Phosphoinositide 3-kinase in disease: timing, location, and scaffolding.

Abstract:

:When PI3Ks are deregulated by aberrant surface receptors or modulators, accumulation of PtdIns(3,4,5)P3 leads to increased cell growth, proliferation and contact-independent survival. The PI3K/PKB/TOR axis controls protein synthesis and growth, while PtdIns(3,4,5)P3-mediated activation of Rho GTPases directs cell motility. PI3K activity has been linked to the formation of tumors, metastasis, chronic inflammation, allergy and cardiovascular disease. Although increased PtdIns(3,4,5)P3 is a well-established cause of disease, it is seldom known which PI3K isoform is implied. Recent work has demonstrated that PI3Kgamma contributes to the control of cAMP levels in the cardiac system, where the protein acts as a scaffold, but not as a lipid kinase.

journal_name

Curr Opin Cell Biol

authors

Wymann MP,Marone R

doi

10.1016/j.ceb.2005.02.011

subject

Has Abstract

pub_date

2005-04-01 00:00:00

pages

141-9

issue

2

eissn

0955-0674

issn

1879-0410

pii

S0955-0674(05)00024-4

journal_volume

17

pub_type

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