Homo sapiens	28-32
19229826-6	2009	RESULTS: Fur and MGly at concentrations reported in traditional PDSs (Fur 0.8 microM; MGly 35 microM) significantly up-regulated eNOS mRNA and tended to down-regulate AQP1 mRNA in cultured endothelial cells.	Pyruvaldehyde	17-21	nitric oxide synthase 3	Homo sapiens	129-133
18845121-2	2009	They can be oxidized by semicarbazide-sensitive amine oxidase (SSAO), leading to the production of toxic aldehydes such as formaldehyde and methylglyoxal as well as hydrogen peroxide and ammonia.	Pyruvaldehyde	140-153	amine oxidase copper containing 2	Homo sapiens	24-61
18845121-2	2009	They can be oxidized by semicarbazide-sensitive amine oxidase (SSAO), leading to the production of toxic aldehydes such as formaldehyde and methylglyoxal as well as hydrogen peroxide and ammonia.	Pyruvaldehyde	140-153	amine oxidase copper containing 2	Homo sapiens	63-67
19229826-6	2009	RESULTS: Fur and MGly at concentrations reported in traditional PDSs (Fur 0.8 microM; MGly 35 microM) significantly up-regulated eNOS mRNA and tended to down-regulate AQP1 mRNA in cultured endothelial cells.	Pyruvaldehyde	17-21	aquaporin 1 (Colton blood group)	Homo sapiens	167-171
19229826-6	2009	RESULTS: Fur and MGly at concentrations reported in traditional PDSs (Fur 0.8 microM; MGly 35 microM) significantly up-regulated eNOS mRNA and tended to down-regulate AQP1 mRNA in cultured endothelial cells.	Pyruvaldehyde	86-90	nitric oxide synthase 3	Homo sapiens	129-133
18980529-4	2008	METHODS: Procedures for rapid in vitro glycation of COLI and FN used methylglyoxal (MG).	Pyruvaldehyde	69-82	fibronectin 1	Homo sapiens	61-63
19012752-4	2009	In this study, we have, for the first time, demonstrated the effect of MGO on the gp130 cytokine-induced signal transducer and activator of transcription 3 (STAT3) responses in RT4 schwannoma, PC12 pheochromocytoma and U87MG glioma cells.	Pyruvaldehyde	71-74	interleukin 6 cytokine family signal transducer	Homo sapiens	82-87
19012752-4	2009	In this study, we have, for the first time, demonstrated the effect of MGO on the gp130 cytokine-induced signal transducer and activator of transcription 3 (STAT3) responses in RT4 schwannoma, PC12 pheochromocytoma and U87MG glioma cells.	Pyruvaldehyde	71-74	signal transducer and activator of transcription 3	Homo sapiens	105-155
19012752-4	2009	In this study, we have, for the first time, demonstrated the effect of MGO on the gp130 cytokine-induced signal transducer and activator of transcription 3 (STAT3) responses in RT4 schwannoma, PC12 pheochromocytoma and U87MG glioma cells.	Pyruvaldehyde	71-74	signal transducer and activator of transcription 3	Homo sapiens	157-162
19012752-5	2009	At dose that very mildly affects cell viability, MGO rapidly induces endocytotic degradation of gp130, which involves the di-leucine internalization motif in the cytoplasmic domain of gp130, without affecting other growth factor receptors.	Pyruvaldehyde	49-52	interleukin 6 cytokine family signal transducer	Homo sapiens	96-101
19012752-5	2009	At dose that very mildly affects cell viability, MGO rapidly induces endocytotic degradation of gp130, which involves the di-leucine internalization motif in the cytoplasmic domain of gp130, without affecting other growth factor receptors.	Pyruvaldehyde	49-52	interleukin 6 cytokine family signal transducer	Homo sapiens	184-189
19012752-6	2009	Concomitant inhibition of basal and interleukin-6-induced STAT3 activation was observed following pre-treatment with MGO.	Pyruvaldehyde	117-120	interleukin 6	Homo sapiens	36-49
19012752-6	2009	Concomitant inhibition of basal and interleukin-6-induced STAT3 activation was observed following pre-treatment with MGO.	Pyruvaldehyde	117-120	signal transducer and activator of transcription 3	Homo sapiens	58-63
19012752-7	2009	The inhibitory effect of MGO on the gp130/STAT3 signaling was prevented by the pre-treatment with an advanced glycation endproduct scavenger aminoguanidine.	Pyruvaldehyde	25-28	interleukin 6 cytokine family signal transducer	Homo sapiens	36-41
19012752-7	2009	The inhibitory effect of MGO on the gp130/STAT3 signaling was prevented by the pre-treatment with an advanced glycation endproduct scavenger aminoguanidine.	Pyruvaldehyde	25-28	signal transducer and activator of transcription 3	Homo sapiens	42-47
19012752-8	2009	Finally, these deleterious effects of MGO on STAT3 signaling led to down-regulation of a STAT3 target gene, Bcl-2, and sensitized cellular toxicity induced by H(2)O(2) and etoposide.	Pyruvaldehyde	38-41	signal transducer and activator of transcription 3	Homo sapiens	45-50
19012752-8	2009	Finally, these deleterious effects of MGO on STAT3 signaling led to down-regulation of a STAT3 target gene, Bcl-2, and sensitized cellular toxicity induced by H(2)O(2) and etoposide.	Pyruvaldehyde	38-41	signal transducer and activator of transcription 3	Homo sapiens	89-94
19012752-8	2009	Finally, these deleterious effects of MGO on STAT3 signaling led to down-regulation of a STAT3 target gene, Bcl-2, and sensitized cellular toxicity induced by H(2)O(2) and etoposide.	Pyruvaldehyde	38-41	BCL2 apoptosis regulator	Homo sapiens	108-113
18842828-5	2008	MGO induced mRNA and protein expression of cyclooxygenase (COX)-2 in a concentration (0-420 microM)- and time (6-24 h)-dependent manner.	Pyruvaldehyde	0-3	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	43-65
18842828-7	2008	Acute treatment with MGO (20 min) induced concentration-dependent (0-420 microM) activation of JNK and p38 MAP kinase but not ERK or NF-kappaB.	Pyruvaldehyde	21-24	mitogen-activated protein kinase 14	Homo sapiens	103-106
18842828-8	2008	Both the JNK inhibitor SP600125 and the p38 inhibitor SB203580 prevented the MGO induction of COX-2.	Pyruvaldehyde	77-80	mitogen-activated protein kinase 14	Homo sapiens	40-43
18842828-8	2008	Both the JNK inhibitor SP600125 and the p38 inhibitor SB203580 prevented the MGO induction of COX-2.	Pyruvaldehyde	77-80	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	94-99
18842828-11	2008	Present results indicated that MGO mediates JNK- and p38-dependent EC inflammatory responses, which might be independent of oxidative stress.	Pyruvaldehyde	31-34	mitogen-activated protein kinase 14	Homo sapiens	53-56
18812164-6	2008	We found that methylglyoxal activates the protein kinase Gcn2 to phosphorylate eIF2alpha.	Pyruvaldehyde	14-27	serine/threonine-protein kinase GCN2	Saccharomyces cerevisiae S288C	57-61
18812164-8	2008	We found that adaptation to methylglyoxal was impaired in gcn4Delta cells, indicating the expression of certain genes regulated by Gcn4 to be important for the adaptive response to methylglyoxal.	Pyruvaldehyde	28-41	amino acid starvation-responsive transcription factor GCN4	Saccharomyces cerevisiae S288C	131-135
18812164-8	2008	We found that adaptation to methylglyoxal was impaired in gcn4Delta cells, indicating the expression of certain genes regulated by Gcn4 to be important for the adaptive response to methylglyoxal.	Pyruvaldehyde	181-194	amino acid starvation-responsive transcription factor GCN4	Saccharomyces cerevisiae S288C	131-135
18980529-12	2008	CONCLUSIONS: MG treatment efficiently glycated COLI and FN, providing a new tool to study the effects of diabetes on periodontal disease.	Pyruvaldehyde	13-15	fibronectin 1	Homo sapiens	56-58
19012752-9	2009	Our data indicate that MGO affects cell viability via desensitization of gp130/STAT3 signaling, which is the key signaling pathway for cell survival, and thereby promotes cytotoxicity.	Pyruvaldehyde	23-26	interleukin 6 cytokine family signal transducer	Homo sapiens	73-78
19012752-9	2009	Our data indicate that MGO affects cell viability via desensitization of gp130/STAT3 signaling, which is the key signaling pathway for cell survival, and thereby promotes cytotoxicity.	Pyruvaldehyde	23-26	signal transducer and activator of transcription 3	Homo sapiens	79-84
18617020-8	2008	IFN-gamma, which is a regulatory molecule of iNOS pathway also showed an elevated level by methylglyoxal.	Pyruvaldehyde	91-104	interferon gamma	Mus musculus	0-9
18617020-8	2008	IFN-gamma, which is a regulatory molecule of iNOS pathway also showed an elevated level by methylglyoxal.	Pyruvaldehyde	91-104	nitric oxide synthase 2, inducible	Mus musculus	45-49
18344542-7	2008	However, subsequent treatment with 1.0 mM MGO not only restored the chaperone function but increased it by approximately 40% and approximately 60% beyond that of unmodified alphaA-crystallin, as measured with citrate synthase and insulin aggregation assays, respectively.	Pyruvaldehyde	42-45	citrate synthase	Homo sapiens	209-225
18855266-3	2008	In insulin-resistant states, like obesity and type 2 diabetes, altered glucose metabolism may lead to increased formation of methylglyoxal and other ketoaldehydes.	Pyruvaldehyde	125-138	insulin	Homo sapiens	3-10
18565324-7	2008	MGO-induced cell death was apoptosis since MGO increased cleaved caspase-3 expression.	Pyruvaldehyde	0-3	caspase 3	Homo sapiens	65-74
18565324-7	2008	MGO-induced cell death was apoptosis since MGO increased cleaved caspase-3 expression.	Pyruvaldehyde	43-46	caspase 3	Homo sapiens	65-74
18565324-9	2008	These results indicate that telmisartan prevents MGO-induced apoptosis by inhibiting caspase-3 activation, which might explain at least in part the beneficial effects of telimisartan against diabetes-related cardiovascular diseases.	Pyruvaldehyde	49-52	caspase 3	Homo sapiens	85-94
18695250-6	2008	In cells, GLO1 plays a critical role in the detoxification of 2-oxoaldehydes, such as methylglyoxal.	Pyruvaldehyde	86-99	glyoxalase I	Homo sapiens	10-14
18706441-6	2008	Our findings indicated that methylglyoxal-induced Neuro-2A cell apoptosis was mediated through the possible glycation mechanism of oxidative stress, activation of the MAPK signaling pathway (p38 and JNK) and oxidation-sensitive protein expression (PKC and p47(phox)) and methylglyoxal-derived N-epsilon-(carboxymethyl)lysine (CML) formation.	Pyruvaldehyde	28-41	mitogen-activated protein kinase 14	Mus musculus	191-194
18706441-6	2008	Our findings indicated that methylglyoxal-induced Neuro-2A cell apoptosis was mediated through the possible glycation mechanism of oxidative stress, activation of the MAPK signaling pathway (p38 and JNK) and oxidation-sensitive protein expression (PKC and p47(phox)) and methylglyoxal-derived N-epsilon-(carboxymethyl)lysine (CML) formation.	Pyruvaldehyde	28-41	mitogen-activated protein kinase 8	Mus musculus	199-202
18706441-6	2008	Our findings indicated that methylglyoxal-induced Neuro-2A cell apoptosis was mediated through the possible glycation mechanism of oxidative stress, activation of the MAPK signaling pathway (p38 and JNK) and oxidation-sensitive protein expression (PKC and p47(phox)) and methylglyoxal-derived N-epsilon-(carboxymethyl)lysine (CML) formation.	Pyruvaldehyde	28-41	NSFL1 (p97) cofactor (p47)	Mus musculus	256-265
18827464-6	2008	MG induced the collapse of mitochondrial membrane potential, an index of apoptosis, and the elevation of caspase-3 activity, an apoptotic execution enzyme, leading to cell death.	Pyruvaldehyde	0-2	caspase 3	Homo sapiens	105-114
18827464-7	2008	Flow cytometric analyses with annexin-V and propidium iodide double staining revealed that cells exposed to a lethal dose of MG displayed features characteristic of apoptosis.	Pyruvaldehyde	125-127	annexin A5	Homo sapiens	30-39
18616999-4	2008	Herein, we report the effect of glucose or methylglyoxal-induced oxidative modifications on BSA or HSA protein structures and on THP1 monocyte physiology.	Pyruvaldehyde	43-56	GLI family zinc finger 2	Homo sapiens	129-133
18481334-6	2008	The data indicated that methylglyoxal induced mouse Neuro-2A neuroblastoma (Neuro-2A) cell apoptosis via alternation of mitochondria membrane potential and Bax/Bcl-2 ratio, activation of caspase-3, and cleavage of poly (ADP-ribose) polymerase.	Pyruvaldehyde	24-37	BCL2-associated X protein	Mus musculus	156-159
18481334-6	2008	The data indicated that methylglyoxal induced mouse Neuro-2A neuroblastoma (Neuro-2A) cell apoptosis via alternation of mitochondria membrane potential and Bax/Bcl-2 ratio, activation of caspase-3, and cleavage of poly (ADP-ribose) polymerase.	Pyruvaldehyde	24-37	B cell leukemia/lymphoma 2	Mus musculus	160-165
18481334-6	2008	The data indicated that methylglyoxal induced mouse Neuro-2A neuroblastoma (Neuro-2A) cell apoptosis via alternation of mitochondria membrane potential and Bax/Bcl-2 ratio, activation of caspase-3, and cleavage of poly (ADP-ribose) polymerase.	Pyruvaldehyde	24-37	caspase 3	Mus musculus	187-196
18481334-6	2008	The data indicated that methylglyoxal induced mouse Neuro-2A neuroblastoma (Neuro-2A) cell apoptosis via alternation of mitochondria membrane potential and Bax/Bcl-2 ratio, activation of caspase-3, and cleavage of poly (ADP-ribose) polymerase.	Pyruvaldehyde	24-37	poly (ADP-ribose) polymerase family, member 1	Mus musculus	214-242
18481334-7	2008	Furthermore, the results demonstrated that activation of mitogen-activated protein kinase signal pathways (JNK and p38) participated in the methylglyoxal-induced Neuro-2A cell apoptosis process.	Pyruvaldehyde	140-153	mitogen-activated protein kinase 14	Mus musculus	115-118
18437350-7	2008	RESULTS: Aminoguanidine, pyridoxamine, metformin and alagebrium all decreased the methylglyoxal-mediated glycation of the ApoA-I in discoidal rHDL and conserved the ability of the particles to act as substrates for LCAT.	Pyruvaldehyde	82-95	apolipoprotein A1	Homo sapiens	122-128
18413187-9	2008	Glyoxalase I (Glo1) is the initial enzyme involved in the detoxification of MG.	Pyruvaldehyde	76-78	glyoxalase I	Homo sapiens	0-12
18413187-9	2008	Glyoxalase I (Glo1) is the initial enzyme involved in the detoxification of MG.	Pyruvaldehyde	76-78	glyoxalase I	Homo sapiens	14-18
18596836-9	2008	The fact that glyoxalase I activity and the level of glutathione, a cofactor of glyoxalase I, were high in the livers of the 3"-MDAB-fed rats can explain the elevated levels of methylglyoxal and D-lactate in the liver.	Pyruvaldehyde	177-190	glyoxalase 1	Rattus norvegicus	14-26
18596836-9	2008	The fact that glyoxalase I activity and the level of glutathione, a cofactor of glyoxalase I, were high in the livers of the 3"-MDAB-fed rats can explain the elevated levels of methylglyoxal and D-lactate in the liver.	Pyruvaldehyde	177-190	glyoxalase 1	Rattus norvegicus	80-92
18437350-7	2008	RESULTS: Aminoguanidine, pyridoxamine, metformin and alagebrium all decreased the methylglyoxal-mediated glycation of the ApoA-I in discoidal rHDL and conserved the ability of the particles to act as substrates for LCAT.	Pyruvaldehyde	82-95	lecithin-cholesterol acyltransferase	Homo sapiens	215-219
18437350-4	2008	METHODS: Inhibition of ApoA-I glycation was assessed by incubating aminoguanidine, pyridoxamine, metformin and alagebrium with mixtures of methylglyoxal and discoidal reconstituted HDL (rHDL) containing phosphatidylcholine and ApoA-I, ([A-I]rHDL).	Pyruvaldehyde	139-152	apolipoprotein A1	Homo sapiens	23-29
18437350-6	2008	The reversal of ApoA-I glycation was investigated by pre-incubating discoidal (A-I)rHDL with methylglyoxal, then incubating the modified rHDL with aminoguanidine, pyridoxamine or alagebrium.	Pyruvaldehyde	93-106	apolipoprotein A1	Homo sapiens	16-22
18533362-3	2008	The physiologically most important substrate methylglyoxal is converted by glyoxalase I into S-D-lactoyl-glutathione in the first reaction.	Pyruvaldehyde	45-58	glyoxalase I	Homo sapiens	75-87
18448828-2	2008	MG is efficiently metabolized by the glyoxalase system where MG is converted by glyoxalase I (GLO I) to S-D-lactoylglutathione.	Pyruvaldehyde	0-2	glyoxalase 1	Rattus norvegicus	80-92
18448828-2	2008	MG is efficiently metabolized by the glyoxalase system where MG is converted by glyoxalase I (GLO I) to S-D-lactoylglutathione.	Pyruvaldehyde	0-2	glyoxalase 1	Rattus norvegicus	94-99
18448828-2	2008	MG is efficiently metabolized by the glyoxalase system where MG is converted by glyoxalase I (GLO I) to S-D-lactoylglutathione.	Pyruvaldehyde	61-63	glyoxalase 1	Rattus norvegicus	80-92
18448828-2	2008	MG is efficiently metabolized by the glyoxalase system where MG is converted by glyoxalase I (GLO I) to S-D-lactoylglutathione.	Pyruvaldehyde	61-63	glyoxalase 1	Rattus norvegicus	94-99
18448838-3	2008	The natural degradation product of glucose, methylglyoxal, was able to induce the aggregation of vimentin.	Pyruvaldehyde	44-57	vimentin	Homo sapiens	97-105
18258440-1	2008	Glyoxalase I (GLO I) is the rate-limiting enzyme for detoxification of methylglyoxal (MG), a side product of glycolysis, which is able to induce apoptosis.	Pyruvaldehyde	71-84	glyoxalase I	Homo sapiens	0-12
18258440-1	2008	Glyoxalase I (GLO I) is the rate-limiting enzyme for detoxification of methylglyoxal (MG), a side product of glycolysis, which is able to induce apoptosis.	Pyruvaldehyde	71-84	glyoxalase I	Homo sapiens	14-19
18258440-1	2008	Glyoxalase I (GLO I) is the rate-limiting enzyme for detoxification of methylglyoxal (MG), a side product of glycolysis, which is able to induce apoptosis.	Pyruvaldehyde	86-88	glyoxalase I	Homo sapiens	0-12
18258440-1	2008	Glyoxalase I (GLO I) is the rate-limiting enzyme for detoxification of methylglyoxal (MG), a side product of glycolysis, which is able to induce apoptosis.	Pyruvaldehyde	86-88	glyoxalase I	Homo sapiens	14-19
17721990-6	2008	Co-treatment of HUVECs with 5 microM MG and 20 mM glucose significantly increased cytoplasmic free calcium levels, activation of nitric oxide synthase (NOS), caspase-3 and -9, cytochrome c release, and apoptotic cell death.	Pyruvaldehyde	37-39	nitric oxide synthase 2	Homo sapiens	129-150
17721990-6	2008	Co-treatment of HUVECs with 5 microM MG and 20 mM glucose significantly increased cytoplasmic free calcium levels, activation of nitric oxide synthase (NOS), caspase-3 and -9, cytochrome c release, and apoptotic cell death.	Pyruvaldehyde	37-39	caspase 3	Homo sapiens	158-174
17721990-6	2008	Co-treatment of HUVECs with 5 microM MG and 20 mM glucose significantly increased cytoplasmic free calcium levels, activation of nitric oxide synthase (NOS), caspase-3 and -9, cytochrome c release, and apoptotic cell death.	Pyruvaldehyde	37-39	cytochrome c, somatic	Homo sapiens	176-188
18221415-4	2008	The decrease in enzymatic activity promotes accumulation of MG-derived adducts and oxidative stress markers, which cause further inhibition of glyoxalase-1 expression.	Pyruvaldehyde	60-62	Glyoxalase 1	Caenorhabditis elegans	143-155
18762725-5	2008	We further investigated the intracellular mechanisms mediating the MG-induced PGE2 synthesis, focusing particularly on cyclooxygenase-2 (COX-2) and the MAPK superfamily.	Pyruvaldehyde	67-69	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	119-135
18762725-5	2008	We further investigated the intracellular mechanisms mediating the MG-induced PGE2 synthesis, focusing particularly on cyclooxygenase-2 (COX-2) and the MAPK superfamily.	Pyruvaldehyde	67-69	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	137-142
18762725-5	2008	We further investigated the intracellular mechanisms mediating the MG-induced PGE2 synthesis, focusing particularly on cyclooxygenase-2 (COX-2) and the MAPK superfamily.	Pyruvaldehyde	67-69	mitogen activated protein kinase 3	Rattus norvegicus	152-156
18762725-6	2008	Our results indicated that MG induced PGE2 production in a dose-dependent manner, accompanied by augmentation of COX-2 mRNA expression.	Pyruvaldehyde	27-29	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	113-118
18762725-7	2008	This MG-induced PGE2 production was significantly suppressed by inhibiting either ERK1/2 or p38 MAPK, implicating involvement of the MAPK superfamily.	Pyruvaldehyde	5-7	mitogen activated protein kinase 3	Rattus norvegicus	82-88
18762725-7	2008	This MG-induced PGE2 production was significantly suppressed by inhibiting either ERK1/2 or p38 MAPK, implicating involvement of the MAPK superfamily.	Pyruvaldehyde	5-7	mitogen activated protein kinase 3	Rattus norvegicus	96-100
17941823-4	2008	We have investigated the role of MGO modification of four model client proteins (insulin, alpha-lactalbumin, alcohol dehydrogenase and gamma-crystallin) in their aggregation and structure and the ability of human alphaA-crystallin to chaperone them.	Pyruvaldehyde	33-36	insulin	Homo sapiens	81-88
17941823-5	2008	We found that MGO modification (10-1000 microM) decreased the chemical aggregation of insulin and alpha-lactalbumin and thermal aggregation of alcohol dehydrogenase and gamma-crystallin.	Pyruvaldehyde	14-17	insulin	Homo sapiens	86-93
17941823-5	2008	We found that MGO modification (10-1000 microM) decreased the chemical aggregation of insulin and alpha-lactalbumin and thermal aggregation of alcohol dehydrogenase and gamma-crystallin.	Pyruvaldehyde	14-17	lactalbumin alpha	Homo sapiens	98-115
17941823-5	2008	We found that MGO modification (10-1000 microM) decreased the chemical aggregation of insulin and alpha-lactalbumin and thermal aggregation of alcohol dehydrogenase and gamma-crystallin.	Pyruvaldehyde	14-17	aldo-keto reductase family 1 member A1	Homo sapiens	143-164
18533366-4	2008	MG has effects on insulin secretion from pancreatic beta-cells and is a major precursor of advanced glycation endproducts (AGE).	Pyruvaldehyde	0-2	insulin	Homo sapiens	18-25
17596537-4	2007	Formaldehyde and methylglyoxal are produced via SSAO-catalyzed deamination of methylamine and aminoacetone, respectively.	Pyruvaldehyde	17-30	amine oxidase copper containing 2	Homo sapiens	48-52
17869161-6	2008	We also investigate methylglyoxal-induced modulation of brain derived neurotrophic factor and proinflammatory cytokines.	Pyruvaldehyde	20-33	brain-derived neurotrophic factor	Rattus norvegicus	56-89
18946510-1	2008	BACKGROUND: Glyoxalases (Glo1 and Glo2) are involved in the glycolytic pathway by detoxifying the reactive methylglyoxal (MGO) into D-lactate in a two-step reaction using glutathione (GSH) as cofactor.	Pyruvaldehyde	122-125	glyoxalase I	Homo sapiens	25-29
18946510-1	2008	BACKGROUND: Glyoxalases (Glo1 and Glo2) are involved in the glycolytic pathway by detoxifying the reactive methylglyoxal (MGO) into D-lactate in a two-step reaction using glutathione (GSH) as cofactor.	Pyruvaldehyde	122-125	hydroxyacylglutathione hydrolase	Homo sapiens	34-38
18946510-9	2008	CONCLUSIONS/SIGNIFICANCE: The results described herein provide new insights into curcumin"s biological activities as they indicate that inhibition of Glo1 by curcumin may result in non-tolerable levels of MGO and GSH, which, in turn, modulate various metabolic cellular pathways including depletion of cellular ATP and GSH content.	Pyruvaldehyde	205-208	glyoxalase I	Homo sapiens	150-154
17660951-6	2007	When 3T3-L1 adipocytes were treated directly with MG, the impaired insulin signaling was also observed, indicated by decreased insulin-induced insulin-receptor substrate-1 (IRS-1) tyrosine phosphorylation and the decreased kinase activity of phosphatidylinositol (PI) 3-kinase (PI3K).	Pyruvaldehyde	50-52	insulin receptor substrate 1	Rattus norvegicus	173-178
17660951-7	2007	The ability of NAC to block MG-impairment of PI3K activity and IRS-1 phosphorylation further confirmed the role of MG in the development of insulin resistance.	Pyruvaldehyde	28-30	insulin receptor substrate 1	Rattus norvegicus	63-68
17919454-7	2007	In addition, we found that methylglyoxal inhibits human protein tyrosine phosphatase 1B (PTP1B) also.	Pyruvaldehyde	27-40	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	56-87
17919454-7	2007	In addition, we found that methylglyoxal inhibits human protein tyrosine phosphatase 1B (PTP1B) also.	Pyruvaldehyde	27-40	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	89-94
17894456-3	2007	Results revealed that glyoxal (GO) and methylglyoxal (MGO) resulting from the glycative and autoxidative reactions of the high blood sugar glucose (G) evoked a huge production of ROS and NO, which in turn increased the production of peroxynitrite, combined with the activation of the nuclear factor kappaB (NFkappaB), leading to cell apoptosis.	Pyruvaldehyde	39-52	nuclear factor kappa B subunit 1	Homo sapiens	284-305
17894456-3	2007	Results revealed that glyoxal (GO) and methylglyoxal (MGO) resulting from the glycative and autoxidative reactions of the high blood sugar glucose (G) evoked a huge production of ROS and NO, which in turn increased the production of peroxynitrite, combined with the activation of the nuclear factor kappaB (NFkappaB), leading to cell apoptosis.	Pyruvaldehyde	39-52	nuclear factor kappa B subunit 1	Homo sapiens	307-315
17894456-3	2007	Results revealed that glyoxal (GO) and methylglyoxal (MGO) resulting from the glycative and autoxidative reactions of the high blood sugar glucose (G) evoked a huge production of ROS and NO, which in turn increased the production of peroxynitrite, combined with the activation of the nuclear factor kappaB (NFkappaB), leading to cell apoptosis.	Pyruvaldehyde	54-57	nuclear factor kappa B subunit 1	Homo sapiens	284-305
17894456-3	2007	Results revealed that glyoxal (GO) and methylglyoxal (MGO) resulting from the glycative and autoxidative reactions of the high blood sugar glucose (G) evoked a huge production of ROS and NO, which in turn increased the production of peroxynitrite, combined with the activation of the nuclear factor kappaB (NFkappaB), leading to cell apoptosis.	Pyruvaldehyde	54-57	nuclear factor kappa B subunit 1	Homo sapiens	307-315
17504976-3	2007	METHODS AND MAIN FINDINGS: Nontoxic concentrations of GO or MGO altered the PDGF-induced PDGFRbeta-phosphorylation, ERK1/2-activation, and nuclear translocation, and the subsequent proliferation of mesenchymal cells (smooth muscle cells and skin fibroblasts).	Pyruvaldehyde	60-63	platelet derived growth factor receptor, beta polypeptide	Mus musculus	89-98
17504976-3	2007	METHODS AND MAIN FINDINGS: Nontoxic concentrations of GO or MGO altered the PDGF-induced PDGFRbeta-phosphorylation, ERK1/2-activation, and nuclear translocation, and the subsequent proliferation of mesenchymal cells (smooth muscle cells and skin fibroblasts).	Pyruvaldehyde	60-63	mitogen-activated protein kinase 3	Mus musculus	116-122
17504976-9	2007	CONCLUSIONS: These data indicate that MGO and GO induce desensitization of PDGFRbeta that helps to reduce mesenchymal cell proliferation.	Pyruvaldehyde	38-41	platelet derived growth factor receptor, beta polypeptide	Mus musculus	75-84
17663721-0	2007	Chk2 kinase is required for methylglyoxal-induced G2/M cell-cycle checkpoint arrest: implication of cell-cycle checkpoint regulation in diabetic oxidative stress signaling.	Pyruvaldehyde	28-41	checkpoint kinase 2	Homo sapiens	0-4
17617381-0	2007	Methylglyoxal suppresses TNF-alpha-induced NF-kappaB activation by inhibiting NF-kappaB DNA-binding.	Pyruvaldehyde	0-13	tumor necrosis factor	Homo sapiens	25-34
17617381-0	2007	Methylglyoxal suppresses TNF-alpha-induced NF-kappaB activation by inhibiting NF-kappaB DNA-binding.	Pyruvaldehyde	0-13	nuclear factor kappa B subunit 1	Homo sapiens	43-52
17617381-0	2007	Methylglyoxal suppresses TNF-alpha-induced NF-kappaB activation by inhibiting NF-kappaB DNA-binding.	Pyruvaldehyde	0-13	nuclear factor kappa B subunit 1	Homo sapiens	78-87
17617381-5	2007	In this study, we show that methylglyoxal inhibits TNF-induced NF-kappaB activation and NF-kappaB-dependent reporter gene expression by inhibiting the DNA binding capacity of NF-kappaB p65.	Pyruvaldehyde	28-41	tumor necrosis factor	Homo sapiens	51-54
17617381-5	2007	In this study, we show that methylglyoxal inhibits TNF-induced NF-kappaB activation and NF-kappaB-dependent reporter gene expression by inhibiting the DNA binding capacity of NF-kappaB p65.	Pyruvaldehyde	28-41	nuclear factor kappa B subunit 1	Homo sapiens	63-72
17617381-5	2007	In this study, we show that methylglyoxal inhibits TNF-induced NF-kappaB activation and NF-kappaB-dependent reporter gene expression by inhibiting the DNA binding capacity of NF-kappaB p65.	Pyruvaldehyde	28-41	nuclear factor kappa B subunit 1	Homo sapiens	88-97
17617381-5	2007	In this study, we show that methylglyoxal inhibits TNF-induced NF-kappaB activation and NF-kappaB-dependent reporter gene expression by inhibiting the DNA binding capacity of NF-kappaB p65.	Pyruvaldehyde	28-41	nuclear factor kappa B subunit 1	Homo sapiens	88-97
17617381-5	2007	In this study, we show that methylglyoxal inhibits TNF-induced NF-kappaB activation and NF-kappaB-dependent reporter gene expression by inhibiting the DNA binding capacity of NF-kappaB p65.	Pyruvaldehyde	28-41	RELA proto-oncogene, NF-kB subunit	Homo sapiens	185-188
17617381-6	2007	Methylglyoxal slightly delayed, but did not inhibit, TNF-induced degradation of IkappaBalpha and strongly inhibited TNF-induced NF-kappaB-dependent re-synthesis of IkappaBalpha.	Pyruvaldehyde	0-13	NFKB inhibitor alpha	Homo sapiens	80-92
17617381-6	2007	Methylglyoxal slightly delayed, but did not inhibit, TNF-induced degradation of IkappaBalpha and strongly inhibited TNF-induced NF-kappaB-dependent re-synthesis of IkappaBalpha.	Pyruvaldehyde	0-13	tumor necrosis factor	Homo sapiens	116-119
17617381-6	2007	Methylglyoxal slightly delayed, but did not inhibit, TNF-induced degradation of IkappaBalpha and strongly inhibited TNF-induced NF-kappaB-dependent re-synthesis of IkappaBalpha.	Pyruvaldehyde	0-13	nuclear factor kappa B subunit 1	Homo sapiens	128-137
17617381-6	2007	Methylglyoxal slightly delayed, but did not inhibit, TNF-induced degradation of IkappaBalpha and strongly inhibited TNF-induced NF-kappaB-dependent re-synthesis of IkappaBalpha.	Pyruvaldehyde	0-13	NFKB inhibitor alpha	Homo sapiens	164-176
