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PMID	12663085 ( )
Title	Glycation--a sweet tempter for neuronal death.
Abstract	Glycation, one of the post-translational modifications of proteins, is a nonenzymatic reaction initiated by the primary addition of a sugar aldehyde or ketone to the amino groups of proteins. In the early stage of glycation, the synthesis of intermediates leading to the formation of Amadori compounds occurs. In the late stage, advanced glycation end products (AGE) are irreversibly formed after a complex cascade of reactions. Several AGEs have been characterized chemically, while other new compounds remain to be identified. To date, studies of the contribution of glycation to diseases have been primarily focused on its relationship to diabetes and diabetes-related complications. However, glucose-induced damage is not limited to diabetic patients. Although it does not cause rapid or remarkable cell damage, glycation advances slowly and accompanies every fundamental process of cellular metabolism. It has recently become clear that glycation also affects physiological aging and neurodegenerative diseases such as Alzheimer's disease and amyotrophic lateral sclerosis. Glycation alters the biological activity of proteins and their degradation processes. Protein cross-linking by AGE results in the formation of detergent-insoluble and protease-resistant aggregates. Such aggregates may interfere with both axonal transport and intracellular protein traffic in neurons. In addition, glycation reactions lead to the production of reactive oxygen species. Conversely, glycation is promoted by oxidative stress. We speculate on the presence of synergism between glycation and oxidative stress. In this review, we provide an outline of glycation and propose some possible mechanisms of its cytotoxicity and defense systems against it. Nishi 7, Kita-ku, Sapporo, Japan. skikuti@med.hokudai.ac.jp

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Targets by SciMiner Summary

HUGO ID	Symbol	Target Name	#Occur	ActualStr
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	37	superoxide dismutase 1 \| SOD-1-related \| SOD-1-positive \|
2728	DDOST	dolichyl-diphosphooligosaccharide-protein glycosyltransferase	9	AGE-R1 \| OST48 \| age r1 \|
6893	MAPT	microtubule-associated protein tau	9	tau \|
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	8	NOS \| NOSs \| iNOS \| nitric oxide synthase \|
613	APOE	apolipoprotein E	6	apoE \| apoprotein \|
5013	HMOX1	heme oxygenase (decycling) 1	5	HO-1 \| ho 1 \|
249	ADH1A	alcohol dehydrogenase 1A (class I), alpha polypeptide	5	aldehyde reductase \|
9411	PRKCSH	protein kinase C substrate 80K-H	5	80k h protein \| AGE-R2 \|
14374	NLRP1	NLR family, pyrin domain containing 1	4	NAC \|
620	APP	amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)	3	amyloid \|
399	ALB	albumin	3	albumin \|
10417	RPS27A	ribosomal protein S27a	2	ubiquitin \|
7734	NEFM	neurofilament, medium polypeptide 150kDa	2	NF-M \| nf m \|
7739	NEFL	neurofilament, light polypeptide 68kDa	2	nf l \| NF-L \|
7737	NEFH	neurofilament, heavy polypeptide 200kDa	2	NF-H \|
2197	COL1A1	collagen, type I, alpha 1	2	collagen \|
2206	COL4A4	collagen, type IV, alpha 4	1	collagen iv \|
1516	CAT	catalase	1	catalase \|
4805	HAGH	hydroxyacylglutathione hydrolase	1	glyoxalase ii \|
381	AKR1B1	aldo-keto reductase family 1, member B1 (aldose reductase)	1	aldose reductase \|
4323	GLO1	glyoxalase I	1	glyoxalase i \|
11892	TNF	tumor necrosis factor (TNF superfamily, member 2)	1	tumor necrosis factor \|
6563	LGALS3	lectin, galactoside-binding, soluble, 3	1	galectin 3 \|
9508	PSEN1	presenilin 1 (Alzheimer disease 3)	1	presenilin 1 \|
12405	TTR	transthyretin (prealbumin, amyloidosis type I)	1	transthyretin \|
9393	PRKCA	protein kinase C, alpha	1	protein kinase c \|

Targets by SciMiner Full list

HUGO ID	Symbol	Name	ActualStr	Score	FlankingText
2197	COL1A1	collagen, type I, alpha 1	collagen	0.3	Pentosidine increases in skin collagen and lens crystallin rectilinearly with age
7739	NEFL	neurofilament, light polypeptide 68kDa	NF-L	1.6	have three isoforms which are referred to as light (NF-L), NF-L medium (NF-M), NF-M and heavy chains (NF-H) NF-H
