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Titolo:
WILD-TYPE P53 AND V-SRC EXERT OPPOSING INFLUENCES ON HUMAN VASCULAR ENDOTHELIAL GROWTH-FACTOR GENE-EXPRESSION
Autore:
MUKHOPADHYAY D; TSIOKAS L; SUKHATME VP;
Indirizzi:
BETH ISRAEL HOSP,330 BROOKLINE AVE BOSTON MA 02215 BETH ISRAEL HOSP BOSTON MA 02215 HARVARD UNIV,SCH MED BOSTON MA 02215
Titolo Testata:
Cancer research
fascicolo: 24, volume: 55, anno: 1995,
pagine: 6161 - 6165
SICI:
0008-5472(1995)55:24<6161:WPAVEO>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXTRACELLULAR-MATRIX; TUMOR ANGIOGENESIS; RAT-CELLS; TRANSFORMATION; PROTEIN; ANTIGEN; PRODUCT; REPRESSION; MODULATION; PP60C-SRC;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
43
Recensione:
Indirizzi per estratti:
Citazione:
D. Mukhopadhyay et al., "WILD-TYPE P53 AND V-SRC EXERT OPPOSING INFLUENCES ON HUMAN VASCULAR ENDOTHELIAL GROWTH-FACTOR GENE-EXPRESSION", Cancer research, 55(24), 1995, pp. 6161-6165

Abstract

Angiogenesis, the development of new capillaries, is tightly controlled by the balance of positive and negative regulatory pathways. A newly described angiogenic factor, vascular endothelial growth factor/vascular permeability factor (VEGF/VPF), binds exclusively to endothelial cells and promotes their proliferation. Here we have studied the role of p53, a tumor suppressor, and v-Src, an oncogene on VEGF regulation. Wild-type p53 down-regulated endogenous VEGF mRNA level, as well as VEGF promoter activity, in a dose-dependent manner, whereas mutant forms of p53 had no effect. Overexpression of v-Src, known to up-regulate VEGF expression, activated a VEGF promoter-luciferase construct in a dose-dependent manner, Moreover, v-Src, in the presence of wt-p53, was unable to activate transcription of the VEGF promoter. Collectively, these data suggest that wild-type p53 may play a role in suppressing angiogenesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/12/20 alle ore 15:33:28