17617381-7	2007	The TNF-induced nuclear translocation of NF-kappaB p65 was also delayed, but not inhibited, in the presence of methylglyoxal.	Pyruvaldehyde	111-124	tumor necrosis factor	Homo sapiens	4-7
17617381-7	2007	The TNF-induced nuclear translocation of NF-kappaB p65 was also delayed, but not inhibited, in the presence of methylglyoxal.	Pyruvaldehyde	111-124	nuclear factor kappa B subunit 1	Homo sapiens	41-50
17617381-7	2007	The TNF-induced nuclear translocation of NF-kappaB p65 was also delayed, but not inhibited, in the presence of methylglyoxal.	Pyruvaldehyde	111-124	RELA proto-oncogene, NF-kB subunit	Homo sapiens	51-54
17617381-10	2007	Furthermore, overexpression of p65 inhibited TNF-induced cell death; however, in the presence of exogenously added methylglyoxal, overexpression of p65 caused far greater TNF-induced cell death.	Pyruvaldehyde	115-128	RELA proto-oncogene, NF-kB subunit	Homo sapiens	148-151
17617381-10	2007	Furthermore, overexpression of p65 inhibited TNF-induced cell death; however, in the presence of exogenously added methylglyoxal, overexpression of p65 caused far greater TNF-induced cell death.	Pyruvaldehyde	115-128	tumor necrosis factor	Homo sapiens	171-174
17617381-11	2007	These findings suggest that methylglyoxal provides another control mechanism for modulating the expression of NF-kappaB-responsive genes and that methylglyoxal may be responsible for tipping the balance towards TNF-induced cell death in cells with constitutive NF-kappaB activation.	Pyruvaldehyde	28-41	nuclear factor kappa B subunit 1	Homo sapiens	110-119
17663721-3	2007	It has been established that MG elicits oxidative stress signaling, leading to the activation of MAP kinases, p38 MAPK and JNK, yet it remains largely unknown about a role of cell-cycle checkpoint regulation in MG-induced signaling.	Pyruvaldehyde	29-31	mitogen-activated protein kinase 14	Homo sapiens	110-113
17663721-3	2007	It has been established that MG elicits oxidative stress signaling, leading to the activation of MAP kinases, p38 MAPK and JNK, yet it remains largely unknown about a role of cell-cycle checkpoint regulation in MG-induced signaling.	Pyruvaldehyde	29-31	mitogen-activated protein kinase 8	Homo sapiens	123-126
17663721-4	2007	Here, we show that checkpoint kinases, Chk1 and Chk2, as well as their upstream ATM kinase are phosphorylated and activated following MG treatment of cultured cells.	Pyruvaldehyde	134-136	checkpoint kinase 1	Homo sapiens	39-43
17663721-4	2007	Here, we show that checkpoint kinases, Chk1 and Chk2, as well as their upstream ATM kinase are phosphorylated and activated following MG treatment of cultured cells.	Pyruvaldehyde	134-136	checkpoint kinase 2	Homo sapiens	48-52
17663721-5	2007	This MG-induced activation of Chk1 and Chk2 were inhibited by either aminoguanidine (AG), an inhibitor of production of advanced glycation end products (AGEs) or N-acetyl-l-cysteine (NAC), an anti-oxidant in dose dependent manners, indicating that oxidative stress via AGEs is involved critically in the activation of Chk1 and Chk2 by MG.	Pyruvaldehyde	5-7	checkpoint kinase 1	Homo sapiens	30-34
17663721-5	2007	This MG-induced activation of Chk1 and Chk2 were inhibited by either aminoguanidine (AG), an inhibitor of production of advanced glycation end products (AGEs) or N-acetyl-l-cysteine (NAC), an anti-oxidant in dose dependent manners, indicating that oxidative stress via AGEs is involved critically in the activation of Chk1 and Chk2 by MG.	Pyruvaldehyde	5-7	checkpoint kinase 2	Homo sapiens	39-43
17663721-5	2007	This MG-induced activation of Chk1 and Chk2 were inhibited by either aminoguanidine (AG), an inhibitor of production of advanced glycation end products (AGEs) or N-acetyl-l-cysteine (NAC), an anti-oxidant in dose dependent manners, indicating that oxidative stress via AGEs is involved critically in the activation of Chk1 and Chk2 by MG.	Pyruvaldehyde	5-7	X-linked Kx blood group	Homo sapiens	183-186
17663721-5	2007	This MG-induced activation of Chk1 and Chk2 were inhibited by either aminoguanidine (AG), an inhibitor of production of advanced glycation end products (AGEs) or N-acetyl-l-cysteine (NAC), an anti-oxidant in dose dependent manners, indicating that oxidative stress via AGEs is involved critically in the activation of Chk1 and Chk2 by MG.	Pyruvaldehyde	5-7	checkpoint kinase 1	Homo sapiens	318-322
17663721-5	2007	This MG-induced activation of Chk1 and Chk2 were inhibited by either aminoguanidine (AG), an inhibitor of production of advanced glycation end products (AGEs) or N-acetyl-l-cysteine (NAC), an anti-oxidant in dose dependent manners, indicating that oxidative stress via AGEs is involved critically in the activation of Chk1 and Chk2 by MG.	Pyruvaldehyde	5-7	checkpoint kinase 2	Homo sapiens	327-331
17663721-6	2007	Furthermore, it was found that cell-cycle synchronized cells exhibited G(2)/M checkpoint arrest following MG treatment, and that siRNA-mediated knock-down of Chk2, but not Chk1, results in a failure of MG-induced G(2)/M arrest.	Pyruvaldehyde	106-108	checkpoint kinase 2	Homo sapiens	158-162
17663721-6	2007	Furthermore, it was found that cell-cycle synchronized cells exhibited G(2)/M checkpoint arrest following MG treatment, and that siRNA-mediated knock-down of Chk2, but not Chk1, results in a failure of MG-induced G(2)/M arrest.	Pyruvaldehyde	202-204	checkpoint kinase 2	Homo sapiens	158-162
17663721-7	2007	Thus, the results indicate a critical role for Chk2 in MG-induced G(2)/M cell-cycle checkpoint arrest.	Pyruvaldehyde	55-57	checkpoint kinase 2	Homo sapiens	47-51
17635749-9	2007	Additionally, SB203580 pretreatment reduced MGO promotion of fibronectin gene activation suggesting that cytosolic p38 activation might affect MGO-induced renal mesangial fibrosis.	Pyruvaldehyde	143-146	fibronectin 1	Rattus norvegicus	61-72
17635749-9	2007	Additionally, SB203580 pretreatment reduced MGO promotion of fibronectin gene activation suggesting that cytosolic p38 activation might affect MGO-induced renal mesangial fibrosis.	Pyruvaldehyde	143-146	mitogen activated protein kinase 14	Rattus norvegicus	115-118
17635749-0	2007	Methylglyoxal-induced fibronectin gene expression through Ras-mediated NADPH oxidase activation in renal mesangial cells.	Pyruvaldehyde	0-13	fibronectin 1	Rattus norvegicus	22-33
17635749-5	2007	RESULTS: Expression of fibronectin induced by MGO was highest after 48 h treatment.	Pyruvaldehyde	46-49	fibronectin 1	Rattus norvegicus	23-34
16969712-3	2007	That MG-induced modification of the chaperone and anti-apoptotic protein (Hsp27) increases its protective functions suggests a possible hormetic response to transient MG production during transient periods of glycolysis in dietary restricted animals.	Pyruvaldehyde	5-7	heat shock protein family B (small) member 1	Homo sapiens	74-79
17635749-7	2007	Pretreatment with diphenylene iodonium significantly suppressed MGO-induced superoxide, TGF-beta1 expression and fibronectin gene expression, indicating that NADPH oxidase is responsible for inducing superoxide formation and subsequently induced renal fibrosis.	Pyruvaldehyde	64-67	transforming growth factor, beta 1	Rattus norvegicus	88-97
17635749-7	2007	Pretreatment with diphenylene iodonium significantly suppressed MGO-induced superoxide, TGF-beta1 expression and fibronectin gene expression, indicating that NADPH oxidase is responsible for inducing superoxide formation and subsequently induced renal fibrosis.	Pyruvaldehyde	64-67	fibronectin 1	Rattus norvegicus	113-124
17635749-8	2007	High MGO rapidly enhanced Ras activation in 1 h and progressively increased cytosolic p38 activation.	Pyruvaldehyde	5-8	mitogen activated protein kinase 14	Rattus norvegicus	86-89
17635749-9	2007	Additionally, SB203580 pretreatment reduced MGO promotion of fibronectin gene activation suggesting that cytosolic p38 activation might affect MGO-induced renal mesangial fibrosis.	Pyruvaldehyde	44-47	fibronectin 1	Rattus norvegicus	61-72
16781798-3	2007	Furthermore, methylglyoxal levels increase under pathophysiological conditions, for example, when trisosephosphate levels are elevated, the expression or activity of glyoxalase I is decreased, as is the case when the concentration of reduced glutathione, the rate-determining co-factor of glyoxalase I, is low.	Pyruvaldehyde	13-26	glyoxalase I	Homo sapiens	166-178
16781798-3	2007	Furthermore, methylglyoxal levels increase under pathophysiological conditions, for example, when trisosephosphate levels are elevated, the expression or activity of glyoxalase I is decreased, as is the case when the concentration of reduced glutathione, the rate-determining co-factor of glyoxalase I, is low.	Pyruvaldehyde	13-26	glyoxalase I	Homo sapiens	289-301
17347135-10	2007	Methylglyoxal significantly increased both the B220(+) and IgE(+)B220(+) cell populations in the draining lymph nodes and total serum IgE levels.	Pyruvaldehyde	0-13	immunoglobulin heavy constant epsilon	Homo sapiens	59-62
17347135-10	2007	Methylglyoxal significantly increased both the B220(+) and IgE(+)B220(+) cell populations in the draining lymph nodes and total serum IgE levels.	Pyruvaldehyde	0-13	immunoglobulin heavy constant epsilon	Homo sapiens	134-137
17347135-11	2007	The four compounds generated by indoor air chemistry were predicted by QSAR and animal modeling to be sensitizers, with the potential for methylglyoxal to induce IgE.	Pyruvaldehyde	138-151	immunoglobulin heavy constant epsilon	Homo sapiens	162-165
16969712-3	2007	That MG-induced modification of the chaperone and anti-apoptotic protein (Hsp27) increases its protective functions suggests a possible hormetic response to transient MG production during transient periods of glycolysis in dietary restricted animals.	Pyruvaldehyde	167-169	heat shock protein family B (small) member 1	Homo sapiens	74-79
17873339-5	2007	In insulin resistance, alterations in glucose and lipid metabolism lead to the production of excess aldehydes including glyoxal and methylglyoxal.	Pyruvaldehyde	132-145	insulin	Homo sapiens	3-10
17216278-9	2007	RESULTS: Methylglyoxal-mediated modifications of the arginine, lysine and tryptophan residues in lipid-free and lipid-associated apoA-I were time- and concentration-dependent.	Pyruvaldehyde	9-22	apolipoprotein A1	Homo sapiens	129-135
17131386-0	2007	Apoptotic signaling in methylglyoxal-treated human osteoblasts involves oxidative stress, c-Jun N-terminal kinase, caspase-3, and p21-activated kinase 2.	Pyruvaldehyde	23-36	mitogen-activated protein kinase 8	Homo sapiens	90-113
17131386-0	2007	Apoptotic signaling in methylglyoxal-treated human osteoblasts involves oxidative stress, c-Jun N-terminal kinase, caspase-3, and p21-activated kinase 2.	Pyruvaldehyde	23-36	caspase 3	Homo sapiens	115-124
17131386-0	2007	Apoptotic signaling in methylglyoxal-treated human osteoblasts involves oxidative stress, c-Jun N-terminal kinase, caspase-3, and p21-activated kinase 2.	Pyruvaldehyde	23-36	p21 (RAC1) activated kinase 2	Homo sapiens	130-152
17131386-4	2007	We further show that MG-induced apoptosis of osteoblasts involves specific apoptotic biochemical changes, including oxidative stress, c-Jun N-terminal kinase (JNK) activation, mitochondrial membrane potential changes, cytochrome C release, increased Bax/Bcl-2 protein ratios, and activation of caspases (caspase-9, caspase-3) and p21-activated protein kinase 2 (PAK2).	Pyruvaldehyde	21-23	mitogen-activated protein kinase 8	Homo sapiens	134-157
17131386-4	2007	We further show that MG-induced apoptosis of osteoblasts involves specific apoptotic biochemical changes, including oxidative stress, c-Jun N-terminal kinase (JNK) activation, mitochondrial membrane potential changes, cytochrome C release, increased Bax/Bcl-2 protein ratios, and activation of caspases (caspase-9, caspase-3) and p21-activated protein kinase 2 (PAK2).	Pyruvaldehyde	21-23	mitogen-activated protein kinase 8	Homo sapiens	159-162
17131386-4	2007	We further show that MG-induced apoptosis of osteoblasts involves specific apoptotic biochemical changes, including oxidative stress, c-Jun N-terminal kinase (JNK) activation, mitochondrial membrane potential changes, cytochrome C release, increased Bax/Bcl-2 protein ratios, and activation of caspases (caspase-9, caspase-3) and p21-activated protein kinase 2 (PAK2).	Pyruvaldehyde	21-23	cytochrome c, somatic	Homo sapiens	218-230
17131386-4	2007	We further show that MG-induced apoptosis of osteoblasts involves specific apoptotic biochemical changes, including oxidative stress, c-Jun N-terminal kinase (JNK) activation, mitochondrial membrane potential changes, cytochrome C release, increased Bax/Bcl-2 protein ratios, and activation of caspases (caspase-9, caspase-3) and p21-activated protein kinase 2 (PAK2).	Pyruvaldehyde	21-23	BCL2 associated X, apoptosis regulator	Homo sapiens	250-253
17131386-4	2007	We further show that MG-induced apoptosis of osteoblasts involves specific apoptotic biochemical changes, including oxidative stress, c-Jun N-terminal kinase (JNK) activation, mitochondrial membrane potential changes, cytochrome C release, increased Bax/Bcl-2 protein ratios, and activation of caspases (caspase-9, caspase-3) and p21-activated protein kinase 2 (PAK2).	Pyruvaldehyde	21-23	BCL2 apoptosis regulator	Homo sapiens	254-259
17131386-4	2007	We further show that MG-induced apoptosis of osteoblasts involves specific apoptotic biochemical changes, including oxidative stress, c-Jun N-terminal kinase (JNK) activation, mitochondrial membrane potential changes, cytochrome C release, increased Bax/Bcl-2 protein ratios, and activation of caspases (caspase-9, caspase-3) and p21-activated protein kinase 2 (PAK2).	Pyruvaldehyde	21-23	caspase 9	Homo sapiens	294-302
17131386-4	2007	We further show that MG-induced apoptosis of osteoblasts involves specific apoptotic biochemical changes, including oxidative stress, c-Jun N-terminal kinase (JNK) activation, mitochondrial membrane potential changes, cytochrome C release, increased Bax/Bcl-2 protein ratios, and activation of caspases (caspase-9, caspase-3) and p21-activated protein kinase 2 (PAK2).	Pyruvaldehyde	21-23	caspase 9	Homo sapiens	304-313
17131386-4	2007	We further show that MG-induced apoptosis of osteoblasts involves specific apoptotic biochemical changes, including oxidative stress, c-Jun N-terminal kinase (JNK) activation, mitochondrial membrane potential changes, cytochrome C release, increased Bax/Bcl-2 protein ratios, and activation of caspases (caspase-9, caspase-3) and p21-activated protein kinase 2 (PAK2).	Pyruvaldehyde	21-23	caspase 3	Homo sapiens	315-324
17131386-4	2007	We further show that MG-induced apoptosis of osteoblasts involves specific apoptotic biochemical changes, including oxidative stress, c-Jun N-terminal kinase (JNK) activation, mitochondrial membrane potential changes, cytochrome C release, increased Bax/Bcl-2 protein ratios, and activation of caspases (caspase-9, caspase-3) and p21-activated protein kinase 2 (PAK2).	Pyruvaldehyde	21-23	p21 (RAC1) activated kinase 2	Homo sapiens	330-360
17131386-4	2007	We further show that MG-induced apoptosis of osteoblasts involves specific apoptotic biochemical changes, including oxidative stress, c-Jun N-terminal kinase (JNK) activation, mitochondrial membrane potential changes, cytochrome C release, increased Bax/Bcl-2 protein ratios, and activation of caspases (caspase-9, caspase-3) and p21-activated protein kinase 2 (PAK2).	Pyruvaldehyde	21-23	p21 (RAC1) activated kinase 2	Homo sapiens	362-366
17131386-5	2007	Treatment of osteoblasts with SP600125, a JNK-specific inhibitor, led to a reduction in MG-induced apoptosis and decreased activation of caspase-3 and PAK2, indicating that JNK activity is upstream of these events.	Pyruvaldehyde	88-90	mitogen-activated protein kinase 8	Homo sapiens	42-45
17131386-5	2007	Treatment of osteoblasts with SP600125, a JNK-specific inhibitor, led to a reduction in MG-induced apoptosis and decreased activation of caspase-3 and PAK2, indicating that JNK activity is upstream of these events.	Pyruvaldehyde	88-90	mitogen-activated protein kinase 8	Homo sapiens	173-176
17131386-6	2007	Experiments using anti-sense oligonucleotides against PAK2 further showed that PAK2 activation is required for MG-induced apoptosis in osteoblasts.	Pyruvaldehyde	111-113	p21 (RAC1) activated kinase 2	Homo sapiens	54-58
17131386-6	2007	Experiments using anti-sense oligonucleotides against PAK2 further showed that PAK2 activation is required for MG-induced apoptosis in osteoblasts.	Pyruvaldehyde	111-113	p21 (RAC1) activated kinase 2	Homo sapiens	79-83
17131386-7	2007	Interestingly, we also found that MG treatment triggered nuclear translocation of NF-kappaB, although the precise regulatory role of NF-kappaB activation in MG-induced apoptosis remains unclear.	Pyruvaldehyde	34-36	nuclear factor kappa B subunit 1	Homo sapiens	82-91
17174344-10	2007	MG-AGE-induced phosphorylation of ERK1/2 and p38 was nullified by neutralizing AGE with specific anti-AGE antibody but not nonspecific antiserum.	Pyruvaldehyde	0-2	mitogen-activated protein kinase 1	Homo sapiens	45-48
17174344-10	2007	MG-AGE-induced phosphorylation of ERK1/2 and p38 was nullified by neutralizing AGE with specific anti-AGE antibody but not nonspecific antiserum.	Pyruvaldehyde	0-2	mitogen-activated protein kinase 3	Homo sapiens	34-40
16427160-14	2007	In conclusion, the decrease of glyoxalase I expression with increasing AD stage might be one reason for methylglyoxal-induced neuronal impairment, apoptosis, and AGE formation in plaques and tangles.	Pyruvaldehyde	104-117	glyoxalase I	Homo sapiens	31-43
17401529-1	2007	Formaldehyde and methylglyoxal are generated via deamination from methylamine and aminoacetone respectively catalyzed by semicarbazide-sensitive amine oxidase (SSAO).	Pyruvaldehyde	17-30	amine oxidase copper containing 2	Homo sapiens	121-158
17401529-1	2007	Formaldehyde and methylglyoxal are generated via deamination from methylamine and aminoacetone respectively catalyzed by semicarbazide-sensitive amine oxidase (SSAO).	Pyruvaldehyde	17-30	amine oxidase copper containing 2	Homo sapiens	160-164
17445870-0	2007	AGEs and methylglyoxal induce apoptosis and expression of Mac-1 on neutrophils resulting in platelet-neutrophil aggregation.	Pyruvaldehyde	9-22	integrin subunit beta 2	Homo sapiens	58-63
17445870-7	2007	However, stimulation with MG resulted in a dose-dependent expression of P-selectin by platelets.	Pyruvaldehyde	26-28	selectin P	Homo sapiens	72-82
17445870-8	2007	Stimulation with AGE-BSA or MG markedly increased dose-dependent expression of Apo2.7 on the neutrophil mitochondria.	Pyruvaldehyde	28-30	TNF receptor superfamily member 10a	Homo sapiens	79-83
17445870-10	2007	CONCLUSIONS: AGE-BSA as well as MG induced apoptosis of neutrophils and enhanced expression of the adhesion molecule Mac-1 resulting in increased formation of platelet-neutrophil aggregates.	Pyruvaldehyde	32-34	integrin subunit beta 2	Homo sapiens	117-122
17074066-3	2006	Formaldehyde and methylglyoxal are produced via deamination of, respectively, methylamine and aminoacetone catalyzed by semicarbazide-sensitive amine oxidase (SSAO, EC 1.4.3.6.	Pyruvaldehyde	17-30	amine oxidase copper containing 2	Homo sapiens	120-157
17994461-5	2007	Superoxide mediated methylglyoxal-induced caspase 3 cleavage.	Pyruvaldehyde	20-33	caspase 3	Rattus norvegicus	42-51
17994461-7	2007	Methylglyoxal rapidly enhanced Ras activation and progressively increased cytosolic P38 and nuclear c-Jun activation.	Pyruvaldehyde	0-13	mitogen activated protein kinase 14	Rattus norvegicus	84-87
17994461-8	2007	Scavenging of superoxide by superoxide dismutase or diphenyloniodium, inhibiting P38 by SB203580, and inhibiting Ras with manumycin A successfully reduced the promoting effect of methylglyoxal on P38 and c-Jun phosphorylation (activation).	Pyruvaldehyde	179-192	mitogen activated protein kinase 14	Rattus norvegicus	81-84
17994461-8	2007	Scavenging of superoxide by superoxide dismutase or diphenyloniodium, inhibiting P38 by SB203580, and inhibiting Ras with manumycin A successfully reduced the promoting effect of methylglyoxal on P38 and c-Jun phosphorylation (activation).	Pyruvaldehyde	179-192	mitogen activated protein kinase 14	Rattus norvegicus	196-199
17994461-10	2007	CONCLUSIONS: This study has shown that methylglyoxal increased Ras modulation of superoxide-mediated P38 activation and c-Jun activation, which resulted in increased apoptosis.	Pyruvaldehyde	39-52	mitogen activated protein kinase 14	Rattus norvegicus	101-104
17074066-3	2006	Formaldehyde and methylglyoxal are produced via deamination of, respectively, methylamine and aminoacetone catalyzed by semicarbazide-sensitive amine oxidase (SSAO, EC 1.4.3.6.	Pyruvaldehyde	17-30	amine oxidase copper containing 2	Homo sapiens	159-163
16950408-7	2006	Moreover, an enhanced iNOS expression was also observed in the cells treated directly with MG which was significantly inhibited when co-application with N-acetyl-l-cysteine.	Pyruvaldehyde	91-93	nitric oxide synthase 2	Homo sapiens	22-26
16337338-10	2006	In addition, incubation with cisplatin induced almost no caspase-3 activation in SW1573 cells while a strong activation was seen in H460 cells; which was significantly reduced by incubation with an inhibitor of glyoxalase I, the enzyme that catalyzes the conversion of methylglyoxal.	Pyruvaldehyde	269-282	glyoxalase I	Homo sapiens	211-223
17030441-4	2006	Ara1p had apparent Km values of approximately 14 mM, 7 mM and 4 mM for methylglyoxal, diacetyl and pentanedione respectively, with corresponding turnover rates of 4.4, 6.9 and 5.9 s(-1) at pH 7.0. pH profiling showed that Ara1p had a pH optimum of 4.5 for the diacetyl reduction reaction.	Pyruvaldehyde	71-85	D-arabinose 1-dehydrogenase (NAD(P)(+)) ARA1	Saccharomyces cerevisiae S288C	0-5
16464860-2	2006	We have recently found that MG activates transcription factors such as Yap1 and Msn2, and triggers a Hog1 mitogen-activated protein kinase cascade in Saccharomyces cerevisiae.	Pyruvaldehyde	28-30	stress-responsive transcriptional activator MSN2	Saccharomyces cerevisiae S288C	80-84
16831876-6	2006	We also found that, upon overexpression, the cytosolic, but not the mitochondrial, GLX2 inhibits the apoptotic response of a cell to methylglyoxal, a by-product of glycolysis.	Pyruvaldehyde	133-146	hydroxyacylglutathione hydrolase	Homo sapiens	83-87
16831876-7	2006	Likewise, we showed that cells deficient in GLX2 are hypersensitive to methylglyoxal-induced apoptosis.	Pyruvaldehyde	71-84	hydroxyacylglutathione hydrolase	Homo sapiens	44-48
16831876-10	2006	Given that methylglyoxal is frequently generated under both physiological and pathological conditions, we postulate that GLX2 serves as a pro-survival factor of the p53 family and plays a critical role in the normal development and in the pathogenesis of various human diseases, including cancer, diabetes, and neurodegenerative diseases.	Pyruvaldehyde	11-24	hydroxyacylglutathione hydrolase	Homo sapiens	121-125
16831876-10	2006	Given that methylglyoxal is frequently generated under both physiological and pathological conditions, we postulate that GLX2 serves as a pro-survival factor of the p53 family and plays a critical role in the normal development and in the pathogenesis of various human diseases, including cancer, diabetes, and neurodegenerative diseases.	Pyruvaldehyde	11-24	tumor protein p53	Homo sapiens	165-168
16671891-8	2006	It is shown that MGX (methylglyoxal), GO (glyoxal) and glycolaldehyde, but not hydroxyacetone and glucose, inhibit catB (cathepsin B), catL (cathepsin L) and catS (cathepsin S) activity in macrophage cell lysates, in a concentration-dependent manner.	Pyruvaldehyde	17-20	cathepsin B	Felis catus	115-119
16671891-8	2006	It is shown that MGX (methylglyoxal), GO (glyoxal) and glycolaldehyde, but not hydroxyacetone and glucose, inhibit catB (cathepsin B), catL (cathepsin L) and catS (cathepsin S) activity in macrophage cell lysates, in a concentration-dependent manner.	Pyruvaldehyde	17-20	cathepsin B	Felis catus	121-132
16671891-8	2006	It is shown that MGX (methylglyoxal), GO (glyoxal) and glycolaldehyde, but not hydroxyacetone and glucose, inhibit catB (cathepsin B), catL (cathepsin L) and catS (cathepsin S) activity in macrophage cell lysates, in a concentration-dependent manner.	Pyruvaldehyde	17-20	procathepsin L	Felis catus	135-139
16671891-8	2006	It is shown that MGX (methylglyoxal), GO (glyoxal) and glycolaldehyde, but not hydroxyacetone and glucose, inhibit catB (cathepsin B), catL (cathepsin L) and catS (cathepsin S) activity in macrophage cell lysates, in a concentration-dependent manner.	Pyruvaldehyde	17-20	procathepsin L	Felis catus	141-152
16671891-8	2006	It is shown that MGX (methylglyoxal), GO (glyoxal) and glycolaldehyde, but not hydroxyacetone and glucose, inhibit catB (cathepsin B), catL (cathepsin L) and catS (cathepsin S) activity in macrophage cell lysates, in a concentration-dependent manner.	Pyruvaldehyde	17-20	cathepsin S	Felis catus	164-175
16671891-8	2006	It is shown that MGX (methylglyoxal), GO (glyoxal) and glycolaldehyde, but not hydroxyacetone and glucose, inhibit catB (cathepsin B), catL (cathepsin L) and catS (cathepsin S) activity in macrophage cell lysates, in a concentration-dependent manner.	Pyruvaldehyde	22-35	cathepsin B	Felis catus	115-119
16671891-8	2006	It is shown that MGX (methylglyoxal), GO (glyoxal) and glycolaldehyde, but not hydroxyacetone and glucose, inhibit catB (cathepsin B), catL (cathepsin L) and catS (cathepsin S) activity in macrophage cell lysates, in a concentration-dependent manner.	Pyruvaldehyde	22-35	cathepsin B	Felis catus	121-132
16671891-8	2006	It is shown that MGX (methylglyoxal), GO (glyoxal) and glycolaldehyde, but not hydroxyacetone and glucose, inhibit catB (cathepsin B), catL (cathepsin L) and catS (cathepsin S) activity in macrophage cell lysates, in a concentration-dependent manner.	Pyruvaldehyde	22-35	procathepsin L	Felis catus	135-139
16671891-8	2006	It is shown that MGX (methylglyoxal), GO (glyoxal) and glycolaldehyde, but not hydroxyacetone and glucose, inhibit catB (cathepsin B), catL (cathepsin L) and catS (cathepsin S) activity in macrophage cell lysates, in a concentration-dependent manner.	Pyruvaldehyde	22-35	procathepsin L	Felis catus	141-152
16671891-8	2006	It is shown that MGX (methylglyoxal), GO (glyoxal) and glycolaldehyde, but not hydroxyacetone and glucose, inhibit catB (cathepsin B), catL (cathepsin L) and catS (cathepsin S) activity in macrophage cell lysates, in a concentration-dependent manner.	Pyruvaldehyde	22-35	cathepsin S	Felis catus	164-175
16756764-0	2006	Oxidative modification of human ceruloplasmin by methylglyoxal: an in vitro study.	Pyruvaldehyde	49-62	ceruloplasmin	Homo sapiens	32-45
16756764-3	2006	In this in vitro study, we investigated the effect of MG on the structure and function of ceruloplasmin (CP) a serum oxidase carrier of copper ions in the human.	Pyruvaldehyde	54-56	ceruloplasmin	Homo sapiens	90-103
16756764-3	2006	In this in vitro study, we investigated the effect of MG on the structure and function of ceruloplasmin (CP) a serum oxidase carrier of copper ions in the human.	Pyruvaldehyde	54-56	ceruloplasmin	Homo sapiens	105-107
16756764-4	2006	When CP was incubated with MG, the protein showed increased electrophoretic mobility which represented the aggregates at a high concentration of MG (100 mM).	Pyruvaldehyde	27-29	ceruloplasmin	Homo sapiens	5-7
16756764-8	2006	It is suggested that oxidative damage of CP by MG may induce perturbations of the copper transport system and subsequently lead to harmful intracellular condition.	Pyruvaldehyde	47-49	ceruloplasmin	Homo sapiens	41-43
16644685-0	2006	Methylglyoxal impairs the insulin signaling pathways independently of the formation of intracellular reactive oxygen species.	Pyruvaldehyde	0-13	insulin	Homo sapiens	26-33
16644685-6	2006	We analyzed the impact of methylglyoxal on insulin-induced signaling in L6 muscle cells.	Pyruvaldehyde	26-39	insulin	Homo sapiens	43-50
16644685-7	2006	We demonstrate that a short exposure to methylglyoxal induces an inhibition of insulin-stimulated phosphorylation of protein kinase B and extracellular-regulated kinase 1/2, without affecting insulin receptor tyrosine phosphorylation.	Pyruvaldehyde	40-53	insulin	Homo sapiens	79-86
16644685-9	2006	Our data suggest that an increase in intracellular methylglyoxal content hampers a key molecule, thereby leading to inhibition of insulin-induced signaling.	Pyruvaldehyde	51-64	insulin	Homo sapiens	130-137
16505483-5	2006	However, treatment with a combination of high glucose and S-p-bromobenzylglutathione cyclopentyl diester, a competitive inhibitor of glyoxalase I, resulted in apoptosis along with a dramatic increase in MGO.	Pyruvaldehyde	203-206	glyoxalase I	Homo sapiens	133-145
16464860-2	2006	We have recently found that MG activates transcription factors such as Yap1 and Msn2, and triggers a Hog1 mitogen-activated protein kinase cascade in Saccharomyces cerevisiae.	Pyruvaldehyde	28-30	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	71-75
16615138-5	2006	Modification by MGO enhanced the chaperone function of both pHsp27 and native Hsp27, but the effect on Hsp27 was at least three-times greater than on pHsp27.	Pyruvaldehyde	16-19	heat shock protein family B (small) member 1	Homo sapiens	61-66
