anti-Aldehyde Dehydrogenase 2 Family (Mitochondrial) (ALDH2) Antibodies

Rabbit Aldehyde Dehydrogenase 2 Family (Mitochondrial) (ALDH2) interaction partners

1. ALDH-2 is involved in the remote ischemic preconditioning pathway.

Human Aldehyde Dehydrogenase 2 Family (Mitochondrial) (ALDH2) interaction partners

1. Patients with ALDH2 504lys variant were less associated with alcoholic liver disease compared to those with ALDH2 504glu using both genotypic and allelic analyses.

2. Our study suggested that ALDH2 rs671 L-genotypes are protective factors for hypertension in Han Chinese. Consumption of fried food accelerated the development of hypertension in individuals with poor metabolism of acetaldehyde.

3. ALDH2 genotype is associated with the tolerability and side affects to alcohol in paclitaxel in Japanese breast cancer patients.

4. The ALDH-2 rs671 polymorphism is a protective factor for essential hypertension susceptibility in man and individuals independently of alcohol consumption in Asians.

5. ALDH2 rs671 polymorphism is associated with the overall cancer risk in Asians (Meta-Analysis)

6. The results of this study demonstrated that the slow-metabolizing ADH1B Arg/Arg genotype and inactive heterozygous ALDH2 Glu/Lys genotype were positive determinants for the development of fatty liver diagnosed by ultrasonography in alcohol-dependent Japanese men.

7. Patients with T2DM and mutations in ALDH2 gene had higher levels of formaldehyde and more severe dementia.

8. Associations of complementation group, ALDH2 genotype, and clonal abnormalities with hematological outcome in Japanese patients with Fanconi anemia.

9. the present study suggested that ALDHbr cell counts in the cryopreserved attached segments may serve as a quality assessment indicator for cord blood units prior to umbilical cord blood transplantation.

10. A significant association between ALDH2 polymorphism (rs671) and gastric cancer risk.A significant interaction between ALDH2 polymorphism and alcohol drinking regarding gastric cancer risk.

11. Our results highlight that ALDH2 impairment accelerates the acquisition of a premature senescent phenotype, a change likely to be associated with the observed reduction of mitochondrial respiration and reserve capacity.

12. we identified three novel SNPs associated with ferritin in ALDH2. Men carrying the mutated genotype of rs671 have lower serum ferritin levels.

13. common variants of ADH1B and ALDH2 are independently associated with gout. Our findings likewise suggest that genotyping these variants can be useful for the evaluation of gout risk.

14. ALDH2 polymorphism is associated with Gastric and esophageal cancer.

15. The use of aldehyde dehydrogenase (ALDH) for isolating and identifying sub-populations of mesenchymal stromal cells (MSCs) with specific gene profile may represent an alternative method to provide solutions for targeted therapeutic applications.

16. The analysis of the effect of the individual SNPs(PON1, IL-6, ITGB3, and ALDH2 ) and GRS groups on different lipid profile parameters revealed no significant association of any of the tested SNPs with any lipid parameter, however, the GRS groups showed marginally significant for TC and highly significant association for TG, LDL-c and HDL-c

17. In a Chinese Han population with dyslipidemia, individuals with A/A or A/G genotypes of rs671 in the Aldehyde Dehydrogenase, Mitochondrial gene have a higher coronary artery disease risk, if they lack physical activity and take fried food regularly, than individuals with G/G genotypes.

18. aldehyde dehydrogenase 2 (ALDH2) is found to be transcriptionally regulated by VHL and contributes to enhanced anthracyclines cytotoxicity in clear cell renal cell carcinoma cells.

19. ardiac-specific expression of the human ALDH2 gene in mice augmented myocardial ALDH2 activity but did not improve cardiac function in response to pressure overload. After 12 weeks of transverse aortic constriction , ALDH2 transgenic mice had larger hearts than their wild-type littermates and lower capillary density

20. Study revealed that the rs10744777 polymorphism in ALDH2 was an independent risk factor for ischemic stroke in Chinese male, but not in Chinese female.

Cow (Bovine) Aldehyde Dehydrogenase 2 Family (Mitochondrial) (ALDH2) interaction partners

1. ALDH2-catalyzed NO formation is necessary and sufficient for nitroglycerin bioactivation in vascular smooth muscle cells.