7734	NEFM	neurofilament, medium polypeptide 150kDa	NF-M	1.6	which are referred to as light (NF-L), NF-L medium (NF-M), NF-M and heavy chains (NF-H) NF-H
7737	NEFH	neurofilament, heavy polypeptide 200kDa	NF-H	0.6	light (NF-L), NF-L medium (NF-M), NF-M and heavy chains (NF-H) NF-H
7737	NEFH	neurofilament, heavy polypeptide 200kDa	NF-H	0.6	The tail domain of NF-H has multiple repeats of Lys_amp_#x2013 Ser_amp_#x2013 Pro (KSP), KSP accounting
6893	MAPT	microtubule-associated protein tau	tau	0.9	Inclusion bodies and intracellular deposits associated with tau are implicated in AD and other neurodegenerative diseases
6893	MAPT	microtubule-associated protein tau	tau	0.9	The glycation of tau has also been extensively studied with regard to AD 49
6893	MAPT	microtubule-associated protein tau	tau	0.9	probed in soluble and insoluble PHF (paired paired helical filaments -tau from AD brains using anti-CML antibody
6893	MAPT	microtubule-associated protein tau	tau	0.9	The results demonstrated that tau becomes glycated in PHF-tau and that the glycation may play
6893	MAPT	microtubule-associated protein tau	tau	0.9	Glycated tau exhibited a loss of capacity in the promotion of microtubule
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	Since mutations of the superoxide dismutase-1 (SOD-1) SOD-1 gene were first identified in 1993 it has been considered
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	Bredesen advocated the possibility that SOD-1 even plays a role in sporadic ALS 7
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	The glycation of SOD-1 under diabetic conditions has been studied extensively by Taniguchi et
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	Glycation prompts the degradation of SOD-1 70
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	the lens of diabetic rats glycation and the degradation of SOD-1 were clearly recognized 104
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	Mutant SOD-1 is more easily glycated than normal SOD-1 and would therefore
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	Mutant SOD-1 is more easily glycated than normal SOD-1 and would therefore be more rapidly degraded
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	In addition mutant SOD-1 has a low affinity for copper
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	Copper released from mutant or glycated SOD-1 would promote the generation of hydroxyl radicals by the Fenton
2728	DDOST	dolichyl-diphosphooligosaccharide-protein glycosyltransferase	AGE-R1	3.3	receptor function three proteins have been reported as AGE-binding proteins AGE-R1 (oligosaccharyl oligosaccharyl transferase complex protein 48 (OST48)), OST48 AGE-R2 (80K-H
2728	DDOST	dolichyl-diphosphooligosaccharide-protein glycosyltransferase	OST48	3.0	AGE-binding proteins AGE-R1 (oligosaccharyl oligosaccharyl transferase complex protein 48 (OST48)), OST48 AGE-R2 (80K-H 80K-H protein and AGE-R3 (galectin-3) galectin-3
9411	PRKCSH	protein kinase C substrate 80K-H	AGE-R2	3.5	proteins AGE-R1 (oligosaccharyl oligosaccharyl transferase complex protein 48 (OST48)), OST48 AGE-R2 (80K-H 80K-H protein and AGE-R3 (galectin-3) galectin-3
620	APP	amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)	amyloid	1.0	al demonstrated that RAGE and SR mediate cell adhesion to amyloid _amp_#x3b2 protein (A_amp_#x3b2;) A_amp_#x3b2 and induction of oxidative stress 118
5013	HMOX1	heme oxygenase (decycling) 1	HO-1	1.0	AGE coexisted with hemeoxygenase-1 (HO-1) HO-1 on neurofibrillary tangles 119
5013	HMOX1	heme oxygenase (decycling) 1	HO-1	1.0	Since HO-1 is induced under oxidative stress it was speculated that reactive
6893	MAPT	microtubule-associated protein tau	tau	0.9	it was speculated that reactive oxygen species were produced by tau modified with AGE leading to the induction of HO-1
5013	HMOX1	heme oxygenase (decycling) 1	HO-1	1.0	by tau modified with AGE leading to the induction of HO-1
6893	MAPT	microtubule-associated protein tau	tau	0.9	In vitro glycation of A_amp_#x3b2 tau and apoprotein E (apoE), apoE and their effects were investigated
613	APOE	apolipoprotein E	apoprotein	1.0	In vitro glycation of A_amp_#x3b2 tau and apoprotein E (apoE), apoE and their effects were investigated
613	APOE	apolipoprotein E	apoE	1.0	In vitro glycation of A_amp_#x3b2 tau and apoprotein E (apoE), apoE and their effects were investigated
