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Titolo:
STRUCTURE AND FUNCTION OF A NEW STAT-INDUCED STAT INHIBITOR
Autore:
NAKA T; NARAZAKI M; HIRATA M; MATSUMOTO T; MINAMOTO S; AONO A; NISHIMOTO N; KAJITA T; TAGA T; YOSHIZAKI K; AKIRA S; KISHIMOTO T;
Indirizzi:
OSAKA UNIV,SCH MED,DEPT MED 3,2-2 YAMADAOKA SUITA OSAKA 565 JAPAN OSAKA UNIV,SCH MED,DEPT MED 3 SUITA OSAKA 565 JAPAN INT REAGENTS CORP,CTR RES & DEV,NISHI KU KOBE 65122 JAPAN TOKYO MED & DENT UNIV,MED RES INST,DEPT MOL CELL BIOL,CHIYODA KU TOKYO 101 JAPAN HYOGO MED UNIV,DEPT BIOCHEM NISHINOMIYA HYOGO 663 JAPAN OSAKA UNIV,SCH HLTH & SPORTS SCI SUITA OSAKA 565 JAPAN
Titolo Testata:
Nature
fascicolo: 6636, volume: 387, anno: 1997,
pagine: 924 - 929
SICI:
0028-0836(1997)387:6636<924:SAFOAN>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
TYROSINE PHOSPHORYLATION; TRANSCRIPTION FACTOR; SIGNAL-TRANSDUCTION; CYTOKINE RECEPTORS; ACTIVATION; INTERLEUKIN-6; PATHWAYS; GP130; FAMILY; IL-3;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
27
Recensione:
Indirizzi per estratti:
Citazione:
T. Naka et al., "STRUCTURE AND FUNCTION OF A NEW STAT-INDUCED STAT INHIBITOR", Nature, 387(6636), 1997, pp. 924-929

Abstract

The signalling pathway that comprises JAK kinases and STAT proteins (for signal transducer and activator of transcription) is important forrelaying signals from various cytokines outside the cell to the inside(1-3). The feedback mechanism responsible for switching off the cytokine signal has not been elucidated. We now report the cloning and characterization of an inhibitor of STAT activation which we name SSI-1 (for STAT-induced STAT inhibitor-1). We found that SSI-1 messenger RNA was induced by the cytokines interleukins 4 and 6 (IL-4, IL-6), leukaemia-inhibitory factor (LIF), and granulocyte colony-stimulating factor (G-CSF). Stimulation by IL-6 or LIF of murine myeloid leukaemia cells (M1 cells) induced SSI-1 mRNA expression which was blocked by transfection of a dominant-negative mutant of Stat3, indicating that the SSI-1gene is a target of Stat3 (refs 4-7). Forced overexpression of SSI-1 complementary DNA interfered with IL-6- and LIF-mediated apoptosis andmacrophage differentiation of M1 cells, as well as IL-6 induced tyrosine-phosphorylation of a receptor glycoprotein component, gp130, and of Stat3. When SSI-1 is overexpressed in COS7 cells, it can associate with the kinases Jak2 and Tyk2, These findings indicate that SSI-1 is responsible for negative-feedback regulation of the JAK-STAT pathway induced by cytokine stimulation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/07/20 alle ore 05:07:00