User:JonSDSUGrad/Sandbox/TEST6 AKT1

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v-akt murine thymoma viral oncogene homolog 1

PDB rendering based on 1h10.

Available structures: 1h10, 1unp, 1unq, 1unr, 2uvm

Identifiers

Symbol(s)

AKT1; AKT; MGC99656; PKB; PRKBA; RAC; RAC-ALPHA

External IDs

OMIM: 164730 MGI: 87986 HomoloGene: 3785

Gene ontology
Molecular Function:	• protein import into nucleus, translocation • nucleotide binding • protein kinase activity • protein serine/threonine kinase activity • sugar:hydrogen ion symporter activity • ATP binding • nucleus • cytoplasm • spindle • carbohydrate metabolic process • glycogen biosynthetic process • glucose metabolic process • regulation of translation • protein amino acid phosphorylation • nitric oxide biosynthetic process • transport • apoptosis • inflammatory response • signal transduction • G-protein coupled receptor protein signaling pathway • germ cell development • insulin receptor signaling pathway • apoptotic mitochondrial changes • response to heat • response to hormone stimulus • glucose transport • protein ubiquitination • transferase activity • lamellipodium • protein catabolic process • anagen • identical protein binding • regulation of survival gene product activity • protein amino acid autophosphorylation • insulin-like growth factor receptor signaling pathway

Orthologs

Human

Mouse

n/a

Refseq

NM_001014431 (mRNA)
NP_001014431 (protein)

NM_009652 (mRNA)
NP_033782 (protein)

Location

Chr 14: 104.31 - 104.33 Mb

Chr 12: 113.1 - 113.12 Mb

Pubmed search

[1]

[2]

[edit] Summary

The serine-threonine protein kinase encoded by the AKT1 gene 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. Multiple alternatively spliced transcript variants have been found for this gene.^[1]