The Ras-ERK and PI3K-mTOR Pathways: Cross-talk and Compensation
By Michelle C. Mendoza, E. E. Er, J. Blenis. TIBS -Trends in Biochemical Sciences. Regular ed, 2011
1,789 citations recorded by the source corpus.
The Ras-ERK (extracellular signal-regulated kinase) and PI3K (phosphatidylinositol 3-kinase)-mTOR (mammalian target of rapamycin) signaling pathways are the cell’s 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 crosstalk and its significance in cancer therapeutics are now becoming clear.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/4c6dc48b7b6901ee0076cea53a486cff899ae8c4
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Citations in the corpus
- Mechanisms and pathways of growth failure in primordial dwarfism. (2011, background): “The ERK1/2 pathway also stimulates global protein synthesis and hence cellular growth through stimulation of rapamycin (mTOR) signaling (Carriere et al. 2008; Mendoza et al. 2011).”
- Predicting ligand-dependent tumors from multi-dimensional signaling features (2017, result): “3c) compared to the other growth factors in the screen.(27,28) Further, the CellTiter-Glo® assay relies on metabolic function and hence can be limited as readout for IGF-1 stimulation.”
- A Comprehensive Review on MAPK: A Promising Therapeutic Target in Cancer (2019, background): “The mTOR complexes are key modulators of cell growth and proliferation, able to respond to GF stimulation (in a similar manner to MAPK) and finally orchestrate protein translation [49].”