Aberrant activation of fundamental cellular processes, such as proliferation, migration and survival, underlies the development of numerous human pathophysiologies, including cancer. One of the most frequently hyperactivated pathways in cancer is the phosphoinositide 3-kinase (PI3K)/Akt signalling cascade. Three isoforms of the serine/threonine protein kinase Akt (Akt1, Akt2 and Akt3) function to regulate cell survival, growth, proliferation and metabolism. Strikingly, non-redundant and even opposing functions of Akt isoforms in the regulation of phenotypes associated with malignancy in humans have been described. However, the mechanisms by which Akt isoform-specificity is conferred are largely unknown. In the present review, we highlight recent findings that have contributed to our understanding of the complexity of Akt isoform-specific signalling and discussed potential mechanisms by which this isoform-specificity is conferred. An understanding of the mechanisms of Akt isoform-specificity has important implications for the development of isoform-specific Akt inhibitors and will be critical to finding novel targets to treat disease.
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Conference Article|
September 18 2014
Signalling specificity in the Akt pathway in breast cancer
Abbe R. Clark;
Abbe R. Clark
*Department of Pathology and Cancer Center, Beth Israel Deaconess Medical Center, Boston, MA 02215, U.S.A.
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Alex Toker
Alex Toker
1
*Department of Pathology and Cancer Center, Beth Israel Deaconess Medical Center, Boston, MA 02215, U.S.A.
1To whom correspondence should be addressed (email atoker@bidmc.harvard.edu).
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Publisher: Portland Press Ltd
Received:
May 30 2014
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2014 Biochemical Society
2014
Biochem Soc Trans (2014) 42 (5): 1349–1355.
Article history
Received:
May 30 2014
Citation
Abbe R. Clark, Alex Toker; Signalling specificity in the Akt pathway in breast cancer. Biochem Soc Trans 1 October 2014; 42 (5): 1349–1355. doi: https://doi.org/10.1042/BST20140160
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