PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
29496360-10	2018	Expression of antimicrobial peptides such as LL-37 and beta-defensin-2 was also increased by exposure to glyoxal in the skin of both naive and AD rats.	Glyoxal	105-112	defensin beta 2	Rattus norvegicus	55-70
29972203-5	2018	Furthermore, treatment with glyoxal resulted in a small change in RAGE expression while CML did not alter its expression.	Glyoxal	28-35	long intergenic non-protein coding RNA 914	Homo sapiens	66-70
29633837-16	2018	This can accelerate interconversion of different conformers (e.g., anti and syn) of atmospheric species, such as glyoxal, depending on their polarity.	Glyoxal	113-120	synemin	Homo sapiens	76-79
33418767-3	2018	Here, various chemically stabilized LPC derived biomaterials were generated using three cross-linking agents: glutaraldehyde, oxaldehyde, and 1-ethyl-3-(3-(dimethylamino)propyl)carbodiimide.	Glyoxal	126-136	proprotein convertase subtilisin/kexin type 7	Homo sapiens	36-39
29484088-10	2017	Expression of ceramide synthase 3 (CERS3) was significantly decreased while fatty acid elongase 3 was increased by glyoxal in a dose dependent manner.	Glyoxal	115-122	ceramide synthase 3	Homo sapiens	14-33
29400466-0	2018	Influence of Transketolase-Catalyzed Reactions on the Formation of Glycolaldehyde and Glyoxal Specific Posttranslational Modifications under Physiological Conditions.	Glyoxal	86-93	transketolase	Homo sapiens	13-26
29400466-2	2018	In vitro experiments with recombinant human TK reduced glycolaldehyde and glyoxal induced carbonyl stress and thereby suppressed the formation of advanced glycation endproducts up to 70% due to the enzyme-catalyzed conversion of glycolaldehyde to erythrulose.	Glyoxal	74-81	transketolase	Homo sapiens	44-46
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.	Glyoxal	52-59	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.	Glyoxal	61-63	casein beta	Homo sapiens	139-150
29196060-2	2018	miR-365 was identified in a previously constructed library from glyoxal-treated rat Muller cell.	Glyoxal	64-71	microRNA 365b	Rattus norvegicus	0-7
29196060-10	2018	miR-365 expression was confirmed in the glyoxal-treated rat Muller cell line (glyoxal-treated rMC-1).	Glyoxal	40-47	microRNA 365b	Rattus norvegicus	0-7
29196060-10	2018	miR-365 expression was confirmed in the glyoxal-treated rat Muller cell line (glyoxal-treated rMC-1).	Glyoxal	78-85	microRNA 365b	Rattus norvegicus	0-7
29196060-12	2018	The increased miR-365 participated in Muller cell gliosis through oxidative stress aggravation, as observed in glyoxal-treated rMC-1 and DR rats before 6 weeks.	Glyoxal	111-118	microRNA 365b	Rattus norvegicus	14-21
28886871-4	2018	Immunoblots of affinity-purified DAF from erythrocytes of patients with diabetes showed pentosidine, glyoxal-AGEs, carboxymethyllysine, and argpyrimidine.	Glyoxal	101-108	CD55 molecule (Cromer blood group)	Homo sapiens	33-36
28391827-9	2017	Four Spanish wines and five Spanish beers have been analysed and the results showed that the levels of glyoxal are comprised between 2.8-9.5mgL-1.	Glyoxal	103-110	LLGL scribble cell polarity complex component 1	Homo sapiens	140-145
28299531-5	2017	Mass spectrometric studies revealed formation of glyoxal-derived fluorescent AGE adduct pentosidine between Lys-145 and Arg-139 residues of Mb.	Glyoxal	49-56	myoglobin	Homo sapiens	140-142
28299531-2	2017	Considering the significance of protein modification by glyoxal-derived AGEs, we investigated the in vitro effect of glyoxal (200 muM) on the monomeric heme protein myoglobin (Mb) (100 muM) after incubation for one week at 25  C. Glyoxal-treated Mb exhibited increased absorbance around the Soret region, decreased alpha-helicity and thermal stability compared to control Mb.	Glyoxal	117-124	myoglobin	Homo sapiens	165-174
28299531-2	2017	Considering the significance of protein modification by glyoxal-derived AGEs, we investigated the in vitro effect of glyoxal (200 muM) on the monomeric heme protein myoglobin (Mb) (100 muM) after incubation for one week at 25  C. Glyoxal-treated Mb exhibited increased absorbance around the Soret region, decreased alpha-helicity and thermal stability compared to control Mb.	Glyoxal	117-124	myoglobin	Homo sapiens	176-178
28013050-1	2017	We discovered recently that Parkinsonism-associated DJ-1 and its bacterial homologs function as protein deglycases that repair glyoxal- and methylglyoxal-glycated proteins.	Glyoxal	127-134	Parkinsonism associated deglycase	Homo sapiens	52-56
27520463-3	2016	METHODS: Flow cytometry was combined with either: 1) immunocytochemical staining to detect glyoxal induced formation of Nepsilon-carboxymethyllysine (CML)-modifications of intracellular proteins (AGEs) and changes in the production of stress response proteins; or 2) vital staining to determine apoptosis rates (annexin V binding), formation of intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and changes in intracellular pH upon treatment of cells with glyoxal.	Glyoxal	91-98	annexin A5	Homo sapiens	312-321
27520463-9	2016	Apoptosis related caspase 3 activation increased in a dose dependent manner after glyoxal incubation.	Glyoxal	82-89	caspase 3	Homo sapiens	18-27
27520463-11	2016	Furthermore, VEGF-A165a mRNA expression and VEGF-A protein production were significantly increased after incubation with glyoxal in ARPE-19 cells.	Glyoxal	121-128	vascular endothelial growth factor A	Homo sapiens	13-19
29619286-7	2016	In addition, we find that AM3B shows better agreement on both formaldehyde and the correlation between glyoxal and formaldehyde (RGF = [GLYX]/[HCHO]), resulting from the suppression of delta-isoprene peroxy radicals (delta-ISOPO2).	Glyoxal	103-110	ral guanine nucleotide dissociation stimulator	Homo sapiens	129-132
29619286-8	2016	We also find that MCM v3.3.1 may underestimate glyoxal production from isoprene oxidation, in part due to an underestimated yield from the reaction of IEPOX peroxy radicals (IEPOXOO) with HO2.	Glyoxal	47-54	heme oxygenase 2	Homo sapiens	188-191
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.	Glyoxal	136-143	albumin	Homo sapiens	78-91
27288931-0	2016	The food processing contaminant glyoxal promotes tumour growth in the multiple intestinal neoplasia (Min) mouse model.	Glyoxal	32-39	APC, WNT signaling pathway regulator	Mus musculus	70-99
27288931-0	2016	The food processing contaminant glyoxal promotes tumour growth in the multiple intestinal neoplasia (Min) mouse model.	Glyoxal	32-39	APC, WNT signaling pathway regulator	Mus musculus	101-104
27337067-4	2016	The analysis of the transgenic cell lines showed that tomato SlAKR4B has enzyme activities toward d-galacturonic acid as well as glyceraldehyde and glyoxal, suggesting that the SlAKR4B gene encodes a functional enzyme in tomato.	Glyoxal	148-155	aldo-keto reductase 4B	Solanum lycopersicum	61-68
27337067-4	2016	The analysis of the transgenic cell lines showed that tomato SlAKR4B has enzyme activities toward d-galacturonic acid as well as glyceraldehyde and glyoxal, suggesting that the SlAKR4B gene encodes a functional enzyme in tomato.	Glyoxal	148-155	aldo-keto reductase 4B	Solanum lycopersicum	177-184
26410776-5	2015	However, methylglyoxal induced significant structural changes in HSA compared with glyoxal and glyceraldehydes.	Glyoxal	15-22	albumin	Homo sapiens	65-68
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.	Glyoxal	136-143	albumin	Homo sapiens	93-96
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.	Glyoxal	91-98	Parkinsonism associated deglycase	Homo sapiens	32-36
26311324-5	2015	We detected increased O-GlcNAc levels and increased ROS production in the glyoxal-treated HRECs.	Glyoxal	74-81	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	22-30
26244639-0	2015	Modification of beta-Defensin-2 by Dicarbonyls Methylglyoxal and Glyoxal Inhibits Antibacterial and Chemotactic Function In Vitro.	Glyoxal	65-72	defensin beta 4A	Homo sapiens	16-31
25611968-0	2015	Glyoxal Oxidation Mechanism: Implications for the Reactions HCO + O2 and OCHCHO + HO2.	Glyoxal	0-7	heme oxygenase 2	Homo sapiens	82-85
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(-/+)).	Glyoxal	27-34	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(-/+)).	Glyoxal	27-34	glyoxalase 1	Mus musculus	216-220