6893	MAPT	microtubule-associated protein tau	tau	0.9	In addition to hyperphosphorylation the glycation of tau leads to the formation of paired helical filaments in AD
613	APOE	apolipoprotein E	apoE	1.0	The glycation of apoE impairs its binding to heparin 93
6893	MAPT	microtubule-associated protein tau	tau	0.9	AGE-modified tau produced reactive oxygen species in cultured cells and also caused
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	iNOS	2.7	Wong et al reported that AGE-positive astrocytes and microglia expressing iNOS were found in AD brains and concluded that the activation
620	APP	amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)	amyloid	1.0	In this study most of the amyloid core of a subset of senile plaques showed no staining
613	APOE	apolipoprotein E	apoE	1.0	major proteins of the CSF of AD patients including albumin apoE and transthyretin
613	APOE	apolipoprotein E	apoE	1.0	from plasma 90% of transthyretin synthesized by choroid plexus and apoE derived from astrocytes
613	APOE	apolipoprotein E	apoE	1.0	to in vitro glycation than does normal apoE3 while glycated apoE maintains its high binding affinity to A_amp_#x3b2 -peptide
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	NOS	2.7	by antioxidants aminoguanidine and inhibitors of nitric oxide synthase (NOS) NOS
2197	COL1A1	collagen, type I, alpha 1	collagen	0.3	survival of cultured DRG neurons were significantly reduced on glycated collagen IV and laminin 54
14374	NLRP1	NLR family, pyrin domain containing 1	NAC	0.3	of MG and 3-DG was attenuated by N -acetylcysteine (NAC) NAC
14374	NLRP1	NLR family, pyrin domain containing 1	NAC	0.3	NAC can raise intracellular GSH levels and thereby provide cells with
14374	NLRP1	NLR family, pyrin domain containing 1	NAC	0.3	In addition NAC also reacts with MG directly and reversibly to form the
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	NOS	2.7	glycation AG has antioxidant properties 81 and also inhibits inducible NOS (iNOS) iNOS 100
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	iNOS	2.7	has antioxidant properties 81 and also inhibits inducible NOS (iNOS) iNOS 100
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	iNOS	2.7	properties 81 and also inhibits inducible nitric oxide synthase (iNOS) iNOS 100
620	APP	amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)	amyloid	1.0	al reported preliminary findings suggesting that cross-link breakers can disaggregate amyloid deposits 111
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	Familial ALS and SOD-1
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	evidence that more than 50 mutations in the gene for SOD-1 the cytosolic copper/zinc-binding copper zinc-binding dimeric form of a protective
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	A discussion of FALS with SOD-1 mutations is complicated because transgenic expression of different SOD-1 mutants
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	with SOD-1 mutations is complicated because transgenic expression of different SOD-1 mutants in both mice and rats causes an ALS-like syndrome
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	mice and rats causes an ALS-like syndrome independently of whether SOD-1 catalytic activity is changed
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	These observations suggest that a novel gain-of-function effect of mutant SOD-1 may have a pathogenic role in FALS 33 and 85
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	First an increase in the peroxidase activity of mutant SOD-1 leading to hydroxyl radical production was assumed while several authors
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	argued against the copper-mediated theory of motor neuron degeneration in SOD-1 mutant mice 101
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	Finally mutant SOD-1 has a tendency to form aggregates spontaneously 31 and 89
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	phosphorylated neurofilament protein are the characteristic markers of FALS with SOD-1 mutations
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	Shibata et al 83 demonstrated the presence of intense SOD-1 immunoreactivity in the NHIs of FALS patients with a heterozygous
