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Titolo:
VHL induces renal cell differentiation and growth arrest through integration of cell-cell and cell-extracellular matrix signaling
Autore:
Davidowitz, EJ; Schoenfeld, AR; Burk, RD;
Indirizzi:
Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Dept Microbiol & Immunol, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 Immunol, Bronx, NY 10461 USA Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Dept Pediat, Bronx,NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 pt Pediat, Bronx,NY 10461 USA Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Dept Epidemiol & Social Med, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 cial Med, Bronx, NY 10461 USA Albert Einstein Coll Med, Albert Einstein Comprehens Canc Ctr, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 Canc Ctr, Bronx, NY 10461 USA
Titolo Testata:
MOLECULAR AND CELLULAR BIOLOGY
fascicolo: 3, volume: 21, anno: 2001,
pagine: 865 - 874
SICI:
0270-7306(200102)21:3<865:VIRCDA>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-SUPPRESSOR GENE; POLYCYSTIC KIDNEY-DISEASE; HIPPEL-LINDAU GENE; AMINOPEPTIDASE-N PROMOTER; UBIQUITIN LIGASE; ADHESION MOLECULES; PRODUCT; PROTEIN; CARCINOMA; COMPLEX;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Burk, RD Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Dept Microbiol & Immunol, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 Bronx, NY 10461 USA
Citazione:
E.J. Davidowitz et al., "VHL induces renal cell differentiation and growth arrest through integration of cell-cell and cell-extracellular matrix signaling", MOL CELL B, 21(3), 2001, pp. 865-874

Abstract

Mutations in the von Hippel-Lindau (VHL) gene are involved in the family cancer syndrome for which it is named and the development of sporadic renal cell cancer (RCC), Reintroduction of VHL into RCC cells lacking functional VHL [VHL(-)] can suppress their growth in nude mice, but not under standardtissue culture conditions, To examine the hypothesis that the tumor suppressor function of VHL requires signaling through contact with extracellular matrix (ECM), 786-O VHL(-) RCC cells and isogenic sublines stably expressing VHL gene products [VHL(+)] were grown on ECMs, Cell-cell and cell-ECM signalings were required to elicit VHL-dependent differences in growth and differentiation. VHL(+) cells differentiated into organized epithelial sheets,whereas VHL(-) cells were branched and disorganized. VHL(+) cells growth to high density on collagen I underwent growth arrest, whereas VHL(-) cells continued to proliferate. Integrin levels were up-regulated in VHL(-) cells, and cell adhesion was down-regulated in VHL(+) cells during growth at high cell density. Hepatocyte nuclear factor Icu, a transcription factor and global activator of proximal tubule-specific genes in the nephron, was markedly up-regulated in VHL(+) cells grown at high cell density. These data indicate that VHL can induce renal cell differentiation and mediate growth arrest through integration of cell-cell and cell-ECM signals.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/01/21 alle ore 06:24:13