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(-/+)).	Glyoxal	27-34	glyoxalase 1	Mus musculus	216-220
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(-/+)).	Glyoxal	147-149	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(-/+)).	Glyoxal	147-149	glyoxalase 1	Mus musculus	41-45
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.	Glyoxal	91-98	Parkinsonism associated deglycase	Homo sapiens	37-42
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.	Glyoxal	61-68	major histocompatibility complex, class I-related	Homo sapiens	255-258
25478901-0	2015	Multiphase chemistry of glyoxal: revised kinetics of the alkyl radical reaction with molecular oxygen and the reaction of glyoxal with OH, NO3, and SO4- in aqueous solution.	Glyoxal	24-31	NBL1, DAN family BMP antagonist	Homo sapiens	139-142
25478901-0	2015	Multiphase chemistry of glyoxal: revised kinetics of the alkyl radical reaction with molecular oxygen and the reaction of glyoxal with OH, NO3, and SO4- in aqueous solution.	Glyoxal	122-129	NBL1, DAN family BMP antagonist	Homo sapiens	139-142
24721423-2	2014	The monoclonal anti-myoglobin antibody (ab-Mb) was covalently immobilized using glyoxal on a film of polyethyleneimine-coated gold nanoparticles (AuNP-PEI).	Glyoxal	80-87	myoglobin	Homo sapiens	20-29
24721423-2	2014	The monoclonal anti-myoglobin antibody (ab-Mb) was covalently immobilized using glyoxal on a film of polyethyleneimine-coated gold nanoparticles (AuNP-PEI).	Glyoxal	80-87	myoglobin	Homo sapiens	43-45
24896370-1	2014	The zero-phonon line (ZPL) and the sideband in the vibronic spectrum of a single glyoxal molecule inside a (3)He droplet are analyzed within the framework of the Lax formalism.	Glyoxal	81-88	lymphocyte transmembrane adaptor 1	Homo sapiens	162-165
24920125-2	2014	Glyoxal and MG are detoxified by the sequential activities of glyoxalase 1 (GLO1) and glyoxalase 2.	Glyoxal	0-7	glyoxalase 1	Mus musculus	62-74
24920125-2	2014	Glyoxal and MG are detoxified by the sequential activities of glyoxalase 1 (GLO1) and glyoxalase 2.	Glyoxal	0-7	glyoxalase 1	Mus musculus	76-80
24613676-3	2014	Here we have studied the structural alterations as well as the sites and nature of amino acid modifications of two heme proteins, hemoglobin and myoglobin on incubation with glyoxal for seven days at 25 C. In comparison with normal hemoglobin (HbA0), glyoxal-treated hemoglobin (GHbA0) exhibits decreased absorbance around 280 nm, reduced intrinsic fluorescence and lower surface hydrophobicity.	Glyoxal	174-181	myoglobin	Homo sapiens	145-154
24613676-4	2014	However, glyoxal-treated myoglobin (GMb) exhibits the opposite effects in these respects when compared to normal myoglobin (Mb).	Glyoxal	9-16	myoglobin	Homo sapiens	25-34
24613676-5	2014	Glyoxal increases the thermal stability of hemoglobin, while it decreases the stability of myoglobin.	Glyoxal	0-7	myoglobin	Homo sapiens	91-100
24613676-7	2014	On the other hand, glyoxal modifies Lys-133 and Lys-145 to carboxymethyllysine and Arg-31 to hydroimidazolone adducts in myoglobin.	Glyoxal	19-26	myoglobin	Homo sapiens	121-130
24161001-1	2013	An asymmetric intramolecular Cannizzaro reaction of aryl and alkyl glyoxals with alcohols has been realized with an unprecedented high level of enantioselectivity, on the basis of a newly developed congested TOX ligand and a gradual liberation protocol of active glyoxals from glyoxal monohydrates.	Glyoxal	67-75	thymocyte selection associated high mobility group box	Homo sapiens	208-211
24747646-0	2014	Kinetics of glycoxidation of bovine serum albumin by methylglyoxal and glyoxal and its prevention by various compounds.	Glyoxal	59-66	albumin	Homo sapiens	36-49
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.	Glyoxal	148-155	glyoxalase I	Homo sapiens	105-109
24078189-1	2014	In this study, an enzymatic procedure for the determination of glycine (Gly) was developed by using a column containing immobilized glutamate dehydrogenase (GDH) on glyoxal agarose beads.	Glyoxal	165-172	glutamate dehydrogenase 1	Homo sapiens	132-155
24078189-1	2014	In this study, an enzymatic procedure for the determination of glycine (Gly) was developed by using a column containing immobilized glutamate dehydrogenase (GDH) on glyoxal agarose beads.	Glyoxal	165-172	glutamate dehydrogenase 1	Homo sapiens	157-160
24078189-6	2014	The interaction between GDH and glyoxal agarose beads was analyzed by Fourier transform infrared (FTIR) spectroscopy.	Glyoxal	32-39	glutamate dehydrogenase 1	Homo sapiens	24-27
24161001-1	2013	An asymmetric intramolecular Cannizzaro reaction of aryl and alkyl glyoxals with alcohols has been realized with an unprecedented high level of enantioselectivity, on the basis of a newly developed congested TOX ligand and a gradual liberation protocol of active glyoxals from glyoxal monohydrates.	Glyoxal	263-271	thymocyte selection associated high mobility group box	Homo sapiens	208-211
23090025-2	2013	Conformational changes on ovalbumin at various concentrations of glyoxal, ethylene glycol (EG) and polyethylene glycol-400 (PEG-400) were investigated by fluorescence spectroscopy, circular dichroism, attenuated total reflection Fourier transform infra red spectroscopy, 8-anilino-1-naphthalenesulfonic acid and thioflavin T assay.	Glyoxal	65-72	ovalbumin (SERPINB14)	Gallus gallus	26-35
23264566-4	2013	To more efficiently characterize the complete catalog of ADAR events in the mammalian transcriptome we developed a high-throughput protocol to identify A > I editing sites, which exploits the capacity of glyoxal to protect guanosine, but not inosine, from RNAse T1 treatment, thus facilitating extraction of RNA fragments with inosine bases at their termini for high-throughput sequencing.	Glyoxal	207-214	adenosine deaminase RNA specific	Homo sapiens	57-61
23624124-1	2013	Caenorhabditis elegans DJR-1.2, a homolog of human DJ-1, has recently been demonstrated to be a novel glyoxalase and protects worms against glyoxals.	Glyoxal	140-148	Glutathione-independent glyoxalase DJR-1.2	Caenorhabditis elegans	23-30
23624124-1	2013	Caenorhabditis elegans DJR-1.2, a homolog of human DJ-1, has recently been demonstrated to be a novel glyoxalase and protects worms against glyoxals.	Glyoxal	140-148	Parkinsonism associated deglycase	Homo sapiens	51-55
23624124-3	2013	The induction of DJR-1.2 led to increased glyoxalase activity in the dauer state, thereby increasing protection against glyoxals.	Glyoxal	120-128	Glutathione-independent glyoxalase DJR-1.2	Caenorhabditis elegans	17-24
23651081-11	2013	When the wild-type DJ-1d enzyme was expressed in E. coli, the bacteria became resistant to glyoxals.	Glyoxal	91-99	Class I glutamine amidotransferase-like superfamily protein	Arabidopsis thaliana	19-24
23090025-3	2013	A partially folded state of ovalbumin at 50 % v/v glyoxal was detected that preceded the onset of the aggregation process at the maximum concentration (90 % v/v) of this aldehyde.	Glyoxal	50-57	ovalbumin (SERPINB14)	Gallus gallus	28-37
23090025-5	2013	Maximum aggregation of ovalbumin was observed at 80 % v/v PEG-400, followed by 70 % v/v EG and 90 % v/v glyoxal.	Glyoxal	104-111	ovalbumin (SERPINB14)	Gallus gallus	23-32
22245096-6	2012	Five different types of AGEs were generated by bovine serum albumin incubation with glyoxal, methylglyoxal, glucose, fructose, and ribose.	Glyoxal	84-91	albumin	Homo sapiens	54-67
23163806-2	2012	The aim of this study was to investigate types and site of PTM of glyoxal-derived advanced glycation end-products-in the neuropeptide substance P by ultrahigh-resolution Fourier transform ion cyclotron resonance (FTICR), mass spectrometry, and tandem mass spectrometry (MS/MS) experiments.	Glyoxal	66-73	tachykinin precursor 1	Homo sapiens	134-145
22523093-4	2012	The presence of DJ-1 protected mouse embryonic fibroblast and dopaminergically derived SH-SY5Y cells from treatments of glyoxals.	Glyoxal	120-128	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	16-20
22523093-5	2012	Likewise, C. elegans lacking cDJR-1.1, a DJ-1 homolog expressed primarily in the intestine, protected worms from glyoxal-induced death.	Glyoxal	113-120	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	41-45
