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ADH5 encodes class V alcohol dehydrogenase, which is a member of the alcohol dehydrogenase family. Zusätzlich bieten wir Ihnen Alcohol Dehydrogenase 5 (Class III), chi Polypeptide Proteine (30) und Alcohol Dehydrogenase 5 (Class III), chi Polypeptide Kits (5) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal ADH5 Primary Antibody für ELISA, WB - ABIN188741
Adinolfi, Adinolfi, Hopkinson: Immunological and biochemical characterization of the human alcohol dehydrogenase chi-ADH isozyme. in Annals of human genetics 1984
It was concluded that in HepG2 cells, ADH5 is a source of formate for de novo purine biosynthesis, especially during folate deficiency when folate-dependent formate production is limited.
Local structural differences between human class V ADH (zeige AVP Antikörper) and other human ADHs includes a for class V ADH (zeige AVP Antikörper) unique and conserved Lys51, a position directly involved in the catalytic mechanism in other ADHs, and nine other class V ADH (zeige AVP Antikörper)-specific residues.
GSNOR expression has different effect on neuronal viability in dependence on the stimulus applied, and plays opposite roles in SH-SY5Y models of Parkinson's disease and amyotrophic lateral sclerosis
ADH5 counteracts neuronal differentiation of neural stem cells and this effect can be reversed by pharmacological inhibition of ADH5.
Results show that polymorphism of ADH6 (zeige ADH6 Antikörper) gene leads to heavy drinking in women.
common ADH (zeige AVP Antikörper) variants conferred risk for both schizophrenia in African-Americans and autism in European-Americans.
A decrease in ADH (zeige AVP Antikörper) IB, rather than GSNOR, correlates with human lung cancer.
study compared individuals occupationally exposed to formaldehyde and controls to effects of XRCC3 (zeige XRCC3 Antikörper) Thr241Met, ADH5 Val309Ile and Asp353Glu polymorphisms; ADH5 polymorphisms did not show significant association with genotoxicity biomarkers
Data suggest that GSNOR deficiency, through dysregulated S-nitrosylation, may promote hepatocellular carcinoma, possibly by inactivating a DNA repair system.
Significant associations were found however, for reactions to alcohol with a SNP in ADH5 (rs6827292, p = .001) and a SNP just upstream of ADH5 (rs6819724, p = .0007) that is in strong LD with rs6827292.
Report inhibition of GSNOR activity by nebivolol leading to accumulation of nitrosothiols in cells, and this is associated with an enhanced vasodilation by S-nitrosoglutathione.
Increased GSNOR expression during aging decreases S-nitrosation of CaMKIIalpha (zeige CAMK2 Antikörper) and reduces CaMKIIalpha (zeige CAMK2 Antikörper) synaptosomal accumulation.
These data indicate a role for GSNOR in the host response to malaria infection and suggest that strategies to disrupt its activity will improve clinical outcomes.
GSNOR may act as a "brake" on skeletal muscle contractile performance under physiological conditions by modulating nitrosylation/denitrosylation balance.
Loss of GSNOR confers enhanced post-MI cardiac regenerative activity, characterized by enhanced turnover of cardiomyocytes and cardiac stem cells.
Results show that ADH5 removes endogenous formaldehyde to prevent DNA adducts, and protects with FANCD2 (zeige FANCD2 Antikörper), hematopoietic stem cells, hepatocytes, and nephrons from endogenous DNA damage.
S-nitrosoglutathione reductase-dependent modification of PPARgamma (zeige PPARG Antikörper) alters the balance between adipocyte and osteoblast differentiation and provides checkpoint regulation of the lineage bifurcation of these 2 lineages.
These findings provide novel insights into the involvement of GSNOR and S-nitrosylation in neuromuscular atrophy and neuropathic pain that are associated with pathological states.
Overexpression of ADH5 reduces both development and adult neuronal differentiation of neurons. This effect depends on the catalytic activity of ADH5 and involves ADH5-mediated denitrosation of histone deacetylase 2 (HDAC2 (zeige HDAC2 Antikörper)).
GSNOR appears to play a crucial role in controlling pulmonary and systemic infection by K. pneumoniae.
This gene encodes a member of the alcohol dehydrogenase family. Members of this family metabolize a wide variety of substrates, including ethanol, retinol, other aliphatic alcohols, hydroxysteroids, and lipid peroxidation products. The encoded protein forms a homodimer. It has virtually no activity for ethanol oxidation, but exhibits high activity for oxidation of long-chain primary alcohols and for oxidation of S-hydroxymethyl-glutathione, a spontaneous adduct between formaldehyde and glutathione. This enzyme is an important component of cellular metabolism for the elimination of formaldehyde, a potent irritant and sensitizing agent that causes lacrymation, rhinitis, pharyngitis, and contact dermatitis. The human genome contains several non-transcribed pseudogenes related to this gene.
, alcohol dehydrogenase (class III), chi polypeptide
, alcohol dehydrogenase class chi chain
, alcohol dehydrogenase class-3
, alcohol dehydrogenase class-III
, formaldehyde dehydrogenase
, glutathione-dependent formaldehyde dehydrogenase
, alcohol dehydrogenase 1C (class I), gamma polypeptide
, class III alcohol dehydrogenase
, alcohol dehydrogenase 2
, alcohol dehydrogenase B2
, class III alcohol dehydrogenase, chi subunit
, S-nitrosoglutathione reductase
, alcohol dehydrogenase 5 (class III), chi polypeptide L homeolog
, alcohol dehydrogenase class 3
, alcohol dehydrogenase 4 (class II), pi polypeptide