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Titolo:
Tuberous sclerosis gene products in proliferation control
Autore:
Hengstschlager, M; Rodman, DM; Miloloza, A; Hengstschlager-Ottnad, E; Rosner, M; Kubista, M;
Indirizzi:
Univ Vienna, A-1090 Vienna, Austria Univ Vienna Vienna Austria A-1090Univ Vienna, A-1090 Vienna, Austria Univ Colorado, Hlth Sci Ctr, Cardiovasc Pulm Res Lab, Ctr Genet Lung Dis, Denver, CO 80262 USA Univ Colorado Denver CO USA 80262 tr Genet Lung Dis, Denver, CO 80262 USA
Titolo Testata:
MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH
fascicolo: 3, volume: 488, anno: 2001,
pagine: 233 - 239
SICI:
1383-5742(200106)488:3<233:TSGPIP>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
EKER RAT MODEL; TUBEROUS-SCLEROSIS-2 TSC2 GENE; DOMINANTLY INHERITED CANCER; KINASE INHIBITOR P27; CELL-CYCLE CONTROL; RENAL-CARCINOMA; DNA-SYNTHESIS; HAMARTIN; SUPPRESSION; MUTATION;
Keywords:
tuberous sclerosis; TSC1; TSC2; proliferation; cell cycle;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Hengstschlager, M Univ Vienna, Wahringer Gurtel 18-20, A-1090 Vienna, Austria Univ Vienna Wahringer Gurtel 18-20 Vienna Austria A-1090
Citazione:
M. Hengstschlager et al., "Tuberous sclerosis gene products in proliferation control", MUT RES-R M, 488(3), 2001, pp. 233-239

Abstract

Two genes, TSC1 and TSC2, have been shown to be responsible for tuberous sclerosis (TSC). The detection of loss of heterozygosity of TSC1 or TSC2 in hamartomas, the growths characteristically occurring in TSC patients, suggested a tumor suppressor function for their gene products hamartin and tuberin. Studies analyzing ectopically modulated expression of TSC2 in human androdent cells together with the finding that a homolog of TSC2 regulates the Drosophila cell cycle suggest that TSC is a disease of proliferation/cellcycle control. We discuss this question including very recent data obtained from analyzing mice expressing a modulated TSC2 transgene, and from studying the effects of deregulated TSC1 expression. Elucidation of the cellularfunctions of these proteins will form the basis of a better understanding of how mutations in these genes cause the disease and for the development of new therapeutic strategies. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 11:59:21