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Titolo:
Cyclin D1 is required for transformation by activated Neu and is induced through an E2F-dependent signaling pathway
Autore:
Lee, RJ; Albanese, C; Fu, MF; DAmico, M; Lin, B; Watanabe, G; Haines, GK; Siegel, PM; Hung, MC; Yarden, Y; Horowitz, JM; Muller, WJ; Pestell, RG;
Indirizzi:
Albert Einstein Coll Med, Albert Einstein Canc Ctr, Dept Med, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 Dept Med, Bronx, NY 10461 USA Albert Einstein Coll Med, Albert Einstein Canc Ctr, Dept Dev & Mol Biol, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 Mol Biol, Bronx, NY 10461 USA N Carolina State Univ, Coll Vet Med, Dept Anat Physiol Sci & Radiol, Raleigh, NC 27606 USA N Carolina State Univ Raleigh NC USA 27606 Radiol, Raleigh, NC 27606 USA Northwestern Univ, Sch Med, Dept Pathol, Chicago, IL 60611 USA Northwestern Univ Chicago IL USA 60611 Dept Pathol, Chicago, IL 60611 USA McMaster Univ, Dept Pathol, Hamilton, ON L8S 4K1, Canada McMaster Univ Hamilton ON Canada L8S 4K1 ol, Hamilton, ON L8S 4K1, Canada Univ Texas, MD Anderson Canc Ctr, Dept Tumor Biol, Houston, TX 77030 USA Univ Texas Houston TX USA 77030 r, Dept Tumor Biol, Houston, TX 77030 USA Weizmann Inst Sci, Dept Bioregulat, IL-76100 Rehovot, Israel Weizmann InstSci Rehovot Israel IL-76100 ulat, IL-76100 Rehovot, Israel
Titolo Testata:
MOLECULAR AND CELLULAR BIOLOGY
fascicolo: 2, volume: 20, anno: 2000,
pagine: 672 - 683
SICI:
0270-7306(200001)20:2<672:CDIRFT>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
BREAST-CANCER CELLS; TRANSCRIPTION FACTOR SP1; NIH 3T3 CELLS; RAS TRANSFORMATION; TRANSGENIC MICE; GENE-EXPRESSION; KINASE-ACTIVITY; DEPENDENT KINASE-4; ESTROGEN-RECEPTOR; DOWN-REGULATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
83
Recensione:
Indirizzi per estratti:
Indirizzo: Pestell, RG Albert Einstein Coll Med, Albert Einstein Canc Ctr, Dept Med, Chanin 302,1300 Morris Pk Ave, Bronx, NY 10461 USA Albert Einstein Coll MedChanin 302,1300 Morris Pk Ave Bronx NY USA 10461
Citazione:
R.J. Lee et al., "Cyclin D1 is required for transformation by activated Neu and is induced through an E2F-dependent signaling pathway", MOL CELL B, 20(2), 2000, pp. 672-683

Abstract

The neu (c-erbB-2) proto-oncogene encodes a tyrosine kinase receptor that is overexpressed in 20 to 30% of human breast tumors. Herein, cyclin D1 protein levels were increased in mammary tumors induced by overexpression of wild-type Neu or activating mutants of Neu in transgenic mice and in MCF7 cells overexpressing transforming Neu, Analyses of 12 Neu mutants in MCF7 cells indicated important roles for specific C-terminal autophosphorylation sites and the extracellular domain in cyclin D1 promoter activation. Induction of cyclin D1 by NeuT involved Ras, Rac, Rho, extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38, but not phosphatidylinositol 3-kinase, NeuT induction of the cyclin D1 promoter required the E2F and Spl DNA binding sites and was inhibited by dominant negative E2F-1 or DP-1, Neu-induced transformation was inhibited by a cyclin D1 antisense or dominant negative E2F-1 construct in Rat-1 cells. Growth of NeuT-transformed mammaryadenocarcinoma cells in nude mice was blocked by the cyclin D1 antisense construct. These results demonstrate that E2F-1 mediates a Neu-signaling cascade to cyclin D1 and identify cyclin D1 as a critical downstream target ofneu-induced transformation.

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Documento generato il 28/09/20 alle ore 04:38:56