2. ACADM and ALDH2 were predicted to be the target genes of miR-224

3. analysis of bioactivation of nitroglycerin by purified mitochondrial and cytosolic aldehyde dehydrogenases ALDH1 and ALDH2

Mouse (Murine) Aldehyde Dehydrogenase 2 Family (Mitochondrial) (ALDH2) interaction partners

1. Studied protective role of aldehyde dehydrogenase 2 (ALDH2) in association with signal pathways in high fat diet induced obesity and cardiomyopathy.

2. esults suggested that ALDH2 may rescue against doxorubicin cardiac toxicity possibly through a TRPV1-mediated protection of mitochondrial integrity.

3. These results suggested that decrease and deficiency of ALDH2 activity would significantly increase the sensitivity to ETBE-induced genotoxicity as well as hepatotoxic effects after exposure even to low concentrations of ethyl tertiary butyl ether .

4. ALDH2 deficiency attenuates compensatory cardiac hypertrophy through regulating Akt but not PI3K phosphorylation early after transverse aorta constriction. In vitro, phosphorylation of Akt was significantly accentuated and PTEN expression was reduced while PI3K phosphorylation remained unchanged in stretched cardiomyocytes pretreated by Alda-1 (a small-molecule activator of ALDH2).

5. data revealed that ALDH2 enzyme may suppress myocardial autophagy possibly through a complex JNK-Bcl-2 and IKKbeta-AMPK-dependent mechanism en route to accentuation of myocardial remodeling and contractile dysfunction in aging.

6. results thus suggest that ALDH2 is indispensable for the favorable cardiac effect of low-to-moderate alcohol consumption and ALDH2 deficiency may lead to unexpected cardiac dysfunctions via enhancing myocardial apoptosis and necroptosis.

7. ALDH2 activation improved ethanol-induced cardiac damage and decreased angiotensin and angiotensin II in hearts.

8. ALDH2 overexpression inhibited the expression of c-Jun N-terminal kinase (JNK)-1, activated protein 1 (AP-1), insulin receptor substrate 1 (IRS-1), 4- hydroxynonenal, caspase 3, transforming growth factor beta1, and collagen I and III, and enhanced Akt phosphorylation.

9. Study found ALDH2*2 diabetic mice exhibit diastolic dysfunction and preserved systolic function at rest, similar to clinical heart failure of preserved ejection fraction.

10. ALDH2 deficiency reduced the therapeutic effect of ALDHbr cells in the mice model of ischemic hind limb due to decreased anaerobic glycolysis and increased mitochondrial ROS generation.

11. osteoblast differentiation is impaired in the absence of Aldh2 gene.

12. ALDH2 plays a protective role in cyclophosphamide-induced acute hepatotoxicity via attenuating oxidative stress and detoxifying reactive aldehydes.

13. Deficiency in ALDH2 activity may contribute to increased cisplatin sensitivity and cytotoxicity by producing more ROS by the treatment.

14. our data suggest that ALDH2 serves as an indispensable cardioprotective factor against insulin resistance-induced cardiomyopathy with a mechanism possibly associated with facilitation of the Sirt3-dependent PGC-1alpha deacetylation.

15. Findings suggested that ALDH2 can influence atherosclerotic plaque development and vulnerability, and inflammation via MAPK, NF-kappaB and AP-1 signaling pathways.

16. ALDH2 deficiency triggers decompensation of metabolic reserves and energy metabolism disturbances in early diabetic hearts.

17. Results show that ALDH2 is required for a normal adipogenesis and its expression in white adipose tissue is negatively correlated with obesity. Also, the study provides evidence that PKCepsilon-ALDH2 pathway positively regulates adipocyte differentiation by regulation of PPARgamma transcriptional activity.

18. In knock-in mice in which ALDH2 enzymatic activity is maximally reduced, cardio-protection in ischemic-reperfused hearts is lacking.

19. Mitochondrial aldehyde dehydrogenase 2 (ALDH2) overexpression attenuates exhaustive exercise-induced mitochondrial oxidative stress

20. ALDH2-catalyzed NO formation is necessary and sufficient for nitroglycerin bioactivation in vascular smooth muscle cells.