Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. STKE, 7 December 1999
Vol. 1999, Issue 11, p. tw2
[DOI: 10.1126/stke.1999.11.tw2]

EDITORS' CHOICE

Apoptosis Presence of p53 May Count in Cell Survival

Adhesion of cells to the extracellular matrix regulates cell survival through the activation of cell surface integrins and their associated signaling pathways. The laminin receptor α6β4 is one example of an integrin that appears to both promote cell survival and induce apoptosis, depending on the cell type. Bachelder et al. examined how this integrin mediates both responses in various carcinoma cell lines and found that when cells were deficient in the p53 tumor suppressor protein, α6β4 promoted cell survival through activation of the serine-threonine kinase AKT/Protein Kinase B (PKB). However, when p53 was expressed, activation of this integrin induced apoptosis instead. AKT/PKB inactivation occurred, in the presence of p53, through cleavage events that were initiated by caspase 3, an enzyme implicated in other p53-dependent apoptotic pathways. These findings suggest the contradictory functions of α6β4 may be associated with the presence of p53. Hence, it is possible that AKT/PKB is a mechanistic link in some cell types between tumor suppressor function and integrin signaling.

Bachelder, R.E., Ribick, M.J., Marchetti, A., Falcioni, R., Soddu, S., Davis, K.R., and Mercurio, A.M. (1999) p53 inhibits α6β4 integrin survival signaling by promoting the caspase 3-dependent cleavage of AKT/PKB. J. Cell Biol. 147: 1063-1072. [Abstract] [Full Text]

Citation: Presence of p53 May Count in Cell Survival. Sci. STKE 1999, tw2 (1999).


To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882