Ignet

Gene Information

Gene symbol: ALDH9A1

Gene name: aldehyde dehydrogenase 9 family, member A1

HGNC ID: 412

Synonyms: E3

Related Genes

#	Gene Symbol	Number of hits
1	AATF	1 hits
2	ACE	1 hits
3	ADH1B	1 hits
4	ADH4	1 hits
5	ADIPOQ	1 hits
6	AGTR1	1 hits
7	AKR1B1	1 hits
8	ALDH1A1	1 hits
9	ALDH2	1 hits
10	APOE	1 hits
11	ARD1A	1 hits
12	ATF3	1 hits
13	AVPR2	1 hits
14	BCHE	1 hits
15	BRD2	1 hits
16	CAT	1 hits
17	CYP2B6	1 hits
18	GLO1	1 hits
19	GSTA1	1 hits
20	GSTCD	1 hits
21	IFNG	1 hits
22	IGF1	1 hits
23	INS	1 hits
24	ITLN1	1 hits
25	MAOA	1 hits
26	NQO1	1 hits
27	PDGFB	1 hits
28	PDGFRA	1 hits
29	PRSS1	1 hits
30	SH2D3C	1 hits
31	SOD3	1 hits
32	SPINK1	1 hits
33	TBXAS1	1 hits
34	TGFB1	1 hits