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	to Val substitution at codon 4 (Ala4Val) Ala4Val in the SOD-1 gene
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	Of added interest is a recent report that mutant SOD-1 expressed in cultured cells abnormally aggregates in the cytoplasm 12.1.3
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	heterozygous Ala to Val substitution at codon 4 in the SOD-1 gene 83
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	No focal collection of either CML or SOD-1 was found in neurons of the controls
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	In the light of evidence that SOD-1 is a protein that is susceptible to the Maillard reaction
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	Maillard reaction the finding of the coexistence of CML and SOD-1 in NHIs points to the possibility that CML-modified SOD-1 is
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	and SOD-1 in NHIs points to the possibility that CML-modified SOD-1 is deposited in NHIs
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	with familial ALS have been shown to contain not only SOD-1 but also phosphorylated NFP and ubiquitin
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	The decreased activity of SOD-1 by glycation is not necessarily considered to be the sole
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1-positive	1.4	Kato et al 35 and 37 found SOD-1-positive inclusions in astrocytes (astrocytic astrocytic hyaline inclusions or AHIs as
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	as in neurons (NHIs) NHIs in patients with FALS with SOD-1 mutations and in transgenic mice expressing human SOD-1 with the
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	FALS with SOD-1 mutations and in transgenic mice expressing human SOD-1 with the G85R mutation
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	conducted in the spinal cords of FALS patients with the SOD-1 mutation (A4V) A4V in sporadic ALS patients and in age-matched
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	NOSs	2.7	pentosidine were negative for stress-response proteins (SRPs), SRPs HNE acrolein NOSs and nitrotyrosine as representative markers of oxidative stress 35
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1-related	1.4	of pyrraline and imidazolone supports the non-oxidative mechanism in the SOD-1-related degeneration of motor neurons
2728	DDOST	dolichyl-diphosphooligosaccharide-protein glycosyltransferase	AGE-R1	3.3	receptors (other other than RAGE reported in the human brain AGE-R1 (oligosaccharyltransferase oligosaccharyltransferase family and AGE-R2 (substrate substrate of protein kinase
9411	PRKCSH	protein kinase C substrate 80K-H	AGE-R2	3.5	reported in the human brain AGE-R1 (oligosaccharyltransferase oligosaccharyltransferase family and AGE-R2 (substrate substrate of protein kinase C have been found in
2728	DDOST	dolichyl-diphosphooligosaccharide-protein glycosyltransferase	AGE-R1	3.3	and three FALS and three control brains with antibodies against AGE-R1 and AGE-R2 13
9411	PRKCSH	protein kinase C substrate 80K-H	AGE-R2	3.5	and three FALS and three control brains with antibodies against AGE-R1 and AGE-R2 13
9411	PRKCSH	protein kinase C substrate 80K-H	AGE-R2	3.5	FALS and three control brains with antibodies against AGE-R1 and AGE-R2 13
2728	DDOST	dolichyl-diphosphooligosaccharide-protein glycosyltransferase	AGE-R1	3.3	They found that AGE-R1 immunoreactivity was co-localized with those of AGE SOD-1 and neurofilaments
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD-1	2.7	found that AGE-R1 immunoreactivity was co-localized with those of AGE SOD-1 and neurofilaments 12.7
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	SOD	1.7	SOD and catalase activities were not changed suggesting that specific defects
14374	NLRP1	NLR family, pyrin domain containing 1	NAC	0.3	To test this possibility we added glutathione-augmenting agents such as NAC and glutathione ethyl ester (GEE) GEE 24 h before MG
10417	RPS27A	ribosomal protein S27a	ubiquitin	1.0	protein cross linkage results in aggregates which then form intracellular protease resistant and ubiquitin proteasome resistant deposits consequently inhibiting the intracellular transport of materials.