16615138-5	2006	Modification by MGO enhanced the chaperone function of both pHsp27 and native Hsp27, but the effect on Hsp27 was at least three-times greater than on pHsp27.	Pyruvaldehyde	16-19	heat shock protein family B (small) member 1	Homo sapiens	78-83
16615138-8	2006	MGO-modified Hsp27 had an even greater effect (62% inhibition).	Pyruvaldehyde	0-3	heat shock protein family B (small) member 1	Homo sapiens	13-18
16615138-9	2006	SP-induced reactive oxygen species in HLE-B3 cells was significantly lower in cells transferred with MGO-modified Hsp27 when compared to native Hsp27.	Pyruvaldehyde	101-104	heat shock protein family B (small) member 1	Homo sapiens	114-119
16615138-10	2006	In vitro incubation experiments showed that MGO-modified Hsp27 reduced the activity of caspase-9, and MGO-modified pHsp27 reduced activities of both caspase-9 and caspase-3.	Pyruvaldehyde	44-47	heat shock protein family B (small) member 1	Homo sapiens	57-62
16615138-10	2006	In vitro incubation experiments showed that MGO-modified Hsp27 reduced the activity of caspase-9, and MGO-modified pHsp27 reduced activities of both caspase-9 and caspase-3.	Pyruvaldehyde	44-47	caspase 9	Homo sapiens	87-96
16615138-10	2006	In vitro incubation experiments showed that MGO-modified Hsp27 reduced the activity of caspase-9, and MGO-modified pHsp27 reduced activities of both caspase-9 and caspase-3.	Pyruvaldehyde	102-105	caspase 9	Homo sapiens	149-158
16615138-10	2006	In vitro incubation experiments showed that MGO-modified Hsp27 reduced the activity of caspase-9, and MGO-modified pHsp27 reduced activities of both caspase-9 and caspase-3.	Pyruvaldehyde	102-105	caspase 3	Homo sapiens	163-172
16615138-11	2006	Based on these results, we propose that Hsp27 becomes a better anti-apoptotic protein after modification by MGO, which may be due to multiple mechanisms that include enhancement of chaperone function, reduction in oxidative stress, and inhibition of activity of caspases.	Pyruvaldehyde	108-111	heat shock protein family B (small) member 1	Homo sapiens	40-45
16615138-11	2006	Based on these results, we propose that Hsp27 becomes a better anti-apoptotic protein after modification by MGO, which may be due to multiple mechanisms that include enhancement of chaperone function, reduction in oxidative stress, and inhibition of activity of caspases.	Pyruvaldehyde	108-111	caspase 9	Homo sapiens	262-270
16615138-12	2006	Our results suggest that MGO modification and phosphorylation of Hsp27 may have important consequences for lens transparency and cataract development.	Pyruvaldehyde	25-28	heat shock protein family B (small) member 1	Homo sapiens	65-70
16583141-1	2006	Glyoxalase I is the first enzyme in a two-enzyme glyoxalase system that metabolizes physiological methylglyoxal (MGO).	Pyruvaldehyde	98-111	glyoxalase 1	Mus musculus	0-12
16583141-1	2006	Glyoxalase I is the first enzyme in a two-enzyme glyoxalase system that metabolizes physiological methylglyoxal (MGO).	Pyruvaldehyde	113-116	glyoxalase 1	Mus musculus	0-12
16804064-6	2006	Pharmacological scavenging of methylglyoxal prevented anoikis and maintained angiogenesis, and inhibition of methylglyoxal metabolism with a cell permeable glyoxalase I inhibitor provoked these responses in normoglycemia.	Pyruvaldehyde	109-122	glyoxalase I	Homo sapiens	156-168
16723378-0	2006	Structural and functional changes in human insulin induced by methylglyoxal.	Pyruvaldehyde	62-75	insulin	Homo sapiens	43-50
16723378-2	2006	The present study investigated whether MG, a highly reactive metabolite of glucose, induced structural and functional changes of insulin.	Pyruvaldehyde	39-41	insulin	Homo sapiens	129-136
16723378-4	2006	Tandem MS analysis of insulin B-chain adducts confirmed attachment of MG at an arginine residue.	Pyruvaldehyde	70-72	insulin	Homo sapiens	22-29
16723378-10	2006	In conclusion, MG modifies insulin by attaching to internal arginine residue in beta-chain of insulin.	Pyruvaldehyde	15-17	insulin	Homo sapiens	27-34
16723378-10	2006	In conclusion, MG modifies insulin by attaching to internal arginine residue in beta-chain of insulin.	Pyruvaldehyde	15-17	insulin	Homo sapiens	94-101
16555297-5	2006	To simulate a reduced glyoxalase I activity, we applied an inhibitor of glyoxalase I, p-bromobenzylglutathione cyclopentyl diester (pBrBzGSCp(2)), to SH-SY5Y neuroblastoma cells to induce chronically elevated methylglyoxal concentrations.	Pyruvaldehyde	209-222	glyoxalase I	Homo sapiens	72-84
16555297-10	2006	Also, pretreatment with the inhibitor okadaic acid prevented tau dephosphorylation, indicating that methylglyoxal activates PP-2A.	Pyruvaldehyde	100-113	microtubule associated protein tau	Homo sapiens	61-64
16555297-10	2006	Also, pretreatment with the inhibitor okadaic acid prevented tau dephosphorylation, indicating that methylglyoxal activates PP-2A.	Pyruvaldehyde	100-113	protein phosphatase 2 phosphatase activator	Homo sapiens	124-129
16722033-11	2006	RESULTS: In rats receiving PD fluids containing more than 0.66 mmol/L MGO, peritoneal function decreased significantly and levels of type IV collagen-7S and MMP-2 in drained dialysate increased significantly.	Pyruvaldehyde	70-73	matrix metallopeptidase 2	Rattus norvegicus	157-162
16722033-12	2006	In the 20-mmol/L MGO-treated rats, loss of body weight, expression of VEGF, thickening of the peritoneum, and formation of abdominal cocoon were induced.	Pyruvaldehyde	17-20	vascular endothelial growth factor A	Rattus norvegicus	70-74
16464860-2	2006	We have recently found that MG activates transcription factors such as Yap1 and Msn2, and triggers a Hog1 mitogen-activated protein kinase cascade in Saccharomyces cerevisiae.	Pyruvaldehyde	28-30	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	101-105
16464860-3	2006	Regarding the activation of Hog1 by MG, we found that Sln1, an osmosensor possessing histidine kinase activity, functions as a sensor of MG (Maeta, K., Izawa, S., and Inoue, Y.	Pyruvaldehyde	36-38	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	28-32
16464860-3	2006	Regarding the activation of Hog1 by MG, we found that Sln1, an osmosensor possessing histidine kinase activity, functions as a sensor of MG (Maeta, K., Izawa, S., and Inoue, Y.	Pyruvaldehyde	137-139	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	28-32
16464860-8	2006	Spc1, a stress-activated protein kinase (SAPK), was phosphorylated following the treatment with MG.	Pyruvaldehyde	96-98	signal peptidase complex subunit 1	Homo sapiens	0-4
16464860-11	2006	The phosphorylation of Spc1 following MG treatment was observed in phk1Deltaphk2Deltaphk3Delta and spy1Delta cells, but not in mcs4Delta cells.	Pyruvaldehyde	38-40	signal peptidase complex subunit 1	Homo sapiens	23-27
16375719-7	2005	Chronic hyperglycemia exacerbated baseline and MG-induced apoptosis that corresponded to exaggerated loss of cytosolic and mitochondrial redox balance, impaired glucose 6-phosphate dehydrogenase (G6PD) activity, and enhanced basal expression of apoptosis protease activator factor-1 (Apaf-1).	Pyruvaldehyde	47-49	apoptotic peptidase activating factor 1	Rattus norvegicus	245-282
16430697-3	2006	In kinetic studies L. major and human enzymes were active with methylglyoxal derivatives of several thiols, but showed opposite substrate selectivities: N1-glutathionylspermidine hemithioacetal is 40-fold better with L. major GLO1, whereas glutathione hemithioacetal is 300-fold better with human GLO1.	Pyruvaldehyde	63-76	glyoxalase I	Homo sapiens	226-230
16504566-7	2006	We observed that a rapid and detectable decrease in Raf-1 protein levels was induced by methylglyoxal, which was accelerated by treating with a Raf-1 activator, phorbol-12-myristate-13-acetate, and by expressing active forms of Raf-1 and Ras.	Pyruvaldehyde	88-101	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	52-57
16504566-7	2006	We observed that a rapid and detectable decrease in Raf-1 protein levels was induced by methylglyoxal, which was accelerated by treating with a Raf-1 activator, phorbol-12-myristate-13-acetate, and by expressing active forms of Raf-1 and Ras.	Pyruvaldehyde	88-101	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	144-149
16504566-7	2006	We observed that a rapid and detectable decrease in Raf-1 protein levels was induced by methylglyoxal, which was accelerated by treating with a Raf-1 activator, phorbol-12-myristate-13-acetate, and by expressing active forms of Raf-1 and Ras.	Pyruvaldehyde	88-101	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	144-149
16504566-8	2006	Moreover, immunoprecipitation and immunoblotting assays showed that co-treatment of cells with methylglyoxal and phorbol-12-myristate-13-acetate caused dramatic ubiquitination in both total intracellular proteins and Raf-1.	Pyruvaldehyde	95-108	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	217-222
16375719-7	2005	Chronic hyperglycemia exacerbated baseline and MG-induced apoptosis that corresponded to exaggerated loss of cytosolic and mitochondrial redox balance, impaired glucose 6-phosphate dehydrogenase (G6PD) activity, and enhanced basal expression of apoptosis protease activator factor-1 (Apaf-1).	Pyruvaldehyde	47-49	apoptotic peptidase activating factor 1	Rattus norvegicus	284-290
16375719-8	2005	Reduced glucose availability in hyperglycemia-adapted nPC12 cells induced by acute lowering of glucose or by dehydroepiandrosterone (DHEA, G6PD inhibitor) further enhanced MG-induced apoptosis in association with greater cytosolic and mitochondrial redox and G6PD impairment and elevated basal Apaf-1 expression.	Pyruvaldehyde	172-174	glucose-6-phosphate dehydrogenase	Rattus norvegicus	139-143
15887245-6	2005	Curcumin inhibited the MG-induced DNA fragmentation, caspase-3 activation, cleavage of PARP, mitochondrial cytochrome c release, and JNK activation.	Pyruvaldehyde	23-25	caspase 3	Mus musculus	53-62
15887245-6	2005	Curcumin inhibited the MG-induced DNA fragmentation, caspase-3 activation, cleavage of PARP, mitochondrial cytochrome c release, and JNK activation.	Pyruvaldehyde	23-25	poly (ADP-ribose) polymerase family, member 1	Mus musculus	87-91
15887245-6	2005	Curcumin inhibited the MG-induced DNA fragmentation, caspase-3 activation, cleavage of PARP, mitochondrial cytochrome c release, and JNK activation.	Pyruvaldehyde	23-25	mitogen-activated protein kinase 8	Mus musculus	133-136
16260349-5	2005	The results indicate that transition metals play a significant role in the formation of MG and 3-DG via oxidative stress and SSAO activity.	Pyruvaldehyde	88-90	amine oxidase, copper containing 3	Rattus norvegicus	125-129
16168380-4	2005	For this study, human serum albumin (HSA)-AGEs derived from different concentrations of glucose, methyl glyoxal, and glyoxylic acid were used.	Pyruvaldehyde	97-111	albumin	Homo sapiens	22-35
16292231-4	2005	These are glucose which leads to glyoxal and to methylglyoxal which in turn reacts with innumerable targets in the organism (including insulin) unless prevented from doing so by detoxifying mechanisms (e.g., glyoxalases).	Pyruvaldehyde	48-61	insulin	Homo sapiens	135-142
16249455-7	2005	Decreased glyceraldehyde-3-phosphate dehydrogenase activity also correlated with increased methylglyoxal levels (P = 0.003) in the NHS cohort.	Pyruvaldehyde	91-104	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	10-50
16037232-0	2005	Methylglyoxal can modify GAPDH activity and structure.	Pyruvaldehyde	0-13	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	25-30
15952936-10	2005	Moreover, methylglyoxal-modified alpha-crystallin, which occurs in aged and diabetic cataract lenses, was less efficient in the reactivation of denaturant inactivated G6PD.	Pyruvaldehyde	10-23	glucose-6-phosphate dehydrogenase	Homo sapiens	167-171
16046286-2	2005	Deamination of aminoacetone by semicarbazide-sensitive amine oxidase (SSAO) leads to production of methylglyoxal.	Pyruvaldehyde	99-112	amine oxidase, copper containing 3	Mus musculus	31-68
16046286-2	2005	Deamination of aminoacetone by semicarbazide-sensitive amine oxidase (SSAO) leads to production of methylglyoxal.	Pyruvaldehyde	99-112	amine oxidase, copper containing 3	Mus musculus	70-74
16077126-5	2005	Quantitative assessment of the metabolites produced in vitro from the crude extracts of these mutants and biochemical study with purified AKRs indicated that the yafB, yqhE, yeaE, and yghZ genes are involved in the conversion of MG to acetol in the presence of NADPH.	Pyruvaldehyde	229-231	plasmid partition protein A	Escherichia coli	162-166
16077126-7	2005	The results imply that the glutathione-independent detoxification of MG can occur through multiple pathways, consisting of yafB, yqhE, yeaE, and yghZ genes, leading to the generation of acetol.	Pyruvaldehyde	69-71	plasmid partition protein A	Escherichia coli	123-127
15814533-9	2005	RESULTS: ZO-1 expression in HPMC was downregulated in a time- and dose-dependent manner following culture with subtoxic concentrations of GDPs (FurA, M-Glx and 3,4-DGE).	Pyruvaldehyde	150-155	tight junction protein 1	Homo sapiens	9-13
16037232-8	2005	Reduction in GAPDH activity was rapidly decreasing by 69.2% by two hours with 1 mM MG.	Pyruvaldehyde	83-85	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	13-18
16037232-10	2005	With MALDI, GAPDH mass increased from 36.012 kDa to 37.071 after exposure to 50 microM MG and to 40.625 following 1 mM MG.	Pyruvaldehyde	87-89	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	12-17
16037232-10	2005	With MALDI, GAPDH mass increased from 36.012 kDa to 37.071 after exposure to 50 microM MG and to 40.625 following 1 mM MG.	Pyruvaldehyde	119-121	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	12-17
16037232-12	2005	GAPDH can be modified by methylglyoxal intracellular concentrations close to those previously observed in vivo, with measurable changes in isoelectric point and mass.	Pyruvaldehyde	25-38	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	0-5
16037232-13	2005	These modifications can lead to decreased enzyme activity, suggesting that conditions associated with elevated intracellular MG could modify GAPDH activity in vivo.	Pyruvaldehyde	125-127	glyceraldehyde-3-phosphate dehydrogenase	Oryctolagus cuniculus	141-146
16037234-0	2005	Methylglyoxal induces apoptosis through oxidative stress-mediated activation of p38 mitogen-activated protein kinase in rat Schwann cells.	Pyruvaldehyde	0-13	mitogen activated protein kinase 14	Rattus norvegicus	80-83
16037234-4	2005	Furthermore, MG induced phosphorylation of MKK3/MKK6, an upstream molecule in the p38 MAPK pathway.	Pyruvaldehyde	13-15	mitogen activated protein kinase kinase 3	Rattus norvegicus	43-47
16037234-4	2005	Furthermore, MG induced phosphorylation of MKK3/MKK6, an upstream molecule in the p38 MAPK pathway.	Pyruvaldehyde	13-15	mitogen-activated protein kinase kinase 6	Rattus norvegicus	48-52
16037234-4	2005	Furthermore, MG induced phosphorylation of MKK3/MKK6, an upstream molecule in the p38 MAPK pathway.	Pyruvaldehyde	13-15	mitogen activated protein kinase 14	Rattus norvegicus	82-85
16037234-5	2005	N-acetyl-L-cysteine, an antioxidant, successfully suppressed the activity of the p38 MAPK signaling pathway along with the inhibition of apoptosis, indicating the involvement of oxidative stress in the MG-induced apoptosis via the p38 MAPK pathway.	Pyruvaldehyde	202-204	mitogen activated protein kinase 14	Rattus norvegicus	81-84
16037234-5	2005	N-acetyl-L-cysteine, an antioxidant, successfully suppressed the activity of the p38 MAPK signaling pathway along with the inhibition of apoptosis, indicating the involvement of oxidative stress in the MG-induced apoptosis via the p38 MAPK pathway.	Pyruvaldehyde	202-204	mitogen activated protein kinase 14	Rattus norvegicus	231-234
16037235-3	2005	We have studied the effect of MGO modification of fibronectin on retinal capillary cell viability.	Pyruvaldehyde	30-33	fibronectin 1	Homo sapiens	50-61
16037235-4	2005	Our studies show that pericytes grown on MGO-modified fibronectin (FN) undergo enhanced apoptosis through the p38MAPK-mediated oxidative pathway and that alphaB-crystallin, a stress protein present in pericytes, can protect them from MGO-mediated apoptosis.	Pyruvaldehyde	41-44	fibronectin 1	Homo sapiens	54-65
16037235-4	2005	Our studies show that pericytes grown on MGO-modified fibronectin (FN) undergo enhanced apoptosis through the p38MAPK-mediated oxidative pathway and that alphaB-crystallin, a stress protein present in pericytes, can protect them from MGO-mediated apoptosis.	Pyruvaldehyde	41-44	fibronectin 1	Homo sapiens	67-69
16037235-4	2005	Our studies show that pericytes grown on MGO-modified fibronectin (FN) undergo enhanced apoptosis through the p38MAPK-mediated oxidative pathway and that alphaB-crystallin, a stress protein present in pericytes, can protect them from MGO-mediated apoptosis.	Pyruvaldehyde	234-237	fibronectin 1	Homo sapiens	67-69
16037241-3	2005	As reactive intermediates of AGE formation, neurotoxic reactive dicarbonyl compounds such as glyoxal and methylglyoxal have been identified.	Pyruvaldehyde	105-118	renin binding protein	Homo sapiens	29-32
16037241-4	2005	One of the most effective detoxification systems for methylglyoxal and glyoxal is the glutathione-dependent glyoxalase system, consisting of glyoxalase I and glyoxalase II.	Pyruvaldehyde	53-66	glyoxalase I	Homo sapiens	141-153
16037241-4	2005	One of the most effective detoxification systems for methylglyoxal and glyoxal is the glutathione-dependent glyoxalase system, consisting of glyoxalase I and glyoxalase II.	Pyruvaldehyde	53-66	hydroxyacylglutathione hydrolase	Homo sapiens	158-171
15965083-6	2005	We report that curcumin prevented MG-induced cell death and apoptotic biochemical changes such as mitochondrial release of cytochrome c, caspase-3 activation, and cleavage of PARP (poly [ADP-ribose] polymerase).	Pyruvaldehyde	34-36	caspase 3	Homo sapiens	137-146
15965083-6	2005	We report that curcumin prevented MG-induced cell death and apoptotic biochemical changes such as mitochondrial release of cytochrome c, caspase-3 activation, and cleavage of PARP (poly [ADP-ribose] polymerase).	Pyruvaldehyde	34-36	poly(ADP-ribose) polymerase 1	Homo sapiens	175-179
15965083-6	2005	We report that curcumin prevented MG-induced cell death and apoptotic biochemical changes such as mitochondrial release of cytochrome c, caspase-3 activation, and cleavage of PARP (poly [ADP-ribose] polymerase).	Pyruvaldehyde	34-36	cytochrome c, somatic	Homo sapiens	123-135
15965083-6	2005	We report that curcumin prevented MG-induced cell death and apoptotic biochemical changes such as mitochondrial release of cytochrome c, caspase-3 activation, and cleavage of PARP (poly [ADP-ribose] polymerase).	Pyruvaldehyde	34-36	poly(ADP-ribose) polymerase 1	Homo sapiens	181-209
15520007-0	2005	Methylglyoxal, a metabolite derived from glycolysis, functions as a signal initiator of the high osmolarity glycerol-mitogen-activated protein kinase cascade and calcineurin/Crz1-mediated pathway in Saccharomyces cerevisiae.	Pyruvaldehyde	0-13	DNA-binding transcription factor CRZ1	Saccharomyces cerevisiae S288C	174-178
15773992-1	2005	A sudden overaccumulation of methylglyoxal (MG) induces, in Saccharomyces cerevisiae, the expression of MG-protective genes, including GPD1, GLO1 and GRE3.	Pyruvaldehyde	29-42	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	135-139
15773992-1	2005	A sudden overaccumulation of methylglyoxal (MG) induces, in Saccharomyces cerevisiae, the expression of MG-protective genes, including GPD1, GLO1 and GRE3.	Pyruvaldehyde	29-42	lactoylglutathione lyase GLO1	Saccharomyces cerevisiae S288C	141-145
15773992-1	2005	A sudden overaccumulation of methylglyoxal (MG) induces, in Saccharomyces cerevisiae, the expression of MG-protective genes, including GPD1, GLO1 and GRE3.	Pyruvaldehyde	29-42	trifunctional aldehyde reductase/xylose reductase/glucose 1-dehydrogenase (NADP(+))	Saccharomyces cerevisiae S288C	150-154
15773992-1	2005	A sudden overaccumulation of methylglyoxal (MG) induces, in Saccharomyces cerevisiae, the expression of MG-protective genes, including GPD1, GLO1 and GRE3.	Pyruvaldehyde	44-46	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	135-139
15773992-1	2005	A sudden overaccumulation of methylglyoxal (MG) induces, in Saccharomyces cerevisiae, the expression of MG-protective genes, including GPD1, GLO1 and GRE3.	Pyruvaldehyde	44-46	lactoylglutathione lyase GLO1	Saccharomyces cerevisiae S288C	141-145
15773992-1	2005	A sudden overaccumulation of methylglyoxal (MG) induces, in Saccharomyces cerevisiae, the expression of MG-protective genes, including GPD1, GLO1 and GRE3.	Pyruvaldehyde	44-46	trifunctional aldehyde reductase/xylose reductase/glucose 1-dehydrogenase (NADP(+))	Saccharomyces cerevisiae S288C	150-154
15773992-4	2005	Strains lacking the MAPK Hog1p, the upstream component Ssk1p or the HOG-dependent nuclear factor Msn1p, showed a reduction in the mRNA accumulation of MG-responsive genes after MG addition.	Pyruvaldehyde	151-153	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	25-30
15773992-4	2005	Strains lacking the MAPK Hog1p, the upstream component Ssk1p or the HOG-dependent nuclear factor Msn1p, showed a reduction in the mRNA accumulation of MG-responsive genes after MG addition.	Pyruvaldehyde	151-153	mitogen-activated protein kinase kinase kinase SSK1	Saccharomyces cerevisiae S288C	55-60
15773992-4	2005	Strains lacking the MAPK Hog1p, the upstream component Ssk1p or the HOG-dependent nuclear factor Msn1p, showed a reduction in the mRNA accumulation of MG-responsive genes after MG addition.	Pyruvaldehyde	151-153	Msn1p	Saccharomyces cerevisiae S288C	97-102
15281912-0	2005	Argpyrimidine, a methylglyoxal-derived advanced glycation end-product in familial amyloidotic polyneuropathy.	Pyruvaldehyde	17-30	fibroblast activation protein alpha	Homo sapiens	73-108
15520007-5	2005	Two osmosensors, Sln1 and Sho1, have been identified to function upstream of the HOG-MAP kinase cascade, and we reveal that MG initiates the signal transduction to this MAP kinase cascade through the Sln1 branch.	Pyruvaldehyde	124-126	histidine kinase	Saccharomyces cerevisiae S288C	17-21
15520007-5	2005	Two osmosensors, Sln1 and Sho1, have been identified to function upstream of the HOG-MAP kinase cascade, and we reveal that MG initiates the signal transduction to this MAP kinase cascade through the Sln1 branch.	Pyruvaldehyde	124-126	osmosensor SHO1	Saccharomyces cerevisiae S288C	26-30
15520007-5	2005	Two osmosensors, Sln1 and Sho1, have been identified to function upstream of the HOG-MAP kinase cascade, and we reveal that MG initiates the signal transduction to this MAP kinase cascade through the Sln1 branch.	Pyruvaldehyde	124-126	histidine kinase	Saccharomyces cerevisiae S288C	200-204
15520007-6	2005	We also demonstrate that MG activates the Msn2 transcription factor.	Pyruvaldehyde	25-27	stress-responsive transcriptional activator MSN2	Saccharomyces cerevisiae S288C	42-46
15520007-7	2005	Moreover, MG activated the uptake of Ca(2+) in yeast cells, thereby stimulating the calcineurin/Crz1-mediated Ca(2+) signaling pathway.	Pyruvaldehyde	10-12	DNA-binding transcription factor CRZ1	Saccharomyces cerevisiae S288C	96-100
15475166-2	2004	Detoxification of MG occurs through the glyoxalase system incorporating glyoxalase-1 (GLO1) and glyoxalase-2.	Pyruvaldehyde	18-20	glyoxalase I	Homo sapiens	86-90
15759051-6	2005	Moreover, MG activated NF-kappaB p65, indicated by an increased immuno cytochemistry stain for NF-kappaB p65 located in the nucleus after the treatment of mesenteric artery SMCs with MG. MG-induced activation of NF-kappaB p65 was inhibited by NAC.	Pyruvaldehyde	10-12	synaptotagmin 1	Rattus norvegicus	33-36
15759051-6	2005	Moreover, MG activated NF-kappaB p65, indicated by an increased immuno cytochemistry stain for NF-kappaB p65 located in the nucleus after the treatment of mesenteric artery SMCs with MG. MG-induced activation of NF-kappaB p65 was inhibited by NAC.	Pyruvaldehyde	10-12	synaptotagmin 1	Rattus norvegicus	105-108
15759051-6	2005	Moreover, MG activated NF-kappaB p65, indicated by an increased immuno cytochemistry stain for NF-kappaB p65 located in the nucleus after the treatment of mesenteric artery SMCs with MG. MG-induced activation of NF-kappaB p65 was inhibited by NAC.	Pyruvaldehyde	10-12	synaptotagmin 1	Rattus norvegicus	105-108
15759051-7	2005	In summary, MG significantly increases oxidative stress and activates NF-kappaB p65 in mesenteric artery SMCs.	Pyruvaldehyde	12-14	synaptotagmin 1	Rattus norvegicus	80-83
15496428-6	2004	HAGH functions in a pathway to detoxify methylglyoxal, a compound present in coffee and alcoholic beverages and produced as a by-product of oxidative stress.	Pyruvaldehyde	40-53	hydroxyacylglutathione hydrolase	Homo sapiens	0-4
15544624-6	2004	2-furaldehyde (FurA), methylglyoxal (M-Glx) and 3,4-dideoxy-glucosone-3-Ene (3,4-DGE) increased the expression of AGE-R1 and RAGE, the receptors that are associated with toxic effects.	Pyruvaldehyde	22-35	dolichyl-diphosphooligosaccharide--protein glycosyltransferase non-catalytic subunit	Homo sapiens	114-120
15544624-6	2004	2-furaldehyde (FurA), methylglyoxal (M-Glx) and 3,4-dideoxy-glucosone-3-Ene (3,4-DGE) increased the expression of AGE-R1 and RAGE, the receptors that are associated with toxic effects.	Pyruvaldehyde	22-35	long intergenic non-protein coding RNA 914	Homo sapiens	125-129
15544624-6	2004	2-furaldehyde (FurA), methylglyoxal (M-Glx) and 3,4-dideoxy-glucosone-3-Ene (3,4-DGE) increased the expression of AGE-R1 and RAGE, the receptors that are associated with toxic effects.	Pyruvaldehyde	37-42	dolichyl-diphosphooligosaccharide--protein glycosyltransferase non-catalytic subunit	Homo sapiens	114-120
15544624-6	2004	2-furaldehyde (FurA), methylglyoxal (M-Glx) and 3,4-dideoxy-glucosone-3-Ene (3,4-DGE) increased the expression of AGE-R1 and RAGE, the receptors that are associated with toxic effects.	Pyruvaldehyde	37-42	long intergenic non-protein coding RNA 914	Homo sapiens	125-129
15367692-0	2004	Activity of the Yap1 transcription factor in Saccharomyces cerevisiae is modulated by methylglyoxal, a metabolite derived from glycolysis.	Pyruvaldehyde	86-99	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	16-20
15454255-1	2004	The inhibition of glyoxalase I leads to antitumour activity through the accumulation of methylglyoxal.	Pyruvaldehyde	88-101	glyoxalase I	Homo sapiens	18-30
19003265-2	2004	Trypan blue cell counts of 6-well cultures incubated for 24 h with various methylglyoxal concentrations revealed inhibition of cell growth at 300 muM and higher, with a median inhibitory concentration of 490+/-20 muM.	Pyruvaldehyde	75-88	latexin	Homo sapiens	146-149
19003265-2	2004	Trypan blue cell counts of 6-well cultures incubated for 24 h with various methylglyoxal concentrations revealed inhibition of cell growth at 300 muM and higher, with a median inhibitory concentration of 490+/-20 muM.	Pyruvaldehyde	75-88	latexin	Homo sapiens	213-216
15367692-7	2004	A Yap1 mutant possessing only one cysteine residue in the c-CRD but no cysteine in the n-CRD and deletion of the basic leucine zipper domain can concentrate in the nucleus with MG treatment.	Pyruvaldehyde	177-179	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	2-6
15367692-8	2004	However, substitution of all the cysteine residues in Yap1 abolishes the ability of this transcription factor to concentrate in the nucleus following MG treatment.	Pyruvaldehyde	150-152	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	54-58
15367692-9	2004	The redox status of Yap1 is substantially unchanged, and protein(s) interaction with Yap1 through disulfide bond is hardly detected in cells treated with MG.	Pyruvaldehyde	154-156	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	85-89
15367692-11	2004	Moreover, we show that nucleocytoplasmic localization of Yap1 closely correlates with growth phase and intracellular MG level.	Pyruvaldehyde	117-119	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	57-61
15329410-1	2004	Glyoxalase I forms part of the glyoxalase pathway that detoxifies reactive aldehydes such as methylglyoxal, using the spontaneously formed glutathione hemithioacetal as substrate.	Pyruvaldehyde	93-106	glyoxalase I	Homo sapiens	0-12
15240103-0	2004	Methylglyoxal induces apoptosis through activation of p38 MAPK in rat Schwann cells.	Pyruvaldehyde	0-13	mitogen activated protein kinase 14	Rattus norvegicus	54-57
18943070-10	2004	These data suggest that GLX-I may play an important role in controlling MG levels inside kernels, thereby contributing to the lower levels of aflatoxins found in resistant maize genotypes.	Pyruvaldehyde	72-74	glyoxylase 1	Zea mays	24-29
15240103-3	2004	MG induced apoptosis in SCs in a dose-dependent manner, accompanied by a reduction of intracellular glutathione content and activation of the p38 MAPK.	Pyruvaldehyde	0-2	mitogen activated protein kinase 14	Rattus norvegicus	142-145
15240103-4	2004	Inhibiting the p38 MAPK activation by SB203580 successfully suppressed the MG-induced apoptosis in SCs.	Pyruvaldehyde	75-77	mitogen activated protein kinase 14	Rattus norvegicus	15-18
15240103-6	2004	These results suggest a potential role for MG in SC injury through oxidative stress-mediated p38 MAPK activation under diabetic conditions, and it may serve as a novel insight into therapeutic strategies for diabetic neuropathy.	Pyruvaldehyde	43-45	mitogen activated protein kinase 14	Rattus norvegicus	93-96
14991464-6	2004	We show that chicken egg albumin-AGEs prepared with glucose and chicken egg albumin-AGEs prepared with methylglyoxal dose-dependently induce TNF-alpha release.	Pyruvaldehyde	103-116	lipopolysaccharide induced TNF factor	Gallus gallus	141-150
