PKB/AKT: functional insights from genetic models
By M. Scheid, J. Woodgett. Nature reviews. Molecular cell biology, 2001
640 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/2ad8bf53d285df0d589bfa09a83a563aa850e540
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Citations in the corpus
- Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale. (2010, background): “These authors proposed that the loss of p38 activity resulted in an increase in AKT activity, a known inducer of physiological hypertrophy.”
- Role for Akt3/Protein Kinase Bγ in Attainment of Normal Brain Size (2005, background): “Now that experiments with fruit flies and mice have convincingly demonstrated a role for the PI3K/Akt pathway in the control of cell and compartment size, the question arises of how specificity is achieved given the large number of regulatory processes for which Akt appears to function as an essenti”
- SIN1/MIP1 maintains rictor-mTOR complex integrity and regulates Akt phosphorylation and substrate specificity. (2006, background): “Akt plays a central role in controlling cell growth, proliferation, survival, and differentiation by phosphorylating a diverse number of protein substrates that contain a minimal consensus sequence of RXRXXS/T (Scheid and Woodgett, 2001).”
- PI3K/Akt: getting it right matters (2008, background): “Numerous studies have since examined oncogenic amplifications of different Akt genes in primary human tumors and cancer cells (for review, see Brazil and Hemmings, 2001; Scheid and Woodgett, 2001).”
- Upstream and downstream of mTOR. (2004, background): “The rate-limiting step in Akt activation is the binding of PIP3 to the pleckstrin homology (PH) domain of Akt and the subsequent translocation of Akt to the plasma membrane (Kandel and Hay 1999; Brazil and Hemmings 2001; Scheid and Woodgett 2001).”