7739	NEFL	neurofilament, light polypeptide 68kDa	nf l	1.0	neurofilaments have three isoforms which are referred to as light nf l medium nf m and heavy chains nf h .
7734	NEFM	neurofilament, medium polypeptide 150kDa	nf m	1.0	neurofilaments have three isoforms which are referred to as light nf l medium nf m and heavy chains nf h .
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	superoxide dismutase 1	1.0	since mutations of the superoxide dismutase 1 sod 1 gene were first identified in 1993 it has been considered a possible cause of familial als fals [ 76 ].
6563	LGALS3	lectin, galactoside-binding, soluble, 3	galectin 3	1.0	e as yet unknown with regard to receptor function three proteins have been reported as age binding proteins: age r1 oligosaccharyl transferase complex protein 48 ost48 age r2 80k h protein and age r3 galectin 3 .
2728	DDOST	dolichyl-diphosphooligosaccharide-protein glycosyltransferase	age r1	1.0	although many are as yet unknown with regard to receptor function three proteins have been reported as age binding proteins: age r1 oligosaccharyl transferase complex protein 48 ost48 age r2 80k h protein and age r3 galectin 3 .
9411	PRKCSH	protein kinase C substrate 80K-H	80k h protein	1.0	although many are as yet unknown with regard to receptor function three proteins have been reported as age binding proteins: age r1 oligosaccharyl transferase complex protein 48 ost48 age r2 80k h protein and age r3 galectin 3 .
11892	TNF	tumor necrosis factor (TNF superfamily, member 2)	tumor necrosis factor	1.0	a_amp_#x3b2; induces the production of tumor necrosis factor _amp_#x3b1; by microglia.
9508	PSEN1	presenilin 1 (Alzheimer disease 3)	presenilin 1	1.0	m_amp_#xfc;nch et al. reported that the accumulation of intracellular age was observed in up to 95% of pyramidal neurons in patients with presenilin 1 mutations [ 60 ].
5013	HMOX1	heme oxygenase (decycling) 1	ho 1	1.0	age coexisted with hemeoxygenase 1 ho 1 on neurofibrillary tangles [ 119 ].
5013	HMOX1	heme oxygenase (decycling) 1	ho 1	1.0	since ho 1 is induced under oxidative stress it was speculated that reactive oxygen species were produced by tau modified with age leading to the induction of ho 1.
399	ALB	albumin	albumin	1.0	an increased accumulation of amadori products was found in all major proteins of the csf of ad patients including albumin apoe and transthyretin.
399	ALB	albumin	albumin	1.0	glycation in albumin normalized on protein quantity was nearly 1.5 times greater in ad patients than in controls total csf glycation of the samples was 8.9 and 3.1 arbitrary units/_amp_#x3bc;g of protein respectively .
399	ALB	albumin	albumin	1.0	this demonstrated that increased csf glycation in ad is not due to a specific protein modification because all major csf proteins of different origin are involved in the process albumin from plasma 90% of transthyretin synthesized by choroid plexus and apoe derived from astrocytes .
12405	TTR	transthyretin (prealbumin, amyloidosis type I)	transthyretin	1.0	demonstrated that increased csf glycation in ad is not due to a specific protein modification because all major csf proteins of different origin are involved in the process albumin from plasma 90% of transthyretin synthesized by choroid plexus and apoe derived from astrocytes .