Related Sentences

#	PMID	Sentence
1	6412739	Levels of lens aldose reductase, aldehyde dehydrogenase activity, and erythrocyte NADPH-oxidising (or glyceraldehyde reductase) activity were determined in 17 diabetic and 16 nondiabetic patients undergoing cataract extraction.
2	6412739	Lens aldose reductase and aldehyde dehydrogenase activities were significantly lower in diabetics than in nondiabetics.
3	6412739	Levels of lens aldose reductase, aldehyde dehydrogenase activity, and erythrocyte NADPH-oxidising (or glyceraldehyde reductase) activity were determined in 17 diabetic and 16 nondiabetic patients undergoing cataract extraction.
4	6412739	Lens aldose reductase and aldehyde dehydrogenase activities were significantly lower in diabetics than in nondiabetics.
5	9105779	In particular, monozygotic twin studies have indicated a higher rate of concordance in non-insulin-dependent (NIDDM) than in insulin-dependent diabetes mellitus (IDDM).
6	9105779	In IDDM, 8 susceptibility loci have been identified, notably the HLA complex and insulin promotor gene.
7	9105779	Rigorous family studies have identified monogenic subtypes representing 10-15% of all NIDDM: MODY2 related to glucokinase gene mutations, MODY1 and MODY3 secondary to mutation of hepatic nuclear factors, and diabetes resulting from deletion or mutation of mitochondrial DNA.
8	9105779	Finally, susceptibility genes for the increased severity and frequency of vascular complications have been identified, such as angiotensin converting enzyme, aldose reductase and aldehyde dehydrogenase genes.
9	9575688	A case control study on male primary hepatocellular carcinoma(HCC) and hepatitis B or C virus and some potential risk factors, e.g. blood transfusion, aldehyde dehydrogenase 2(ALDH2) genotype and drinking habits, was performed using two controls, i.e. a hospital control(HC) and a community control(CC) in Fukuoka and Saga Prefectures.
10	9752691	[Aldehyde dehydrogenase 2(ALDH2) gene polymorphism in NIDDM patients with chronic renal failure].
11	9752691	In order to investigate the influence of aldehyde dehydrogenase 2(ALDH2) genotype in the pathogenesis of nephropathy due to non-insulin dependent diabetes mellitus (NIDDM), genotyping of ALDH2 was measured using the PCR-RFLP method in patients with NIDDM on chronic hemodialysis (HD).
12	9752691	[Aldehyde dehydrogenase 2(ALDH2) gene polymorphism in NIDDM patients with chronic renal failure].
13	9752691	In order to investigate the influence of aldehyde dehydrogenase 2(ALDH2) genotype in the pathogenesis of nephropathy due to non-insulin dependent diabetes mellitus (NIDDM), genotyping of ALDH2 was measured using the PCR-RFLP method in patients with NIDDM on chronic hemodialysis (HD).
14	10812837	Polymorphism and the induction/inhibition of drug-metabolizing enzymes, such as cytochrome P450, aldehyde dehydrogenase (ALDH), glutathione S-transferase (GST), N-acetyltransferase (NAT), and NAD(P)H-quinone oxidoreductase (NQO1), were reviewed in relation to susceptibility to disease and to inter-individual difference in biological monitorings.
15	10812837	Investigation of such situations has generated data implicating GSTT1, GSTM1, NAT2, and NQO1 polymorphisms in biological monitoring of some chemicals; the ALDH2 polymorphism is the likely link between the genotype and the metabolism of low molecular aliphatic aldehydes.
16	12452318	About half of Japanese show an extremely high sensitivity to alcohol (ethanol), which is due to a missense mutation from glutamic acid (Glu) to lysine (Lys) at codon 487 in an isoenzyme of aldehyde dehydrogenase (ALDH2) with a low Km.
17	12604221	Methylglyoxal metabolism and diabetic complications: roles of aldose reductase, glyoxalase-I, betaine aldehyde dehydrogenase and 2-oxoaldehyde dehydrogenase.
18	15131119	White adipose tissue of FIRKO mice is also characterized by a polarization into two major populations of adipocytes, one small (<50 microm) and one large (>100 microm), which differ with regard to basal triglyceride synthesis and lipolysis, as well as in the expression of fatty acid synthase, sterol regulatory element-binding protein 1c, and CCAAT/enhancer-binding protein alpha (C/EBP-alpha).
19	15131119	These alterations exhibited 10 defined patterns and occurred in response to two distinct regulatory effects. 63 genes were identified as changed in expression depending primarily upon adipocyte size, including C/EBP-alpha, C/EBP-delta, superoxide dismutase 3, and the platelet-derived growth factor receptor. 48 genes were regulated primarily by impairment of insulin signaling, including transforming growth factor beta, interferon gamma, insulin-like growth factor I receptor, activating transcription factor 3, aldehyde dehydrogenase 2, and protein kinase Cdelta.
20	15131119	These data suggest an intrinsic heterogeneity of adipocytes with differences in gene expression related to adipocyte size and insulin signaling.
21	15318096	ALDH2/ADH2 polymorphism associated with vasculopathy and neuropathy in type 2 diabetes.
22	15318096	A mechanism of CPAF has been regarded as the inhibition of aldehyde dehydrogenase 2 (ALDH2) by an N-alkyl-substituted derivative of chlorpropamide, and the expression of these mutations of ALDH2 and alcohol dehydrogenase 2 (ADH2) could determine the alcohol tolerance among the Japanese population.
23	15318096	Therefore, we hypothesized that expression of different ALDH2 and ADH2 polymorphisms may induce differences in vascular complications in diabetes and conducted two studies.
24	15318096	To know the association of ALDH2/AHD2 polymorphism with diabetic vasculopathy and neuropathy, a total of 158 patients with type 2 diabetes were divided into four groups on the basis of ALDH2 "activity" and ADH2 "superactivity."