15161867-2	2004	METHODS: Primary cultures of bovine retinal pericytes (BRPs) were seeded on either normal fibronectin (FN) or FN modified by methylglyoxal (MGO) and glyoxal (GO).	Pyruvaldehyde	125-138	fibronectin 1	Bos taurus	110-112
15161867-2	2004	METHODS: Primary cultures of bovine retinal pericytes (BRPs) were seeded on either normal fibronectin (FN) or FN modified by methylglyoxal (MGO) and glyoxal (GO).	Pyruvaldehyde	140-143	fibronectin 1	Bos taurus	110-112
15161867-7	2004	RESULTS: Cultures seeded on MGO- or GO-modified FN showed a significant reduction in the number of viable cells, an increase in the number of apoptotic cells, and increased caspase-3 activity, which correlated with the extent of FN modification.	Pyruvaldehyde	28-31	caspase 3	Rattus norvegicus	173-182
15051519-0	2004	Methylglyoxal induces oxidative stress-dependent cell injury and up-regulation of interleukin-1beta and nerve growth factor in cultured hippocampal neuronal cells.	Pyruvaldehyde	0-13	interleukin 1 beta	Homo sapiens	82-99
15040952-4	2004	Here, we show that in Saccharomyces cerevisiae, MG exposure increased the internal MG content and activated the expression of GLO1 and GRE3, two genes involved in MG detoxification; GPD1, the gene for glycerol synthesis; and TPS1 and TPS2, the trehalose pathway genes.	Pyruvaldehyde	48-50	lactoylglutathione lyase GLO1	Saccharomyces cerevisiae S288C	126-130
15040952-4	2004	Here, we show that in Saccharomyces cerevisiae, MG exposure increased the internal MG content and activated the expression of GLO1 and GRE3, two genes involved in MG detoxification; GPD1, the gene for glycerol synthesis; and TPS1 and TPS2, the trehalose pathway genes.	Pyruvaldehyde	48-50	trifunctional aldehyde reductase/xylose reductase/glucose 1-dehydrogenase (NADP(+))	Saccharomyces cerevisiae S288C	135-139
15040952-4	2004	Here, we show that in Saccharomyces cerevisiae, MG exposure increased the internal MG content and activated the expression of GLO1 and GRE3, two genes involved in MG detoxification; GPD1, the gene for glycerol synthesis; and TPS1 and TPS2, the trehalose pathway genes.	Pyruvaldehyde	48-50	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	182-186
15040952-4	2004	Here, we show that in Saccharomyces cerevisiae, MG exposure increased the internal MG content and activated the expression of GLO1 and GRE3, two genes involved in MG detoxification; GPD1, the gene for glycerol synthesis; and TPS1 and TPS2, the trehalose pathway genes.	Pyruvaldehyde	48-50	alpha,alpha-trehalose-phosphate synthase (UDP-forming) TPS1	Saccharomyces cerevisiae S288C	225-229
15040952-4	2004	Here, we show that in Saccharomyces cerevisiae, MG exposure increased the internal MG content and activated the expression of GLO1 and GRE3, two genes involved in MG detoxification; GPD1, the gene for glycerol synthesis; and TPS1 and TPS2, the trehalose pathway genes.	Pyruvaldehyde	48-50	trehalose-phosphatase TPS2	Saccharomyces cerevisiae S288C	234-238
15040952-7	2004	Furthermore, a gpd1 gpd2 double mutant showed enhanced MG contents compared with the wild-type.	Pyruvaldehyde	55-57	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	15-19
15040952-7	2004	Furthermore, a gpd1 gpd2 double mutant showed enhanced MG contents compared with the wild-type.	Pyruvaldehyde	55-57	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD2	Saccharomyces cerevisiae S288C	20-24
15040952-9	2004	In agreement with this, MG-instigated GPD1 activation was enhanced in strains lacking GLO1, and this effect correlated with the internal MG content.	Pyruvaldehyde	24-26	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	38-42
15040952-9	2004	In agreement with this, MG-instigated GPD1 activation was enhanced in strains lacking GLO1, and this effect correlated with the internal MG content.	Pyruvaldehyde	24-26	lactoylglutathione lyase GLO1	Saccharomyces cerevisiae S288C	86-90
14978257-0	2004	Phorbol 12-myristate 13-acetate protects Jurkat cells from methylglyoxal-induced apoptosis by preventing c-Jun N-terminal kinase-mediated leakage of cytochrome c in an extracellular signal-regulated kinase-dependent manner.	Pyruvaldehyde	59-72	mitogen-activated protein kinase 8	Homo sapiens	105-128
14978257-0	2004	Phorbol 12-myristate 13-acetate protects Jurkat cells from methylglyoxal-induced apoptosis by preventing c-Jun N-terminal kinase-mediated leakage of cytochrome c in an extracellular signal-regulated kinase-dependent manner.	Pyruvaldehyde	59-72	cytochrome c, somatic	Homo sapiens	149-161
14978257-2	2004	We showed previously that Jurkat cells treated with MG rapidly undergo apoptosis via c-Jun N-terminal kinase (JNK) activation.	Pyruvaldehyde	52-54	mitogen-activated protein kinase 8	Homo sapiens	85-108
14978257-2	2004	We showed previously that Jurkat cells treated with MG rapidly undergo apoptosis via c-Jun N-terminal kinase (JNK) activation.	Pyruvaldehyde	52-54	mitogen-activated protein kinase 8	Homo sapiens	110-113
14978257-5	2004	Taken together, these results suggest that PMA-induced ERK activation can protect Jurkat cells from methylglyoxal-induced apoptosis and that activated ERK exerts its antiapoptotic effects on mitochondria by inhibiting activated JNK-induced permeabilization of the outer mitochondrial membrane.	Pyruvaldehyde	100-113	mitogen-activated protein kinase 1	Homo sapiens	55-58
14641072-5	2003	Formation of hyperphosphorylated and cross-linked microtubule-associated protein tau aggregates, especially tau dimers as the first step in tangle formation, can be induced in vitro by the combination of okadaic acid, a PP2A phosphatase inhibitor, and methylglyoxal.	Pyruvaldehyde	252-265	microtubule associated protein tau	Homo sapiens	81-84
14556652-1	2004	GlxI (glyoxalase I) isomerizes the hemithioacetal formed between glutathione and methylglyoxal.	Pyruvaldehyde	81-94	glyoxalase I	Homo sapiens	0-4
14675555-5	2004	If glucose metabolism through the glycolytic pathway is impaired, as in insulin resistance, there will be a build-up of glyceraldehyde, glyceraldehyde-3-phosphate and dihydroxyacetone phosphate with further metabolism to methylglyoxal, a highly reactive ketoaldehyde.	Pyruvaldehyde	221-234	insulin	Homo sapiens	72-79
14757937-7	2003	Our findings showed that A beta/CTF aggregation and cytotoxicity may be profoundly altered by aldehydes associated with diabetes and that in the case of MG, this process is suppressed by alpha-tocopherol.	Pyruvaldehyde	153-155	amyloid beta precursor protein	Homo sapiens	25-31
14641060-17	2003	Glyoxalase I has a critical role in the prevention of glycation reactions mediated by methylglyoxal, glyoxal and other alpha-oxoaldehydes in vivo.	Pyruvaldehyde	86-99	glyoxalase I	Homo sapiens	0-12
12962499-9	2003	MG similarly enhances chaperone function of another small heat shock protein, Hsp27.	Pyruvaldehyde	0-2	heat shock protein family B (small) member 1	Homo sapiens	78-83
14556850-6	2003	To this purpose, we comparatively evaluated the signaling transduction pathway elicited by methylglyoxal in human glioblastoma (ADF) and neuroblastoma (SH-SY 5Y) cells.	Pyruvaldehyde	91-104	destrin, actin depolymerizing factor	Homo sapiens	128-131
14556850-8	2003	However, SH-SY 5Y cells show higher sensitivity to methylglyoxal challenge due to a defective antioxidant and detoxifying ability that, preventing these cells from an efficient scavenging action, elicits extensive caspase-9 dependent apoptosis.	Pyruvaldehyde	51-64	caspase 9	Homo sapiens	214-223
14577607-6	2003	These data suggest that the carbohydrates or glyceraldehyde were metabolised to form carbonyls such as MG which depleted erythrocyte GSH as a result of catalysis by glyoxalase I.	Pyruvaldehyde	103-105	glyoxalase I	Homo sapiens	165-177
12359232-1	2002	Semicarbazide-sensitive amine oxidase (SSAO) catalyzes formation of methylglyoxal (MG) from aminoacetone; MG then reacts with proteins to form advanced glycation end products or AGEs.	Pyruvaldehyde	68-81	amine oxidase, copper containing 3	Rattus norvegicus	0-37
12815061-5	2003	Incubation of isolated mitochondria with MG for a short period of time (5 min), followed by removal of excess free MG, prevented both ganglioside GD3- and Ca2+-induced PTP opening and the ensuing membrane depolarization, swelling, and cytochrome c release.	Pyruvaldehyde	41-43	GRDX	Homo sapiens	146-149
12815061-5	2003	Incubation of isolated mitochondria with MG for a short period of time (5 min), followed by removal of excess free MG, prevented both ganglioside GD3- and Ca2+-induced PTP opening and the ensuing membrane depolarization, swelling, and cytochrome c release.	Pyruvaldehyde	41-43	cytochrome c, somatic	Homo sapiens	235-247
12815061-5	2003	Incubation of isolated mitochondria with MG for a short period of time (5 min), followed by removal of excess free MG, prevented both ganglioside GD3- and Ca2+-induced PTP opening and the ensuing membrane depolarization, swelling, and cytochrome c release.	Pyruvaldehyde	115-117	GRDX	Homo sapiens	146-149
12965214-7	2003	Additional studies showed that MGO-induced modification of Hsp27 decreased its binding to cytochrome c. Our results suggest that Hsp27 is a major target for MGO modification in mesangial cells.	Pyruvaldehyde	31-34	heat shock protein family B (small) member 1	Rattus norvegicus	59-64
12965214-7	2003	Additional studies showed that MGO-induced modification of Hsp27 decreased its binding to cytochrome c. Our results suggest that Hsp27 is a major target for MGO modification in mesangial cells.	Pyruvaldehyde	31-34	heat shock protein family B (small) member 1	Rattus norvegicus	129-134
12965214-7	2003	Additional studies showed that MGO-induced modification of Hsp27 decreased its binding to cytochrome c. Our results suggest that Hsp27 is a major target for MGO modification in mesangial cells.	Pyruvaldehyde	157-160	heat shock protein family B (small) member 1	Rattus norvegicus	59-64
12965214-7	2003	Additional studies showed that MGO-induced modification of Hsp27 decreased its binding to cytochrome c. Our results suggest that Hsp27 is a major target for MGO modification in mesangial cells.	Pyruvaldehyde	157-160	heat shock protein family B (small) member 1	Rattus norvegicus	129-134
12605598-15	2003	The activities of two important enzymes, namely glyoxalase I and creatine kinase, which act upon glutathione plus methylglyoxal and creatine respectively, were also measured in different PMS.	Pyruvaldehyde	114-127	glyoxalase 1	Mus musculus	48-60
12938820-7	2003	Furthermore, MCs were exposed to a single dose of MGO or 3-DG and analyzed for apoptosis, proliferation by MTT assay, and [3H]-thymidine incorporation.	Pyruvaldehyde	50-53	olfactory receptor family 7 subfamily E member 66 pseudogene	Homo sapiens	54-61
12938820-14	2003	Cell-bound ELISA showed a two- to three-fold induction of expression of VCAM-1 by MGO and 3-DG; the expression of ICAM-1 and CD44 was not changed.	Pyruvaldehyde	82-85	vascular cell adhesion molecule 1	Homo sapiens	72-78
12647305-0	2003	Involvement of MEKK1/ERK/P21Waf1/Cip1 signal transduction pathway in inhibition of IGF-I-mediated cell growth response by methylglyoxal.	Pyruvaldehyde	122-135	mitogen-activated protein kinase kinase kinase 1	Homo sapiens	15-20
12647305-0	2003	Involvement of MEKK1/ERK/P21Waf1/Cip1 signal transduction pathway in inhibition of IGF-I-mediated cell growth response by methylglyoxal.	Pyruvaldehyde	122-135	mitogen-activated protein kinase 1	Homo sapiens	21-24
12647305-0	2003	Involvement of MEKK1/ERK/P21Waf1/Cip1 signal transduction pathway in inhibition of IGF-I-mediated cell growth response by methylglyoxal.	Pyruvaldehyde	122-135	cyclin dependent kinase inhibitor 1A	Homo sapiens	33-37
12647305-0	2003	Involvement of MEKK1/ERK/P21Waf1/Cip1 signal transduction pathway in inhibition of IGF-I-mediated cell growth response by methylglyoxal.	Pyruvaldehyde	122-135	insulin like growth factor 1	Homo sapiens	83-88
12647305-3	2003	In this study, we investigated the effect of MG on IGF-I-induced cell proliferation and the mechanism of the effect in two cell lines, a human embryonic kidney cell line (HEK293), and a mouse fibroblast cell line (NIH3T3).	Pyruvaldehyde	45-47	insulin like growth factor 1	Homo sapiens	51-56
12631075-8	2003	SB203580, a specific inhibitor of p38 MAPK also suppressed the MG-induced apoptosis in rat mesangial cells.	Pyruvaldehyde	63-65	mitogen activated protein kinase 14	Rattus norvegicus	34-37
12631075-9	2003	CONCLUSIONS: These results suggest a potential role for MG in glomerular injury through p38 MAPK activation under diabetic conditions and may serve as a novel insight into the therapeutic strategies for diabetic nephropathy.	Pyruvaldehyde	56-58	mitogen activated protein kinase 14	Rattus norvegicus	88-91
12604218-1	2003	Methylglyoxal (MG), a reactive dicarbonyl produced during glucose metabolism, is known as a preferred substrate of aldose reductase (AR; AKR1B1) that concomitantly catalyzes the reduction of glucose in the polyol pathway.	Pyruvaldehyde	0-13	aldo-keto reductase family 1 member B	Homo sapiens	115-131
12604218-1	2003	Methylglyoxal (MG), a reactive dicarbonyl produced during glucose metabolism, is known as a preferred substrate of aldose reductase (AR; AKR1B1) that concomitantly catalyzes the reduction of glucose in the polyol pathway.	Pyruvaldehyde	0-13	aldo-keto reductase family 1 member B	Homo sapiens	133-135
12604218-1	2003	Methylglyoxal (MG), a reactive dicarbonyl produced during glucose metabolism, is known as a preferred substrate of aldose reductase (AR; AKR1B1) that concomitantly catalyzes the reduction of glucose in the polyol pathway.	Pyruvaldehyde	0-13	aldo-keto reductase family 1 member B	Homo sapiens	137-143
12604218-1	2003	Methylglyoxal (MG), a reactive dicarbonyl produced during glucose metabolism, is known as a preferred substrate of aldose reductase (AR; AKR1B1) that concomitantly catalyzes the reduction of glucose in the polyol pathway.	Pyruvaldehyde	15-17	aldo-keto reductase family 1 member B	Homo sapiens	115-131
12604218-1	2003	Methylglyoxal (MG), a reactive dicarbonyl produced during glucose metabolism, is known as a preferred substrate of aldose reductase (AR; AKR1B1) that concomitantly catalyzes the reduction of glucose in the polyol pathway.	Pyruvaldehyde	15-17	aldo-keto reductase family 1 member B	Homo sapiens	133-135
12604218-1	2003	Methylglyoxal (MG), a reactive dicarbonyl produced during glucose metabolism, is known as a preferred substrate of aldose reductase (AR; AKR1B1) that concomitantly catalyzes the reduction of glucose in the polyol pathway.	Pyruvaldehyde	15-17	aldo-keto reductase family 1 member B	Homo sapiens	137-143
12604218-5	2003	MG-induced a dose- and time-dependent increase in AR mRNA levels to a maximum of 4.5-fold.	Pyruvaldehyde	0-2	aldo-keto reductase family 1 member B	Homo sapiens	50-52
12604218-7	2003	Pretreatment of SMC with N-acetyl-L-cysteine significantly suppressed the MG-induced AR expression, while DL-buthionine-(S,R)-sulfoximine further augmented the MG-induced increase in AR mRNA level.	Pyruvaldehyde	74-76	aldo-keto reductase family 1 member B	Homo sapiens	85-87
12604218-7	2003	Pretreatment of SMC with N-acetyl-L-cysteine significantly suppressed the MG-induced AR expression, while DL-buthionine-(S,R)-sulfoximine further augmented the MG-induced increase in AR mRNA level.	Pyruvaldehyde	160-162	aldo-keto reductase family 1 member B	Homo sapiens	183-185
12604218-10	2003	In contrast, the p38 kinase pathway appears to mediate MG-induced AR expression.	Pyruvaldehyde	55-57	aldo-keto reductase family 1 member B	Homo sapiens	66-68
12604218-11	2003	The cytotoxic effect of MG was significantly enhanced in the presence of the AR inhibitor ponalrestat, indicating a protective role of AR against MG-induced cell damage.	Pyruvaldehyde	24-26	aldo-keto reductase family 1 member B	Homo sapiens	77-79
12604218-11	2003	The cytotoxic effect of MG was significantly enhanced in the presence of the AR inhibitor ponalrestat, indicating a protective role of AR against MG-induced cell damage.	Pyruvaldehyde	24-26	aldo-keto reductase family 1 member B	Homo sapiens	135-137
12604218-11	2003	The cytotoxic effect of MG was significantly enhanced in the presence of the AR inhibitor ponalrestat, indicating a protective role of AR against MG-induced cell damage.	Pyruvaldehyde	146-148	aldo-keto reductase family 1 member B	Homo sapiens	77-79
12604218-11	2003	The cytotoxic effect of MG was significantly enhanced in the presence of the AR inhibitor ponalrestat, indicating a protective role of AR against MG-induced cell damage.	Pyruvaldehyde	146-148	aldo-keto reductase family 1 member B	Homo sapiens	135-137
12504894-5	2003	Levels of the dicarbonyl methylglyoxal (MGO) are elevated in diabetic plasma and MGO-modified bovine serum albumin (MGO-BSA) can trigger cellular uptake of TNF.	Pyruvaldehyde	40-43	tumor necrosis factor	Mus musculus	156-159
12504894-5	2003	Levels of the dicarbonyl methylglyoxal (MGO) are elevated in diabetic plasma and MGO-modified bovine serum albumin (MGO-BSA) can trigger cellular uptake of TNF.	Pyruvaldehyde	81-84	tumor necrosis factor	Mus musculus	156-159
12504894-6	2003	Therefore we tested the hypothesis that MGO-modified proteins may cause TNFalpha secretion in macrophage-like RAW 264.7 cells.	Pyruvaldehyde	40-43	tumor necrosis factor	Mus musculus	72-80
12504894-19	2003	Our findings suggest that the presence of chronically elevated levels of MGO-modified bovine serum albumin may contribute to elevated levels of TNFalpha in diabetes.	Pyruvaldehyde	73-76	tumor necrosis factor	Mus musculus	144-152
12686132-6	2003	The SSAO-catalyzed deamination of endogenous substrates, that is, methylamine and aminoacetone, led to production of toxic formaldehyde and methylglyoxal, hydrogen peroxide and ammonia, respectively.	Pyruvaldehyde	140-153	amine oxidase, copper containing 3	Mus musculus	4-8
12631075-0	2003	Methylglyoxal induces apoptosis through activation of p38 mitogen-activated protein kinase in rat mesangial cells.	Pyruvaldehyde	0-13	mitogen activated protein kinase 14	Rattus norvegicus	54-90
12631075-6	2003	RESULTS: MG induced apoptosis in rat mesangial cells in a dose-dependent manner and was accompanied by the activation of p38alpha isoform.	Pyruvaldehyde	9-11	mitogen activated protein kinase 14	Rattus norvegicus	121-129
12601626-1	2003	A time-delayed fluorescence immunoassay was developed for the determination of serum levels of methylglyoxal (MG)-derived hydroimidazolone using a monoclonal antiserum raised against Nalpha-acetyl-Ndelta-(5-hydro-5-methyl)-4-imidazolone, Europium-labeled anti-mouse IgG antiserum as indicator, and MG modified bovine serum albumin (BSA) as standard.	Pyruvaldehyde	95-108	albumin	Homo sapiens	317-330
12527413-0	2003	Glyceraldehyde-3-phosphate dehydrogenase activity as an independent modifier of methylglyoxal levels in diabetes.	Pyruvaldehyde	80-93	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-40
12527413-3	2003	Using a human red blood cell (RBC) culture, we examined the effect of modifying GAPDH activity on MG production.	Pyruvaldehyde	98-100	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	80-85
12527413-4	2003	With the inhibitor koningic acid (KA), we showed a linear, concentration-dependent GAPDH inhibition, with 5 microM KA leading to a 79% reduction of GAPDH activity and a sixfold increase in MG. Changes in redox state produced by elevated pH also resulted in a 2.4-fold increase in MG production at pH 7.5 and a 13.4-fold increase at pH 7.8.	Pyruvaldehyde	189-191	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	83-88
12527413-5	2003	We found substantial inter-individual variation in DHAP and MG levels and an inverse relationship between GAPDH activity and MG production (R=0.57, P=0.005) in type 2 diabetes.	Pyruvaldehyde	125-127	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	106-111
12527413-6	2003	A similar relationship between GAPDH activity and MG was observed in vivo in type 1 diabetes (R=0.29, P=0.0018).	Pyruvaldehyde	50-52	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	31-36
12527413-8	2003	We postulate that modification of GAPDH by environmental factors or genetic dysregulation and the resultant differences in MG production could at least partially account for this observation.	Pyruvaldehyde	123-125	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	34-39
12359232-1	2002	Semicarbazide-sensitive amine oxidase (SSAO) catalyzes formation of methylglyoxal (MG) from aminoacetone; MG then reacts with proteins to form advanced glycation end products or AGEs.	Pyruvaldehyde	68-81	amine oxidase, copper containing 3	Rattus norvegicus	39-43
12359232-2	2002	Because of its potential to generate MG, SSAO may contribute to AGE-associated vascular complications of aging and diabetes.	Pyruvaldehyde	37-39	amine oxidase, copper containing 3	Rattus norvegicus	41-45
12359232-8	2002	We believe that SSAO can enhance AGE synthesis in the macrovasculature of diabetic individuals by production of MG.	Pyruvaldehyde	112-114	amine oxidase, copper containing 3	Rattus norvegicus	16-20
11955284-4	2002	The D-lactate translocators and the D-lactate dehydrogenase could account for the removal of the toxic methylglyoxal from cytosol, as well as for D-lactate-dependent gluconeogenesis.	Pyruvaldehyde	103-116	lactate dehydrogenase D	Rattus norvegicus	36-59
12110033-2	2002	The present study utilized the glyoxalase I (GLO I) system as a new approach to lower in vitro the peritoneal fluid content of RCOs such as methylglyoxal (MGO), glyoxal (GO) and 3-deoxyglucosone (3-DG).	Pyruvaldehyde	140-153	glyoxalase I	Homo sapiens	31-43
12110033-2	2002	The present study utilized the glyoxalase I (GLO I) system as a new approach to lower in vitro the peritoneal fluid content of RCOs such as methylglyoxal (MGO), glyoxal (GO) and 3-deoxyglucosone (3-DG).	Pyruvaldehyde	140-153	glyoxalase I	Homo sapiens	45-50
12110033-2	2002	The present study utilized the glyoxalase I (GLO I) system as a new approach to lower in vitro the peritoneal fluid content of RCOs such as methylglyoxal (MGO), glyoxal (GO) and 3-deoxyglucosone (3-DG).	Pyruvaldehyde	155-158	glyoxalase I	Homo sapiens	31-43
12110033-2	2002	The present study utilized the glyoxalase I (GLO I) system as a new approach to lower in vitro the peritoneal fluid content of RCOs such as methylglyoxal (MGO), glyoxal (GO) and 3-deoxyglucosone (3-DG).	Pyruvaldehyde	155-158	glyoxalase I	Homo sapiens	45-50
12110033-10	2002	Together with GLO I, it promptly decreased GO and MGO levels but was less efficient toward 3-DG.	Pyruvaldehyde	50-53	glyoxalase I	Homo sapiens	14-19
12110033-11	2002	After incubation with glucose PD fluid, GSH together with GLO I had the same effect on MGO, GO, and 3-DG levels.	Pyruvaldehyde	87-90	glyoxalase I	Homo sapiens	58-63
12110033-12	2002	Addition of transfected cell supernatant or tissue extracts overexpressing GLO I, together with GSH to either GO, MGO, or 3-DG solutions, promptly and markedly reduced GO and MGO but not 3-DG levels.	Pyruvaldehyde	114-117	glyoxalase I	Homo sapiens	75-80
12110033-12	2002	Addition of transfected cell supernatant or tissue extracts overexpressing GLO I, together with GSH to either GO, MGO, or 3-DG solutions, promptly and markedly reduced GO and MGO but not 3-DG levels.	Pyruvaldehyde	175-178	glyoxalase I	Homo sapiens	75-80
12110033-13	2002	CONCLUSIONS: GLO I together with GSH efficiently lowers glucose-derived RCOs, especially GO and MGO, both in conventional glucose PD fluids and in RCO solutions.	Pyruvaldehyde	96-99	glyoxalase I	Homo sapiens	13-18
11988071-2	2002	Serum albumin derivatives modified to minimal and high extents by methylglyoxal and glucose in vitro have been used in many studies as model AGE proteins.	Pyruvaldehyde	66-79	albumin	Homo sapiens	6-13
12076520-11	2002	In contrast, V79-GSTA5 cells were more sensitive to methyl glyoxal, suggesting that a methyl glyoxal-glutathione conjugate is more toxic that the parental compound.	Pyruvaldehyde	52-66	glutathione S-transferase alpha 5	Rattus norvegicus	17-22
11988071-6	2002	Human serum albumin (HSA) glycated minimally by methylglyoxal in vitro contained mainly MG-H1 with minor amounts of THP and argpyrimidine.	Pyruvaldehyde	48-61	albumin	Homo sapiens	12-19
11988071-8	2002	HSA glycated highly by methylglyoxal contained mainly argpyrimidine, MG-H1 and THP, with minor amounts of CEL and MOLD.	Pyruvaldehyde	23-36	uromodulin	Homo sapiens	69-82
11988071-11	2002	Most AGEs in albumin glycated minimally by methylglyoxal and glucose were identified.	Pyruvaldehyde	43-56	albumin	Homo sapiens	13-20
12002523-5	2002	Glycating agents, methylglyoxal (MG) and glyceraldehyde (Glyc), caused an increase in the formation of advanced glycation endproducts (AGEs) in native and denatured GAPDH and AAT.	Pyruvaldehyde	18-31	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	165-170
11961137-0	2002	Substrate-induced up-regulation of aldose reductase by methylglyoxal, a reactive oxoaldehyde elevated in diabetes.	Pyruvaldehyde	55-68	aldo-keto reductase family 1 member B1	Rattus norvegicus	35-51
11961137-1	2002	Methylglyoxal (MG), a reactive dicarbonyl produced during glucose metabolism, induced a dose- and time-dependent increase in aldose reductase (AR) mRNA level in rat aortic smooth muscle cells (SMCs).	Pyruvaldehyde	0-13	aldo-keto reductase family 1 member B1	Rattus norvegicus	125-141
11961137-1	2002	Methylglyoxal (MG), a reactive dicarbonyl produced during glucose metabolism, induced a dose- and time-dependent increase in aldose reductase (AR) mRNA level in rat aortic smooth muscle cells (SMCs).	Pyruvaldehyde	0-13	aldo-keto reductase family 1 member B1	Rattus norvegicus	143-145
11961137-1	2002	Methylglyoxal (MG), a reactive dicarbonyl produced during glucose metabolism, induced a dose- and time-dependent increase in aldose reductase (AR) mRNA level in rat aortic smooth muscle cells (SMCs).	Pyruvaldehyde	15-17	aldo-keto reductase family 1 member B1	Rattus norvegicus	125-141
11961137-1	2002	Methylglyoxal (MG), a reactive dicarbonyl produced during glucose metabolism, induced a dose- and time-dependent increase in aldose reductase (AR) mRNA level in rat aortic smooth muscle cells (SMCs).	Pyruvaldehyde	15-17	aldo-keto reductase family 1 member B1	Rattus norvegicus	143-145
11961137-3	2002	The enzyme catalyzes the reduction of glucose in the polyol pathway, as well as that of MG, which is known to be a preferred substrate of AR.	Pyruvaldehyde	88-90	aldo-keto reductase family 1 member B1	Rattus norvegicus	138-140
11897769-7	2002	Addition of exogenous methylglyoxal to the cultures induced a greater increase in oxidative stress and advanced glycation end products in cells from hypertensive rats compared with normotensive rats and significantly decreased the activities of glutathione reductase and glutathione peroxidase in cells of both rat strains.	Pyruvaldehyde	22-35	glutathione-disulfide reductase	Rattus norvegicus	245-266
11897769-9	2002	Our study demonstrates an elevated methylglyoxal level and advanced glycation end products in cells from hypertensive rats, and methylglyoxal increases oxidative stress, activates NF-kappaB, and enhances ICAM-1 expression.	Pyruvaldehyde	128-141	intercellular adhesion molecule 1	Rattus norvegicus	204-210
11978653-3	2002	Therefore, we studied the effects of two AGE precursors, glyoxal (GO) and methylglyoxal (MGO), on the epidermal growth factor receptor (EGFR) signaling pathway in cultured cells.	Pyruvaldehyde	74-87	epidermal growth factor receptor	Homo sapiens	102-134
11978653-3	2002	Therefore, we studied the effects of two AGE precursors, glyoxal (GO) and methylglyoxal (MGO), on the epidermal growth factor receptor (EGFR) signaling pathway in cultured cells.	Pyruvaldehyde	74-87	epidermal growth factor receptor	Homo sapiens	136-140
11978653-3	2002	Therefore, we studied the effects of two AGE precursors, glyoxal (GO) and methylglyoxal (MGO), on the epidermal growth factor receptor (EGFR) signaling pathway in cultured cells.	Pyruvaldehyde	89-92	epidermal growth factor receptor	Homo sapiens	102-134
11978653-3	2002	Therefore, we studied the effects of two AGE precursors, glyoxal (GO) and methylglyoxal (MGO), on the epidermal growth factor receptor (EGFR) signaling pathway in cultured cells.	Pyruvaldehyde	89-92	epidermal growth factor receptor	Homo sapiens	136-140
11978653-8	2002	Aminoguanidine, an inhibitor of AGE formation, partially prevented the EGFR dysfunction induced by GO and MGO.	Pyruvaldehyde	106-109	epidermal growth factor receptor	Homo sapiens	71-75
11961137-4	2002	A maximum of 4.5-fold induction of AR mRNA by MG was accompanied by elevated enzyme activity and protein levels and was completely abolished in the presence of cycloheximide or actinomycin D.	Pyruvaldehyde	46-48	aldo-keto reductase family 1 member B1	Rattus norvegicus	35-37
11961137-5	2002	Pretreatment of SMCs with N-acetyl-L-cysteine significantly suppressed the MG-induced AR expression, whereas DL-buthionine-(S,R)-sulfoximine further augmented the MG-induced increase in AR mRNA level.	Pyruvaldehyde	75-77	aldo-keto reductase family 1 member B1	Rattus norvegicus	86-88
11961137-5	2002	Pretreatment of SMCs with N-acetyl-L-cysteine significantly suppressed the MG-induced AR expression, whereas DL-buthionine-(S,R)-sulfoximine further augmented the MG-induced increase in AR mRNA level.	Pyruvaldehyde	163-165	aldo-keto reductase family 1 member B1	Rattus norvegicus	186-188
11961137-8	2002	The cytotoxic effect of MG on SMCs was significantly enhanced in the presence of the AR inhibitor ponalrestat, indicating a protective role of AR against MG-induced cell damage.	Pyruvaldehyde	24-26	aldo-keto reductase family 1 member B1	Rattus norvegicus	85-87