4323	GLO1	glyoxalase I	glyoxalase i	1.0	glyoxalase i catalyzes the conversion of mg to s lactoylglutathione which in turn is converted to lactate by glyoxalase ii [ 91 ].
4805	HAGH	hydroxyacylglutathione hydrolase	glyoxalase ii	1.0	glyoxalase i catalyzes the conversion of mg to s lactoylglutathione which in turn is converted to lactate by glyoxalase ii [ 91 ].
249	ADH1A	alcohol dehydrogenase 1A (class I), alpha polypeptide	aldehyde reductase	1.0	2 3 dg induced toxicity in pc12 cells which was suppressed by the overexpression of aldehyde reductase [ 102 ].
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	nitric oxide synthase	1.0	the cytotoxic effects were attenuated by antioxidants aminoguanidine and inhibitors of nitric oxide synthase nos .
2206	COL4A4	collagen, type IV, alpha 4	collagen iv	1.0	4 neurite production and neuronal survival of cultured drg neurons were significantly reduced on glycated collagen iv and laminin [ 54 ].
249	ADH1A	alcohol dehydrogenase 1A (class I), alpha polypeptide	aldehyde reductase	1.0	1 enzyme systems such as aldehyde reductase and glyoxalase detoxify 3 dg and mg which are the building blocks of age.
381	AKR1B1	aldo-keto reductase family 1, member B1 (aldose reductase)	aldose reductase	1.0	aldehyde reductase has been identified as a detoxication enzyme of 3 dg and mg and has homology to aldose reductase.
249	ADH1A	alcohol dehydrogenase 1A (class I), alpha polypeptide	aldehyde reductase	1.0	aldehyde reductase has been identified as a detoxication enzyme of 3 dg and mg and has homology to aldose reductase.
249	ADH1A	alcohol dehydrogenase 1A (class I), alpha polypeptide	aldehyde reductase	1.0	in pc12 cells overexpressing aldehyde reductase 3 dg toxicity was suppressed as described above [ 102 ].
249	ADH1A	alcohol dehydrogenase 1A (class I), alpha polypeptide	aldehyde reductase	1.0	aldehyde reductase however can be glycated and its enzymatic activity attenuated [ 103 ].
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	nitric oxide synthase	1.0	in addition to its suppressive effect on glycation ag has antioxidant properties [ 81 ] and also inhibits inducible nitric oxide synthase inos [ 100 ].
10417	RPS27A	ribosomal protein S27a	ubiquitin	1.0	neuronal hyaline inclusions nhis abnormal intracellular structures that appear in the soma and neurites of some of the surviving lower motor neurons and contain ubiquitin and phosphorylated neurofilament protein are the characteristic markers of fals with sod 1 mutations.
9393	PRKCA	protein kinase C, alpha	protein kinase c	1.0	among the three types of age receptors other than rage reported in the human brain age r1 oligosaccharyltransferase family and age r2 substrate of protein kinase c have been found in neurons while age r3 is restricted to glial cells.
2728	DDOST	dolichyl-diphosphooligosaccharide-protein glycosyltransferase	age r1	1.0	among the three types of age receptors other than rage reported in the human brain age r1 oligosaccharyltransferase family and age r2 substrate of protein kinase c have been found in neurons while age r3 is restricted to glial cells.
2728	DDOST	dolichyl-diphosphooligosaccharide-protein glycosyltransferase	age r1	1.0	al. investigated the distributions of these receptors in conglomerates of cortical motor neurons in eight als brains five sporadic als and three fals and three control brains with antibodies against age r1 and age r2 [ 13 ].
2728	DDOST	dolichyl-diphosphooligosaccharide-protein glycosyltransferase	age r1	1.0	they found that age r1 immunoreactivity was co localized with those of age sod 1 and neurofilaments. 12.7.
1516	CAT	catalase	catalase	1.0	sod and catalase activities were not changed suggesting that specific defects of the gsh system are more important in als.