PIK3CA

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PIK3CA

A gene on chromosome 3q26.3 that encodes the 110-kDa catalytic subunit of phosphatidylinositol 3-kinase, which uses ATP to phosphorylate phosphatidylinositol, phosphatidylinositol4P and phosphatidylinositol(4,5)P2.
 
Molecular pathology
PIK3CA is oncogenic and been implicated in cervical cancers.
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They studied chordoma tumours from 104 patients and found that 16 per cent of the tumour samples had genetic changes, or mutations, in PI3K signalling genes.
5] Nonstandard abbreviations: PIP3, phosphatidylinositol 3,4,5-trisphosphate; PKB, protein kinase B; PI3K, phosphatidylinositol 3-kinase; APC, anaphase-promoting complex.
Previous investigations also revealed that CPT inhibited signaling pathways of PI3K and mTOR, and regulated expression of downstream molecules, which led to attenuation of cancer development (Ge et al.
On the other hand, a number of recent studies have indicated that "ischemia/reperfusion injury salvage," including PI3K and Akt activation, played a vital role in the process of myocardium I/R [50, 51].
Verastem identified that the dual inhibition of both mTORC1/2 and PI3K preferentially kills cancer stem cells through the use of the company's in vitro cancer stem cell screening platform and multiple in vivo models of human cancer.
Such forward-looking statements include those regarding the Company's expectations about: the timing of data and updates from clinical trials of its PI3K and Hsp90 programs; its ability to execute on its strategic plans; the therapeutic potential of its PI3K inhibitors and retaspimycin HCl; its 2013 research and development goals, including without limitation clinical and nonclinical development plans, for its PI3K program and its Hsp90 program; and dose optimization strategies.
326]Ile and the two silent polymorphs appeared to have no functional effect on the insulin stimulated PI3K activity.
NRAS, BRAF, and PI3K activating mutations, (5) as well as loss of PTEN (6-9) may also render anti-EGFR-based therapy ineffective, although this is less well established than for KRAS mutations.
The combination therapy targets the RAS/RAF/MEK and PI3K pathways, which are among the most commonly mutated in cancer.
Similarly, reduced expression of signalling pathway components such as phosphatase and tensin homologue (PTEN) involved in negative regulation of PI3K signalling, by dephosphorylating PIP3 in this signal transduction pathway, may prevent the anti-tumour effects of the antibody.
La via de la PI3K es estimulada fisiologicamente como consecuencia de la activacion de receptores de membrana tirosina kinasa, los cuales autofosforilan y fosforilan el sustrato del receptor de insulina (IRS); este ultimo, a la vez, fosforilara la subunidad p85 de la PI3K (Figura 1).
On inhibition of the PI3K activity there was absence of phosphorylation of downstream effectors in the limbal epithelial cells from the explant culture over the intact HAM.