22523093-6	2012	Sub-lethal doses of glyoxals caused significant degeneration of the dopaminergic neurons in C. elegans lacking cDJR-1.2, another DJ-1 homolog expressed primarily in the head region, including neurons.	Glyoxal	20-28	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	129-133
22293583-5	2012	Cross-linking of gelatin with glyoxal via Schiff bases significantly increased thermal stability and decreased the solubility of the MSs, leading to a significant decrease in the initial release of IGF-1.	Glyoxal	30-37	insulin-like growth factor 1	Mus musculus	198-203
22328670-0	2012	Genomic rearrangements leading to overexpression of aldo-keto reductase YafB of Escherichia coli confer resistance to glyoxal.	Glyoxal	118-125	plasmid partition protein A	Escherichia coli	72-76
22328670-5	2012	Glyoxal resistances of the mutants are correlated with the levels of yafB transcripts as well as the activities of aldo-keto reductase.	Glyoxal	0-7	plasmid partition protein A	Escherichia coli	69-73
22328670-6	2012	An overproduction of YafB in the glyoxal-resistant mutant lacking the putative NsrR-binding site provides evidence that the yafB gene is negatively regulated by this protein.	Glyoxal	33-40	plasmid partition protein A	Escherichia coli	21-25
22328670-6	2012	An overproduction of YafB in the glyoxal-resistant mutant lacking the putative NsrR-binding site provides evidence that the yafB gene is negatively regulated by this protein.	Glyoxal	33-40	plasmid partition protein A	Escherichia coli	124-128
22328670-7	2012	We also observed that the expression of yafB is enhanced with an increased concentration of glyoxal as well as a mutation in the fnr gene, encoding a putative regulator.	Glyoxal	92-99	plasmid partition protein A	Escherichia coli	40-44
21174464-0	2011	Kinetics and mechanism of the glyoxal + HO2 reaction: conversion of HO2 to OH by carbonyls.	Glyoxal	30-37	heme oxygenase 2	Homo sapiens	40-43
21768101-8	2011	Treatment with either cytochalasin D or glyoxal, a cellular AGE, indicated that both actin depolymerization and AGE contribute to desmin disorganization.	Glyoxal	40-47	desmin	Mus musculus	130-136
21768101-9	2011	Heat shock-induced phosphorylation of alphaB-crystallin provides a transient protection of desmin against glyoxal in a p38 MAPK-dependent manner.	Glyoxal	106-113	crystallin, alpha B	Mus musculus	38-55
21768101-9	2011	Heat shock-induced phosphorylation of alphaB-crystallin provides a transient protection of desmin against glyoxal in a p38 MAPK-dependent manner.	Glyoxal	106-113	desmin	Mus musculus	91-97
21768101-9	2011	Heat shock-induced phosphorylation of alphaB-crystallin provides a transient protection of desmin against glyoxal in a p38 MAPK-dependent manner.	Glyoxal	106-113	mitogen-activated protein kinase 14	Mus musculus	119-127
21334317-11	2011	GO-caused cytotoxicity and protein carbonylation were also increased with ALDH2-inhibited hepatocytes whereas such an increase was only observed with MGO in GSH-depleted hepatocytes.	Glyoxal	0-2	aldehyde dehydrogenase 2 family member	Homo sapiens	74-79
21782982-0	2011	pH stability of the stromelysin-1 catalytic domain and its mechanism of interaction with a glyoxal inhibitor.	Glyoxal	91-98	matrix metallopeptidase 3	Homo sapiens	20-33
21782982-6	2011	At pH 5.5-6.5 the glyoxal inhibitor is a potent inhibitor of stromelysin-1 (K(i)=~1muM).	Glyoxal	18-25	matrix metallopeptidase 3	Homo sapiens	61-74
21782982-6	2011	At pH 5.5-6.5 the glyoxal inhibitor is a potent inhibitor of stromelysin-1 (K(i)=~1muM).	Glyoxal	18-25	latexin	Homo sapiens	83-86
21650468-2	2011	AGE-modified proteins, namely, GO-AGEs, were prepared by incubating bovine serum albumin (BSA) with glyoxal (GO) for 7 days.	Glyoxal	31-33	albumin	Mus musculus	75-88
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).	Glyoxal	129-136	glyoxalase 1	Mus musculus	0-4
21174464-0	2011	Kinetics and mechanism of the glyoxal + HO2 reaction: conversion of HO2 to OH by carbonyls.	Glyoxal	30-37	heme oxygenase 2	Homo sapiens	68-71
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%.	Glyoxal	24-31	glyoxalase 1	Rattus norvegicus	12-17
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).	Glyoxal	45-47	superoxide dismutase 1	Homo sapiens	252-255
20955686-1	2010	A series of substrate-based alpha-keto-beta-aldehyde (glyoxal) sequences have been synthesised and evaluated as inhibitors of the caspase family of cysteine proteases.	Glyoxal	54-61	caspase 1	Homo sapiens	130-137
20397192-0	2010	Carbonyl compounds methylglyoxal and glyoxal affect interleukin-8 secretion in intestinal cells by superoxide anion generation and activation of MAPK p38.	Glyoxal	25-32	C-X-C motif chemokine ligand 8	Homo sapiens	52-65
20397192-0	2010	Carbonyl compounds methylglyoxal and glyoxal affect interleukin-8 secretion in intestinal cells by superoxide anion generation and activation of MAPK p38.	Glyoxal	25-32	mitogen-activated protein kinase 3	Homo sapiens	145-149
20397192-0	2010	Carbonyl compounds methylglyoxal and glyoxal affect interleukin-8 secretion in intestinal cells by superoxide anion generation and activation of MAPK p38.	Glyoxal	25-32	mitogen-activated protein kinase 1	Homo sapiens	150-153
20397192-5	2010	MAPK p38 and extracellular signal-regulated kinase (ERK) were phosphorylated in these cells after having been stimulated by MG and GL.	Glyoxal	131-133	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.	Glyoxal	131-133	mitogen-activated protein kinase 1	Homo sapiens	13-50
21196299-3	2011	The expression levels of TNF-alpha, IL-1beta, IL-6 and VEGF in cultured rat Muller cells were enhanced by 1 mM glyoxal.	Glyoxal	111-118	tumor necrosis factor	Rattus norvegicus	25-34
21196299-3	2011	The expression levels of TNF-alpha, IL-1beta, IL-6 and VEGF in cultured rat Muller cells were enhanced by 1 mM glyoxal.	Glyoxal	111-118	interleukin 1 beta	Rattus norvegicus	36-44
21196299-3	2011	The expression levels of TNF-alpha, IL-1beta, IL-6 and VEGF in cultured rat Muller cells were enhanced by 1 mM glyoxal.	Glyoxal	111-118	interleukin 6	Rattus norvegicus	46-50
21196299-3	2011	The expression levels of TNF-alpha, IL-1beta, IL-6 and VEGF in cultured rat Muller cells were enhanced by 1 mM glyoxal.	Glyoxal	111-118	vascular endothelial growth factor A	Rattus norvegicus	55-59
20828700-1	2010	Non-enzymatic posttranslational modifications of bovine serum albumin (BSA) by various oxo-compounds (glucose, ribose, glyoxal and glutardialdehyde) have been investigated using high-performance liquid chromatography (HPLC) and capillary zone electrophoresis (CZE).	Glyoxal	119-126	albumin	Homo sapiens	56-69
20397192-5	2010	MAPK p38 and extracellular signal-regulated kinase (ERK) were phosphorylated in these cells after having been stimulated by MG and GL.	Glyoxal	131-133	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).	Glyoxal	45-47	C-X-C motif chemokine ligand 8	Homo sapiens	56-60
19628748-1	2010	PURPOSE: To characterize the neuroprotective mechanisms of erythropoietin (EPO) against the stress of glyoxal-advanced glycation end products (AGEs) in retinal neuronal cells.	Glyoxal	102-109	erythropoietin	Rattus norvegicus	59-73
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).	Glyoxal	45-47	superoxide dismutase 1	Homo sapiens	230-250
20200221-9	2010	IL-6 and IL-8 were also significantly elevated after exposure to diacetyl, glyoxal, and methyl glyoxal.	Glyoxal	75-82	interleukin 6	Homo sapiens	0-4
20200221-9	2010	IL-6 and IL-8 were also significantly elevated after exposure to diacetyl, glyoxal, and methyl glyoxal.	Glyoxal	75-82	C-X-C motif chemokine ligand 8	Homo sapiens	9-13
20200221-9	2010	IL-6 and IL-8 were also significantly elevated after exposure to diacetyl, glyoxal, and methyl glyoxal.	Glyoxal	95-102	interleukin 6	Homo sapiens	0-4
20200221-9	2010	IL-6 and IL-8 were also significantly elevated after exposure to diacetyl, glyoxal, and methyl glyoxal.	Glyoxal	95-102	C-X-C motif chemokine ligand 8	Homo sapiens	9-13
19628748-1	2010	PURPOSE: To characterize the neuroprotective mechanisms of erythropoietin (EPO) against the stress of glyoxal-advanced glycation end products (AGEs) in retinal neuronal cells.	Glyoxal	102-109	erythropoietin	Rattus norvegicus	75-78
