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PMID: 21531565 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review

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

Trends in biochemical sciences ·Vol. 36 ·No. 6 ·2011-06-00 ·Pages 320-8

Mendoza MC, Er EE, Blenis J

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.

MeSH Terms
Extracellular Signal-Regulated MAP Kinases/metabolism Humans Phosphatidylinositol 3-Kinase/metabolism Signal Transduction TOR Serine-Threonine Kinases/metabolism ras Proteins/metabolism
Chemicals
Phosphatidylinositol 3-Kinase TOR Serine-Threonine Kinases Extracellular Signal-Regulated MAP Kinases ras Proteins
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Mendoza Michelle C
Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Er E Emrah
Blenis John
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Article Info
Journal
Trends in biochemical sciences
Abbr.
Trends Biochem Sci
ISSN
0968-0004
Published
2011-06-00
Epub
2011-00-30
Pages
320-8
Language
English
Region
England
NLM ID
7610674
PMCID
PMC3112285
Subset
IM
Grants
NIGMS NIH HHS · R01 GM051405 · United States
NCI NIH HHS · R37 CA046595 · United States
NCI NIH HHS · R37 CA046595-26 · United States
NCI NIH HHS · R37CA46595 · United States
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