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Erschienen in: Breast Cancer Research 2/2011

01.12.2011 | Oral presentation

The phosphatidylinositol-3 kinase/mTOR pathway: new agents

verfasst von: CL Arteaga

Erschienen in: Breast Cancer Research | Sonderheft 2/2011

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Excerpt

The phosphatidylinositol-3 kinase (PI3K) pathway is overall the most frequently mutated pathway in cancer, with mutation and/or amplification of the genes encoding the PI3K catalytic subunits p110α (PIK3CA) and p110β (PIK3CB), the PI3K regulatory subunit p85α (PIK3R1), receptor tyrosine kinases (RTKs) such as HER2 (ERBB2) and FGFR1, the PI3K activator K-Ras, the PI3K effectors AKT1, AKT2, and PDK1, and loss of the lipid phosphatases PTEN and INPP4B. PI3K is activated by growth factor RTKs and G-protein-coupled receptors (GPCRs). PI3K activates Akt, which, in turn, phosphorylates and inactivates Tuberin (TSC2), a GTPase-activating protein of the Ras homologue Rheb. Inactivation of Tuberin allows GTP-bound Rheb to accumulate and activate the mTOR/Raptor (TORC1) complex, which regulates protein synthesis and cell growth. mTOR also couples with Rictor to form the TORC2 complex, which phosphorylates and activates AKT. …
Metadaten
Titel
The phosphatidylinositol-3 kinase/mTOR pathway: new agents
verfasst von
CL Arteaga
Publikationsdatum
01.12.2011
Verlag
BioMed Central
Erschienen in
Breast Cancer Research / Ausgabe Sonderheft 2/2011
Elektronische ISSN: 1465-542X
DOI
https://doi.org/10.1186/bcr3007

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