19628748-9	2010	EPO protected the retinal cells from glyoxal-AGE-induced injury in a time- and dose-dependent fashion.	Glyoxal	37-44	erythropoietin	Rattus norvegicus	0-3
19628748-11	2010	Glyoxal upregulated Bax expression but suppressed Bcl-xL expression and BAD phosphorylation.	Glyoxal	0-7	BCL2 associated X, apoptosis regulator	Rattus norvegicus	20-23
19628748-11	2010	Glyoxal upregulated Bax expression but suppressed Bcl-xL expression and BAD phosphorylation.	Glyoxal	0-7	Bcl2-like 1	Rattus norvegicus	50-56
19628748-14	2010	CONCLUSIONS: These data demonstrate that exogenous EPO significantly attenuates the retinal neuronal cell death induced by glyoxal-AGEs by promoting antiapoptotic and suppressing apoptotic proteins.	Glyoxal	123-130	erythropoietin	Rattus norvegicus	51-54
19778056-3	2009	Taking into account the non-oxidative mechanism of pyrazine formation, the data indicated that all of the ethyl-substituted pyrazines identified in the glyoxal/alanine model system incorporated C-2" and C-3" atoms of alanine, and not that of free acetaldehyde, as the ethyl group carbon atoms.	Glyoxal	152-159	complement C2	Homo sapiens	194-197
19778542-6	2009	However, an increase in SSB content in PARP-1 null cell DNA, as indicated by glyoxal gel electrophoresis under neutral conditions, suggested the presence of BER intermediates.	Glyoxal	77-84	Sjogren syndrome antigen B	Gallus gallus	24-27
19778542-6	2009	However, an increase in SSB content in PARP-1 null cell DNA, as indicated by glyoxal gel electrophoresis under neutral conditions, suggested the presence of BER intermediates.	Glyoxal	77-84	poly(ADP-ribose) polymerase 1	Gallus gallus	39-45
19924942-6	2009	Our measurements of evaporation fractions can be used to estimate the global aerosol formation potential of glyoxal and methylglyoxal via self-reactions at 1 and 1.6 Tg C yr(-1), respectively.	Glyoxal	108-115	transglutaminase 2	Homo sapiens	166-170
19778056-3	2009	Taking into account the non-oxidative mechanism of pyrazine formation, the data indicated that all of the ethyl-substituted pyrazines identified in the glyoxal/alanine model system incorporated C-2" and C-3" atoms of alanine, and not that of free acetaldehyde, as the ethyl group carbon atoms.	Glyoxal	152-159	complement C3	Homo sapiens	203-206
19778056-6	2009	On the basis of the proposed mechanism, the glyoxal interaction with alanine through a decarboxylative aldol addition reaction can lead to the formation of 1,2-butanedione with the terminal ethyl carbon atoms originating from C-2" and C-3" atoms of alanine, and the similar interaction of 1,2-butanedione with a second molecule of alanine can lead to the formation of 3,4-hexanedione with both terminal ethyl carbon atoms originating from C-2" and C-3" atoms of alanine.	Glyoxal	44-51	complement C2	Homo sapiens	226-229
19778056-6	2009	On the basis of the proposed mechanism, the glyoxal interaction with alanine through a decarboxylative aldol addition reaction can lead to the formation of 1,2-butanedione with the terminal ethyl carbon atoms originating from C-2" and C-3" atoms of alanine, and the similar interaction of 1,2-butanedione with a second molecule of alanine can lead to the formation of 3,4-hexanedione with both terminal ethyl carbon atoms originating from C-2" and C-3" atoms of alanine.	Glyoxal	44-51	complement C3	Homo sapiens	235-238
19778056-6	2009	On the basis of the proposed mechanism, the glyoxal interaction with alanine through a decarboxylative aldol addition reaction can lead to the formation of 1,2-butanedione with the terminal ethyl carbon atoms originating from C-2" and C-3" atoms of alanine, and the similar interaction of 1,2-butanedione with a second molecule of alanine can lead to the formation of 3,4-hexanedione with both terminal ethyl carbon atoms originating from C-2" and C-3" atoms of alanine.	Glyoxal	44-51	complement C2	Homo sapiens	439-442
19778056-6	2009	On the basis of the proposed mechanism, the glyoxal interaction with alanine through a decarboxylative aldol addition reaction can lead to the formation of 1,2-butanedione with the terminal ethyl carbon atoms originating from C-2" and C-3" atoms of alanine, and the similar interaction of 1,2-butanedione with a second molecule of alanine can lead to the formation of 3,4-hexanedione with both terminal ethyl carbon atoms originating from C-2" and C-3" atoms of alanine.	Glyoxal	44-51	complement C3	Homo sapiens	448-451
19522522-1	2009	Quantum yields, Phi, for the production of the formyl radical, HCO, in the photolysis of glyoxal were determined at 85 wavelengths, lambda, in the range of 290-420 nm at pressures between 50 and 550 Torr (N(2)) at 298 K using pulsed-laser photolysis combined with cavity ring-down spectroscopy detection of HCO.	Glyoxal	89-96	glucose-6-phosphate isomerase	Homo sapiens	16-19
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.	Glyoxal	47-54	synuclein alpha	Homo sapiens	166-174
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.	Glyoxal	33-35	catalase	Homo sapiens	419-427
18983988-0	2009	Hepatocyte cytotoxicity induced by hydroperoxide (oxidative stress model) or glyoxal (carbonylation model): prevention by bioactive nut extracts or catechins.	Glyoxal	77-84	NUT midline carcinoma, family member 1	Rattus norvegicus	132-135
18983988-3	2009	This study was conducted to evaluate the cytoprotectiveness of various nut extracts and bioactive compounds found in nuts for decreasing cytotoxicity, lipid peroxidation and protein carbonylation in cell toxicity models of diabetes-related carbonyl (glyoxal) and oxidative stress (hydroperoxide).	Glyoxal	250-257	NUT midline carcinoma, family member 1	Rattus norvegicus	71-74
18983988-11	2009	Our results suggest (a) that bioactive nut constituents in the non-lipophilic extracts were more effective than lipophilic extracts for cytoprotection against hydroperoxide induced oxidative stress, (b) catechin compounds under physiological conditions were likely effective at preventing glyoxal cytotoxicity by trapping glyoxal or reversing early stage carbonylation (Schiff base formation).	Glyoxal	289-296	NUT midline carcinoma, family member 1	Rattus norvegicus	39-42
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.	Glyoxal	57-59	synuclein alpha	Homo sapiens	166-174
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.	Glyoxal	22-29	nuclear factor kappa B subunit 1	Homo sapiens	284-305
18624919-6	2008	We found that glyoxal and H(2)O(2) increased accumulation of CML-modified proteins and ROS production and decreased pHi and MTMP in cell bodies of multipolar ganglion cell layer.	Glyoxal	14-21	glucose-6-phosphate isomerase	Rattus norvegicus	116-119
18448824-2	2008	The incubations were performed under atmospheric and high hydrostatic pressure (400 MPa), and, at the same time, beta-casein was reacted with glyoxal.	Glyoxal	142-149	casein beta	Homo sapiens	113-124
18801604-4	2009	CL-20 degradation was accompanied by the formation of formate, glyoxal, nitrite, ammonium, and nitrous oxide.	Glyoxal	63-70	epithelial membrane protein 1	Homo sapiens	0-5
18464885-7	2008	N-acetyl-L-cysteine (L-NAC) at 1 mM significantly suppressed the glyoxal-induced embryonal toxicity.	Glyoxal	65-72	synuclein alpha	Homo sapiens	23-26
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.	Glyoxal	22-29	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.	Glyoxal	31-33	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.	Glyoxal	31-33	nuclear factor kappa B subunit 1	Homo sapiens	307-315
17408936-6	2007	The presence of PEO chains slightly decreased the diffusivity of glyoxal due to obstruction effects.	Glyoxal	65-72	twinkle mtDNA helicase	Homo sapiens	16-19
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).	Glyoxal	54-56	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).	Glyoxal	54-56	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.	Glyoxal	39-41	platelet derived growth factor receptor, beta polypeptide	Mus musculus	75-84
17943239-6	2007	Subsequent treatment of the WI- 38 conditioned medium with the dicarbonyl compound glyoxal, a highly reactive precursor of the AGE formation, resulted in a dose-dependent reduction of the MMP-2 activity.	Glyoxal	83-90	matrix metallopeptidase 2	Homo sapiens	188-193
