AKT1

From Wikipedia, the free encyclopedia

V-akt murine thymoma viral oncogene homolog 1, also known as AKT1, is a human gene.

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:	• nucleotide binding • protein kinase activity • protein serine/threonine kinase activity • sugar:hydrogen ion symporter activity • ATP binding • transferase activity • identical protein binding
Cellular Component:	• nucleus • cytoplasm • spindle • lamellipodium
Biological Process:	• protein import into nucleus, translocation • 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 • protein catabolic process • anagen • regulation of survival gene product activity • protein amino acid autophosphorylation • insulin-like growth factor receptor signaling pathway

RNA expression pattern

More reference expression data

Orthologs

Human

Mouse

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]

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]

Mice lacking Akt1 display a 25% reduction in body mass, indicating that Akt1 is critical for transmiting growth promoting signals, most likel via the igf1 receptor. Mice lacking atk1 are also resistant to cancer: they experience considerable delay in tumor growth initiated by the large T antigen or the Neu oncogene.

[edit] References

^ Entrez Gene: AKT1 v-akt murine thymoma viral oncogene homolog 1.

[edit] Further reading

Hemmings BA (1997). "Akt signaling: linking membrane events to life and death decisions.". Science 275 (5300): 628–30. PMID 9019819.
Vanhaesebroeck B, Alessi DR (2000). "The PI3K-PDK1 connection: more than just a road to PKB.". Biochem. J. 346 Pt 3: 561–76. PMID 10698680.
Chan TO, Rittenhouse SE, Tsichlis PN (2000). "AKT/PKB and other D3 phosphoinositide-regulated kinases: kinase activation by phosphoinositide-dependent phosphorylation.". Annu. Rev. Biochem. 68: 965–1014. doi:10.1146/annurev.biochem.68.1.965. PMID 10872470.
Pekarsky Y, Hallas C, Croce CM (2001). "Molecular basis of mature T-cell leukemia.". JAMA 286 (18): 2308–14. PMID 11710897.
Dickson LM, Rhodes CJ (2004). "Pancreatic beta-cell growth and survival in the onset of type 2 diabetes: a role for protein kinase B in the Akt?". Am. J. Physiol. Endocrinol. Metab. 287 (2): E192–8. doi:10.1152/ajpendo.00031.2004. PMID 15271644.
Manning BD (2004). "Balancing Akt with S6K: implications for both metabolic diseases and tumorigenesis.". J. Cell Biol. 167 (3): 399–403. doi:10.1083/jcb.200408161. PMID 15533996.
Shinohara M, Chung YJ, Saji M, Ringel MD (2007). "AKT in thyroid tumorigenesis and progression.". Endocrinology 148 (3): 942–7. doi:10.1210/en.2006-0937. PMID 16946008.