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Titolo:
TSC1 and TSC2 tumor suppressors antagonize insulin signaling in cell growth
Autore:
Gao, XS; Pan, DJ;
Indirizzi:
Univ Texas, SW Med Ctr, Dept Physiol, Dallas, TX 75390 USA Univ Texas Dallas TX USA 75390 ed Ctr, Dept Physiol, Dallas, TX 75390 USA
Titolo Testata:
GENES & DEVELOPMENT
fascicolo: 11, volume: 15, anno: 2001,
pagine: 1383 - 1392
SICI:
0890-9369(20010601)15:11<1383:TATTSA>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
SCLEROSIS GENE-2 PRODUCT; TUBEROUS SCLEROSIS; EMBRYONIC LETHALITY; DROSOPHILA HOMOLOG; PHOSPHOINOSITIDE 3-KINASE; RENAL CARCINOGENESIS; SIZE CONTROL; PROTEIN; IDENTIFICATION; PROLIFERATION;
Keywords:
cell size; tumor suppressor; insulin signaling; Akt;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Pan, DJ Univ Texas, SW Med Ctr, Dept Physiol, Dallas, TX 75390 USA Univ Texas Dallas TX USA 75390 Dept Physiol, Dallas, TX 75390 USA
Citazione:
X.S. Gao e D.J. Pan, "TSC1 and TSC2 tumor suppressors antagonize insulin signaling in cell growth", GENE DEV, 15(11), 2001, pp. 1383-1392

Abstract

Tuberous sclerosis is a human disease caused by mutations in the TSC1 or the TSC2 tumor suppressor gene. Previous studies of a Drosophila TSC2 homolog suggested a role for the TSC genes in maintaining DNA content, with loss of TSC2 leading to polyploidy and increased cell size. We have isolated mutations in the Drosophila homolog of the TSC1 gene. We show that TSC1 and TSC2 form a complex and function in a common pathway to control cellular growth. Unlike previous studies, our work shows that TSC1(-) or TSC2 cells are diploid. We find that, strikingly, the heterozygosity of TSC1 or TSC2 is sufficient to rescue the lethality of loss-of-function insulin receptor mutants. Further genetic analyses suggest that the TSC genes act in a parallel pathway that converges on the insulin pathway downstream from Akt. Taken together, our studies identified the TSC tumor suppressors as novel negative regulators of insulin signaling.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 09:07:08