17655273-10	2007	Aliphatic aldehydes such as glyoxal, acetaldehyde, and propanal are relatively weak inactivators of PTP1B under the conditions employed here.	Glyoxal	28-35	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	100-105
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.	Glyoxal	38-40	cathepsin B	Felis catus	115-119
17873339-5	2007	In insulin resistance, alterations in glucose and lipid metabolism lead to the production of excess aldehydes including glyoxal and methylglyoxal.	Glyoxal	120-127	insulin	Homo sapiens	3-10
16427160-4	2007	AGE precursor compounds such as methylglyoxal and glyoxal were cellulary detoxified by the glyoxalase system, consisting of glyoxalases I and II.	Glyoxal	38-45	glyoxalase I	Homo sapiens	124-144
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.	Glyoxal	38-40	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.	Glyoxal	38-40	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.	Glyoxal	38-40	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.	Glyoxal	38-40	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.	Glyoxal	28-35	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.	Glyoxal	28-35	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.	Glyoxal	28-35	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.	Glyoxal	28-35	procathepsin L	Felis catus	141-152
15983222-4	2005	Treating cells with glycolaldehyde (GA) and glyoxal (GO) strongly inhibited ABCA1-dependent transport of cholesterol from cells to apoA-I, while methylglyoxal had little effect.	Glyoxal	44-51	ATP binding cassette subfamily A member 1	Sus scrofa	76-81
16392851-5	2006	Furthermore, the 193 nm photolysis of glyoxal, (CHO)2, has been proven to be an efficient HCO source.	Glyoxal	38-45	EBP cholestenol delta-isomerase	Homo sapiens	48-53
15983222-4	2005	Treating cells with glycolaldehyde (GA) and glyoxal (GO) strongly inhibited ABCA1-dependent transport of cholesterol from cells to apoA-I, while methylglyoxal had little effect.	Glyoxal	44-51	apolipoprotein A1	Sus scrofa	131-137
15983222-4	2005	Treating cells with glycolaldehyde (GA) and glyoxal (GO) strongly inhibited ABCA1-dependent transport of cholesterol from cells to apoA-I, while methylglyoxal had little effect.	Glyoxal	53-55	ATP binding cassette subfamily A member 1	Sus scrofa	76-81
15983222-4	2005	Treating cells with glycolaldehyde (GA) and glyoxal (GO) strongly inhibited ABCA1-dependent transport of cholesterol from cells to apoA-I, while methylglyoxal had little effect.	Glyoxal	53-55	apolipoprotein A1	Sus scrofa	131-137
16037241-3	2005	As reactive intermediates of AGE formation, neurotoxic reactive dicarbonyl compounds such as glyoxal and methylglyoxal have been identified.	Glyoxal	93-100	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.	Glyoxal	59-66	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.	Glyoxal	59-66	hydroxyacylglutathione hydrolase	Homo sapiens	158-171
15343506-5	2004	Moreover, estrogen receptor detection in GL-fixed specimens was diminished compared to formalin and did require antigen retrieval.	Glyoxal	41-43	estrogen receptor 1	Homo sapiens	10-27
15822816-9	2005	Immunoblots of immunoprecipitated GLT-1 disclosed GLT-1 CML adduct formation in the glyoxal-exposed cells.	Glyoxal	84-91	solute carrier family 1 member 2	Rattus norvegicus	50-55
15822816-10	2005	Our results indicate that glyoxal modifies GLT-1 to form CML and simultaneously deprives its glutamate uptake activity.	Glyoxal	26-33	solute carrier family 1 member 2	Rattus norvegicus	43-48
15669350-3	2004	In the absence of O2, CL-20 underwent a rapid decomposition with the concurrent formation of nitrite to ultimately produce nitrous oxide, ammonium, formate, glyoxal, and glycolate.	Glyoxal	157-164	epithelial membrane protein 1	Homo sapiens	22-27
15822816-0	2005	Glyoxal inactivates glutamate transporter-1 in cultured rat astrocytes.	Glyoxal	0-7	solute carrier family 1 member 2	Rattus norvegicus	20-43
15822816-5	2005	In considering these documents, it is important to determine whether GLT-1 protein modification by glyoxal might cause reduced GLT-1 activity.	Glyoxal	99-106	solute carrier family 1 member 2	Rattus norvegicus	69-74
15822816-5	2005	In considering these documents, it is important to determine whether GLT-1 protein modification by glyoxal might cause reduced GLT-1 activity.	Glyoxal	99-106	solute carrier family 1 member 2	Rattus norvegicus	127-132
15822816-9	2005	Immunoblots of immunoprecipitated GLT-1 disclosed GLT-1 CML adduct formation in the glyoxal-exposed cells.	Glyoxal	84-91	solute carrier family 1 member 2	Rattus norvegicus	34-39
15652820-1	2005	Non-enzymatic posttranslational modifications of bovine serum albumin (BSA) by oxo-compounds, particularly glucose, ribose, glyoxal and glutardialdehyde, have been investigated using a set of modern chromatographic and electrophoretic separation methods.	Glyoxal	124-131	albumin	Homo sapiens	56-69
15237193-2	2004	Glyoxal is a highly reactive glycating agent involved in the formation of AGEs and is known to induce apoptosis, as revealed by the upregulation of caspase-3 and fractin (caspase-3 being a key enzyme activated during the late stage of apoptosis and fractin being a caspase-cleaved actin fragment).	Glyoxal	0-7	caspase 3	Homo sapiens	148-157
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).	Glyoxal	131-138	fibronectin 1	Bos taurus	110-112
15309567-5	2004	Incubation of insulin with glyoxal proved the protein-bound formation of pyrazinones, with the N-terminus of the B-chain as the main target.	Glyoxal	27-34	insulin	Homo sapiens	14-21
15237193-2	2004	Glyoxal is a highly reactive glycating agent involved in the formation of AGEs and is known to induce apoptosis, as revealed by the upregulation of caspase-3 and fractin (caspase-3 being a key enzyme activated during the late stage of apoptosis and fractin being a caspase-cleaved actin fragment).	Glyoxal	0-7	caspase 3	Homo sapiens	171-180
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.	Glyoxal	92-99	glyoxalase I	Homo sapiens	0-12
12644946-8	2003	CML, bax and active caspase-3 increased after incubation with glyoxal.	Glyoxal	62-69	BCL2 associated X, apoptosis regulator	Rattus norvegicus	5-8
12483325-18	2002	The cells were immunoreactive for active caspase-3 after glyoxal in a dose-dependent manner.	Glyoxal	57-64	caspase 3	Rattus norvegicus	41-50
12644946-8	2003	CML, bax and active caspase-3 increased after incubation with glyoxal.	Glyoxal	62-69	caspase 3	Rattus norvegicus	20-29
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).	Glyoxal	31-38	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).	Glyoxal	156-158	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).	Glyoxal	156-158	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.	Glyoxal	43-45	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.	Glyoxal	88-90	glyoxalase I	Homo sapiens	58-63
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.	Glyoxal	89-91	glyoxalase I	Homo sapiens	13-18
11705701-0	2001	Glyoxal and methylglyoxal induce lyoxal and methyglyoxal induce aggregation and inactivation of ERK in human endothelial cells.	Glyoxal	0-7	mitogen-activated protein kinase 1	Homo sapiens	96-99
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.	Glyoxal	57-64	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.	Glyoxal	57-64	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.	Glyoxal	66-68	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.	Glyoxal	66-68	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.	Glyoxal	99-101	epidermal growth factor receptor	Homo sapiens	71-75
11952331-6	2002	The alpha-hydroxylation of NHMOR at either C-3 or C-5 to give glyoxal or glycolaldehyde, respectively, occurs at respective rates 3-6 times that of the alpha-hydroxylation of NDELA.	Glyoxal	62-69	complement C3	Rattus norvegicus	43-46
11952331-6	2002	The alpha-hydroxylation of NHMOR at either C-3 or C-5 to give glyoxal or glycolaldehyde, respectively, occurs at respective rates 3-6 times that of the alpha-hydroxylation of NDELA.	Glyoxal	62-69	complement C5	Rattus norvegicus	50-53
11559702-4	2001	In addition, the activity of glucose-6-phosphate dehydrogenase, a crucial enzyme for the regulation of the intracellular redox status, was dramatically reduced in glyoxal-treated cells.	Glyoxal	163-170	glucose-6-phosphate dehydrogenase	Homo sapiens	29-62