11961137-8	2002	The cytotoxic effect of MG on SMCs was significantly enhanced in the presence of the AR inhibitor ponalrestat, indicating a protective role of AR against MG-induced cell damage.	Pyruvaldehyde	24-26	aldo-keto reductase family 1 member B1	Rattus norvegicus	143-145
11961137-8	2002	The cytotoxic effect of MG on SMCs was significantly enhanced in the presence of the AR inhibitor ponalrestat, indicating a protective role of AR against MG-induced cell damage.	Pyruvaldehyde	154-156	aldo-keto reductase family 1 member B1	Rattus norvegicus	143-145
11961137-9	2002	Taken together, these observations indicated that substrate-induced induction of AR by MG during hyperglycemic conditions may hinder vascular remodeling and accelerate the development of vascular lesions in diabetes.	Pyruvaldehyde	87-89	aldo-keto reductase family 1 member B1	Rattus norvegicus	81-83
12002523-5	2002	Glycating agents, methylglyoxal (MG) and glyceraldehyde (Glyc), caused an increase in the formation of advanced glycation endproducts (AGEs) in native and denatured GAPDH and AAT.	Pyruvaldehyde	33-35	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	165-170
11705701-7	2001	Evidence was provided that GO/MGO upregulated MKP-1 activity that in turn dephosphorylated possibly co-aggregated phospho-ERK efficiently for inactivation.	Pyruvaldehyde	30-33	dual specificity phosphatase 1	Homo sapiens	46-51
11848206-2	2002	In this study, we found that cytochrome c added to incubation mixtures containing guanidino compounds and methylglyoxal in phosphate buffer solution (pH 7.4) resulted in reduction of cytochrome c.	Pyruvaldehyde	106-119	cytochrome c, somatic	Homo sapiens	29-41
11848206-2	2002	In this study, we found that cytochrome c added to incubation mixtures containing guanidino compounds and methylglyoxal in phosphate buffer solution (pH 7.4) resulted in reduction of cytochrome c.	Pyruvaldehyde	106-119	cytochrome c, somatic	Homo sapiens	183-195
11707430-0	2002	Methylglyoxal enhances cisplatin-induced cytotoxicity by activating protein kinase Cdelta.	Pyruvaldehyde	0-13	protein kinase C delta	Homo sapiens	68-89
11707430-2	2002	We report that the circulating glucose metabolite, methylglyoxal (MGO), enhances cisplatin-induced apoptosis by activating protein kinase Cdelta (PKCdelta).	Pyruvaldehyde	51-64	protein kinase C delta	Homo sapiens	123-144
11707430-2	2002	We report that the circulating glucose metabolite, methylglyoxal (MGO), enhances cisplatin-induced apoptosis by activating protein kinase Cdelta (PKCdelta).	Pyruvaldehyde	51-64	protein kinase C delta	Homo sapiens	146-154
11707430-2	2002	We report that the circulating glucose metabolite, methylglyoxal (MGO), enhances cisplatin-induced apoptosis by activating protein kinase Cdelta (PKCdelta).	Pyruvaldehyde	66-69	protein kinase C delta	Homo sapiens	123-144
11707430-2	2002	We report that the circulating glucose metabolite, methylglyoxal (MGO), enhances cisplatin-induced apoptosis by activating protein kinase Cdelta (PKCdelta).	Pyruvaldehyde	66-69	protein kinase C delta	Homo sapiens	146-154
11707430-6	2002	MGO and cisplatin increased PKCdelta activity by 4-fold, and this effect was blocked by the PKCdelta inhibitor rottlerin but not by NAC.	Pyruvaldehyde	0-3	protein kinase C delta	Homo sapiens	28-36
11707430-6	2002	MGO and cisplatin increased PKCdelta activity by 4-fold, and this effect was blocked by the PKCdelta inhibitor rottlerin but not by NAC.	Pyruvaldehyde	0-3	protein kinase C delta	Homo sapiens	92-100
11707430-8	2002	Finally, MGO and cisplatin induced c-Abl activation and c-Abl:PKCdelta association.	Pyruvaldehyde	9-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
11707430-8	2002	Finally, MGO and cisplatin induced c-Abl activation and c-Abl:PKCdelta association.	Pyruvaldehyde	9-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-61
11707430-8	2002	Finally, MGO and cisplatin induced c-Abl activation and c-Abl:PKCdelta association.	Pyruvaldehyde	9-12	protein kinase C delta	Homo sapiens	62-70
11707430-9	2002	Rottlerin blocked c-Abl activation, but the c-Abl inhibitor STI-571 increased MGO and cisplatin-induced apoptosis by 50%.	Pyruvaldehyde	78-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
11707430-10	2002	Taken together these data indicate that MGO synergistically enhances cisplatin-induced apoptosis through activation of PKCdelta and that PKCdelta is critical to both cell death and cell survival pathways.	Pyruvaldehyde	40-43	protein kinase C delta	Homo sapiens	119-127
11705701-0	2001	Glyoxal and methylglyoxal induce lyoxal and methyglyoxal induce aggregation and inactivation of ERK in human endothelial cells.	Pyruvaldehyde	12-25	mitogen-activated protein kinase 1	Homo sapiens	96-99
11705701-5	2001	Interestingly, however, GO/MGO caused both aggregation and dephosphorylation of intracellular phospho-ERK for inactivation.	Pyruvaldehyde	27-30	mitogen-activated protein kinase 1	Homo sapiens	102-105
11792832-4	2002	We also show that TNF induces a substantial increase in intracellular levels of methylglyoxal (MG) that leads to the formation of a specific MG-derived advanced glycation end product and that this formation occurs as a consequence of increased ROS production.	Pyruvaldehyde	80-93	tumor necrosis factor	Homo sapiens	18-21
11792832-4	2002	We also show that TNF induces a substantial increase in intracellular levels of methylglyoxal (MG) that leads to the formation of a specific MG-derived advanced glycation end product and that this formation occurs as a consequence of increased ROS production.	Pyruvaldehyde	95-97	tumor necrosis factor	Homo sapiens	18-21
11792832-6	2002	Furthermore, we provide evidence that the TNF-induced phosphorylation of glyoxalase I is not involved in detoxification of MG by means of the glyoxalase system, but that phosphorylated glyoxalase I is on the pathway leading to the formation of a specific MG-derived advanced glycation end product.	Pyruvaldehyde	123-125	tumor necrosis factor	Homo sapiens	42-45
11792832-6	2002	Furthermore, we provide evidence that the TNF-induced phosphorylation of glyoxalase I is not involved in detoxification of MG by means of the glyoxalase system, but that phosphorylated glyoxalase I is on the pathway leading to the formation of a specific MG-derived advanced glycation end product.	Pyruvaldehyde	123-125	glyoxalase I	Homo sapiens	73-85
11792832-6	2002	Furthermore, we provide evidence that the TNF-induced phosphorylation of glyoxalase I is not involved in detoxification of MG by means of the glyoxalase system, but that phosphorylated glyoxalase I is on the pathway leading to the formation of a specific MG-derived advanced glycation end product.	Pyruvaldehyde	255-257	tumor necrosis factor	Homo sapiens	42-45
11792832-6	2002	Furthermore, we provide evidence that the TNF-induced phosphorylation of glyoxalase I is not involved in detoxification of MG by means of the glyoxalase system, but that phosphorylated glyoxalase I is on the pathway leading to the formation of a specific MG-derived advanced glycation end product.	Pyruvaldehyde	255-257	glyoxalase I	Homo sapiens	73-85
11792832-6	2002	Furthermore, we provide evidence that the TNF-induced phosphorylation of glyoxalase I is not involved in detoxification of MG by means of the glyoxalase system, but that phosphorylated glyoxalase I is on the pathway leading to the formation of a specific MG-derived advanced glycation end product.	Pyruvaldehyde	255-257	glyoxalase I	Homo sapiens	185-197
12572858-1	2002	The glyoxalase system, comprised of glyoxalase-I and glyoxalase-II with glutathione as the cofactor, plays an important role in the detoxification of methylglyoxal and other alpha-oxo-aldehydes.	Pyruvaldehyde	150-163	glyoxalase I	Homo sapiens	36-48
12572858-1	2002	The glyoxalase system, comprised of glyoxalase-I and glyoxalase-II with glutathione as the cofactor, plays an important role in the detoxification of methylglyoxal and other alpha-oxo-aldehydes.	Pyruvaldehyde	150-163	hydroxyacylglutathione hydrolase	Homo sapiens	53-66
11705701-7	2001	Evidence was provided that GO/MGO upregulated MKP-1 activity that in turn dephosphorylated possibly co-aggregated phospho-ERK efficiently for inactivation.	Pyruvaldehyde	30-33	mitogen-activated protein kinase 1	Homo sapiens	122-125
11705701-8	2001	These results together suggest that GO and MGO trigger a novel pathway for chemical reaction-mediated downregulation of ERK.	Pyruvaldehyde	43-46	mitogen-activated protein kinase 1	Homo sapiens	120-123
11459475-1	2001	The structure of the active site of human glyoxalase I and the reaction mechanism of the enzyme-catalyzed conversion of the thiohemiacetal, formed from methylglyoxal and glutathione, to S-D-lactoylglutathione has been investigated by ab initio quantum chemical calculations.	Pyruvaldehyde	152-165	glyoxalase I	Homo sapiens	42-54
11489834-1	2001	PURPOSE: Glyoxalase I (GLO1) is an enzyme that plays a role in the detoxification of methylglyoxal, a side-product of glycolysis.	Pyruvaldehyde	85-98	glyoxalase I	Homo sapiens	9-21
11489834-1	2001	PURPOSE: Glyoxalase I (GLO1) is an enzyme that plays a role in the detoxification of methylglyoxal, a side-product of glycolysis.	Pyruvaldehyde	85-98	glyoxalase I	Homo sapiens	23-27
11498280-0	2001	Superoxide-mediated early oxidation and activation of ASK1 are important for initiating methylglyoxal-induced apoptosis process.	Pyruvaldehyde	88-101	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	54-58
11498280-2	2001	Our previous studies demonstrated that MG induced apoptosis in Jurkat cells by activating the c-Jun N-terminal kinase (JNK) signal transduction pathway, which induced an obvious decrease in mitochondrial membrane potential, followed by caspase-3 activation.	Pyruvaldehyde	39-41	mitogen-activated protein kinase 8	Homo sapiens	94-117
11498280-2	2001	Our previous studies demonstrated that MG induced apoptosis in Jurkat cells by activating the c-Jun N-terminal kinase (JNK) signal transduction pathway, which induced an obvious decrease in mitochondrial membrane potential, followed by caspase-3 activation.	Pyruvaldehyde	39-41	mitogen-activated protein kinase 8	Homo sapiens	119-122
11498280-2	2001	Our previous studies demonstrated that MG induced apoptosis in Jurkat cells by activating the c-Jun N-terminal kinase (JNK) signal transduction pathway, which induced an obvious decrease in mitochondrial membrane potential, followed by caspase-3 activation.	Pyruvaldehyde	39-41	caspase 3	Homo sapiens	236-245
11498280-3	2001	Here, we observed that MG-induced apoptosis was associated with both rapid production of superoxide anion (O(2)(-)) followed by a marked increase in ROS and striking and temporal activation of ASK1.	Pyruvaldehyde	23-25	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	193-197
11498280-7	2001	Correspondingly, MG-mediated ASK1 activation was enhanced by diethyldithiocarbamate (DDC).	Pyruvaldehyde	17-19	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	29-33
11498280-9	2001	These results suggest that activating ASK1 at the early stage linking to production of O(2)(-) is crucial for subsequent progression of apoptosis in MG-treated Jurkat cells.	Pyruvaldehyde	149-151	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	38-42
11425486-7	2001	We then found that MGO, but not GO, reduced the intracellular glutathione level, and that cysteine, but not cystine, inhibited the MGO-mediated activation of ERK, JNK, p38 MAPK, or c-Jun more extensively than did lysine or arginine.	Pyruvaldehyde	131-134	mitogen-activated protein kinase 1	Homo sapiens	158-161
11525399-8	2001	Furthermore, addition of NaCl or H2O2 to exponential-phase cells triggers an initial transient increase in the intracellular level of methylglyoxal, which is dependent on the Gre3p and Glo1p function.	Pyruvaldehyde	134-147	trifunctional aldehyde reductase/xylose reductase/glucose 1-dehydrogenase (NADP(+))	Saccharomyces cerevisiae S288C	175-180
11525399-8	2001	Furthermore, addition of NaCl or H2O2 to exponential-phase cells triggers an initial transient increase in the intracellular level of methylglyoxal, which is dependent on the Gre3p and Glo1p function.	Pyruvaldehyde	134-147	lactoylglutathione lyase GLO1	Saccharomyces cerevisiae S288C	185-190
11425486-3	2001	Depending on their concentrations, GO and MGO promoted phosphorylations of ERK1 and ERK2, which were blocked by the protein-tyrosine kinase (PTK) inhibitors herbimycin A and staurosporine, thereby being PTK-dependent.	Pyruvaldehyde	42-45	mitogen-activated protein kinase 3	Homo sapiens	75-79
11425486-3	2001	Depending on their concentrations, GO and MGO promoted phosphorylations of ERK1 and ERK2, which were blocked by the protein-tyrosine kinase (PTK) inhibitors herbimycin A and staurosporine, thereby being PTK-dependent.	Pyruvaldehyde	42-45	mitogen-activated protein kinase 1	Homo sapiens	84-88
11425486-7	2001	We then found that MGO, but not GO, reduced the intracellular glutathione level, and that cysteine, but not cystine, inhibited the MGO-mediated activation of ERK, JNK, p38 MAPK, or c-Jun more extensively than did lysine or arginine.	Pyruvaldehyde	131-134	mitogen-activated protein kinase 1	Homo sapiens	168-171
11425486-3	2001	Depending on their concentrations, GO and MGO promoted phosphorylations of ERK1 and ERK2, which were blocked by the protein-tyrosine kinase (PTK) inhibitors herbimycin A and staurosporine, thereby being PTK-dependent.	Pyruvaldehyde	42-45	EPH receptor A8	Homo sapiens	116-139
11425486-9	2001	These results demonstrated that GO and MGO triggered two distinct signal cascades, one for PTK-dependent control of ERK and another for PTK-independent redox-linked activation of JNK/p38 MAPK and caspases in HUVECs, depending on the structure of the carbon skeleton of the chemicals.	Pyruvaldehyde	39-42	EPH receptor A8	Homo sapiens	91-94
11425486-3	2001	Depending on their concentrations, GO and MGO promoted phosphorylations of ERK1 and ERK2, which were blocked by the protein-tyrosine kinase (PTK) inhibitors herbimycin A and staurosporine, thereby being PTK-dependent.	Pyruvaldehyde	42-45	EPH receptor A8	Homo sapiens	141-144
11425486-3	2001	Depending on their concentrations, GO and MGO promoted phosphorylations of ERK1 and ERK2, which were blocked by the protein-tyrosine kinase (PTK) inhibitors herbimycin A and staurosporine, thereby being PTK-dependent.	Pyruvaldehyde	42-45	EPH receptor A8	Homo sapiens	203-206
11425486-9	2001	These results demonstrated that GO and MGO triggered two distinct signal cascades, one for PTK-dependent control of ERK and another for PTK-independent redox-linked activation of JNK/p38 MAPK and caspases in HUVECs, depending on the structure of the carbon skeleton of the chemicals.	Pyruvaldehyde	39-42	mitogen-activated protein kinase 1	Homo sapiens	116-119
11425486-4	2001	GO and MGO also induced phosphorylations of JNK, p38 MAPK, and c-Jun, either PTK-dependently (GO) or -independently (MGO).	Pyruvaldehyde	7-10	mitogen-activated protein kinase 1	Homo sapiens	49-52
11425486-4	2001	GO and MGO also induced phosphorylations of JNK, p38 MAPK, and c-Jun, either PTK-dependently (GO) or -independently (MGO).	Pyruvaldehyde	7-10	mitogen-activated protein kinase 3	Homo sapiens	53-57
11425486-9	2001	These results demonstrated that GO and MGO triggered two distinct signal cascades, one for PTK-dependent control of ERK and another for PTK-independent redox-linked activation of JNK/p38 MAPK and caspases in HUVECs, depending on the structure of the carbon skeleton of the chemicals.	Pyruvaldehyde	39-42	EPH receptor A8	Homo sapiens	136-139
11425486-4	2001	GO and MGO also induced phosphorylations of JNK, p38 MAPK, and c-Jun, either PTK-dependently (GO) or -independently (MGO).	Pyruvaldehyde	7-10	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	63-68
11425486-4	2001	GO and MGO also induced phosphorylations of JNK, p38 MAPK, and c-Jun, either PTK-dependently (GO) or -independently (MGO).	Pyruvaldehyde	7-10	EPH receptor A8	Homo sapiens	77-80
11425486-4	2001	GO and MGO also induced phosphorylations of JNK, p38 MAPK, and c-Jun, either PTK-dependently (GO) or -independently (MGO).	Pyruvaldehyde	117-120	mitogen-activated protein kinase 1	Homo sapiens	49-52
11425486-4	2001	GO and MGO also induced phosphorylations of JNK, p38 MAPK, and c-Jun, either PTK-dependently (GO) or -independently (MGO).	Pyruvaldehyde	117-120	mitogen-activated protein kinase 3	Homo sapiens	53-57
11425486-4	2001	GO and MGO also induced phosphorylations of JNK, p38 MAPK, and c-Jun, either PTK-dependently (GO) or -independently (MGO).	Pyruvaldehyde	117-120	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	63-68
11425486-9	2001	These results demonstrated that GO and MGO triggered two distinct signal cascades, one for PTK-dependent control of ERK and another for PTK-independent redox-linked activation of JNK/p38 MAPK and caspases in HUVECs, depending on the structure of the carbon skeleton of the chemicals.	Pyruvaldehyde	39-42	mitogen-activated protein kinase 1	Homo sapiens	183-186
11425486-5	2001	Next, we found that MGO, but not GO, induced degradation of poly(ADP-ribose) polymerase (PARP) as the intracellular substrate of caspase-3.	Pyruvaldehyde	20-23	poly(ADP-ribose) polymerase 1	Homo sapiens	60-87
11425486-5	2001	Next, we found that MGO, but not GO, induced degradation of poly(ADP-ribose) polymerase (PARP) as the intracellular substrate of caspase-3.	Pyruvaldehyde	20-23	poly(ADP-ribose) polymerase 1	Homo sapiens	89-93
11425486-9	2001	These results demonstrated that GO and MGO triggered two distinct signal cascades, one for PTK-dependent control of ERK and another for PTK-independent redox-linked activation of JNK/p38 MAPK and caspases in HUVECs, depending on the structure of the carbon skeleton of the chemicals.	Pyruvaldehyde	39-42	mitogen-activated protein kinase 3	Homo sapiens	187-191
11425486-5	2001	Next, we found that MGO, but not GO, induced degradation of poly(ADP-ribose) polymerase (PARP) as the intracellular substrate of caspase-3.	Pyruvaldehyde	20-23	caspase 3	Homo sapiens	129-138
11425486-6	2001	Curcumin and SB203580, which inhibit JNK and p38 MAPK signaling pathways, but not herbimycin A/staurosporine, prevented the MGO-induced PARP degradation.	Pyruvaldehyde	124-127	mitogen-activated protein kinase 1	Homo sapiens	45-48
11139585-7	2001	As expected, both native Glb33 purified from rice seeds and the recombinant protein had glyoxalase I activity that catalyzes condensation of methylglyoxal and glutathione into S-lactoylglutathione.	Pyruvaldehyde	141-154	glyoxalase I	Homo sapiens	88-100
11425486-6	2001	Curcumin and SB203580, which inhibit JNK and p38 MAPK signaling pathways, but not herbimycin A/staurosporine, prevented the MGO-induced PARP degradation.	Pyruvaldehyde	124-127	mitogen-activated protein kinase 3	Homo sapiens	49-53
11425486-6	2001	Curcumin and SB203580, which inhibit JNK and p38 MAPK signaling pathways, but not herbimycin A/staurosporine, prevented the MGO-induced PARP degradation.	Pyruvaldehyde	124-127	poly(ADP-ribose) polymerase 1	Homo sapiens	136-140
11266660-1	2001	Semicarbazide-sensitive amine oxidase (SSAO) catalyzes the deamination of methylamine and aminoacetone to produce toxic aldehydes, i.e. formaldehyde and methylglyoxal, as well as hydrogen peroxide and ammonia.	Pyruvaldehyde	153-166	amine oxidase copper containing 2	Homo sapiens	0-37
11315838-8	2001	Significant postprandial increases in MG, 3-DG, and D-lactate occurred after the STM.	Pyruvaldehyde	38-40	sulfotransferase family 1A member 3	Homo sapiens	81-84
11266660-1	2001	Semicarbazide-sensitive amine oxidase (SSAO) catalyzes the deamination of methylamine and aminoacetone to produce toxic aldehydes, i.e. formaldehyde and methylglyoxal, as well as hydrogen peroxide and ammonia.	Pyruvaldehyde	153-166	amine oxidase copper containing 2	Homo sapiens	39-43
10913283-1	2000	The metalloenzyme glyoxalase I (GlxI) converts the nonenzymatically produced hemimercaptal of cytotoxic methylglyoxal and glutathione to nontoxic S-D-lactoylglutathione.	Pyruvaldehyde	104-117	glyoxalase I	Homo sapiens	32-36
11368170-1	2001	Glyoxalase I, a member of the metalloglutathione (GSH) transferase superfamily, plays a critical detoxification role in cells by catalyzing the conversion of cytotoxic methylglyoxal (as the diastereomeric GSH-thiohemiacetals) to S-D-lactoylglutathione via a 1,2-hydrogen transfer.	Pyruvaldehyde	168-181	glyoxalase I	Homo sapiens	0-12
11306074-3	2001	Aldose reductase catalyzes the reduction of methylglyoxal efficiently (k(cat)=142 min(-1) and k(cat)/K(m)=1.8x10(7) M(-1) min(-1)).	Pyruvaldehyde	44-57	aldo-keto reductase family 1 member B	Homo sapiens	0-16
11306074-4	2001	In the presence of physiological concentrations of glutathione, methylglyoxal is significantly converted into the hemithioacetal, which is the actual substrate of glyoxalase-I.	Pyruvaldehyde	64-77	glyoxalase I	Homo sapiens	163-175
11306074-5	2001	However, in the presence of glutathione, the efficiency of reduction of methylglyoxal, catalyzed by aldose reductase, also increases.	Pyruvaldehyde	72-85	aldo-keto reductase family 1 member B	Homo sapiens	100-116
11306074-8	2001	The relative importance of aldose reductase and glyoxalase-I in the metabolic disposal of methylglyoxal is highly dependent upon the concentration of glutathione, owing to the non-catalytic pre-enzymatic reaction between methylglyoxal and glutathione.	Pyruvaldehyde	90-103	aldo-keto reductase family 1 member B	Homo sapiens	27-43
11306074-8	2001	The relative importance of aldose reductase and glyoxalase-I in the metabolic disposal of methylglyoxal is highly dependent upon the concentration of glutathione, owing to the non-catalytic pre-enzymatic reaction between methylglyoxal and glutathione.	Pyruvaldehyde	90-103	glyoxalase I	Homo sapiens	48-60
11306074-8	2001	The relative importance of aldose reductase and glyoxalase-I in the metabolic disposal of methylglyoxal is highly dependent upon the concentration of glutathione, owing to the non-catalytic pre-enzymatic reaction between methylglyoxal and glutathione.	Pyruvaldehyde	221-234	aldo-keto reductase family 1 member B	Homo sapiens	27-43
11306074-8	2001	The relative importance of aldose reductase and glyoxalase-I in the metabolic disposal of methylglyoxal is highly dependent upon the concentration of glutathione, owing to the non-catalytic pre-enzymatic reaction between methylglyoxal and glutathione.	Pyruvaldehyde	221-234	glyoxalase I	Homo sapiens	48-60
9787766-1	1998	Methylglyoxal was demonstrated to be a substrate for the isozymes E1, E2 and E3 of human aldehyde dehydrogenase.	Pyruvaldehyde	0-13	small nucleolar RNA, H/ACA box 73A	Homo sapiens	66-111
10828676-6	2000	Induction of apoptosis by MG was indicated by partial degradation of poly(ADP-ribose) polymerase and further confirmed by discrete DNA fragmentation detected on an agarose gel.	Pyruvaldehyde	26-28	poly(ADP-ribose) polymerase 1	Homo sapiens	69-96
10752532-4	2000	Exposure of HPMC to acetaldehyde, formaldehyde, glyoxal, methylglyoxal, furaldehyde, but not to 5-hydroxymethyl-furfural, resulted in dose-dependent inhibition of cell growth, viability, and interleukin-1beta (IL-1beta)-stimulated IL-6 release; for several GDP, this suppression was significantly greater compared with L929 cells.	Pyruvaldehyde	57-70	interleukin 1 beta	Mus musculus	191-208
10752532-4	2000	Exposure of HPMC to acetaldehyde, formaldehyde, glyoxal, methylglyoxal, furaldehyde, but not to 5-hydroxymethyl-furfural, resulted in dose-dependent inhibition of cell growth, viability, and interleukin-1beta (IL-1beta)-stimulated IL-6 release; for several GDP, this suppression was significantly greater compared with L929 cells.	Pyruvaldehyde	57-70	interleukin 1 beta	Mus musculus	210-218
10723098-2	2000	This study examines molecular mechanisms in the MG-induced signal transduction leading to apoptosis, focusing particularly on the role of JNK activation.	Pyruvaldehyde	48-50	mitogen-activated protein kinase 8	Homo sapiens	138-141
10723098-4	2000	A caspase inhibitor, Z-DEVD-fmk, completely blocked MG-induced poly(ADP-ribose)polymerase (PARP) cleavage and apoptosis, showing the critical role of caspase activation.	Pyruvaldehyde	52-54	poly(ADP-ribose) polymerase 1	Homo sapiens	63-89
10723098-4	2000	A caspase inhibitor, Z-DEVD-fmk, completely blocked MG-induced poly(ADP-ribose)polymerase (PARP) cleavage and apoptosis, showing the critical role of caspase activation.	Pyruvaldehyde	52-54	poly(ADP-ribose) polymerase 1	Homo sapiens	91-95
10723098-5	2000	Inhibition of JNK activity by a JNK inhibitor, curcumin, remarkably reduced MG-induced caspase-3 activation, PARP cleavage, and apoptosis.	Pyruvaldehyde	76-78	mitogen-activated protein kinase 8	Homo sapiens	14-17
10723098-5	2000	Inhibition of JNK activity by a JNK inhibitor, curcumin, remarkably reduced MG-induced caspase-3 activation, PARP cleavage, and apoptosis.	Pyruvaldehyde	76-78	mitogen-activated protein kinase 8	Homo sapiens	32-35
10723098-5	2000	Inhibition of JNK activity by a JNK inhibitor, curcumin, remarkably reduced MG-induced caspase-3 activation, PARP cleavage, and apoptosis.	Pyruvaldehyde	76-78	caspase 3	Homo sapiens	87-96
10723098-5	2000	Inhibition of JNK activity by a JNK inhibitor, curcumin, remarkably reduced MG-induced caspase-3 activation, PARP cleavage, and apoptosis.	Pyruvaldehyde	76-78	poly(ADP-ribose) polymerase 1	Homo sapiens	109-113
10723098-7	2000	Correspondingly, loss of the mitochondrial membrane potential induced by MG was decreased by the dominant negative JNK.	Pyruvaldehyde	73-75	mitogen-activated protein kinase 8	Homo sapiens	115-118
10972486-1	2000	PURPOSE: The enediol analogue S-(N-p-chlorophenyl-N-hydroxycarbamoyl)glutathione (CHG) is a powerful, mechanism-based, competitive inhibitor of the methylglyoxal-detoxifying enzyme glyoxalase I.	Pyruvaldehyde	148-161	glyoxalase 1	Mus musculus	181-193
10548540-5	1999	Addition of t-BOC-lysine and human serum albumin increased the rate of formation of alpha-oxoaldehydes - except glyoxal and methylglyoxal concentrations were low with albumin, as expected from the high reactivity of glyoxal and methylglyoxal with arginine residues.	Pyruvaldehyde	124-137	albumin	Homo sapiens	41-48
10548540-5	1999	Addition of t-BOC-lysine and human serum albumin increased the rate of formation of alpha-oxoaldehydes - except glyoxal and methylglyoxal concentrations were low with albumin, as expected from the high reactivity of glyoxal and methylglyoxal with arginine residues.	Pyruvaldehyde	124-137	albumin	Homo sapiens	167-174
10548540-5	1999	Addition of t-BOC-lysine and human serum albumin increased the rate of formation of alpha-oxoaldehydes - except glyoxal and methylglyoxal concentrations were low with albumin, as expected from the high reactivity of glyoxal and methylglyoxal with arginine residues.	Pyruvaldehyde	228-241	albumin	Homo sapiens	41-48
10497785-1	1999	The deamination of methylamine and aminoacetone by semicarbazide-sensitive amine oxidase (SSAO) produces formaldehyde and methylglyoxal, respectively, which have been presumed to be involved in diabetic complications.	Pyruvaldehyde	122-135	amine oxidase, copper containing 3	Rattus norvegicus	51-88
10497785-1	1999	The deamination of methylamine and aminoacetone by semicarbazide-sensitive amine oxidase (SSAO) produces formaldehyde and methylglyoxal, respectively, which have been presumed to be involved in diabetic complications.	Pyruvaldehyde	122-135	amine oxidase, copper containing 3	Rattus norvegicus	90-94
10497785-6	1999	A potent selective SSAO inhibitor, (E)-2-(4-fluorophenethyl)-3-fluoroallylamine hydrochloride (MDL-72974A), reduced the formation of formaldehyde, methylglyoxal, and malondialdehyde.	Pyruvaldehyde	147-160	amine oxidase, copper containing 3	Rattus norvegicus	19-23
10206549-1	1999	The inhibition of glyoxalase I enzyme to increase cellular levels of methylglyoxal has been developed as a rationale for the production of anticancer agents.	Pyruvaldehyde	69-82	glyoxalase I	Homo sapiens	18-30
10352726-0	1999	The cytotoxicity of methylglyoxal and 3-deoxyglucosone is decreased in the aldehyde reductase gene-transfected cells.	Pyruvaldehyde	20-33	aldo-keto reductase family 1 member A1	Homo sapiens	75-93
9737992-2	1998	Glycation of bovine serum albumin by methylglyoxal generated the protein-bound free radical, probably the cation radical of the cross-linked Schiff base, as observed in the reaction of methylglyoxal with L-alanine (Yim, H.-S., Kang, S.-O., Hah, Y. C., Chock, P. B., and Yim, M. B.	Pyruvaldehyde	37-50	albumin	Homo sapiens	20-33
9737992-2	1998	Glycation of bovine serum albumin by methylglyoxal generated the protein-bound free radical, probably the cation radical of the cross-linked Schiff base, as observed in the reaction of methylglyoxal with L-alanine (Yim, H.-S., Kang, S.-O., Hah, Y. C., Chock, P. B., and Yim, M. B.	Pyruvaldehyde	185-198	albumin	Homo sapiens	20-33
9737992-6	1998	The glycated bovine serum albumin showed increased electrophoretic mobility suggesting that the basic residues, such as lysine, were modified by methylglyoxal.	Pyruvaldehyde	145-158	albumin	Homo sapiens	20-33
10942318-6	2000	The protective effect of methylglyoxal against ethanol-induced damage to the gastric wall mucosa may be mediated through its effect on mucous production, proteins, nucleic acids, NP-SH groups and its free-radical scavenging property under the influence of polyamines stimulated by ornithine decarboxylase activity (ODC).	Pyruvaldehyde	25-38	ornithine decarboxylase 1	Rattus norvegicus	281-304
