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Titolo:
Src family kinases are required for prolactin induction of cell proliferation
Autore:
Vara, JAF; Caceres, AD; Silva, A; Martin-Perez, J;
Indirizzi:
CSIC, Ctr Invest Biol, E-28029 Madrid, Spain CSIC Madrid Spain E-28029CSIC, Ctr Invest Biol, E-28029 Madrid, Spain CSIC, Inst Invest Biomed, E-28029 Madrid, Spain CSIC Madrid Spain E-28029 SIC, Inst Invest Biomed, E-28029 Madrid, Spain
Titolo Testata:
MOLECULAR BIOLOGY OF THE CELL
fascicolo: 7, volume: 12, anno: 2001,
pagine: 2171 - 2183
SICI:
1059-1524(200107)12:7<2171:SFKARF>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-TYROSINE KINASES; SIGNAL-TRANSDUCTION PATHWAYS; COLONY-STIMULATING FACTOR; C-SRC; PHOSPHATIDYLINOSITOL 3-KINASE; GROWTH-HORMONE; T-LYMPHOCYTES; PHOSPHOTYROSINE PHOSPHATASE; PROMOTER ACTIVATION; POSITIVE REGULATOR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
72
Recensione:
Indirizzi per estratti:
Indirizzo: Martin-Perez, J CSIC, Ctr Invest Biol, Arturo Duperier 4, E-28029 Madrid, Spain CSIC Arturo Duperier 4 Madrid Spain E-28029 Madrid, Spain
Citazione:
J.A.F. Vara et al., "Src family kinases are required for prolactin induction of cell proliferation", MOL BIOL CE, 12(7), 2001, pp. 2171-2183

Abstract

Prolactin (PRL) is a pleiotropic cytokine promoting cellular proliferationand differentiation. Because PRL activates the Src family of tyrosine kinases (SFK), we have studied the role of these kinases in PRL cell proliferation signaling. PRL induced [H-3]thymidine incorporation upon transient transfection of BaF-3 cells with the PRL receptor. This effect was inhibited bycotransfection with the dominant negative mutant of c-Src (K > A295/Y > F527, SrcDM). The role of SFK in PRL-induced proliferation was confirmed in the BaF-3 PRL receptor-stable transfectant, W53 cells, where PRL induced Fynand Lyn activation. The SFK-selective inhibitors PP1/PP2 and herbimycin A blocked PRL-dependent cell proliferation by arresting the W53 cells in G1, with no evident apoptosis. In parallel, PP1/PP2 inhibited PRL induction of cell growth-related genes c-fos, c-jun, c-myc, and odc. These inhibitors have no effect on PRL-mediated activation of Ras/Mapk and Jak/Start pathways. In contrast, they inhibited the PRL-dependent stimulation of the SFKs substrate Sam68, the phosphorylation of the tyrosine phosphatase Shp2, and the PI3K-dependent Akt and p70S6k serine kinases. Consistently, transient expression of SrcDM in W53 cells also blocked PRL activation of Akt. These results demonstrate that activation of SFKs is required for cell proliferation induced by PRL.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 23:47:37