11705701-8	2001	These results together suggest that GO and MGO trigger a novel pathway for chemical reaction-mediated downregulation of ERK.	Glyoxal	36-38	mitogen-activated protein kinase 1	Homo sapiens	120-123
11705701-5	2001	Interestingly, however, GO/MGO caused both aggregation and dephosphorylation of intracellular phospho-ERK for inactivation.	Glyoxal	24-26	mitogen-activated protein kinase 1	Homo sapiens	102-105
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.	Glyoxal	27-29	dual specificity phosphatase 1	Homo sapiens	46-51
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.	Glyoxal	27-29	mitogen-activated protein kinase 1	Homo sapiens	122-125
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.	Glyoxal	35-37	mitogen-activated protein kinase 3	Homo sapiens	75-79
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.	Glyoxal	32-34	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.	Glyoxal	35-37	mitogen-activated protein kinase 1	Homo sapiens	84-88
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.	Glyoxal	32-34	mitogen-activated protein kinase 1	Homo sapiens	116-119
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.	Glyoxal	35-37	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.	Glyoxal	32-34	EPH receptor A8	Homo sapiens	136-139
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.	Glyoxal	32-34	mitogen-activated protein kinase 1	Homo sapiens	183-186
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.	Glyoxal	35-37	EPH receptor A8	Homo sapiens	141-144
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.	Glyoxal	32-34	mitogen-activated protein kinase 3	Homo sapiens	187-191
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.	Glyoxal	35-37	EPH receptor A8	Homo sapiens	203-206
11425486-4	2001	GO and MGO also induced phosphorylations of JNK, p38 MAPK, and c-Jun, either PTK-dependently (GO) or -independently (MGO).	Glyoxal	0-2	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).	Glyoxal	0-2	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).	Glyoxal	0-2	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).	Glyoxal	0-2	EPH receptor A8	Homo sapiens	77-80
9846896-4	1998	Like the glycoxidation products, N(epsilon)-(carboxymethyl)lysine (CML) and glyoxal-lysine dimer (GOLD) which are formed on reaction of glyoxal with protein, CEL and MOLD increase in lens proteins and skin collagen with age.	Glyoxal	76-83	carboxyl ester lipase	Homo sapiens	158-161
11017913-7	2000	To examine the role of apoptosis in epithelial lung cells we investigated glyoxal-dependent changes in pro- and antiapoptotic mediators bax and activated caspase-3, and galectin-3 and bcl-2, respectively.	Glyoxal	74-81	BCL2 associated X, apoptosis regulator	Homo sapiens	136-139
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.	Glyoxal	66-73	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.	Glyoxal	66-73	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.	Glyoxal	88-95	vascular endothelial growth factor A	Rattus norvegicus	0-4
10025661-3	1999	Glyoxal induced cross-linking of a number of cellular proteins, including glycosylphosphatidylinositol (GPI)-anchored cell surface Thy-1.	Glyoxal	0-7	thymus cell antigen 1, theta	Mus musculus	131-136
11131093-8	2000	Increasing concentrations of glyoxal induced an increase in the number of apoptotic cells which were identified by the immunoreactivity for active caspase-3.	Glyoxal	29-36	caspase 3	Homo sapiens	147-156
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.	Glyoxal	112-119	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.	Glyoxal	130-137	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.	Glyoxal	130-137	albumin	Homo sapiens	167-174
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.	Glyoxal	20-27	glyoxalase 1	Mus musculus	119-131
8930762-1	1996	A reversed-phase (C18) HPLC method with diode-array detection was developed for the separation and determination of methylglyoxal bis(amidinohydrazone) (mitoguazone) and seven closely related aliphatic analogs thereof, namely the bis(amidinohydrazones) of glyoxal, dimethylglyoxal, ethylmethylglyoxal, methylpropylglyoxal, butylmethylglyoxal, diethylglyoxal and dipropylglyoxal.	Glyoxal	122-129	Bardet-Biedl syndrome 9	Homo sapiens	18-21
9438984-1	1997	Human Cu,Zn-superoxide dismutase (SOD) was incubated with various intermediates of the Maillard reaction and glycolytic pathway (arabinose, glyoxal, glycolaldehyde, glyceraldehyde, glyceraldehyde 3-phosphate, and dihydroxyacetone) and some reducing sugars (sorbose, xylose, and ribose).	Glyoxal	140-147	superoxide dismutase 1	Homo sapiens	6-32
9438984-1	1997	Human Cu,Zn-superoxide dismutase (SOD) was incubated with various intermediates of the Maillard reaction and glycolytic pathway (arabinose, glyoxal, glycolaldehyde, glyceraldehyde, glyceraldehyde 3-phosphate, and dihydroxyacetone) and some reducing sugars (sorbose, xylose, and ribose).	Glyoxal	140-147	superoxide dismutase 1	Homo sapiens	34-37
11672185-3	1998	The entire sequence lies in the preparation of nonracemic 3-hydroxy beta-lactams through the highly diastereoselective Staudinger reaction of hydroxyketene equivalents with chiral alpha-oxyaldehyde-derived imines, followed by TEMPO radical assisted cycloexpansion to the corresponding NCA and subsequent peptide coupling with alpha-amino acid esters.	Glyoxal	142-155	CEA cell adhesion molecule 6	Homo sapiens	285-288
9744543-8	1998	When glyoxal was reacted with various combinations of deoxynucleosides for a prolonged period, dG-glyoxal-dC (GgC), dG-glyoxal-dA (GgA), dG-glyoxal-dG (GgG) and dC-glyoxal-dC (CgC) cross-links were detected, although structures were not assigned unequivocally.	Glyoxal	5-12	gamma-glutamylcyclotransferase	Homo sapiens	110-113
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.	Glyoxal	99-106	glutathione S-transferase pi 1	Rattus norvegicus	25-30
8526867-5	1995	Determination of the apparent Km reveals that AFAR has highest affinity for 9,10-phenanthrenequinone and succinic semialdehyde, and low affinity for glyoxal and DL-glyceraldehyde.	Glyoxal	149-156	aldo-keto reductase family 7 member A3	Rattus norvegicus	46-50
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.	Glyoxal	146-153	catenin beta like 1	Homo sapiens	44-47
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.	Glyoxal	81-88	glyoxalase 1	Mus musculus	0-12
34971698-0	2021	Glyoxal induces senescence in human keratinocytes through oxidative stress and activation of the AKT/FOXO3a/p27KIP1 pathway.	Glyoxal	0-7	AKT serine/threonine kinase 1	Homo sapiens	97-100
34971698-0	2021	Glyoxal induces senescence in human keratinocytes through oxidative stress and activation of the AKT/FOXO3a/p27KIP1 pathway.	Glyoxal	0-7	forkhead box O3	Homo sapiens	101-107
34971698-0	2021	Glyoxal induces senescence in human keratinocytes through oxidative stress and activation of the AKT/FOXO3a/p27KIP1 pathway.	Glyoxal	0-7	cyclin dependent kinase inhibitor 1B	Homo sapiens	108-115
34971698-6	2021	Furthermore, glyoxal-induced senescence bears a unique molecular progression profile: an "early-stage" when AKT-FOXO3a-p27KIP1 pathway mediates cell-cycle arrest, and a "late-stage" senescence maintained by the p16INK4/pRb pathway.	Glyoxal	13-20	AKT serine/threonine kinase 1	Homo sapiens	108-111
34971698-6	2021	Furthermore, glyoxal-induced senescence bears a unique molecular progression profile: an "early-stage" when AKT-FOXO3a-p27KIP1 pathway mediates cell-cycle arrest, and a "late-stage" senescence maintained by the p16INK4/pRb pathway.	Glyoxal	13-20	forkhead box O3	Homo sapiens	112-118
34971698-6	2021	Furthermore, glyoxal-induced senescence bears a unique molecular progression profile: an "early-stage" when AKT-FOXO3a-p27KIP1 pathway mediates cell-cycle arrest, and a "late-stage" senescence maintained by the p16INK4/pRb pathway.	Glyoxal	13-20	cyclin dependent kinase inhibitor 1B	Homo sapiens	119-126
34971698-6	2021	Furthermore, glyoxal-induced senescence bears a unique molecular progression profile: an "early-stage" when AKT-FOXO3a-p27KIP1 pathway mediates cell-cycle arrest, and a "late-stage" senescence maintained by the p16INK4/pRb pathway.	Glyoxal	13-20	cyclin dependent kinase inhibitor 2A	Homo sapiens	211-218