10942318-6	2000	The protective effect of methylglyoxal against ethanol-induced damage to the gastric wall mucosa may be mediated through its effect on mucous production, proteins, nucleic acids, NP-SH groups and its free-radical scavenging property under the influence of polyamines stimulated by ornithine decarboxylase activity (ODC).	Pyruvaldehyde	25-38	ornithine decarboxylase 1	Rattus norvegicus	315-318
10712823-12	2000	In addition, inhibition of glyoxalase I promotes MG accumulation.	Pyruvaldehyde	49-51	glyoxalase 1	Rattus norvegicus	27-39
10666306-6	2000	GmGlyox I was active toward the hemithioacetal adducts formed by reacting methylglyoxal, or phenylglyoxal, with glutathione, homoglutathione, or gamma-glutamylcysteine, showing no preference for homoglutathione adducts over glutathione adducts, even though homoglutathione is the dominant thiol in soybean.	Pyruvaldehyde	74-87	lactoylglutathione lyase	Glycine max	0-9
10606733-2	1999	We test whether glucose degradation products (GDPs) in PD fluids, glyoxal, methylglyoxal and 3-deoxyglucosone, stimulate the production of vascular endothelial growth factor (VEGF), a factor known to enhance vascular permeability and angiogenesis.	Pyruvaldehyde	75-88	vascular endothelial growth factor A	Homo sapiens	139-173
10606733-2	1999	We test whether glucose degradation products (GDPs) in PD fluids, glyoxal, methylglyoxal and 3-deoxyglucosone, stimulate the production of vascular endothelial growth factor (VEGF), a factor known to enhance vascular permeability and angiogenesis.	Pyruvaldehyde	75-88	vascular endothelial growth factor A	Homo sapiens	175-179
10606733-3	1999	VEGF increased in cultured rat mesothelial and human endothelial cells exposed to methylglyoxal, but not to glyoxal or 3-deoxyglucosone.	Pyruvaldehyde	82-95	vascular endothelial growth factor A	Rattus norvegicus	0-4
10564821-1	1999	Glyoxalase-I is a glutathione-binding protein involved in the detoxification of methylglyoxal, a by-product of glycolysis.	Pyruvaldehyde	80-93	glyoxalase I	Homo sapiens	0-12
10510318-5	1999	In contrast, AKR1A1 reduces a broad spectrum of carbonyl-containing compounds, displaying highest specific activity for SSA, 4-carboxybenzaldehyde, 4-nitrobenzaldehyde, pyridine-3-aldehyde, pyridine-4-aldehyde, 4-hydroxynonenal, phenylglyoxal, methylglyoxal, 2,3-hexanedione, 1, 2-NQ, 16-ketoestrone and d-glucuronic acid.	Pyruvaldehyde	244-257	aldo-keto reductase family 1 member A1	Homo sapiens	13-19
10413301-8	1999	The accumulation of glyoxal and MG in toxicant-treated cells was a likely consequence of decreased in situ activity of glyoxalase 1.	Pyruvaldehyde	32-34	glyoxalase 1	Mus musculus	119-131
9925727-6	1999	Consistent with the hypothesis that cell growth inhibition is due to competitive inhibition of glyoxalase I, preincubation of L1210 cells with 2(Et)2 increases the sensitivity of these cells to the inhibitory effects of exogenous methylglyoxal.	Pyruvaldehyde	230-243	glyoxalase 1	Mus musculus	95-107
9846896-3	1998	In addition to reaction with arginine residues to form imidazolone adducts, methylglyoxal reacts with lysine residues in protein to form N(epsilon)-(carboxyethyl)lysine (CEL) and the imidazolium crosslink, methylglyoxal-lysine dimer (MOLD).	Pyruvaldehyde	76-89	carboxyl ester lipase	Homo sapiens	137-174
22358615-4	1998	More importantly, comparative studies involving wild-type Chinese hamster ovary cells and clones overexpressing glyoxalase I indicate that glucose and glutamine, within the range normally found in cell culture media, can cause decreased cell viability mediated solely through increased production of methylglyoxal.	Pyruvaldehyde	300-313	lactoylglutathione lyase	Cricetulus griseus	112-124
9787766-7	1998	Methylglyoxal strongly inhibited the glycolaldehyde activity of the E1 and E2 isozymes.	Pyruvaldehyde	0-13	small nucleolar RNA, H/ACA box 73A	Homo sapiens	68-77
9525289-2	1998	Methylglyoxal inhibits cell growth in a dose-dependent manner and causes an increase in glyceraldehyde 3-phosphate dehydrogenase, and glyoxalase 1 and glyoxalase 2 specific activities.	Pyruvaldehyde	0-13	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	88-128
9486985-2	1998	Glyoxalase-I catalyzes the conversion of MG to S-D-lactoylglutathione, which in turn is converted to D-lactate by glyoxalase-II.	Pyruvaldehyde	41-43	glyoxalase I	Bos taurus	0-12
9486985-2	1998	Glyoxalase-I catalyzes the conversion of MG to S-D-lactoylglutathione, which in turn is converted to D-lactate by glyoxalase-II.	Pyruvaldehyde	41-43	hydroxyacylglutathione hydrolase	Bos taurus	114-127
9538214-0	1998	Overexpression of aldehyde reductase protects PC12 cells from the cytotoxicity of methylglyoxal or 3-deoxyglucosone.	Pyruvaldehyde	82-95	aldo-keto reductase family 1 member A1	Rattus norvegicus	18-36
9538214-7	1998	In the ALR gene-transfected cells, the cytotoxicity of both MG and 3-DG and apoptotic cell death were decreased.	Pyruvaldehyde	60-62	aldo-keto reductase family 1 member A1	Rattus norvegicus	7-10
9446611-12	1998	Methylglyoxal is also synthesized from dihydroxyacetone phosphate; therefore, induction of the GLO1 gene expression by osmotic stress was thought to scavenge methylglyoxal, which increased during glycerol production for adaptation to osmotic stress.	Pyruvaldehyde	0-13	lactoylglutathione lyase GLO1	Saccharomyces cerevisiae S288C	95-99
9572061-3	1998	After deamination by SSAO highly angiotoxic products are formed, methylglyoxal and formaldehyde, respectively.	Pyruvaldehyde	65-78	amine oxidase copper containing 2	Homo sapiens	21-25
9446611-12	1998	Methylglyoxal is also synthesized from dihydroxyacetone phosphate; therefore, induction of the GLO1 gene expression by osmotic stress was thought to scavenge methylglyoxal, which increased during glycerol production for adaptation to osmotic stress.	Pyruvaldehyde	158-171	lactoylglutathione lyase GLO1	Saccharomyces cerevisiae S288C	95-99
9839528-1	1998	Semicarbazide-sensitive amine oxidase (SSAO)-mediated deamination of methylamine and aminoacetone in vitro produces carbonyl compounds, such as formaldehyde and methylglyoxal, which have been proposed to be cytotoxic and may be responsible for some pathological conditions.	Pyruvaldehyde	161-174	amine oxidase, copper containing 3	Rattus norvegicus	0-37
9839528-1	1998	Semicarbazide-sensitive amine oxidase (SSAO)-mediated deamination of methylamine and aminoacetone in vitro produces carbonyl compounds, such as formaldehyde and methylglyoxal, which have been proposed to be cytotoxic and may be responsible for some pathological conditions.	Pyruvaldehyde	161-174	amine oxidase, copper containing 3	Rattus norvegicus	39-43
9191294-0	1997	Induction of TNF alpha and IL-1 beta mRNA in monocytes by methylglyoxal- and advanced glycated endproduct-modified human serum albumin.	Pyruvaldehyde	58-71	tumor necrosis factor	Homo sapiens	13-22
9450641-0	1997	Inactivation of glyceraldehyde-3-phosphate dehydrogenase of human malignant cells by methylglyoxal.	Pyruvaldehyde	85-98	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	16-56
9450641-1	1997	The effect of methylglyoxal on the activity of glyceraldehyde-3-phosphate dehydrogenase (GA3PD) of several normal human tissues and benign and malignant tumors has been tested.	Pyruvaldehyde	14-27	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	47-87
9450641-1	1997	The effect of methylglyoxal on the activity of glyceraldehyde-3-phosphate dehydrogenase (GA3PD) of several normal human tissues and benign and malignant tumors has been tested.	Pyruvaldehyde	14-27	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	89-94
9450641-3	1997	When the effect of methylglyoxal on other two dehydrogenases namely glucose 6-phosphate dehydrogenase (G6PD) and L-lactic dehydrogenase (LDH) of similar cells was tested as controls it has been observed that methylglyoxal has some inactivating effect on G6PD of all the normal, benign and malignant samples tested, whereas, LDH remained completely unaffected.	Pyruvaldehyde	19-32	glucose-6-phosphate dehydrogenase	Homo sapiens	68-101
9450641-3	1997	When the effect of methylglyoxal on other two dehydrogenases namely glucose 6-phosphate dehydrogenase (G6PD) and L-lactic dehydrogenase (LDH) of similar cells was tested as controls it has been observed that methylglyoxal has some inactivating effect on G6PD of all the normal, benign and malignant samples tested, whereas, LDH remained completely unaffected.	Pyruvaldehyde	19-32	glucose-6-phosphate dehydrogenase	Homo sapiens	103-107
9450641-3	1997	When the effect of methylglyoxal on other two dehydrogenases namely glucose 6-phosphate dehydrogenase (G6PD) and L-lactic dehydrogenase (LDH) of similar cells was tested as controls it has been observed that methylglyoxal has some inactivating effect on G6PD of all the normal, benign and malignant samples tested, whereas, LDH remained completely unaffected.	Pyruvaldehyde	19-32	glucose-6-phosphate dehydrogenase	Homo sapiens	254-258
9450641-3	1997	When the effect of methylglyoxal on other two dehydrogenases namely glucose 6-phosphate dehydrogenase (G6PD) and L-lactic dehydrogenase (LDH) of similar cells was tested as controls it has been observed that methylglyoxal has some inactivating effect on G6PD of all the normal, benign and malignant samples tested, whereas, LDH remained completely unaffected.	Pyruvaldehyde	208-221	glucose-6-phosphate dehydrogenase	Homo sapiens	68-101
9450641-3	1997	When the effect of methylglyoxal on other two dehydrogenases namely glucose 6-phosphate dehydrogenase (G6PD) and L-lactic dehydrogenase (LDH) of similar cells was tested as controls it has been observed that methylglyoxal has some inactivating effect on G6PD of all the normal, benign and malignant samples tested, whereas, LDH remained completely unaffected.	Pyruvaldehyde	208-221	glucose-6-phosphate dehydrogenase	Homo sapiens	103-107
9450641-3	1997	When the effect of methylglyoxal on other two dehydrogenases namely glucose 6-phosphate dehydrogenase (G6PD) and L-lactic dehydrogenase (LDH) of similar cells was tested as controls it has been observed that methylglyoxal has some inactivating effect on G6PD of all the normal, benign and malignant samples tested, whereas, LDH remained completely unaffected.	Pyruvaldehyde	208-221	glucose-6-phosphate dehydrogenase	Homo sapiens	254-258
9450641-4	1997	These studies indicate that the inactivating effect of methylglyoxal on GA3PD specifically of the malignant cells may be a common feature of all the malignant cells, and this phenomenon can be used as a simple and rapid device for the detection of malignancy.	Pyruvaldehyde	55-68	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	72-77
9359858-6	1997	The kcat/Km values of the mutant glyoxalase I determined with the hemithioacetal adduct of glutathione and methylglyoxal were reduced to between 10 and 40% of the wild-type value.	Pyruvaldehyde	107-120	glyoxalase I	Homo sapiens	33-45
9218489-0	1997	Selective induction of heparin-binding epidermal growth factor-like growth factor by methylglyoxal and 3-deoxyglucosone in rat aortic smooth muscle cells.	Pyruvaldehyde	85-98	heparin-binding EGF-like growth factor	Rattus norvegicus	23-81
9218489-2	1997	Methylglyoxal (MG) and 3-deoxyglucosone (3-DG), reactive dicarbonyl metabolites in the glyoxalase system and glycation reaction, respectively, selectively induced heparin-binding epidermal growth factor (HB-EGF)-like growth factor mRNA in a dose- and time-dependent manner in rat aortic smooth muscle cells (RASMC).	Pyruvaldehyde	0-13	heparin-binding EGF-like growth factor	Rattus norvegicus	163-202
9218489-2	1997	Methylglyoxal (MG) and 3-deoxyglucosone (3-DG), reactive dicarbonyl metabolites in the glyoxalase system and glycation reaction, respectively, selectively induced heparin-binding epidermal growth factor (HB-EGF)-like growth factor mRNA in a dose- and time-dependent manner in rat aortic smooth muscle cells (RASMC).	Pyruvaldehyde	0-13	heparin-binding EGF-like growth factor	Rattus norvegicus	204-210
9218489-2	1997	Methylglyoxal (MG) and 3-deoxyglucosone (3-DG), reactive dicarbonyl metabolites in the glyoxalase system and glycation reaction, respectively, selectively induced heparin-binding epidermal growth factor (HB-EGF)-like growth factor mRNA in a dose- and time-dependent manner in rat aortic smooth muscle cells (RASMC).	Pyruvaldehyde	15-17	heparin-binding EGF-like growth factor	Rattus norvegicus	163-202
9218489-2	1997	Methylglyoxal (MG) and 3-deoxyglucosone (3-DG), reactive dicarbonyl metabolites in the glyoxalase system and glycation reaction, respectively, selectively induced heparin-binding epidermal growth factor (HB-EGF)-like growth factor mRNA in a dose- and time-dependent manner in rat aortic smooth muscle cells (RASMC).	Pyruvaldehyde	15-17	heparin-binding EGF-like growth factor	Rattus norvegicus	204-210
9218489-10	1997	These results indicate that MG and 3-DG induce HB-EGF by increasing the intracellular peroxide levels.	Pyruvaldehyde	28-30	heparin-binding EGF-like growth factor	Rattus norvegicus	47-53
9191294-0	1997	Induction of TNF alpha and IL-1 beta mRNA in monocytes by methylglyoxal- and advanced glycated endproduct-modified human serum albumin.	Pyruvaldehyde	58-71	interleukin 1 beta	Homo sapiens	27-36
9446106-4	1997	Intervention with aldose reductase inhibitors or aminoguanidine, which is an efficient scavenger of methylglyoxal, in diabetes mellitus may prevent increased methylglyoxal concentration.	Pyruvaldehyde	100-113	aldo-keto reductase family 1 member B	Homo sapiens	18-34
9175718-6	1997	Other reactive endogenous aldehydes such as methylglyoxal, 3-deoxyglucosone, and xylosone inactivated glutathione reductase by an NADPH-independent mechanism, with methylglyoxal being the most reactive.	Pyruvaldehyde	44-57	glutathione-disulfide reductase	Homo sapiens	102-123
9175718-6	1997	Other reactive endogenous aldehydes such as methylglyoxal, 3-deoxyglucosone, and xylosone inactivated glutathione reductase by an NADPH-independent mechanism, with methylglyoxal being the most reactive.	Pyruvaldehyde	164-177	glutathione-disulfide reductase	Homo sapiens	102-123
9446106-4	1997	Intervention with aldose reductase inhibitors or aminoguanidine, which is an efficient scavenger of methylglyoxal, in diabetes mellitus may prevent increased methylglyoxal concentration.	Pyruvaldehyde	158-171	aldo-keto reductase family 1 member B	Homo sapiens	18-34
8824231-7	1996	The gsh2-deficient mutant, which accumulates gamma-glutamylcysteine (an intermediate of glutathione biosynthesis), was also sensitive to methylglyoxal compared with the isogenic wild type strain, although the growth arrest caused by methylglyoxal was partially restored by overexpression of the GLO1 gene.	Pyruvaldehyde	137-150	glutathione synthase	Saccharomyces cerevisiae S288C	4-8
8942396-10	1996	In non-diabetic subjects, erythrocyte glyoxalase I activity correlated positively with methylglyoxal concentration.	Pyruvaldehyde	87-100	glyoxalase I	Homo sapiens	38-50
8640957-6	1996	Methylglyoxal inhibits platelet aggregation induced by several agonists and ATP release induced by thrombin.	Pyruvaldehyde	0-13	coagulation factor II, thrombin	Homo sapiens	99-107
8824231-6	1996	The gsh1-deficient mutant, which could not produce glutathione at all, was hypersensitive to methylglyoxal, and overproduction of the Glo1p did not restore the growth arrest caused by exogenously added methylglyoxal.	Pyruvaldehyde	93-106	glutamate--cysteine ligase	Saccharomyces cerevisiae S288C	4-8
8640957-2	1996	The oxidation effect of methylglyoxal significantly potentiated by thrombin, depends on both the ketoaldehyde and the agonist concentrations.	Pyruvaldehyde	24-37	coagulation factor II, thrombin	Homo sapiens	67-75
8636255-0	1996	Increased levels of methylglyoxal-metabolizing enzymes in mononuclear and polymorphonuclear cells from insulin-dependent diabetic patients with diabetic complications: aldose reductase, glyoxalase I, and glyoxalase II--a clinical research center study.	Pyruvaldehyde	20-33	insulin	Homo sapiens	103-110
8853285-11	1996	Decreased detoxification of methylglyoxal may be induced pharmacologically by glyoxalase I inhibitors which have anti-tumor and anti-malarial activities.	Pyruvaldehyde	28-41	glyoxalase I	Homo sapiens	78-90
8683979-5	1996	These effects confirm and further substantiate the anti-proliferative anti-tumour activity of methylglyoxal in vitro, which may mediate the anti-tumour activity of glyoxalase I inhibitors in vivo.	Pyruvaldehyde	94-107	glyoxalase I	Homo sapiens	164-176
8787553-7	1996	Glyoxalase I inhibitor diesters may, therefore, inhibit tumour growth by inducing the accumulation of methylglyoxal in tumour cells, and induction of apoptosis.	Pyruvaldehyde	102-115	glyoxalase I	Homo sapiens	0-12
8920635-10	1996	Recent studies showing that the endogenously-occurring aliphatic amines methylamine and aminoacetone are metabolized in vitro to formaldehyde and methylglyoxal, respectively, by SSAO in some animal (including human) tissues, suggest the possibility that toxicological consequences upon cellular function could result if such conversions occur in vivo.	Pyruvaldehyde	146-159	amine oxidase copper containing 2	Homo sapiens	178-182
8636255-0	1996	Increased levels of methylglyoxal-metabolizing enzymes in mononuclear and polymorphonuclear cells from insulin-dependent diabetic patients with diabetic complications: aldose reductase, glyoxalase I, and glyoxalase II--a clinical research center study.	Pyruvaldehyde	20-33	aldo-keto reductase family 1 member B	Homo sapiens	168-184
8636255-0	1996	Increased levels of methylglyoxal-metabolizing enzymes in mononuclear and polymorphonuclear cells from insulin-dependent diabetic patients with diabetic complications: aldose reductase, glyoxalase I, and glyoxalase II--a clinical research center study.	Pyruvaldehyde	20-33	glyoxalase I	Homo sapiens	186-198
8636255-0	1996	Increased levels of methylglyoxal-metabolizing enzymes in mononuclear and polymorphonuclear cells from insulin-dependent diabetic patients with diabetic complications: aldose reductase, glyoxalase I, and glyoxalase II--a clinical research center study.	Pyruvaldehyde	20-33	hydroxyacylglutathione hydrolase	Homo sapiens	204-217
7821871-4	1995	The resultant values for GST-P-positive hepatic focus induction were slightly increased with methylglyoxal and decreased with glyoxal and theobromine compared with the corresponding controls.	Pyruvaldehyde	93-106	glutathione S-transferase pi 1	Rattus norvegicus	25-30
7748183-1	1995	Aldose reductase (aldehyde reductase 2) catalyses the conversion of glucose to sorbitol, and methylglyoxal to acetol.	Pyruvaldehyde	93-106	aldose reductase	Bos taurus	0-16
7748183-1	1995	Aldose reductase (aldehyde reductase 2) catalyses the conversion of glucose to sorbitol, and methylglyoxal to acetol.	Pyruvaldehyde	93-106	aldo-keto reductase family 1 member B1	Bos taurus	18-36
7748183-5	1995	ZD5522 follows pure noncompetitive kinetics against bovine lens aldose reductase when either glucose or methylglyoxal is varied (K(is) = K(ii) = 7.2 and 4.3 nM, respectively).	Pyruvaldehyde	104-117	aldose reductase	Bos taurus	64-80
7827133-6	1995	Reaction of methylglyoxal with bovine gamma II-crystallin, which is found mainly in the lens nucleus, could alter the change surface network of the molecule, resulting in aggregation, increased light scattering and hence cataract.	Pyruvaldehyde	12-25	G protein subunit gamma 7	Bos taurus	38-46
7827133-7	1995	Modification of gamma II-crystallin by methylglyoxal produced an overall loss of positive charge and an increase in molecular weight and non-disulfide covalent crosslinking.	Pyruvaldehyde	39-52	G protein subunit gamma 7	Bos taurus	16-24
8575417-0	1995	Methylglyoxal induces hprt mutation and DNA adducts in human T-lymphocytes in vitro.	Pyruvaldehyde	0-13	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	22-26
8584666-4	1995	Recent evidence has accumulated that SSAO may also be involved in metabolizing endogenous aliphatic amines such as methylamine and aminoacetone, focussing attention on the fact that the aldehyde products (formaldehyde and methylglyoxal, respectively) are potentially cytotoxic agents.	Pyruvaldehyde	222-235	amine oxidase copper containing 2	Homo sapiens	37-41
8584667-5	1995	The possibility that SSAO enzymes can convert amine substrates to highly toxic metabolites is illustrated by the production of acrolein from the xenobiotic amine, allylamine and formaldehyde and methylglyoxal from methylamine and aminoacetone, respectively.	Pyruvaldehyde	195-208	amine oxidase copper containing 2	Homo sapiens	21-25
7859825-7	1994	Given the previously reported decrease in the concentration of reduced glutathione in the human lens with age, there is expected to be a marked decrease in in situ activity of glyoxalase I and concomitant susceptibility of human lens proteins to modification by methylglyoxal with age.	Pyruvaldehyde	262-275	glyoxalase I	Homo sapiens	176-188
7986197-4	1994	The mean second order rate constant for the reaction of methylglyoxal with aminoguanidine, kMG.AG = 0.39 +/- 0.06 M-1 sec-1 at pH 7.4 and 37 degrees.	Pyruvaldehyde	56-69	secretory blood group 1, pseudogene	Homo sapiens	118-123
7798229-0	1994	Receptor-mediated endocytic uptake of methylglyoxal-modified serum albumin.	Pyruvaldehyde	38-51	albumin	Mus musculus	61-74
7798229-2	1994	Methylglyoxal binds and irreversibly modifies arginine and lysine residues in bovine serum albumin (BSA) under physiological conditions, producing a protein with an increased net negative charge at physiological pH.	Pyruvaldehyde	0-13	albumin	Mus musculus	85-98
8288025-8	1993	A further significant increase was observed in platelets stimulated with thrombin in the presence of methylglyoxal.	Pyruvaldehyde	101-114	coagulation factor II, thrombin	Homo sapiens	73-81
24190739-2	1994	Methylglyoxal is metabolised to S-D-lactoylglutathione and D-lactate by the glyoxalase system and to hydroxyacetone (95%) and D-lactaldehyde by aldose reductase.	Pyruvaldehyde	0-13	aldo-keto reductase family 1 member B1	Rattus norvegicus	144-160
24190739-5	1994	Aldose reductase inhibitors decrease the concentration of methylglyoxal in experimental diabetic rats to normal levels, aminoguanidine and L-arginine scavenge methylglyoxal; these effects may be involved in their prospective preventive therapy of diabetic complications.	Pyruvaldehyde	58-71	aldo-keto reductase family 1 member B1	Rattus norvegicus	0-16
24190739-5	1994	Aldose reductase inhibitors decrease the concentration of methylglyoxal in experimental diabetic rats to normal levels, aminoguanidine and L-arginine scavenge methylglyoxal; these effects may be involved in their prospective preventive therapy of diabetic complications.	Pyruvaldehyde	159-172	aldo-keto reductase family 1 member B1	Rattus norvegicus	0-16
7931255-3	1994	However SSAO in human and rat vascular homogenates readily converts the aliphatic biogenic amines methylamine and aminoacetone to formaldehyde and methylglyoxal, respectively.	Pyruvaldehyde	147-160	amine oxidase copper containing 2	Homo sapiens	8-12
8399366-1	1993	Glyoxalase-I (Gly-I) is part of the glyoxalase system which converts methylglyoxal to D-lactic acid via an S-D-lactoylglutathione intermediate.	Pyruvaldehyde	69-82	glyoxalase I	Homo sapiens	0-12
8399366-1	1993	Glyoxalase-I (Gly-I) is part of the glyoxalase system which converts methylglyoxal to D-lactic acid via an S-D-lactoylglutathione intermediate.	Pyruvaldehyde	69-82	glyoxalase I	Homo sapiens	14-19
7684374-2	1993	Glyoxalase I (EC 4.4.1.5) catalyzes the transformation of methylglyoxal and glutathione to S-lactoylglutathione.	Pyruvaldehyde	58-71	glyoxalase I	Homo sapiens	0-12
8370454-2	1993	Methylglyoxal, 1,2-propanediol and glycerol are shown to be substrates for sheep liver sorbitol dehydrogenase.	Pyruvaldehyde	0-13	L-iditol 2-dehydrogenase	Ovis aries	87-109
8509219-5	1993	Methylglyoxal has little inactivating effect on glucose 6-phosphate dehydrogenase (G6PD), and no effect on L-lactate dehydrogenase (LDH) of the malignant cells.	Pyruvaldehyde	0-13	glucose-6-phosphate dehydrogenase 2	Mus musculus	83-87
1459997-2	1992	In principle, competitive inhibitors of glyoxalase I that also serve as substrates for the thioester hydrolase glyoxalase II might function as tumor-selective anti-cancer agents, given the role of these enzymes in removing cytotoxic methylglyoxal from cells and the observation that glyoxalase II activity is abnormally low in some types of cancer cells.	Pyruvaldehyde	233-246	glyoxalase I	Homo sapiens	40-52
8509219-6	1993	Glucose-dependent L-lactic acid formation of EAC-cell-free homogenate was strongly inhibited by MG, but when GA3PD of normal cells was added to this homogenate, significant lactate formation was observed even in the presence of MG. Methylglyoxal also inhibited the respiration of EAC-cell mitochondria.	Pyruvaldehyde	232-245	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	109-114
8509219-9	1993	Studies reported herein strongly suggest that the tumoricidal effect of MG is mediated at least in part through the inhibition of mitochondrial respiration and inactivation of GA3PD, and this enzyme may play an important role in the high glycolytic capacity of the malignant cells.	Pyruvaldehyde	72-74	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	176-181
8504817-5	1993	S-p-Nitrobenzoxycarbonylglutathione was a potent competitive inhibitor of glyoxalase II with a Ki value of 1.20 +/- 0.21 microM, and the hemithioacetal formed non-enzymically from the reaction of methylglyoxal with reduced glutathione was a weak competitive inhibitor with a Ki value of 834 +/- 98 microM.	Pyruvaldehyde	196-209	hydroxyacylglutathione hydrolase	Homo sapiens	74-87
8444148-4	1993	Methylglyoxal formation from glycerone phosphate was increased in the presence of triose phosphate isomerase but this may be due to the faster non-enzymatic formation from the glyceraldehyde 3-phosphate isomerisation product.	Pyruvaldehyde	0-13	triosephosphate isomerase 1	Homo sapiens	82-108
8509219-3	1993	Methylglyoxal strongly inactivated glyceraldehyde 3-phosphate dehydrogenase (GA3PD) of the malignant cells, whereas MG has little inactivating effect on this enzyme from several normal sources.	Pyruvaldehyde	0-13	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	35-75
8509219-3	1993	Methylglyoxal strongly inactivated glyceraldehyde 3-phosphate dehydrogenase (GA3PD) of the malignant cells, whereas MG has little inactivating effect on this enzyme from several normal sources.	Pyruvaldehyde	0-13	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	77-82
1459997-2	1992	In principle, competitive inhibitors of glyoxalase I that also serve as substrates for the thioester hydrolase glyoxalase II might function as tumor-selective anti-cancer agents, given the role of these enzymes in removing cytotoxic methylglyoxal from cells and the observation that glyoxalase II activity is abnormally low in some types of cancer cells.	Pyruvaldehyde	233-246	hydroxyacylglutathione hydrolase	Bos taurus	111-124
1440521-1	1992	Under conditions closely approximating those in vivo (100 mM sodium carbonate pH 7.3 with 0.9% NaCl, 37 degrees C), antithrombin III (AT III) and the C1 inhibitor (C1-INH) are inactivated by methylglyoxal (MG) with pseudofirst-order kinetics and second-order rate constants of 25.2 and 7.8 M-1 min-1, respectively.	Pyruvaldehyde	191-204	serpin family C member 1	Homo sapiens	116-132
1440521-1	1992	Under conditions closely approximating those in vivo (100 mM sodium carbonate pH 7.3 with 0.9% NaCl, 37 degrees C), antithrombin III (AT III) and the C1 inhibitor (C1-INH) are inactivated by methylglyoxal (MG) with pseudofirst-order kinetics and second-order rate constants of 25.2 and 7.8 M-1 min-1, respectively.	Pyruvaldehyde	191-204	serpin family C member 1	Homo sapiens	134-140
1440521-1	1992	Under conditions closely approximating those in vivo (100 mM sodium carbonate pH 7.3 with 0.9% NaCl, 37 degrees C), antithrombin III (AT III) and the C1 inhibitor (C1-INH) are inactivated by methylglyoxal (MG) with pseudofirst-order kinetics and second-order rate constants of 25.2 and 7.8 M-1 min-1, respectively.	Pyruvaldehyde	191-204	serpin family G member 1	Homo sapiens	150-162
1440521-1	1992	Under conditions closely approximating those in vivo (100 mM sodium carbonate pH 7.3 with 0.9% NaCl, 37 degrees C), antithrombin III (AT III) and the C1 inhibitor (C1-INH) are inactivated by methylglyoxal (MG) with pseudofirst-order kinetics and second-order rate constants of 25.2 and 7.8 M-1 min-1, respectively.	Pyruvaldehyde	191-204	serpin family G member 1	Homo sapiens	164-170
1440521-1	1992	Under conditions closely approximating those in vivo (100 mM sodium carbonate pH 7.3 with 0.9% NaCl, 37 degrees C), antithrombin III (AT III) and the C1 inhibitor (C1-INH) are inactivated by methylglyoxal (MG) with pseudofirst-order kinetics and second-order rate constants of 25.2 and 7.8 M-1 min-1, respectively.	Pyruvaldehyde	191-204	CD59 molecule (CD59 blood group)	Homo sapiens	294-299
1836354-8	1991	Methylglyoxal (a dicarbonyl which is analogous to hydroxypyruvaldehyde derived from glyceraldehyde autoxidation) proved to have a powerful inhibitory action on ATPase activities.	Pyruvaldehyde	0-13	dynein axonemal heavy chain 8	Homo sapiens	160-166
1537826-7	1992	The aldose reductase-catalyzed reduction of methylglyoxal produces 95% acetol, 5% D-lactaldehyde.	Pyruvaldehyde	44-57	aldo-keto reductase family 1 member B	Homo sapiens	4-20
