AKT1

V-akt murine thymoma viral oncogene homolog 1, also known as AKT1, is a human gene. PBB_Summary
section_title =
summary_text = 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. [cite web | title = Entrez Gene: AKT1 v-akt murine thymoma viral oncogene homolog 1| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=207| accessdate = ]

Mice lacking Akt1 display a 25% reduction in body mass, indicating that Akt1 is critical for transmitting 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.

References

Further reading

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

ee also

*AKT - the AKT family of proteins
*AKT2 - the gene for the second member of the AKT family
*AKT3 - the gene for the third member of the AKT family

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