34971698-6	2021	Furthermore, glyoxal-induced senescence bears a unique molecular progression profile: an "early-stage" when AKT-FOXO3a-p27KIP1 pathway mediates cell-cycle arrest, and a "late-stage" senescence maintained by the p16INK4/pRb pathway.	Glyoxal	13-20	RB transcriptional corepressor 1	Homo sapiens	219-222
34584990-9	2021	A lower plasma glycolate in male GLO-2 KO animals suggests glyoxal production may be a significant contributor to circulating glycolate levels, but not to endogenous oxalate synthesis.	Glyoxal	59-66	hydroxyacyl glutathione hydrolase	Mus musculus	33-38
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.	Glyoxal	161-168	hydroxyacyl glutathione hydrolase	Mus musculus	52-57
34573117-0	2021	Glyoxal-Lysine Dimer, an Advanced Glycation End Product, Induces Oxidative Damage and Inflammatory Response by Interacting with RAGE.	Glyoxal	0-7	MOK protein kinase	Mus musculus	128-132
34240860-2	2021	The initially formed labile glyoxal-imine was previously established as a key intermediate in the formation of the advanced glycation end products N6-carboxymethyl lysine (CML), glyoxal lysine amide (GOLA), glyoxal lysine dimer (GOLD), and N6-glycolyl lysine (GALA).	Glyoxal	28-35	galactosidase alpha	Homo sapiens	260-264
34240860-5	2021	Furthermore, incubations of proteins (6 mg/mL) with 50 mM glyoxal confirmed the cross-linking by GLA, which was additionally identified in acidic hydrolyzed proteins of butter biscuits after HPLC enrichment.	Glyoxal	58-65	galactosidase alpha	Homo sapiens	97-100
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.	Glyoxal	0-7	renin binding protein	Homo sapiens	151-154
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.	Glyoxal	9-11	renin binding protein	Homo sapiens	151-154
35621379-4	2022	Network toxicology results showed that oxidative stress and advanced glycation end products (AGEs)/RAGE signaling pathways played a crucial role in glyoxal toxicity.	Glyoxal	148-155	MOK protein kinase	Homo sapiens	99-103
34208633-3	2021	In this study, a chitosan/gelatin (CS-GE) hydrogel crosslinked by glyoxal was fabricated for sustained release of HPL.	Glyoxal	66-73	galectin 1	Homo sapiens	114-117
35621379-6	2022	Glyoxal activated the AGEs-RAGE signaling pathway, caused the increase of cellular ROS, and activated the p38MAPK and JNK signaling pathways, causing cellular oxidative stress.	Glyoxal	0-7	MOK protein kinase	Homo sapiens	27-31
35621379-6	2022	Glyoxal activated the AGEs-RAGE signaling pathway, caused the increase of cellular ROS, and activated the p38MAPK and JNK signaling pathways, causing cellular oxidative stress.	Glyoxal	0-7	mitogen-activated protein kinase 8	Homo sapiens	118-121
35621379-7	2022	Furthermore, glyoxal caused the activation of the NF-kappaB signaling pathway and increased the expression of TGF-beta1, indicating that glyoxal caused cellular inflammation.	Glyoxal	13-20	nuclear factor kappa B subunit 1	Homo sapiens	50-59
35621379-7	2022	Furthermore, glyoxal caused the activation of the NF-kappaB signaling pathway and increased the expression of TGF-beta1, indicating that glyoxal caused cellular inflammation.	Glyoxal	13-20	transforming growth factor beta 1	Homo sapiens	110-119
35621379-7	2022	Furthermore, glyoxal caused the activation of the NF-kappaB signaling pathway and increased the expression of TGF-beta1, indicating that glyoxal caused cellular inflammation.	Glyoxal	137-144	nuclear factor kappa B subunit 1	Homo sapiens	50-59
35621379-7	2022	Furthermore, glyoxal caused the activation of the NF-kappaB signaling pathway and increased the expression of TGF-beta1, indicating that glyoxal caused cellular inflammation.	Glyoxal	137-144	transforming growth factor beta 1	Homo sapiens	110-119
35621379-10	2022	The results that obtained in cell biology were consistent with network toxicology, which corroborated each other and together indicated that glyoxal induced HEK293 cells damage via the process of oxidative stress, the AGEs-RAGE pathway, and their associated signaling pathways.	Glyoxal	141-148	MOK protein kinase	Homo sapiens	223-227
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.	Glyoxal	54-56	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.	Glyoxal	226-228	NFE2 like bZIP transcription factor 2	Homo sapiens	89-93
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.	Glyoxal	104-112	decapping mRNA 1B	Homo sapiens	71-76
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.	Glyoxal	132-139	decapping mRNA 1B	Homo sapiens	71-76
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.	Glyoxal	119-121	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.	Glyoxal	119-121	NFE2 like bZIP transcription factor 2	Homo sapiens	199-203
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.	Glyoxal	52-59	lysozyme	Homo sapiens	0-8
35194998-2	2022	In the present study, human serum albumin (HSA) as the major transporter of fatty acids was modified with glyoxal under physiological conditions.	Glyoxal	106-113	albumin	Homo sapiens	28-41
3123439-6	1987	These results and previous findings that stomach-tumor promoters such as NaCl, taurocholate, glyoxal, K2S2O5 and formaldehyde induced ODC and DNA synthesis in the pyloric mucosa of the stomach of F344 rats suggest that the inductions of ODC and DNA synthesis in the glandular stomach mucosa are markers of promotive activities of complete carcinogens and tumor promoters in the glandular stomach.	Glyoxal	93-100	ornithine decarboxylase 1	Rattus norvegicus	134-137
3123439-6	1987	These results and previous findings that stomach-tumor promoters such as NaCl, taurocholate, glyoxal, K2S2O5 and formaldehyde induced ODC and DNA synthesis in the pyloric mucosa of the stomach of F344 rats suggest that the inductions of ODC and DNA synthesis in the glandular stomach mucosa are markers of promotive activities of complete carcinogens and tumor promoters in the glandular stomach.	Glyoxal	93-100	ornithine decarboxylase 1	Rattus norvegicus	237-240
1066674-3	1976	The distribution of me3-psoralen crosslinks was determined by electron microscopy after denaturation of the DNA in the presence of glyoxal.	Glyoxal	131-138	malic enzyme 3, NADP(+)-dependent, mitochondrial	Mus musculus	20-23
3939095-6	1985	Small modifications, such as increased hydrophobicity at the glyoxal portion of the parent compound glyoxal bis(guanylhydrazone), greatly enhance the inhibition of adenosylmethionine decarboxylase and diminish the undesirable inhibition of diamine oxidase.	Glyoxal	61-68	amine oxidase copper containing 1	Homo sapiens	240-255
283388-2	1978	alpha-LA mRNA was homogeneous as judged by electrophoresis in urea/agarose gel and in 1.5% agarose gel under glyoxal-denaturation conditions, which gave a molecular weight of 210,000.	Glyoxal	109-116	lactalbumin, alpha	Rattus norvegicus	0-8
33903117-12	2021	AMPK phosphorylation was reduced by glyoxal treatment but it was not responsible for the accumulation of LDs.	Glyoxal	36-43	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	0-4
33933705-0	2021	High-Performance affinity chromatographic studies of repaglinide and nateglinide interactions with normal and glyoxal- or methylglyoxal-modified human albumin serum.	Glyoxal	110-117	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.	Glyoxal	114-121	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.	Glyoxal	123-125	albumin	Homo sapiens	28-35
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.	Glyoxal	44-51	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	10-13
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.	Glyoxal	53-55	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	10-13
33444798-5	2021	Prior studies modeled BP-AGE formation in vitro with glyoxal, a glucose breakdown product, and serum albumin.	Glyoxal	53-60	renin binding protein	Bos taurus	25-28
32746708-7	2021	GO and MGO increased production of pro-inflammatory such as interleukin (IL)-1beta and IL-6) and MUC5AC/5B.	Glyoxal	0-2	interleukin 1 alpha	Homo sapiens	60-82
32746708-7	2021	GO and MGO increased production of pro-inflammatory such as interleukin (IL)-1beta and IL-6) and MUC5AC/5B.	Glyoxal	0-2	interleukin 6	Homo sapiens	87-91
