Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
ADH5 encodes a member of the alcohol dehydrogenase family. Additionally we are shipping Alcohol Dehydrogenase 5 (Class III), chi Polypeptide Proteins (30) and Alcohol Dehydrogenase 5 (Class III), chi Polypeptide Kits (5) and many more products for this protein.
Showing 10 out of 96 products:
Human Polyclonal ADH5 Primary Antibody for ELISA, WB - ABIN188741
Adinolfi, Adinolfi, Hopkinson: Immunological and biochemical characterization of the human alcohol dehydrogenase chi-ADH isozyme. in Annals of human genetics 1984
GSNOR represents the prototype enzyme to disclose how denitrosylation plays a crucial role in tuning NO-bioactivity and how much it deeply impacts on cell homeostasis and human pathophysiology. (Review)
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 (show AVP Antibodies) and other human ADHs includes a for class V ADH (show AVP Antibodies) unique and conserved Lys51, a position directly involved in the catalytic mechanism in other ADHs, and nine other class V ADH (show AVP Antibodies)-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 (show ADH6 Antibodies) gene leads to heavy drinking in women.
common ADH (show AVP Antibodies) variants conferred risk for both schizophrenia in African-Americans and autism in European-Americans.
A decrease in ADH (show AVP Antibodies) IB, rather than GSNOR, correlates with human lung cancer.
study compared individuals occupationally exposed to formaldehyde and controls to effects of XRCC3 (show XRCC3 Antibodies) 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.
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 (show CAMK2 Antibodies) and reduces CaMKIIalpha (show CAMK2 Antibodies) 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 (show FANCD2 Antibodies), hematopoietic stem cells, hepatocytes, and nephrons from endogenous DNA damage.
S-nitrosoglutathione reductase-dependent modification of PPARgamma (show PPARG Antibodies) 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 (show HDAC2 Antibodies)).
GSNOR appears to play a crucial role in controlling pulmonary and systemic infection by K. pneumoniae.
This gene encodes class V alcohol dehydrogenase, which is 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. This gene is expressed in the stomach as well as in the liver, and it contains a glucocorticoid response element upstream of its 5' UTR, which is a steroid hormone receptor binding site. Alternatively spliced transcript variants encoding different isoforms have been found for 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 6
, aldehyde reductase
, 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