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Titolo:
Hyperactive Ras as a therapeutic target in neurofibromatosis type 1
Autore:
Weiss, B; Bollag, G; Shannon, K;
Indirizzi:
Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Onyx Pharmaceut, Small Mol Therapeut, Richmond, CA USA Onyx Pharmaceut Richmond CA USA t, Small Mol Therapeut, Richmond, CA USA
Titolo Testata:
AMERICAN JOURNAL OF MEDICAL GENETICS
fascicolo: 1, volume: 89, anno: 1999,
pagine: 14 - 22
SICI:
0148-7299(19990326)89:1<14:HRAATT>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
NUCLEOTIDE EXCHANGE FACTOR; JUVENILE MYELOMONOCYTIC LEUKEMIA; MALIGNANT MYELOID DISORDERS; PROTEIN-KINASE KINASE; SACCHAROMYCES-CEREVISIAE; NF1 GENE; TRANSGENIC MICE; TYROSINE KINASE; VONRECKLINGHAUSEN NEUROFIBROMATOSIS; FARNESYLTRANSFERASE INHIBITORS;
Keywords:
neurofibromatosis type 1; experimental therapeutics; Ras;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
104
Recensione:
Indirizzi per estratti:
Indirizzo: Shannon, K Univ Calif San Francisco, Dept Pediat, Room HSE 302,Box 0519, San Francisco, CA 94143 USA Univ Calif San Francisco Room HSE 302,Box 0519 San Francisco CA USA 94143
Citazione:
B. Weiss et al., "Hyperactive Ras as a therapeutic target in neurofibromatosis type 1", AM J MED G, 89(1), 1999, pp. 14-22

Abstract

The NF1 gene encodes neurofibromin, a GTPase-activating protein (GAP) for members of the p21(ras) (Ras) family, which negatively regulates Ras outputby accelerating the conversion of active Ras GTP to inactive Ras-GDP. Analysis of tumors from patients with neurofibromatosis type 1 (NF1) has shown biochemical evidence of hyperactive Ras as well as frequent loss of the normal NF1 allele, consistent with its role as a tumor suppressor gene. Taken together, these data suggest that novel therapeutics directed against components of the Ras signaling cascade might provide effective treatments for certain pathological complications of NF1. Here we summarize data that support a role for hyperactive Ras in NF1 disease, including Ras processing, activation,and down-regulation. We review targets for rational drug design, provide preliminary results, and discuss implications for future studies. Am. J. Med. Genet. (Semin. Med. Genet.) 89:14-22, 1999. (C) 1999 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 07:59:20