Suppression of c-Myc-induced apoptosis by Ras signalling through PI(3)K and PKB View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1997-02

AUTHORS

Andrea Kauffmann-Zeh, Pablo Rodriguez-Viciana, Eugen Ulrich, Christopher Gilbert, Paul Coffer, Julian Downward, Gerard Evan

ABSTRACT

The viability of vertebrate cells depends on survival factors which activate signal transduction pathways that suppress apoptosis. Defects in anti-apoptotic signalling pathways are implicated in many pathologies including cancer, in which apoptosis induced by deregulated oncogenes must be forestalled for a tumour to become established. Phosphatidylinositol-3-kinase (PI(3)K) is involved in the intracellular signal transduction of many receptors and has been implicated in the transduction of survival signals in neuronal cells1. We therefore examined the role of PI(3)K, its upstream effector Ras2, and its putative downstream protein kinase effectors PKB/Akt3,4 and p70S6K (ref. 5) in the modulation of apoptosis induced in fibroblasts by the oncoprotein c-Myc. Here we show that Ras activation of PI(3)K suppresses c-Myc-induced apoptosis through the activation of PKB/Akt but not p70S6K. However, we also found that Ras is an effective promoter of apoptosis, through the Raf pathway. Thus Ras activates contradictory intracellular pathways that modulate cell viability. Induction of apoptosis by Ras may be an important factor in limiting the expansion of somatic cells that sustain oncogenic ras mutations.cells More... »

PAGES

544-548

Journal

TITLE

Nature

ISSUE

6616

VOLUME

385

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/385544a0

DOI

http://dx.doi.org/10.1038/385544a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1031372205

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9020362


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