32746708-10	2021	These significantly repressed GO- and MGO-induced expression of pro-inflammatory cytokines (IL-1beta and IL-6) and MUC5AC/5B.	Glyoxal	30-32	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.	Glyoxal	30-32	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.	Glyoxal	30-32	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.	Glyoxal	13-15	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.	Glyoxal	13-15	nuclear factor kappa B subunit 1	Homo sapiens	110-119
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.	Glyoxal	174-181	albumin	Homo sapiens	57-60
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.	Glyoxal	103-110	renin binding protein	Homo sapiens	37-40
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.	Glyoxal	126-128	renin binding protein	Homo sapiens	37-40
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.	Glyoxal	5-7	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.	Glyoxal	174-181	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.	Glyoxal	174-181	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.	Glyoxal	174-181	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.	Glyoxal	183-185	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.	Glyoxal	183-185	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.	Glyoxal	183-185	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.	Glyoxal	183-185	albumin	Homo sapiens	235-238
33304826-1	2020	Glyoxal (GO), a by-product of glucose auto-oxidation, is involved in the glycation of proteins/ lipids and formation of advanced glycation (AGE) and lipoxidation (ALE) end products.	Glyoxal	0-7	renin binding protein	Rattus norvegicus	140-143
32814203-5	2020	The glyoxal:formaldehyde ratio (Rgf), reported for the first time in Australia, was consistently high compared to values elsewhere in the world with a mean of 0.105 +- 0.0503 and tended to increase with increasing anthropogenic influence.	Glyoxal	4-11	ral guanine nucleotide dissociation stimulator	Homo sapiens	32-35
33304826-1	2020	Glyoxal (GO), a by-product of glucose auto-oxidation, is involved in the glycation of proteins/ lipids and formation of advanced glycation (AGE) and lipoxidation (ALE) end products.	Glyoxal	9-11	renin binding protein	Rattus norvegicus	140-143
32244975-8	2020	TGA results showed that the initial ignition temperature of furanic-glyoxal foams is ~200  C higher than that of wood, and the smaller comprehensive combustion index S (about 0.15 x 10-7 (%2 K-3 min-2)) indicates that the foam burns slowly and has poor flammability, that is, it is not easy to burn.	Glyoxal	68-75	CD59 molecule (CD59 blood group)	Homo sapiens	195-200
32800831-11	2020	Ranibizumab and CGP77675 also inhibited the glyoxal-induced phosphorylation of Src and VE-cadherin.	Glyoxal	44-51	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	79-82
32800831-11	2020	Ranibizumab and CGP77675 also inhibited the glyoxal-induced phosphorylation of Src and VE-cadherin.	Glyoxal	44-51	cadherin 5	Rattus norvegicus	87-98
32800831-12	2020	Cellular fractionation showed EPO mitigated the VE-cadherin internalization in glyoxal-treated cells.	Glyoxal	79-86	erythropoietin	Rattus norvegicus	30-33
32800831-12	2020	Cellular fractionation showed EPO mitigated the VE-cadherin internalization in glyoxal-treated cells.	Glyoxal	79-86	cadherin 5	Rattus norvegicus	48-59
31541246-8	2020	Results support the hypotheses that APOE-epsilon4 carriers have shorter telomeres than non-carriers and telomere erosion is increased with higher concentration of glucose, fluorescent AGEs and glyoxal.	Glyoxal	193-200	apolipoprotein E	Homo sapiens	36-40
31677348-5	2020	APOE epsilon4 carriers showed higher levels of cholesterol (p< 0.001), glyoxal (p< 0.001), fluorescent AGEs (p< 0.001), Nepsilon-carboxymethyllysine (p< 0.001) and sRAGE (p= 0.018) when compared to non-carriers.	Glyoxal	74-81	apolipoprotein E	Homo sapiens	0-4
32695253-6	2020	Protein expressions of phospho-AMPKalpha, Sirt1, TXNIP, ZO-1, and Occludin, but not Nrf2, were decreased significantly in the glyoxal-treated group compared to normal controls.	Glyoxal	126-133	sirtuin 1	Homo sapiens	42-47
32695253-6	2020	Protein expressions of phospho-AMPKalpha, Sirt1, TXNIP, ZO-1, and Occludin, but not Nrf2, were decreased significantly in the glyoxal-treated group compared to normal controls.	Glyoxal	126-133	thioredoxin interacting protein	Homo sapiens	49-54
32695253-6	2020	Protein expressions of phospho-AMPKalpha, Sirt1, TXNIP, ZO-1, and Occludin, but not Nrf2, were decreased significantly in the glyoxal-treated group compared to normal controls.	Glyoxal	126-133	tight junction protein 1	Homo sapiens	56-60
32695253-6	2020	Protein expressions of phospho-AMPKalpha, Sirt1, TXNIP, ZO-1, and Occludin, but not Nrf2, were decreased significantly in the glyoxal-treated group compared to normal controls.	Glyoxal	126-133	occludin	Homo sapiens	66-74
32695253-6	2020	Protein expressions of phospho-AMPKalpha, Sirt1, TXNIP, ZO-1, and Occludin, but not Nrf2, were decreased significantly in the glyoxal-treated group compared to normal controls.	Glyoxal	126-133	NFE2 like bZIP transcription factor 2	Homo sapiens	84-88
32255634-7	2020	The main products (and associated relative abundances) originating from unimolecular decay of anti-MVK-oxide and subsequent reaction with O2 are formaldehyde (88 +- 5%), ketene (9 +- 1%) and glyoxal (3 +- 1%).	Glyoxal	191-198	mevalonate kinase	Homo sapiens	99-102
30886207-2	2019	Spectroscopic measurements revealed that Cyt c undergo certain conformational alterations and exposure of heme upon overnight incubation with Gly and MGly.	Glyoxal	142-145	cytochrome c, somatic	Homo sapiens	41-46
31731544-10	2019	RESULTS: Our data show that GO-treatment results in glycation of Wnt3a.	Glyoxal	28-30	Wnt family member 3A	Homo sapiens	65-70
31731544-12	2019	CONCLUSIONS: GO-induced glycation impairs Wnt3a signaling function.	Glyoxal	13-15	Wnt family member 3A	Homo sapiens	42-47
30886207-0	2019	Covalent Modification by Glyoxals Converts Cytochrome c Into its Apoptotically Competent State.	Glyoxal	25-33	cytochrome c, somatic	Homo sapiens	43-55
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.	Glyoxal	107-109	glyoxalase I	Homo sapiens	0-12
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.	Glyoxal	107-109	glyoxalase I	Homo sapiens	14-19
32003651-6	2020	OBJECTIVE: In the present study the in vitro aggregation of human serum albumin (HSA) by using a reactive dicarbonyl glyoxal has been investigated, simultaneously an attempt has been done to inhibit the glyoxal (GO) induced aggregation of (HSA) by caffeic acid (CA).	Glyoxal	106-124	albumin	Homo sapiens	66-79
32003651-6	2020	OBJECTIVE: In the present study the in vitro aggregation of human serum albumin (HSA) by using a reactive dicarbonyl glyoxal has been investigated, simultaneously an attempt has been done to inhibit the glyoxal (GO) induced aggregation of (HSA) by caffeic acid (CA).	Glyoxal	117-124	albumin	Homo sapiens	66-79
32003651-6	2020	OBJECTIVE: In the present study the in vitro aggregation of human serum albumin (HSA) by using a reactive dicarbonyl glyoxal has been investigated, simultaneously an attempt has been done to inhibit the glyoxal (GO) induced aggregation of (HSA) by caffeic acid (CA).	Glyoxal	212-214	albumin	Homo sapiens	66-79
31483932-4	2019	The glyoxal-treated ARPE-19 cells, incubated with EPO, soluble EPO receptor (sEPOR), Go6976, or digoxin, were studied for cell viability and barrier function.	Glyoxal	4-11	erythropoietin	Rattus norvegicus	63-66
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.	Glyoxal	69-71	albumin	Homo sapiens	43-46
31364512-0	2019	Glyoxal induced transition of transferrin to aggregates: Spectroscopic, microscopic and molecular docking insight.	Glyoxal	0-7	transferrin	Homo sapiens	30-41
29932913-2	2018	Here, we show that DJ-1, deglycase 1 and deglycase 2 repair glyoxal- and methylglyoxal-glycated substrates, whereas deglycase 3 principally repairs glyoxal-glycated substrates.	Glyoxal	60-67	Parkinsonism associated deglycase	Homo sapiens	19-52
29932913-2	2018	Here, we show that DJ-1, deglycase 1 and deglycase 2 repair glyoxal- and methylglyoxal-glycated substrates, whereas deglycase 3 principally repairs glyoxal-glycated substrates.	Glyoxal	79-86	Parkinsonism associated deglycase	Homo sapiens	19-52