1567465-0	1992	The metabolism of aminoacetone to methylglyoxal by semicarbazide-sensitive amine oxidase in human umbilical artery.	Pyruvaldehyde	34-47	amine oxidase copper containing 2	Homo sapiens	51-88
2021650-1	1991	Kinetic parameters for triosephosphate isomerase catalysis of the elimination reaction of an equilibrium mixture of dihydroxyacetone phosphate (DHAP) and D-glyceraldehyde-3-phosphate (DGAP) to form methylglyoxal and phosphate ion are reported for the enzyme from rabbit muscle.	Pyruvaldehyde	198-211	triosephosphate isomerase	Oryctolagus cuniculus	23-48
34962083-3	2022	Cell viability, apoptosis and the signaling pathways were measured with MTT, fluorescent staining and western blot experiments, the results showed that MGO could induce oxidative stress and cell inflammation, the level of reactive oxygen species (ROS) increased, and p38MAPK, JNK and NF-kappaB signaling pathways were activated.	Pyruvaldehyde	152-155	mitogen-activated protein kinase 8	Homo sapiens	276-279
34936958-0	2022	Metabolomic analysis indicates that higher drip loss may be related to the production of methylglyoxal as a by-product of glycolysis.	Pyruvaldehyde	89-102	DL	Gallus gallus	43-52
34838714-9	2022	CONCLUSIONS: These data, together with published findings that elevated MG leads to hyperglycemia, suggest the existence of a deleterious positive feedback loop whereby hyperglycemia leads to reduced Glo1 activity, contributing to elevated MG levels, which in turn promote hyperglycemia.	Pyruvaldehyde	72-74	glyoxalase 1	Mus musculus	200-204
34838714-9	2022	CONCLUSIONS: These data, together with published findings that elevated MG leads to hyperglycemia, suggest the existence of a deleterious positive feedback loop whereby hyperglycemia leads to reduced Glo1 activity, contributing to elevated MG levels, which in turn promote hyperglycemia.	Pyruvaldehyde	240-242	glyoxalase 1	Mus musculus	200-204
33971178-0	2021	Methylglyoxal augments uridine diphosphate-induced contraction via activation of p38 mitogen-activated protein kinase in rat carotid artery.	Pyruvaldehyde	0-13	mitogen activated protein kinase 14	Rattus norvegicus	81-117
33779307-6	2021	These treatments induce different levels of intracellular accumulation of AGEs which colocalize with the insulin-sensitive glucose transporter GLUT4 (solute carrier family 2 member 4- SLC2A4) in the cytoplasm; in particular, BSA-MGO reduces glucose uptake.	Pyruvaldehyde	229-232	insulin	Homo sapiens	105-112
33779307-6	2021	These treatments induce different levels of intracellular accumulation of AGEs which colocalize with the insulin-sensitive glucose transporter GLUT4 (solute carrier family 2 member 4- SLC2A4) in the cytoplasm; in particular, BSA-MGO reduces glucose uptake.	Pyruvaldehyde	229-232	solute carrier family 2 member 4	Homo sapiens	143-148
33779307-6	2021	These treatments induce different levels of intracellular accumulation of AGEs which colocalize with the insulin-sensitive glucose transporter GLUT4 (solute carrier family 2 member 4- SLC2A4) in the cytoplasm; in particular, BSA-MGO reduces glucose uptake.	Pyruvaldehyde	229-232	solute carrier family 2 member 4	Homo sapiens	150-182
33779307-6	2021	These treatments induce different levels of intracellular accumulation of AGEs which colocalize with the insulin-sensitive glucose transporter GLUT4 (solute carrier family 2 member 4- SLC2A4) in the cytoplasm; in particular, BSA-MGO reduces glucose uptake.	Pyruvaldehyde	229-232	solute carrier family 2 member 4	Homo sapiens	184-190
34102705-6	2022	Sciadopitysin attenuated intracellular Ca2+ , NOX4 levels, oxidative stress, and MG-protein adduct levels, and increased nuclear Nrf2 and glyoxalase 1 levels in the presence of MG.	Pyruvaldehyde	177-179	NADPH oxidase 4	Homo sapiens	46-50
34102705-6	2022	Sciadopitysin attenuated intracellular Ca2+ , NOX4 levels, oxidative stress, and MG-protein adduct levels, and increased nuclear Nrf2 and glyoxalase 1 levels in the presence of MG.	Pyruvaldehyde	177-179	NFE2 like bZIP transcription factor 2	Homo sapiens	129-133
34710466-13	2022	Glyoxalase 1 catalyzes the detoxification of reactive alpha-oxoaldehydes such as glyoxal and methylglyoxal, is associated with anxiety and activity levels, and its inhibition reduces alcohol intake.	Pyruvaldehyde	93-106	glyoxalase 1	Mus musculus	0-12
34962083-7	2022	Finally, mitochondrial membrane potential (MMP) decreased, fluorescence intensity of Hoechst33258 increased, and the protein expression ratio of Bax/Bcl-2 increased significantly after the treatment of MGO.	Pyruvaldehyde	202-205	BCL2 associated X, apoptosis regulator	Homo sapiens	145-148
34962083-7	2022	Finally, mitochondrial membrane potential (MMP) decreased, fluorescence intensity of Hoechst33258 increased, and the protein expression ratio of Bax/Bcl-2 increased significantly after the treatment of MGO.	Pyruvaldehyde	202-205	BCL2 apoptosis regulator	Homo sapiens	149-154
34790575-2	2021	Methylglyoxal (MG) is a reactive metabolite formed mainly as a by-product in anaerobic glycolysis, metabolized by glyoxalase 1 (Glo1) of the glyoxalase system.	Pyruvaldehyde	0-13	glyoxalase I	Homo sapiens	114-126
34970417-2	2021	Methylglyoxal (MG) induces glycation of fibrinogen, resulting in structural alterations that lead to autoimmune response via the generation of neoepitopes on protein molecules.	Pyruvaldehyde	0-13	fibrinogen beta chain	Homo sapiens	40-50
34970417-2	2021	Methylglyoxal (MG) induces glycation of fibrinogen, resulting in structural alterations that lead to autoimmune response via the generation of neoepitopes on protein molecules.	Pyruvaldehyde	15-17	fibrinogen beta chain	Homo sapiens	40-50
34656697-0	2021	Methylglyoxal affects cognitive behaviour and modulates RAGE and Presenilin-1 expression in hippocampus of aged mice.	Pyruvaldehyde	0-13	presenilin 1	Mus musculus	65-77
34842044-0	2021	Studies on the synergistic action of methylglyoxal and peroxynitrite on structure and function of human serum albumin.	Pyruvaldehyde	37-50	albumin	Homo sapiens	104-117
34842044-5	2021	In certain pathological conditions albumin may be modified by peroxynitrite and methylglyoxal simultaneously.	Pyruvaldehyde	80-93	albumin	Homo sapiens	35-42
34842044-9	2021	Molecular docking model and molecular dynamic simulations showed close interaction and formation of stable complexes between methylglyoxal, peroxynitrite and albumin.	Pyruvaldehyde	125-138	albumin	Homo sapiens	158-165
34842044-12	2021	On the basis of these results, it may be speculated that, albumin modified with endogenously generated methylglyoxal and peroxynitrite might be a driving factor in the progression of heightened inflammatory autoimmune responses.	Pyruvaldehyde	103-116	albumin	Homo sapiens	58-65
34887734-0	2021	TNF-alpha Induces Methylglyoxal Accumulation in Lumbar Herniated Disc of Patients With Radicular Pain.	Pyruvaldehyde	18-31	tumor necrosis factor	Homo sapiens	0-9
34887734-4	2021	In the present study, we found that both MG and tumor necrosis factor-alpha (TNF-alpha) levels in the herniated disc of patients with radicular pain were significantly increased, and the activity of Glyoxalase 1 (GLO1), the rate-limiting enzyme that metabolizes MG, was decreased.	Pyruvaldehyde	262-264	tumor necrosis factor	Homo sapiens	48-75
34887734-4	2021	In the present study, we found that both MG and tumor necrosis factor-alpha (TNF-alpha) levels in the herniated disc of patients with radicular pain were significantly increased, and the activity of Glyoxalase 1 (GLO1), the rate-limiting enzyme that metabolizes MG, was decreased.	Pyruvaldehyde	262-264	tumor necrosis factor	Homo sapiens	77-86
34887734-4	2021	In the present study, we found that both MG and tumor necrosis factor-alpha (TNF-alpha) levels in the herniated disc of patients with radicular pain were significantly increased, and the activity of Glyoxalase 1 (GLO1), the rate-limiting enzyme that metabolizes MG, was decreased.	Pyruvaldehyde	262-264	glyoxalase I	Homo sapiens	199-211
34887734-4	2021	In the present study, we found that both MG and tumor necrosis factor-alpha (TNF-alpha) levels in the herniated disc of patients with radicular pain were significantly increased, and the activity of Glyoxalase 1 (GLO1), the rate-limiting enzyme that metabolizes MG, was decreased.	Pyruvaldehyde	262-264	glyoxalase I	Homo sapiens	213-217
34887734-9	2021	These results suggested that TNF-alpha-induced GLO1 activity decrease contributed to MG accumulation in the herniated disc of patients with radicular pain.	Pyruvaldehyde	85-87	tumor necrosis factor	Homo sapiens	29-38
34887734-9	2021	These results suggested that TNF-alpha-induced GLO1 activity decrease contributed to MG accumulation in the herniated disc of patients with radicular pain.	Pyruvaldehyde	85-87	glyoxalase I	Homo sapiens	47-51
34835243-3	2021	Glyoxalase 1 (GLO1) is the major enzyme metabolizing methylglyoxal, a potent precursor of advanced glycation end-products.	Pyruvaldehyde	53-66	glyoxalase I	Homo sapiens	0-12
34835243-3	2021	Glyoxalase 1 (GLO1) is the major enzyme metabolizing methylglyoxal, a potent precursor of advanced glycation end-products.	Pyruvaldehyde	53-66	glyoxalase I	Homo sapiens	14-18
34516950-6	2021	MGO intake markedly elevated the levels of MGO and fluorescent AGEs in serum and reduced the mRNA expression and activity of glyoxalase (Glo1) in bladder tissues.	Pyruvaldehyde	0-3	glyoxalase 1	Mus musculus	137-141
34774865-9	2021	Considering the increased level of MG in diabetic condition, the current study appears physiologically relevant in terms of understanding AGE-mediated protein modification and subsequent structural changes.	Pyruvaldehyde	35-37	renin binding protein	Homo sapiens	138-141
34880648-0	2021	Methylglyoxal Exacerbates Lipopolysaccharide-Induced Acute Lung Injury via RAGE-Induced ROS Generation: Protective Effects of Metformin.	Pyruvaldehyde	0-13	advanced glycosylation end product-specific receptor	Mus musculus	75-79
34880648-8	2021	MGO treatment significantly increased the airways neutrophil infiltration and mRNA expressions of TNF-alpha and IL-1beta, whereas COX-2 expression remained unchanged.	Pyruvaldehyde	0-3	tumor necrosis factor	Mus musculus	98-107
34880648-8	2021	MGO treatment significantly increased the airways neutrophil infiltration and mRNA expressions of TNF-alpha and IL-1beta, whereas COX-2 expression remained unchanged.	Pyruvaldehyde	0-3	interleukin 1 alpha	Mus musculus	112-120
34880648-9	2021	In lung tissues of LPS-exposed mice, MGO treatment significantly increased the immunostaining and mRNA expression of RAGE, and the ROS levels.	Pyruvaldehyde	37-40	advanced glycosylation end product-specific receptor	Mus musculus	117-121
34880648-12	2021	Conclusion: MGO intake potentiates the LPS-induced ALI, increases RAGE expression and ROS generation, which is normalized by metformin.	Pyruvaldehyde	12-15	advanced glycosylation end product-specific receptor	Mus musculus	66-70
34785142-5	2021	Moreover, it was demonstrated that P2X7R regulated NLRP3 inflammasome signals in methylglyoxal-treated PC12 cells.	Pyruvaldehyde	81-94	NLR family, pyrin domain containing 3	Rattus norvegicus	51-56
34581579-8	2021	Finally, we discovered that intracellular MICA-glutathione metabolites are recognized and exported by the efflux pump MRP1, providing a parallel and perhaps complementary pathway for MGO detoxification working alongside the glyoxalase pathway.	Pyruvaldehyde	183-186	ATP binding cassette subfamily C member 1	Homo sapiens	118-122
34834827-4	2021	In glyI4 mutant plants, a general stress phenotype characterized by compromised MG scavenging, accumulation of reactive oxygen species (ROS), stomatal closure, and reduced fitness was observed.	Pyruvaldehyde	80-82	Lactoylglutathione lyase / glyoxalase I family protein	Arabidopsis thaliana	3-8
34790575-2	2021	Methylglyoxal (MG) is a reactive metabolite formed mainly as a by-product in anaerobic glycolysis, metabolized by glyoxalase 1 (Glo1) of the glyoxalase system.	Pyruvaldehyde	0-13	glyoxalase I	Homo sapiens	128-132
34790575-2	2021	Methylglyoxal (MG) is a reactive metabolite formed mainly as a by-product in anaerobic glycolysis, metabolized by glyoxalase 1 (Glo1) of the glyoxalase system.	Pyruvaldehyde	15-17	glyoxalase I	Homo sapiens	114-126
34790575-2	2021	Methylglyoxal (MG) is a reactive metabolite formed mainly as a by-product in anaerobic glycolysis, metabolized by glyoxalase 1 (Glo1) of the glyoxalase system.	Pyruvaldehyde	15-17	glyoxalase I	Homo sapiens	128-132
34790575-4	2021	Methods: Human Glo1 was overexpressed in HEK293 cells and the effect on anticancer drug potency, drug-induced increase in MG and mechanism of cytotoxicity characterized.	Pyruvaldehyde	122-124	glyoxalase I	Homo sapiens	15-19
34790575-8	2021	Antitumor drugs increased MG to cytotoxic levels which contributed to the cytotoxic, antiproliferative mechanism of action, consistent with Glo1-mediated MDR.	Pyruvaldehyde	26-28	glyoxalase I	Homo sapiens	140-144
34790575-15	2021	High expression of Glo1 contributes to multidrug resistance by shielding the spliceosome from MG modification and decreasing survival in the chemotherapy of breast cancer.	Pyruvaldehyde	94-96	glyoxalase I	Homo sapiens	19-23
34411784-7	2021	Thiourea-induced increased glyoxalase I and glyoxalase II activities are the indications of upregulated methylglyoxal detoxification system.	Pyruvaldehyde	104-117	lactoylglutathione lyase	Cicer arietinum	27-39
34686659-10	2021	Exogenous methylglyoxal (MGO) impaired insulin-stimulated AKT signaling in adipose tissues from WT mice fed a normal chow diet, but not in RAGE-/- mice.	Pyruvaldehyde	10-23	thymoma viral proto-oncogene 1	Mus musculus	58-61
34686659-10	2021	Exogenous methylglyoxal (MGO) impaired insulin-stimulated AKT signaling in adipose tissues from WT mice fed a normal chow diet, but not in RAGE-/- mice.	Pyruvaldehyde	25-28	thymoma viral proto-oncogene 1	Mus musculus	58-61
34669914-3	2021	Glyoxalase system contains enzyme named glyoxalase 1 (GLO1).It is a metabolic pathway which detoxifies alpha-oxo-aldehydes, particularly methylglyoxal (MG).	Pyruvaldehyde	137-150	glyoxalase 1	Mus musculus	40-52
34669914-3	2021	Glyoxalase system contains enzyme named glyoxalase 1 (GLO1).It is a metabolic pathway which detoxifies alpha-oxo-aldehydes, particularly methylglyoxal (MG).	Pyruvaldehyde	137-150	glyoxalase 1	Mus musculus	54-58
34669914-3	2021	Glyoxalase system contains enzyme named glyoxalase 1 (GLO1).It is a metabolic pathway which detoxifies alpha-oxo-aldehydes, particularly methylglyoxal (MG).	Pyruvaldehyde	152-154	glyoxalase 1	Mus musculus	40-52
34669914-3	2021	Glyoxalase system contains enzyme named glyoxalase 1 (GLO1).It is a metabolic pathway which detoxifies alpha-oxo-aldehydes, particularly methylglyoxal (MG).	Pyruvaldehyde	152-154	glyoxalase 1	Mus musculus	54-58
34680107-2	2021	Mitochondrial aldehyde dehydrogenase 2 (ALDH2) detoxifies reactive aldehydes, such as methylglyoxal (MG) and 4-hydroxynonenal (4-HNE), derived from glucose and lipids, respectively.	Pyruvaldehyde	86-99	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	40-45
34680107-2	2021	Mitochondrial aldehyde dehydrogenase 2 (ALDH2) detoxifies reactive aldehydes, such as methylglyoxal (MG) and 4-hydroxynonenal (4-HNE), derived from glucose and lipids, respectively.	Pyruvaldehyde	101-103	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	40-45
34831154-10	2021	Increased secretion of IL-6 and MIF was also observed upon the treatment of dermal fibroblasts with MGO, suggesting that MGO is sufficient for triggering these immunomodulatory responses.	Pyruvaldehyde	100-103	interleukin 6	Homo sapiens	23-27
34831154-10	2021	Increased secretion of IL-6 and MIF was also observed upon the treatment of dermal fibroblasts with MGO, suggesting that MGO is sufficient for triggering these immunomodulatory responses.	Pyruvaldehyde	100-103	macrophage migration inhibitory factor	Homo sapiens	32-35
34831154-10	2021	Increased secretion of IL-6 and MIF was also observed upon the treatment of dermal fibroblasts with MGO, suggesting that MGO is sufficient for triggering these immunomodulatory responses.	Pyruvaldehyde	121-124	interleukin 6	Homo sapiens	23-27
34831154-10	2021	Increased secretion of IL-6 and MIF was also observed upon the treatment of dermal fibroblasts with MGO, suggesting that MGO is sufficient for triggering these immunomodulatory responses.	Pyruvaldehyde	121-124	macrophage migration inhibitory factor	Homo sapiens	32-35
34831154-12	2021	Given that reduced glyoxalase activity results in increased MGO levels, these findings suggested a positive-feedback loop for MGO generation, in which MIF, evoked by MGO, in turn blocks MGO-degrading glyoxalase activity.	Pyruvaldehyde	60-63	macrophage migration inhibitory factor	Homo sapiens	151-154
34831154-12	2021	Given that reduced glyoxalase activity results in increased MGO levels, these findings suggested a positive-feedback loop for MGO generation, in which MIF, evoked by MGO, in turn blocks MGO-degrading glyoxalase activity.	Pyruvaldehyde	126-129	macrophage migration inhibitory factor	Homo sapiens	151-154
34831154-12	2021	Given that reduced glyoxalase activity results in increased MGO levels, these findings suggested a positive-feedback loop for MGO generation, in which MIF, evoked by MGO, in turn blocks MGO-degrading glyoxalase activity.	Pyruvaldehyde	166-169	macrophage migration inhibitory factor	Homo sapiens	151-154
34831154-12	2021	Given that reduced glyoxalase activity results in increased MGO levels, these findings suggested a positive-feedback loop for MGO generation, in which MIF, evoked by MGO, in turn blocks MGO-degrading glyoxalase activity.	Pyruvaldehyde	186-189	macrophage migration inhibitory factor	Homo sapiens	151-154
34654829-9	2021	Furthermore, MGO was positively correlated with markers of systemic inflammation (IL-6, p = 0.004) and the development of ascites (p = 0.013).	Pyruvaldehyde	13-16	interleukin 6	Homo sapiens	82-86
34680099-4	2021	Glycation of ac-alphaSyn by methylglyoxal increases oligomer formation, as visualized by AFM in solution, resulting in decreased dynamics of the monomer amide backbone around the Lys residues, as measured using NMR.	Pyruvaldehyde	28-41	synuclein alpha	Homo sapiens	16-24
34527816-0	2021	Methylglyoxal attenuates isoproterenol-induced increase in uncoupling protein 1 expression through activation of JNK signaling pathway in beige adipocytes.	Pyruvaldehyde	0-13	uncoupling protein 1	Homo sapiens	59-79
34703363-5	2021	Aminoguanidine, the reference drug inhibited caspase-3/7 activity by 56.2% and 54.7% through attenuation of dichlorofluorescin and methylglyoxal, respectively.	Pyruvaldehyde	131-144	caspase 3	Homo sapiens	45-56
34584990-1	2021	Objective: Hydroxyacylglutathione hydrolase (aka as GLO-2) is a component of the glyoxalase pathway involved in the detoxification of the reactive oxoaldehydes, glyoxal and methylglyoxal.	Pyruvaldehyde	173-186	hydroxyacyl glutathione hydrolase	Mus musculus	52-57
34527816-0	2021	Methylglyoxal attenuates isoproterenol-induced increase in uncoupling protein 1 expression through activation of JNK signaling pathway in beige adipocytes.	Pyruvaldehyde	0-13	mitogen-activated protein kinase 8	Homo sapiens	113-116
34527816-3	2021	Here, we show that MG negatively affects the expression of uncoupling protein 1 (UCP1), which is involved in thermogenesis and the regulation of systemic metabolism.	Pyruvaldehyde	19-21	uncoupling protein 1	Homo sapiens	59-79
34527816-3	2021	Here, we show that MG negatively affects the expression of uncoupling protein 1 (UCP1), which is involved in thermogenesis and the regulation of systemic metabolism.	Pyruvaldehyde	19-21	uncoupling protein 1	Homo sapiens	81-85
34527816-5	2021	We found that MG attenuated the increase in Ucp1 expression following treatment with isoproterenol in beige adipocytes.	Pyruvaldehyde	14-16	uncoupling protein 1	Homo sapiens	44-48
34527816-8	2021	We found that JNK inhibition, but not p38, recovered isoproterenol-stimulated Ucp1 expression under MG treatment.	Pyruvaldehyde	100-102	uncoupling protein 1	Homo sapiens	78-82
34527816-9	2021	Altogether, these results suggest an inhibitory role of MG on the thermogenic function of beige adipocytes through the JNK signaling pathway.	Pyruvaldehyde	56-58	mitogen-activated protein kinase 8	Homo sapiens	119-122
34572324-5	2021	HIF1-alpha silencing, the carbonyl-trapping and anti-glycating agent L-carnosine, and the glyoxalase-1 inducer trans-resveratrol reversed HG-induced bioenergetics/biochemical changes and endothelial-monocyte cell inflammation, pointing to methylglyoxal (MGO) as the non-hypoxic stimulus for HIF1-alpha induction.	Pyruvaldehyde	239-252	hypoxia inducible factor 1 subunit alpha	Homo sapiens	291-301
34091674-10	2021	In addition, after 6 wk of quercetin administration, the expressions of GLO I/II and AR in the liver and kidney were significantly upregulated to promote MGO detoxification compared with MGO-treated mice.	Pyruvaldehyde	154-157	aldo-keto reductase family 1, member B3 (aldose reductase)	Mus musculus	85-87
34091674-10	2021	In addition, after 6 wk of quercetin administration, the expressions of GLO I/II and AR in the liver and kidney were significantly upregulated to promote MGO detoxification compared with MGO-treated mice.	Pyruvaldehyde	187-190	aldo-keto reductase family 1, member B3 (aldose reductase)	Mus musculus	85-87
34572324-5	2021	HIF1-alpha silencing, the carbonyl-trapping and anti-glycating agent L-carnosine, and the glyoxalase-1 inducer trans-resveratrol reversed HG-induced bioenergetics/biochemical changes and endothelial-monocyte cell inflammation, pointing to methylglyoxal (MGO) as the non-hypoxic stimulus for HIF1-alpha induction.	Pyruvaldehyde	254-257	hypoxia inducible factor 1 subunit alpha	Homo sapiens	291-301
34572324-5	2021	HIF1-alpha silencing, the carbonyl-trapping and anti-glycating agent L-carnosine, and the glyoxalase-1 inducer trans-resveratrol reversed HG-induced bioenergetics/biochemical changes and endothelial-monocyte cell inflammation, pointing to methylglyoxal (MGO) as the non-hypoxic stimulus for HIF1-alpha induction.	Pyruvaldehyde	239-252	hypoxia inducible factor 1 subunit alpha	Homo sapiens	0-10
34572324-6	2021	Consistently, MGO mimicked the effects of HG on HIF-1alpha induction and was able to induce a switch from oxidative metabolism to glycolysis.	Pyruvaldehyde	14-17	hypoxia inducible factor 1 subunit alpha	Homo sapiens	48-58
34572324-7	2021	Mechanistically, methylglyoxal causes HIF1-alpha stabilization by inhibiting prolyl 4-hydroxylase domain 2 enzyme activity through post-translational glycation.	Pyruvaldehyde	17-30	hypoxia inducible factor 1 subunit alpha	Homo sapiens	38-48
34298821-1	2021	Glyoxalase 1 (GLO1) is an enzyme involved in the detoxification of methylglyoxal (MG), a reactive oncometabolite formed in the context of energy metabolism as a result of high glycolytic flux.	Pyruvaldehyde	67-80	glyoxalase I	Homo sapiens	0-12
34318802-1	2021	An "AND"-logic-gate-based fluorescent probe NAP-DCP-4 with dual reactive sites is reported, which has improved selectivity for methylglyoxal over glyoxal, featuring formaldehyde-enhanced methylglyoxal detection and irreversible and reversible turn-on fluorescence responses at different excitation wavelengths.	Pyruvaldehyde	127-140	catenin beta like 1	Homo sapiens	44-47
34301957-5	2021	Methylglyoxal is generated from substrates of GAPDH, dihydroxyacetone phosphate and glyceraldehyde 3-phosphate.	Pyruvaldehyde	0-13	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	46-51
34301957-8	2021	Thus, trace amounts of phenethylamine alleviate HFD-induced liver damage by regulating methylglyoxal via increase of GAPDH.	Pyruvaldehyde	87-100	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	117-122
34298821-1	2021	Glyoxalase 1 (GLO1) is an enzyme involved in the detoxification of methylglyoxal (MG), a reactive oncometabolite formed in the context of energy metabolism as a result of high glycolytic flux.	Pyruvaldehyde	67-80	glyoxalase I	Homo sapiens	14-18
34298821-1	2021	Glyoxalase 1 (GLO1) is an enzyme involved in the detoxification of methylglyoxal (MG), a reactive oncometabolite formed in the context of energy metabolism as a result of high glycolytic flux.	Pyruvaldehyde	82-84	glyoxalase I	Homo sapiens	0-12
34298821-1	2021	Glyoxalase 1 (GLO1) is an enzyme involved in the detoxification of methylglyoxal (MG), a reactive oncometabolite formed in the context of energy metabolism as a result of high glycolytic flux.	Pyruvaldehyde	82-84	glyoxalase I	Homo sapiens	14-18
34142632-2	2022	Glyoxal (GO) and methylglyoxal (MGO) are reactive intermediates created by food processing and they are precursors of advanced glycation end products (AGE) that cause glycative stress.	Pyruvaldehyde	17-30	renin binding protein	Homo sapiens	151-154
34093768-2	2021	One such upregulated glycolytic enzyme is glyoxalase 1 (GLO 1), which catalyzes the conversion of toxic methylglyoxal to nontoxic S-D-lactoylglutathione.	Pyruvaldehyde	104-117	glyoxalase I	Homo sapiens	42-54
34093768-2	2021	One such upregulated glycolytic enzyme is glyoxalase 1 (GLO 1), which catalyzes the conversion of toxic methylglyoxal to nontoxic S-D-lactoylglutathione.	Pyruvaldehyde	104-117	glyoxalase I	Homo sapiens	56-61
34207084-0	2021	Methylglyoxal-Derived Advanced Glycation End Product (AGE4)-Induced Apoptosis Leads to Mitochondrial Dysfunction and Endoplasmic Reticulum Stress through the RAGE/JNK Pathway in Kidney Cells.	Pyruvaldehyde	0-13	MOK protein kinase	Homo sapiens	158-162
34207084-0	2021	Methylglyoxal-Derived Advanced Glycation End Product (AGE4)-Induced Apoptosis Leads to Mitochondrial Dysfunction and Endoplasmic Reticulum Stress through the RAGE/JNK Pathway in Kidney Cells.	Pyruvaldehyde	0-13	mitogen-activated protein kinase 8	Homo sapiens	163-166
34142632-2	2022	Glyoxal (GO) and methylglyoxal (MGO) are reactive intermediates created by food processing and they are precursors of advanced glycation end products (AGE) that cause glycative stress.	Pyruvaldehyde	32-35	renin binding protein	Homo sapiens	151-154
34084282-8	2021	RESULTS: EGCG inhibited methyl glyoxal (MG)-induced Tau glycation in vitro.	Pyruvaldehyde	24-38	microtubule associated protein tau	Homo sapiens	52-55
34355187-1	2021	The oncoprotein and Parkinson"s disease-associated enzyme DJ-1/PARK7 has emerged as a promiscuous deglycase that can remove methylglyoxal-induced glycation adducts from both proteins and nucleotides.	Pyruvaldehyde	124-137	Parkinsonism associated deglycase	Homo sapiens	58-62
34355187-1	2021	The oncoprotein and Parkinson"s disease-associated enzyme DJ-1/PARK7 has emerged as a promiscuous deglycase that can remove methylglyoxal-induced glycation adducts from both proteins and nucleotides.	Pyruvaldehyde	124-137	Parkinsonism associated deglycase	Homo sapiens	63-68
34199263-4	2021	In the present study, by using gene silencing and specific activators or scavengers, we demonstrated, in mPCa cell models, that methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs), especially 5-hydro-5-methylimidazolone (MG-H1), and its metabolizing enzyme, glyoxalase 1 (Glo1), contribute to maintain an immunosuppressive microenvironment through MG-H1-mediated PD-L1 up-regulation and to promote cancer progression.	Pyruvaldehyde	128-141	glyoxalase I	Homo sapiens	287-299
34199263-4	2021	In the present study, by using gene silencing and specific activators or scavengers, we demonstrated, in mPCa cell models, that methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs), especially 5-hydro-5-methylimidazolone (MG-H1), and its metabolizing enzyme, glyoxalase 1 (Glo1), contribute to maintain an immunosuppressive microenvironment through MG-H1-mediated PD-L1 up-regulation and to promote cancer progression.	Pyruvaldehyde	128-141	glyoxalase I	Homo sapiens	301-305
34199263-4	2021	In the present study, by using gene silencing and specific activators or scavengers, we demonstrated, in mPCa cell models, that methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs), especially 5-hydro-5-methylimidazolone (MG-H1), and its metabolizing enzyme, glyoxalase 1 (Glo1), contribute to maintain an immunosuppressive microenvironment through MG-H1-mediated PD-L1 up-regulation and to promote cancer progression.	Pyruvaldehyde	128-141	CD274 molecule	Homo sapiens	392-397
34199263-4	2021	In the present study, by using gene silencing and specific activators or scavengers, we demonstrated, in mPCa cell models, that methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs), especially 5-hydro-5-methylimidazolone (MG-H1), and its metabolizing enzyme, glyoxalase 1 (Glo1), contribute to maintain an immunosuppressive microenvironment through MG-H1-mediated PD-L1 up-regulation and to promote cancer progression.	Pyruvaldehyde	143-145	glyoxalase I	Homo sapiens	287-299
34199263-4	2021	In the present study, by using gene silencing and specific activators or scavengers, we demonstrated, in mPCa cell models, that methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs), especially 5-hydro-5-methylimidazolone (MG-H1), and its metabolizing enzyme, glyoxalase 1 (Glo1), contribute to maintain an immunosuppressive microenvironment through MG-H1-mediated PD-L1 up-regulation and to promote cancer progression.	Pyruvaldehyde	143-145	glyoxalase I	Homo sapiens	301-305
34199263-4	2021	In the present study, by using gene silencing and specific activators or scavengers, we demonstrated, in mPCa cell models, that methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs), especially 5-hydro-5-methylimidazolone (MG-H1), and its metabolizing enzyme, glyoxalase 1 (Glo1), contribute to maintain an immunosuppressive microenvironment through MG-H1-mediated PD-L1 up-regulation and to promote cancer progression.	Pyruvaldehyde	143-145	CD274 molecule	Homo sapiens	392-397
