Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Trends Biochem Sci. 2011 Jun;36(6):320-8. doi: 10.1016/j.tibs.2011.03.006. Epub 2011 Apr 30.

The Ras-ERK and PI3K-mTOR pathways: cross-talk and compensation.

Author information

  • 1Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.

Abstract

The Ras-extracellular signal-regulated kinase (Ras-ERK) and phosphatidylinositol 3-kinase-mammalian target of rapamycin (PI3K-mTOR) signaling pathways are the chief mechanisms for controlling cell survival, differentiation, proliferation, metabolism, and motility in response to extracellular cues. Components of these pathways were among the first to be discovered when scientists began cloning proto-oncogenes and purifying cellular kinase activities in the 1980s. Ras-ERK and PI3K-mTOR were originally modeled as linear signaling conduits activated by different stimuli, yet even early experiments hinted that they might intersect to regulate each other and co-regulate downstream functions. The extent of this cross-talk and its significance in cancer therapeutics are now becoming clear.

Copyright © 2011 Elsevier Ltd. All rights reserved.

PMID:
21531565
[PubMed - indexed for MEDLINE]
PMCID:
PMC3112285
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Write to the Help Desk