PI 3-kinase, Akt and cell survival.
By Julian Downward. Seminars in Cell and Developmental Biology, 2004
840 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/9562d697f55c1a4e2d7b6d6d40496d274b9063f7
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Citations in the corpus
- A Novel Function of eIF2α Kinases as Inducers of the Phosphoinositide-3 Kinase Signaling Pathway (2007, background): “…possibility is that posttranslational regulation of anti-apoptotic or proapoptotic proteins through Akt/PKB-mediated phosphorylation results in their activation or inactivation, respectively, and thus exerts an antagonistic effect on PKR-mediated apoptosis (Franke et al., 2003; Downward, 2004).”
- Perturbations of the AKT signaling pathway in human cancer (2005, background): “AKT also phosphorylates and inactivates the proapoptotic factors BAD and procaspase-9 (reviewed in Downward, 2004).”
- The regulation of AMPK beta1, TSC2, and PTEN expression by p53: stress, cell and tissue specificity, and the role of these gene products in modulating the IGF-1-AKT-mTOR pathways. (2007, background): “The IGF-I hormone binds to and activates the IGF receptor to recruit and activate the phosphoinositide-3-kinase to the cell membrane ( 13 ).”
- PIK3CA mutations correlate with hormone receptors, node metastasis, and ERBB2, and are mutually exclusive with PTEN loss in human breast carcinoma. (2005, background): “In an elegant ‘‘on/off ’’ switch, the phosphatidylinositol 3-kinase (PI3K) holoenzyme, in response to signals transmitted via growth factor receptor tyrosine kinases, phosphorylates phosphatidylinositol-4,5-bisphosphate at the 3V-OH position of the inositol ring to form PIP3, whereas PTEN catalyzes ”
- Glycogen synthase kinase-3 regulates mitochondrial outer membrane permeabilization and apoptosis by destabilization of MCL-1. (2006, background): “Our findings add to other well-established mechanisms downstream of growth factor stimulation governing apoptosis: the phosphorylation of the BH3-only protein BAD, as well of the transcription factors FOXO1 and FOXO3a, being transcriptional inducers of FasL and BIM, mediate their retention in the cy”