34199263-4	2021	In the present study, by using gene silencing and specific activators or scavengers, we demonstrated, in mPCa cell models, that methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs), especially 5-hydro-5-methylimidazolone (MG-H1), and its metabolizing enzyme, glyoxalase 1 (Glo1), contribute to maintain an immunosuppressive microenvironment through MG-H1-mediated PD-L1 up-regulation and to promote cancer progression.	Pyruvaldehyde	250-253	CD274 molecule	Homo sapiens	392-397
34084282-8	2021	RESULTS: EGCG inhibited methyl glyoxal (MG)-induced Tau glycation in vitro.	Pyruvaldehyde	40-42	microtubule associated protein tau	Homo sapiens	52-55
34084282-9	2021	EGCG potently inhibited MG-induced advanced glycation endproducts formation in neuroblastoma cells as well modulated the localization of AT100 phosphorylated Tau in the cells.	Pyruvaldehyde	24-26	microtubule associated protein tau	Homo sapiens	158-161
34084282-12	2021	CONCLUSIONS: We report EGCG, a green tea polyphenol, as a modulator of in vitro methylglyoxal-induced Tau glycation and its impact on reducing advanced glycation end products in neuroblastoma cells.	Pyruvaldehyde	80-93	microtubule associated protein tau	Homo sapiens	102-105
35398259-7	2022	AKR1C1 and AKR1C4 also showed broad substrate specificity for nonsteroidal carbonyl compounds including endogenous 4-oxo-2-nonenal, 4-hydroxy-nonenal, acrolein, isocaproaldehyde, farnesal, isatin and methylglyoxal, of which 4-oxo-2-nonenal was reduced with the lowest Km value of 0.9microM.	Pyruvaldehyde	200-213	aldo-keto reductase family 1 member C1	Homo sapiens	0-6
34062923-5	2021	The cells were exposed to OP at 50 microM for 24 h prior to the administration of MG at 300 microM for additional 24 h. We found that OP prevented MG-induced glycative stress and DPSCs impairment by restoring the activity of Glyoxalase 1 (Glo1), the major detoxifying enzyme of MG, in a mechanism involving the redox-sensitive transcription factor Nrf2.	Pyruvaldehyde	82-84	glyoxalase I	Homo sapiens	225-237
34062923-5	2021	The cells were exposed to OP at 50 microM for 24 h prior to the administration of MG at 300 microM for additional 24 h. We found that OP prevented MG-induced glycative stress and DPSCs impairment by restoring the activity of Glyoxalase 1 (Glo1), the major detoxifying enzyme of MG, in a mechanism involving the redox-sensitive transcription factor Nrf2.	Pyruvaldehyde	82-84	glyoxalase I	Homo sapiens	239-243
34062923-5	2021	The cells were exposed to OP at 50 microM for 24 h prior to the administration of MG at 300 microM for additional 24 h. We found that OP prevented MG-induced glycative stress and DPSCs impairment by restoring the activity of Glyoxalase 1 (Glo1), the major detoxifying enzyme of MG, in a mechanism involving the redox-sensitive transcription factor Nrf2.	Pyruvaldehyde	82-84	NFE2 like bZIP transcription factor 2	Homo sapiens	348-352
34062923-5	2021	The cells were exposed to OP at 50 microM for 24 h prior to the administration of MG at 300 microM for additional 24 h. We found that OP prevented MG-induced glycative stress and DPSCs impairment by restoring the activity of Glyoxalase 1 (Glo1), the major detoxifying enzyme of MG, in a mechanism involving the redox-sensitive transcription factor Nrf2.	Pyruvaldehyde	147-149	glyoxalase I	Homo sapiens	225-237
34062923-5	2021	The cells were exposed to OP at 50 microM for 24 h prior to the administration of MG at 300 microM for additional 24 h. We found that OP prevented MG-induced glycative stress and DPSCs impairment by restoring the activity of Glyoxalase 1 (Glo1), the major detoxifying enzyme of MG, in a mechanism involving the redox-sensitive transcription factor Nrf2.	Pyruvaldehyde	147-149	glyoxalase I	Homo sapiens	239-243
34062923-5	2021	The cells were exposed to OP at 50 microM for 24 h prior to the administration of MG at 300 microM for additional 24 h. We found that OP prevented MG-induced glycative stress and DPSCs impairment by restoring the activity of Glyoxalase 1 (Glo1), the major detoxifying enzyme of MG, in a mechanism involving the redox-sensitive transcription factor Nrf2.	Pyruvaldehyde	147-149	NFE2 like bZIP transcription factor 2	Homo sapiens	348-352
34062923-5	2021	The cells were exposed to OP at 50 microM for 24 h prior to the administration of MG at 300 microM for additional 24 h. We found that OP prevented MG-induced glycative stress and DPSCs impairment by restoring the activity of Glyoxalase 1 (Glo1), the major detoxifying enzyme of MG, in a mechanism involving the redox-sensitive transcription factor Nrf2.	Pyruvaldehyde	278-280	glyoxalase I	Homo sapiens	225-237
34062923-5	2021	The cells were exposed to OP at 50 microM for 24 h prior to the administration of MG at 300 microM for additional 24 h. We found that OP prevented MG-induced glycative stress and DPSCs impairment by restoring the activity of Glyoxalase 1 (Glo1), the major detoxifying enzyme of MG, in a mechanism involving the redox-sensitive transcription factor Nrf2.	Pyruvaldehyde	278-280	glyoxalase I	Homo sapiens	239-243
34062923-5	2021	The cells were exposed to OP at 50 microM for 24 h prior to the administration of MG at 300 microM for additional 24 h. We found that OP prevented MG-induced glycative stress and DPSCs impairment by restoring the activity of Glyoxalase 1 (Glo1), the major detoxifying enzyme of MG, in a mechanism involving the redox-sensitive transcription factor Nrf2.	Pyruvaldehyde	278-280	NFE2 like bZIP transcription factor 2	Homo sapiens	348-352
34719646-0	2021	Methylglyoxal-Derived Advanced Glycation End Products (AGE4) Promote Cell Proliferation and Survival in Renal Cell Carcinoma Cells through the RAGE/Akt/ERK Signaling Pathways.	Pyruvaldehyde	0-13	advanced glycosylation end-product specific receptor	Homo sapiens	143-147
34719646-0	2021	Methylglyoxal-Derived Advanced Glycation End Products (AGE4) Promote Cell Proliferation and Survival in Renal Cell Carcinoma Cells through the RAGE/Akt/ERK Signaling Pathways.	Pyruvaldehyde	0-13	AKT serine/threonine kinase 1	Homo sapiens	148-151
34719646-0	2021	Methylglyoxal-Derived Advanced Glycation End Products (AGE4) Promote Cell Proliferation and Survival in Renal Cell Carcinoma Cells through the RAGE/Akt/ERK Signaling Pathways.	Pyruvaldehyde	0-13	mitogen-activated protein kinase 1	Homo sapiens	152-155
35245757-3	2022	Comparing the availability of alpha-dicarbonyl compounds generated from the Met/Glc model, methylglyoxal (MGO) was a considerably effective alpha-dicarbonyl compound for the formation of pyrazines during MG-ARP degradation, but glyoxal (GO) produced from MG-ARP did not effectively participate in the corresponding formation of pyrazines due to the asynchrony on the formation of GO and recovered Met.	Pyruvaldehyde	91-104	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	207-210
35245757-3	2022	Comparing the availability of alpha-dicarbonyl compounds generated from the Met/Glc model, methylglyoxal (MGO) was a considerably effective alpha-dicarbonyl compound for the formation of pyrazines during MG-ARP degradation, but glyoxal (GO) produced from MG-ARP did not effectively participate in the corresponding formation of pyrazines due to the asynchrony on the formation of GO and recovered Met.	Pyruvaldehyde	91-104	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	258-261
35398259-7	2022	AKR1C1 and AKR1C4 also showed broad substrate specificity for nonsteroidal carbonyl compounds including endogenous 4-oxo-2-nonenal, 4-hydroxy-nonenal, acrolein, isocaproaldehyde, farnesal, isatin and methylglyoxal, of which 4-oxo-2-nonenal was reduced with the lowest Km value of 0.9microM.	Pyruvaldehyde	200-213	aldo-keto reductase family 1 member C4	Homo sapiens	11-17
35620868-4	2022	Here, we show that MGO accumulation induces an age-dependent impairment of glucose tolerance and glucose-stimulated insulin secretion in mice knockdown for glyoxalase 1 (Glo1KD).	Pyruvaldehyde	19-22	glyoxalase 1	Mus musculus	156-168
35363883-1	2022	Human glyoxalase I (hGLO I) is an enzyme for detoxification of methylglyoxal (MG), and has been considered an attractive target for the development of new anti-cancer drugs.	Pyruvaldehyde	63-76	glyoxalase I	Homo sapiens	6-18
35363883-1	2022	Human glyoxalase I (hGLO I) is an enzyme for detoxification of methylglyoxal (MG), and has been considered an attractive target for the development of new anti-cancer drugs.	Pyruvaldehyde	78-80	glyoxalase I	Homo sapiens	6-18
35219163-11	2022	Moreover, CAD increased Bcl-2 expression and decreased the expression of Bax and cleaved caspase-3 in MGO-treated NRK-52E cells.	Pyruvaldehyde	102-105	BCL2, apoptosis regulator	Rattus norvegicus	24-29
35219163-11	2022	Moreover, CAD increased Bcl-2 expression and decreased the expression of Bax and cleaved caspase-3 in MGO-treated NRK-52E cells.	Pyruvaldehyde	102-105	BCL2 associated X, apoptosis regulator	Rattus norvegicus	73-76
35219163-11	2022	Moreover, CAD increased Bcl-2 expression and decreased the expression of Bax and cleaved caspase-3 in MGO-treated NRK-52E cells.	Pyruvaldehyde	102-105	caspase 3	Rattus norvegicus	89-98
35219163-12	2022	Compared with control group, MGO increased the AGEs formation, the expression of RAGE and p-p65, the levels of TNF-alpha, IL-6, IL-1beta, MDA in NRK-52E cells and reduced the levels of GSH and SOD, while treatment of CAD dose-dependently prevented these results.	Pyruvaldehyde	29-32	synaptotagmin 1	Rattus norvegicus	92-95
35219163-12	2022	Compared with control group, MGO increased the AGEs formation, the expression of RAGE and p-p65, the levels of TNF-alpha, IL-6, IL-1beta, MDA in NRK-52E cells and reduced the levels of GSH and SOD, while treatment of CAD dose-dependently prevented these results.	Pyruvaldehyde	29-32	tumor necrosis factor	Rattus norvegicus	111-120
35219163-12	2022	Compared with control group, MGO increased the AGEs formation, the expression of RAGE and p-p65, the levels of TNF-alpha, IL-6, IL-1beta, MDA in NRK-52E cells and reduced the levels of GSH and SOD, while treatment of CAD dose-dependently prevented these results.	Pyruvaldehyde	29-32	interleukin 6	Rattus norvegicus	122-126
35219163-12	2022	Compared with control group, MGO increased the AGEs formation, the expression of RAGE and p-p65, the levels of TNF-alpha, IL-6, IL-1beta, MDA in NRK-52E cells and reduced the levels of GSH and SOD, while treatment of CAD dose-dependently prevented these results.	Pyruvaldehyde	29-32	interleukin 1 alpha	Rattus norvegicus	128-136
35620868-4	2022	Here, we show that MGO accumulation induces an age-dependent impairment of glucose tolerance and glucose-stimulated insulin secretion in mice knockdown for glyoxalase 1 (Glo1KD).	Pyruvaldehyde	19-22	glyoxalase 1	Mus musculus	170-176
35390441-6	2022	Not only that, subsequent cellular responses resulting from methylglyoxal accumulation, such as oxidative stress, activation of ERK, upregulation of NF-kappaB inflammatory signaling pathway, and elevated pro-inflammatory factor TNF-alpha, were found in the acrylamide-treated cell model.	Pyruvaldehyde	60-73	mitogen-activated protein kinase 1	Mus musculus	128-131
35390441-6	2022	Not only that, subsequent cellular responses resulting from methylglyoxal accumulation, such as oxidative stress, activation of ERK, upregulation of NF-kappaB inflammatory signaling pathway, and elevated pro-inflammatory factor TNF-alpha, were found in the acrylamide-treated cell model.	Pyruvaldehyde	60-73	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	149-158
35390441-6	2022	Not only that, subsequent cellular responses resulting from methylglyoxal accumulation, such as oxidative stress, activation of ERK, upregulation of NF-kappaB inflammatory signaling pathway, and elevated pro-inflammatory factor TNF-alpha, were found in the acrylamide-treated cell model.	Pyruvaldehyde	60-73	tumor necrosis factor	Mus musculus	228-237
35455754-5	2022	The glyoxalase 1 (GLO1) is a detoxifying enzyme and catalyzes the elimination of the cytotoxic product methylglyoxal (MG) by converting it to D-lactate, which is not toxic to tissues.	Pyruvaldehyde	103-116	glyoxalase I	Homo sapiens	4-16
35500286-6	2022	Methylglyoxal is normally scavenged by the glyoxalase system, and ketogenic diet-fed mice displayed increased glyoxalase 1 activity compared to chow-fed control mice.	Pyruvaldehyde	0-13	glyoxalase 1	Mus musculus	110-122
35500286-10	2022	Methylglyoxal increased phospho-ERK-positive cells in the spinal dorsal horn, and this evoked spinal activation was ameliorated by preincubation with acetoacetate or beta-hydroxybutyrate.	Pyruvaldehyde	0-13	mitogen-activated protein kinase 1	Mus musculus	32-35
35420027-1	2022	Trapping of methylglyoxal (MGO), an important precursor of advanced glycation end products (AGEs), is considered an effective therapy for alleviating AGE-induced chronic metabolic diseases.	Pyruvaldehyde	27-30	renin binding protein	Mus musculus	150-153
35625570-11	2022	Tannerella&amp;nbsp;forsythia, a common gram-negative anaerobe periodontal pathogen in the oral biofilm, was observed to produce methylglyoxal (precursor of AGE) in the gingival tissues.	Pyruvaldehyde	129-142	renin binding protein	Homo sapiens	157-160
35455754-5	2022	The glyoxalase 1 (GLO1) is a detoxifying enzyme and catalyzes the elimination of the cytotoxic product methylglyoxal (MG) by converting it to D-lactate, which is not toxic to tissues.	Pyruvaldehyde	103-116	glyoxalase I	Homo sapiens	18-22
35405976-7	2022	Modulation of intracellular GSH levels showed that the cytotoxicity and induction of the Nrf2-mediated pathway by MGO, GO and 3-DG was significantly enhanced by depletion of GSH, while a decrease in Nrf2-activation by MGO and GO but not 3-DG was observed upon an increase of the cellular GSH levels.	Pyruvaldehyde	218-221	NFE2 like bZIP transcription factor 2	Homo sapiens	89-93
35456956-6	2022	Furthermore, the protein abundance of Securin, an inhibitor of sister chromatid separation, was increased following treatment with MGO.	Pyruvaldehyde	131-134	PTTG1 regulator of sister chromatid separation, securin	Homo sapiens	38-45
35505576-1	2022	PURPOSE: The aim of this study was to determine the effect of insulin growth factor binding protein-3 (IGFBP-3) on the inhibition of glucose oxidative stress and promotion of bone formation near the implant site in a rat model of methylglyoxal (MGO)-induced bone loss.	Pyruvaldehyde	230-243	insulin-like growth factor binding protein 3	Rattus norvegicus	62-101
35505576-1	2022	PURPOSE: The aim of this study was to determine the effect of insulin growth factor binding protein-3 (IGFBP-3) on the inhibition of glucose oxidative stress and promotion of bone formation near the implant site in a rat model of methylglyoxal (MGO)-induced bone loss.	Pyruvaldehyde	230-243	insulin-like growth factor binding protein 3	Rattus norvegicus	103-110
35505576-1	2022	PURPOSE: The aim of this study was to determine the effect of insulin growth factor binding protein-3 (IGFBP-3) on the inhibition of glucose oxidative stress and promotion of bone formation near the implant site in a rat model of methylglyoxal (MGO)-induced bone loss.	Pyruvaldehyde	245-248	insulin-like growth factor binding protein 3	Rattus norvegicus	62-101
35505576-1	2022	PURPOSE: The aim of this study was to determine the effect of insulin growth factor binding protein-3 (IGFBP-3) on the inhibition of glucose oxidative stress and promotion of bone formation near the implant site in a rat model of methylglyoxal (MGO)-induced bone loss.	Pyruvaldehyde	245-248	insulin-like growth factor binding protein 3	Rattus norvegicus	103-110
35505576-5	2022	In contrast, IGFBP-3 inhibited oxidative stress and inflammation and enhanced osteogenesis in MGO-treated MC3T3 E1 cells.	Pyruvaldehyde	94-97	insulin-like growth factor binding protein 3	Mus musculus	13-20
35505576-6	2022	In addition, IGFBP-3 promoted bone formation by reducing inflammatory proteins in MGO-administered rats.	Pyruvaldehyde	82-85	insulin-like growth factor binding protein 3	Rattus norvegicus	13-20
35505576-8	2022	CONCLUSIONS: This study demonstrated that IGFBP-3 could be applied as a therapeutic component in dental implants to promote the osseointegration of dental implants in patients with diabetes, which affects MGO levels.	Pyruvaldehyde	205-208	insulin like growth factor binding protein 3	Homo sapiens	42-49
35424850-1	2022	An anthracenecarboximide-guanidine based turn-on fluorescent probe ANC-DCP-1 for selective detection of glyoxals (methylglyoxal and glyoxal, GOS) over formaldehyde under weak acidic conditions around pH 6.0 was reported.	Pyruvaldehyde	114-127	decapping mRNA 1B	Homo sapiens	71-76
35405976-6	2022	Furthermore, in a cell-based reporter gene assay MGO, GO, and 3-DG were able to induce Nrf2-mediated gene expression in a dose-dependent manner.	Pyruvaldehyde	49-52	NFE2 like bZIP transcription factor 2	Homo sapiens	87-91
35405976-7	2022	Modulation of intracellular GSH levels showed that the cytotoxicity and induction of the Nrf2-mediated pathway by MGO, GO and 3-DG was significantly enhanced by depletion of GSH, while a decrease in Nrf2-activation by MGO and GO but not 3-DG was observed upon an increase of the cellular GSH levels.	Pyruvaldehyde	114-117	NFE2 like bZIP transcription factor 2	Homo sapiens	89-93
35405976-7	2022	Modulation of intracellular GSH levels showed that the cytotoxicity and induction of the Nrf2-mediated pathway by MGO, GO and 3-DG was significantly enhanced by depletion of GSH, while a decrease in Nrf2-activation by MGO and GO but not 3-DG was observed upon an increase of the cellular GSH levels.	Pyruvaldehyde	114-117	NFE2 like bZIP transcription factor 2	Homo sapiens	199-203
35365944-11	2022	Altogether, our results indicate that light and ABA signaling cooperate to enhance seed germination by the upregulation of GIG1 to detoxify MG in maturing seeds.	Pyruvaldehyde	140-142	UV-B-insensitive 4-like protein	Arabidopsis thaliana	123-127
34999047-3	2022	Under in vitro conditions, MG altered the tertiary structure of fibrinogen.	Pyruvaldehyde	27-29	fibrinogen beta chain	Homo sapiens	64-74
35418871-0	2022	Enhanced RAGE Expression and Excess Reactive-Oxygen Species Production Mediates Rho Kinase-Dependent Detrusor Overactivity After Methylglyoxal Exposure.	Pyruvaldehyde	129-142	MOK protein kinase	Mus musculus	9-13
35418871-2	2022	In vascular tissues, MGO induces the formation of advanced glycation end products (AGEs) that bounds its receptor RAGE, initiating the downstream tissue injury.	Pyruvaldehyde	21-24	MOK protein kinase	Mus musculus	114-118
35418871-4	2022	We have sought that MGO-induced bladder overactivity is due to activation of AGE-RAGE-reactive-oxygen species (ROS) signaling cascade, leading to Rho kinase activation.	Pyruvaldehyde	20-23	MOK protein kinase	Mus musculus	81-85
35418871-6	2022	Treatment with MGO significantly elevated the serum levels of MGO and fluorescent AGEs, as well as the RAGE immunostaining in the urothelium, detrusor, and vascular endothelium.	Pyruvaldehyde	15-18	MOK protein kinase	Mus musculus	103-107
35418871-10	2022	Gene expressions of L-type Ca2+ channels, RhoA, ROCK-1, and ROCK-2 in bladder tissues were significantly elevated in the MGO group.	Pyruvaldehyde	121-124	ras homolog family member A	Mus musculus	42-46
35418871-10	2022	Gene expressions of L-type Ca2+ channels, RhoA, ROCK-1, and ROCK-2 in bladder tissues were significantly elevated in the MGO group.	Pyruvaldehyde	121-124	Rho-associated coiled-coil containing protein kinase 1	Mus musculus	48-54
35418871-10	2022	Gene expressions of L-type Ca2+ channels, RhoA, ROCK-1, and ROCK-2 in bladder tissues were significantly elevated in the MGO group.	Pyruvaldehyde	121-124	Rho-associated coiled-coil containing protein kinase 2	Mus musculus	60-66
35418871-12	2022	Overall, our data indicate serum MGO accumulation elevates the AGEs levels and activates the RAGE-ROS signaling leading to Rho kinase-induced muscle sensitization, ultimately leading to detrusor overactivity.	Pyruvaldehyde	33-36	MOK protein kinase	Mus musculus	93-97
35013107-0	2022	Metformin prevents methylglyoxal-induced apoptosis by suppressing oxidative stress in vitro and in vivo.	Pyruvaldehyde	19-32	SAFB like transcription modulator	Homo sapiens	0-9
35316449-9	2022	The inhibition of gamma-GCL, adenosine monophosphate-activated protein kinase (AMPK), and phosphoinositide 3-kinase/Akt (PI3K/Akt) suppressed the beneficial effects induced by ISO on the MG-challenged cells.	Pyruvaldehyde	187-189	AKT serine/threonine kinase 1	Homo sapiens	126-129
35316449-10	2022	Moreover, silencing of Nrf2 blocked the ISO-dependent gamma-GCL and GSH upregulation and the effects on the mitochondria of the MG-challenged cells.	Pyruvaldehyde	128-130	NFE2 like bZIP transcription factor 2	Homo sapiens	23-27
35316449-11	2022	Then, ISO caused mitochondrial protection by an AMPK-PI3K/Akt/Nrf2/gamma-GCL/GSH-dependent manner in MG-administrated SH-SY5Y cells.	Pyruvaldehyde	101-103	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	48-52
35316449-11	2022	Then, ISO caused mitochondrial protection by an AMPK-PI3K/Akt/Nrf2/gamma-GCL/GSH-dependent manner in MG-administrated SH-SY5Y cells.	Pyruvaldehyde	101-103	AKT serine/threonine kinase 1	Homo sapiens	58-61
35316449-11	2022	Then, ISO caused mitochondrial protection by an AMPK-PI3K/Akt/Nrf2/gamma-GCL/GSH-dependent manner in MG-administrated SH-SY5Y cells.	Pyruvaldehyde	101-103	NFE2 like bZIP transcription factor 2	Homo sapiens	62-66
35023763-9	2022	In the soleus muscle, the exercise-induced increases in the expression of TLR4, HSP72, and advanced glycation end products receptor 1 were inhibited with MG treatment.	Pyruvaldehyde	154-156	toll-like receptor 4	Mus musculus	74-78
35023763-9	2022	In the soleus muscle, the exercise-induced increases in the expression of TLR4, HSP72, and advanced glycation end products receptor 1 were inhibited with MG treatment.	Pyruvaldehyde	154-156	heat shock protein 1A	Mus musculus	80-85
35061788-0	2022	Fructose and methylglyoxal-induced glycation alters structural and functional properties of salivary proteins, albumin and lysozyme.	Pyruvaldehyde	13-26	albumin	Homo sapiens	111-118
35061788-0	2022	Fructose and methylglyoxal-induced glycation alters structural and functional properties of salivary proteins, albumin and lysozyme.	Pyruvaldehyde	13-26	lysozyme	Homo sapiens	123-131
35013107-13	2022	Collectively, these findings broaden our understanding of the mechanism by which MET regulates apoptosis induced by MGO under oxidative stress conditions, with important implications regarding the potential application of MET for the treatment of diabetic vascular complications.	Pyruvaldehyde	116-119	SAFB like transcription modulator	Homo sapiens	81-84
35013107-13	2022	Collectively, these findings broaden our understanding of the mechanism by which MET regulates apoptosis induced by MGO under oxidative stress conditions, with important implications regarding the potential application of MET for the treatment of diabetic vascular complications.	Pyruvaldehyde	116-119	SAFB like transcription modulator	Homo sapiens	222-225
35013107-4	2022	We reported here that MET prevents MGO-induced apoptosis by suppressing oxidative stress in vitro and in vivo.	Pyruvaldehyde	35-38	SAFB like transcription modulator	Homo sapiens	22-25
35013107-8	2022	Our results revealed that MET prevented MGO-induced HUVEC apoptosis, inhibited apoptosis-associated biochemical changes such as loss of MMP, the elevation of the Bax/Bcl-2 ratio, and activation of cleaved caspase-3, and attenuated MGO-induced mitochondrial morphological alterations in a dose-dependent manner.	Pyruvaldehyde	40-43	SAFB like transcription modulator	Homo sapiens	26-29
35013107-8	2022	Our results revealed that MET prevented MGO-induced HUVEC apoptosis, inhibited apoptosis-associated biochemical changes such as loss of MMP, the elevation of the Bax/Bcl-2 ratio, and activation of cleaved caspase-3, and attenuated MGO-induced mitochondrial morphological alterations in a dose-dependent manner.	Pyruvaldehyde	231-234	SAFB like transcription modulator	Homo sapiens	26-29
35013107-9	2022	MET pretreatment also significantly suppressed MGO-stimulated ROS production, increased signaling through the ROS-mediated PI3K/Akt and Nrf2/HO-1 pathways, and markedly elevated the levels of its downstream antioxidants.	Pyruvaldehyde	47-50	SAFB like transcription modulator	Homo sapiens	0-3
35013107-10	2022	Finally, similar results were obtained in vivo, and we demonstrated that MET prevented MGO-induced oxidative damage, apoptosis, and inflammation.	Pyruvaldehyde	87-90	SAFB like transcription modulator	Homo sapiens	73-76
35013107-11	2022	As expected, MET reversed MGO-induced downregulation of Nrf2 and p-Akt.	Pyruvaldehyde	26-29	SAFB like transcription modulator	Homo sapiens	13-16
35013107-11	2022	As expected, MET reversed MGO-induced downregulation of Nrf2 and p-Akt.	Pyruvaldehyde	26-29	NFE2 like bZIP transcription factor 2	Homo sapiens	56-60
35013107-11	2022	As expected, MET reversed MGO-induced downregulation of Nrf2 and p-Akt.	Pyruvaldehyde	26-29	AKT serine/threonine kinase 1	Homo sapiens	67-70
35013107-12	2022	In addition, a PI3K inhibitor (LY-294002) and a Nrf2 inhibitor (ML385) observably attenuated the protective effects of MET on MGO-induced apoptosis and ROS generation by inhibiting the Nrf2/HO-1 pathways, while a ROS scavenger (NAC) and a permeability transition pores inhibitor (CsA) completely reversed these effects.	Pyruvaldehyde	126-129	NFE2 like bZIP transcription factor 2	Homo sapiens	48-52
35013107-12	2022	In addition, a PI3K inhibitor (LY-294002) and a Nrf2 inhibitor (ML385) observably attenuated the protective effects of MET on MGO-induced apoptosis and ROS generation by inhibiting the Nrf2/HO-1 pathways, while a ROS scavenger (NAC) and a permeability transition pores inhibitor (CsA) completely reversed these effects.	Pyruvaldehyde	126-129	SAFB like transcription modulator	Homo sapiens	119-122
35013107-12	2022	In addition, a PI3K inhibitor (LY-294002) and a Nrf2 inhibitor (ML385) observably attenuated the protective effects of MET on MGO-induced apoptosis and ROS generation by inhibiting the Nrf2/HO-1 pathways, while a ROS scavenger (NAC) and a permeability transition pores inhibitor (CsA) completely reversed these effects.	Pyruvaldehyde	126-129	NFE2 like bZIP transcription factor 2	Homo sapiens	185-189
35013107-12	2022	In addition, a PI3K inhibitor (LY-294002) and a Nrf2 inhibitor (ML385) observably attenuated the protective effects of MET on MGO-induced apoptosis and ROS generation by inhibiting the Nrf2/HO-1 pathways, while a ROS scavenger (NAC) and a permeability transition pores inhibitor (CsA) completely reversed these effects.	Pyruvaldehyde	126-129	heme oxygenase 1	Homo sapiens	190-194
35013107-12	2022	In addition, a PI3K inhibitor (LY-294002) and a Nrf2 inhibitor (ML385) observably attenuated the protective effects of MET on MGO-induced apoptosis and ROS generation by inhibiting the Nrf2/HO-1 pathways, while a ROS scavenger (NAC) and a permeability transition pores inhibitor (CsA) completely reversed these effects.	Pyruvaldehyde	126-129	X-linked Kx blood group	Homo sapiens	228-231
35035668-7	2022	Interestingly, administration of MG significantly impaired cell proliferation, cell migration, and tube formation and decreased protein expression of angiogenesis-related factors, which was rescued by three different MG scavengers, glyoxalase 1 (GLO1), aminoguanidine (AG), and N-acetyl cysteine (NAC).	Pyruvaldehyde	33-35	glyoxalase I	Homo sapiens	232-244
35035668-7	2022	Interestingly, administration of MG significantly impaired cell proliferation, cell migration, and tube formation and decreased protein expression of angiogenesis-related factors, which was rescued by three different MG scavengers, glyoxalase 1 (GLO1), aminoguanidine (AG), and N-acetyl cysteine (NAC).	Pyruvaldehyde	33-35	glyoxalase I	Homo sapiens	246-250
35035668-10	2022	We also noted that administration of MG increased cellular oxidative stress as measured by reactive oxygen species (ROS) generation, enhanced AGE accumulation, and receptor for advanced glycation end-product (RAGE) expression in the cultured HBMECs, which were partially reversed by GLO1, AG, or NAC.	Pyruvaldehyde	37-39	advanced glycosylation end-product specific receptor	Homo sapiens	209-213
35035668-10	2022	We also noted that administration of MG increased cellular oxidative stress as measured by reactive oxygen species (ROS) generation, enhanced AGE accumulation, and receptor for advanced glycation end-product (RAGE) expression in the cultured HBMECs, which were partially reversed by GLO1, AG, or NAC.	Pyruvaldehyde	37-39	glyoxalase I	Homo sapiens	283-287
35035668-11	2022	Taken together, our findings demonstrated that GLO1, AG, or NAC administration can ameliorate MG-induced angiogenesis dysfunction, and this can be mainly attributed to attenuated ROS production, reduced cellular apoptosis, and increased levels of angiogenic factors.	Pyruvaldehyde	94-96	glyoxalase I	Homo sapiens	47-51
34261819-5	2022	HK2 upregulation led to increased production levels of methylglyoxal (MG), a toxic metabolic intermediate of abnormal glycolytic processes.	Pyruvaldehyde	55-68	hexokinase 2	Mus musculus	0-3
34261819-5	2022	HK2 upregulation led to increased production levels of methylglyoxal (MG), a toxic metabolic intermediate of abnormal glycolytic processes.	Pyruvaldehyde	70-72	hexokinase 2	Mus musculus	0-3