The enzyme encoded by this gene is responsible for the catalysis of the 5-beta-reduction of bile acid intermediates and steroid hormones carrying a delta(4)-3-one structure. Deficiency of this enzyme may contribute to hepatic dysfunction. Three transcript variants encoding different isoforms have been found for this gene. Other variants may be present, but their full-length natures have not been determined yet.
A synthesized peptide derived from human AKR7A2, corresponding to a region within the internal amino acids.
A synthesized peptide derived from human AKR7A3, corresponding to a region within the internal amino acids.
A synthetic peptide from human AKT1
A synthesized peptide derived from human Akt, corresponding to a region within the internal amino acids.
A synthesized peptide derived from human AKT1, corresponding to a region within C-terminal amino acids.
A synthesized peptide derived from human AKT1, corresponding to a region within the internal amino acids.
A synthesized peptide derived from human AKT1.
The serine-threonine protein kinase AKT1 is catalytically inactive in serum-starved primary and immortalized fibroblasts. AKT1 and the related AKT2 are activated by platelet-derived growth factor. The activation is rapid and specific, and it is abrogated by mutations in the pleckstrin homology domain of AKT1. It was shown that the activation occurs through phosphatidylinositol 3-kinase. In the developing nervous system AKT is a critical mediator of growth factor-induced neuronal survival. Survival factors can suppress apoptosis in a transcription-independent manner by activating the serine/threonine kinase AKT1, which then phosphorylates and inactivates components of the apoptotic machinery.
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