25	15318096	The frequency of proteinuria and the percentage of proliferative retinopathy among the patients with retinopathy was higher in those with active ALDH2 and superactive ADH2.
26	15318096	We speculated that protein kinase C isoforms up-regulated by 4-hydroxynonenal that was detoxified by ALDH2 and ADH2 may account for the long-term development of diabetic nephropathy and severe retinopathy.
27	15318096	As for neuropathy, the frequency of symptomatic neuropathy was higher in patients with inactive ALDH2 and usual ADH2.
28	15318096	We speculate that increased tissue levels of toxic aldehyde could result from inactive ALDH2 and usual ADH2 expression, which results in the increased level of reactive aldehyde in sensory neuron pathway, thereby causing symptomatic polyneuropathy.
29	16054982	Alcohol and its metabolites (acetaldehyde and fatty acid ethyl esters) can alter metabolic pathways involved in the inflammatory response and carcinogenesis, and they are mediated by one or more of the following mechanisms: (1) premature activation of zymogens; (2) induction of the inflammatory response through activation of nuclear transcription factors, including nuclear factor-kappa and activation protein 1; (3) increased production of reactive oxygen species, resulting in oxidative DNA damage and altered effect of dietary antioxidants; (4) activation of pancreatic stellate cells, which leads to fibrosis; (5) gene mutation in enzymes related to cytochrome P450, glutathione S-transferase, aldehyde dehydrogenase, cationic trypsinogen, and pancreatic secretory trypsin inhibitor; (6) synergistic effects of ethanol and tobacco carcinogen on NNK [nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone] metabolism; and (7) dysregulation of proliferation and apoptosis.
30	17388993	The objective of the present study was to examine the association between a polymorphism of the aldehyde dehydrogenase 2 (ALDH2) gene and lacunar infarcts of the brain.
31	18216179	Association of alcohol dehydrogenase 2 and aldehyde dehydrogenase 2 genotypes with fasting plasma glucose levels in Japanese male and female workers.
32	20797821	Butyrylcholinesterase may have a role in a number of metabolic functions and could affect the expression of insulin resistance syndrome.
33	20797821	We also demonstrated a possible pathogenic role for BChE in the common existence of insulin resistance, type 2 diabetes and Alzheimer's disease by in silico method and followed it up with a diabetic mouse study where cognition was slowed along with changes in BChE levels.
34	20797821	Using ISIS/Draw 2.5SP4, ARGUSLAB 4.0.1 and HEX 5.1. software. 3-D ligands were docked with BChE motif (from PDB).
35	20797821	Protein-protein interaction showed the following intersections with BChE UBE21, CHAT, APOE, AATF, DF ALDH9A1, PDHX, PONI PSME3 and ATP6VOA2.
36	20957334	Aldehyde dehydrogenase 2 (ALDH2) has been considered a key cardioprotective enzyme susceptible to oxidative inactivation.
37	21879339	Reduced aldehyde dehydrogenase activity and arginine vasopressin receptor 2 expression in the kidneys of male TALLYHO/JngJ mice of prediabetic age.
38	21879339	Since Swr/J mice are reported to develop diabetes insipidus and share 86.8% genotype homology with TH mice, the expression level of arginine vasopressin receptor 2 (AVPR2), a candidate protein for diabetes insipidus, was examined and determined to be significantly reduced in the kidneys of prediabetic male TH mice, compared to B6 mice.
39	22155604	The role of ALDH2 and ADH1B polymorphism in alcohol consumption and stroke in Han Chinese.
40	22155604	The genes encoding the enzymes for metabolising alcohol dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (ALDH2) - exhibit genetic polymorphism and ethnic variations.
41	22155604	The goal of this study was to determine whether the polymorphic ADH1B and ALDH2 genes are associated with stroke in male Han Chinese with high alcohol consumption.
42	22155604	Sixty-five stroke patients with a history of heavy drinking (HDS) and 83 stroke patients without such a history (NHDS) were recruited for analysis of the ADH1B and ALDH2 genotypes from the stroke registry in the Tri-Service General Hospital, Taipei, Taiwan, between January 2000 and December 2001.
43	22155604	The allelotypes of ADH1B and ALDH2 were determined using the polymerase chain reaction-restriction fragment length polymorphism method.
44	23550892	Genetic polymorphisms of alcohol dehydrogenase-1B and aldehyde dehydrogenase-2 and liver cirrhosis, chronic calcific pancreatitis, diabetes mellitus, and hypertension among Japanese alcoholic men.
45	23957476	Currently, the lack of a suitable high-throughput cellular assay hinders efforts to identify therapeutic small molecular inhibitors of aldehyde dehydrogenase, such as ALDH1A1.
46	24012905	We explored the hypothesis that exposure of cardiomyocytes to AT-II caused activation of MAO-A and also of catalase and aldehyde dehydrogenase activities, enzymes involved in degrading MAO's end products.
47	24012905	In each group of cells, MAO, catalase and aldehyde dehydrogenase activities were measured radiochemically and spectrophotometrically.
48	24012905	The same enzymes were also measured in HL-1 immortalized cardiomyocytes not exposed and exposed to AT-II (100 nM for 18 h) in the absence and in the presence of irbesartan (1 μM), an AT1 antagonist.
49	24012905	MAO-A catalase and aldehyde dehydrogenase activities were found significantly higher in D, than in N cells.
50	24012905	MAO-A positively correlated with catalase activity in D cells.
51	24012905	MAO-A and aldehyde dehydrogenase but not catalase over-activation, were prevented in DLos cells.
