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Titolo:
Functional cloning of the proto-oncogene brain factor-1 (BF-1) as a smad-binding antagonist of transforming growth factor-beta signaling
Autore:
Rodriguez, C; Huang, LJS; Son, JK; McKee, A; Xiao, Z; Lodish, HF;
Indirizzi:
Whitehead Inst Biomed Res, Cambridge Ctr 9, Cambridge, MA 02142 USA Whitehead Inst Biomed Res Cambridge MA USA 02142 Cambridge, MA 02142 USA MIT, Dept Biol, Cambridge, MA 02139 USA MIT Cambridge MA USA 02139MIT, Dept Biol, Cambridge, MA 02139 USA
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 32, volume: 276, anno: 2001,
pagine: 30224 - 30230
SICI:
0021-9258(20010810)276:32<30224:FCOTPB>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATOR INHIBITOR-1 GENE; TGF-BETA; TRANSCRIPTION FACTORS; RECEPTOR COMPLEX; QIN PROTEIN; EXPRESSION; RESPONSES; SPECIFICITY; ONCOPROTEIN; REPRESSOR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Lodish, HF Whitehead Inst Biomed Res, Cambridge Ctr 9, Cambridge, MA 02142USA Whitehead Inst Biomed Res Cambridge MA USA 02142 MA 02142 USA
Citazione:
C. Rodriguez et al., "Functional cloning of the proto-oncogene brain factor-1 (BF-1) as a smad-binding antagonist of transforming growth factor-beta signaling", J BIOL CHEM, 276(32), 2001, pp. 30224-30230

Abstract

Using the plasminogen activator inhibitor (PAI) promoter to drive the expression of a reporter gene (mouse CD2), we devised a system to clone negative regulators of the transforming growth factor-beta (TGF-beta) signaling pathway. We infected a TGF-beta -responsive cell line (MvLu1) with a retroviral cDNA library, selecting by fluorescence-activated cell sorter single cells displaying low PAI promoter activity in response to TGF-beta. Using thisstrategy we cloned the proto-oncogene brain factor-1 (BF-1). BF-1 represses the PAI promoter in part by associating with both unphosphorylated Smad3 (in the cytoplasm) and phosphorylated Smad3 (in the nucleus), thus preventing its binding to DNA BF-1 also associates with Smad1, -2, and -4, the SmadMH2 domain binds to BF-1, and the C-terminal segment of BF-1 is uniquely and solely required for binding to Smads. Further, BF-1 represses another TGF-beta -induced promoter (p15), it upregulates a TGF-beta -repressed promoter (Cyclin A), and it reverses the growth arrest caused by TGF-beta. Our results suggest that BF-1 is a general inhibitor of TGF-beta signaling and assuch may play a key role during brain development.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 03:52:16