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Titolo:
PTEN expression causes feedback upregulation of insulin receptor substrate2
Autore:
Simpson, L; Li, J; Liaw, D; Hennessy, I; Oliner, J; Christians, F; Parsons, R;
Indirizzi:
Columbia Univ Coll Phys & Surg, Inst Canc Genet, New York, NY 10032 USA Columbia Univ Coll Phys & Surg New York NY USA 10032 w York, NY 10032 USA Affymetrix, Santa Clara, CA 95051 USA Affymetrix Santa Clara CA USA 95051Affymetrix, Santa Clara, CA 95051 USA
Titolo Testata:
MOLECULAR AND CELLULAR BIOLOGY
fascicolo: 12, volume: 21, anno: 2001,
pagine: 3947 - 3958
SICI:
0270-7306(200106)21:12<3947:PECFUO>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
FORKHEAD TRANSCRIPTION FACTOR; TUMOR-SUPPRESSOR GENE; CELL-SURVIVAL; TYROSINE PHOSPHORYLATION; CAENORHABDITIS-ELEGANS; PHOSPHATASE-ACTIVITY; SIGNALING PATHWAY; BREAST-CANCER; SERINE/THREONINE PHOSPHORYLATION; PHOSPHATIDYLINOSITOL 3-KINASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
64
Recensione:
Indirizzi per estratti:
Indirizzo: Parsons, R Columbia Univ Coll Phys & Surg, Inst Canc Genet, 1150 St Nicholas Ave,RussBerrie Pavil,Rm 302, New York, NY 10032 USA Columbia Univ Coll Phys & Surg 1150 St Nicholas Ave,Russ Berrie Pavil,Rm 302 New York NY USA 10032
Citazione:
L. Simpson et al., "PTEN expression causes feedback upregulation of insulin receptor substrate2", MOL CELL B, 21(12), 2001, pp. 3947-3958

Abstract

PTEN is a tumor suppressor that antagonizes phosphatidylinositol-3 kinase (PI3K) by dephosphorylating the D3 position of phosphatidylinositol (3,4,5)-triphosphate (PtdIns-3,4,5-P3). Given the importance of PTEN in regulatingPtdIns-3,4,5-P3 levels, we used Affymetrix GeneChip arrays to identify genes regulated by PTEN. PTEN expression rapidly reduced the activity of Akt, which was followed by a G(1) arrest and eventually apoptosis. The gene encoding insulin receptor substrate 2 (IRS-2), a mediator of insulin signaling,was found to be the most induced gene at all time points. A PI3K-specific inhibitor, LY294002, also upregulated IRS-2, providing evidence that it wasthe suppression of the PI3K pathway that was responsible for the message upregulation. In addition, PTEN, LY294002, and rapamycin, an inhibitor of mammalian target of rapamycin, caused a reduction in the molecular weight of IRS-2 and an increase in the association of IRS-2 with PI3K. Apparently, PTEN inhibits a negative regulator of IRS-2 to upregulate the IRS-2-PI3K interaction. These studies suggest that PtdIns-3,4,5 P3 levels regulate the specific activity and amount of IRS-2 available for insulin signaling.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 07:05:45