52	24012905	Similarly, MAO-A activity, but not catalase and aldehyde dehydrogenase increased significantly in HL-1 cells acutely exposed to AT-II and this increase was prevented when irbesartan, an AT1 antagonist was present.
53	24012905	Over-activation of cardiomyocyte MAO-A activity is among acute (18 h) and short-term (2-weeks of diabetes) cardiac effects of AT-II and a novel target of AT1 antagonists, first line treatments of diabetic cardiomyopathy.
54	24012905	We explored the hypothesis that exposure of cardiomyocytes to AT-II caused activation of MAO-A and also of catalase and aldehyde dehydrogenase activities, enzymes involved in degrading MAO's end products.
55	24012905	In each group of cells, MAO, catalase and aldehyde dehydrogenase activities were measured radiochemically and spectrophotometrically.
56	24012905	The same enzymes were also measured in HL-1 immortalized cardiomyocytes not exposed and exposed to AT-II (100 nM for 18 h) in the absence and in the presence of irbesartan (1 μM), an AT1 antagonist.
57	24012905	MAO-A catalase and aldehyde dehydrogenase activities were found significantly higher in D, than in N cells.
58	24012905	MAO-A positively correlated with catalase activity in D cells.
59	24012905	MAO-A and aldehyde dehydrogenase but not catalase over-activation, were prevented in DLos cells.
60	24012905	Similarly, MAO-A activity, but not catalase and aldehyde dehydrogenase increased significantly in HL-1 cells acutely exposed to AT-II and this increase was prevented when irbesartan, an AT1 antagonist was present.
61	24012905	Over-activation of cardiomyocyte MAO-A activity is among acute (18 h) and short-term (2-weeks of diabetes) cardiac effects of AT-II and a novel target of AT1 antagonists, first line treatments of diabetic cardiomyopathy.
62	24012905	We explored the hypothesis that exposure of cardiomyocytes to AT-II caused activation of MAO-A and also of catalase and aldehyde dehydrogenase activities, enzymes involved in degrading MAO's end products.
63	24012905	In each group of cells, MAO, catalase and aldehyde dehydrogenase activities were measured radiochemically and spectrophotometrically.
64	24012905	The same enzymes were also measured in HL-1 immortalized cardiomyocytes not exposed and exposed to AT-II (100 nM for 18 h) in the absence and in the presence of irbesartan (1 μM), an AT1 antagonist.
65	24012905	MAO-A catalase and aldehyde dehydrogenase activities were found significantly higher in D, than in N cells.
66	24012905	MAO-A positively correlated with catalase activity in D cells.
67	24012905	MAO-A and aldehyde dehydrogenase but not catalase over-activation, were prevented in DLos cells.
68	24012905	Similarly, MAO-A activity, but not catalase and aldehyde dehydrogenase increased significantly in HL-1 cells acutely exposed to AT-II and this increase was prevented when irbesartan, an AT1 antagonist was present.
69	24012905	Over-activation of cardiomyocyte MAO-A activity is among acute (18 h) and short-term (2-weeks of diabetes) cardiac effects of AT-II and a novel target of AT1 antagonists, first line treatments of diabetic cardiomyopathy.
70	24012905	We explored the hypothesis that exposure of cardiomyocytes to AT-II caused activation of MAO-A and also of catalase and aldehyde dehydrogenase activities, enzymes involved in degrading MAO's end products.
71	24012905	In each group of cells, MAO, catalase and aldehyde dehydrogenase activities were measured radiochemically and spectrophotometrically.
72	24012905	The same enzymes were also measured in HL-1 immortalized cardiomyocytes not exposed and exposed to AT-II (100 nM for 18 h) in the absence and in the presence of irbesartan (1 μM), an AT1 antagonist.
73	24012905	MAO-A catalase and aldehyde dehydrogenase activities were found significantly higher in D, than in N cells.
74	24012905	MAO-A positively correlated with catalase activity in D cells.
75	24012905	MAO-A and aldehyde dehydrogenase but not catalase over-activation, were prevented in DLos cells.
76	24012905	Similarly, MAO-A activity, but not catalase and aldehyde dehydrogenase increased significantly in HL-1 cells acutely exposed to AT-II and this increase was prevented when irbesartan, an AT1 antagonist was present.
77	24012905	Over-activation of cardiomyocyte MAO-A activity is among acute (18 h) and short-term (2-weeks of diabetes) cardiac effects of AT-II and a novel target of AT1 antagonists, first line treatments of diabetic cardiomyopathy.
78	24012905	We explored the hypothesis that exposure of cardiomyocytes to AT-II caused activation of MAO-A and also of catalase and aldehyde dehydrogenase activities, enzymes involved in degrading MAO's end products.
79	24012905	In each group of cells, MAO, catalase and aldehyde dehydrogenase activities were measured radiochemically and spectrophotometrically.
80	24012905	The same enzymes were also measured in HL-1 immortalized cardiomyocytes not exposed and exposed to AT-II (100 nM for 18 h) in the absence and in the presence of irbesartan (1 μM), an AT1 antagonist.
81	24012905	MAO-A catalase and aldehyde dehydrogenase activities were found significantly higher in D, than in N cells.
82	24012905	MAO-A positively correlated with catalase activity in D cells.
83	24012905	MAO-A and aldehyde dehydrogenase but not catalase over-activation, were prevented in DLos cells.
84	24012905	Similarly, MAO-A activity, but not catalase and aldehyde dehydrogenase increased significantly in HL-1 cells acutely exposed to AT-II and this increase was prevented when irbesartan, an AT1 antagonist was present.
85	24012905	Over-activation of cardiomyocyte MAO-A activity is among acute (18 h) and short-term (2-weeks of diabetes) cardiac effects of AT-II and a novel target of AT1 antagonists, first line treatments of diabetic cardiomyopathy.