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Titolo:
Differential involvement of p38 mitogen-activated protein kinase and phosphatidyl inositol 3-kinase in the IL-1-mediated NF-kappa B and AP-1 activation
Autore:
Funakoshi, M; Sonoda, Y; Tago, K; Tominaga, S; Kasahara, T;
Indirizzi:
Kyoritsu Coll Pharm, Dept Biochem, Tokyo 1058512, Japan Kyoritsu Coll Pharm Tokyo Japan 1058512 pt Biochem, Tokyo 1058512, Japan Jichi Med Sch, Dept Biochem, Minami Kawachi, Tochigi 3290498, Japan Jichi Med Sch Minami Kawachi Tochigi Japan 3290498 Tochigi 3290498, Japan
Titolo Testata:
INTERNATIONAL IMMUNOPHARMACOLOGY
fascicolo: 3, volume: 1, anno: 2001,
pagine: 595 - 604
SICI:
1567-5769(200103)1:3<595:DIOPMP>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLIOBLASTOMA CELL-LINE; IL-1 RECEPTOR; INTERLEUKIN-1 RECEPTOR; C-JUN; EXPRESSION; PATHWAY; GENE; INDUCTION; SUBUNIT; PHOSPHORYLATION;
Keywords:
IL-1 signaling; PI3-kinase; p38 MAP kinase; TRAF6;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Kasahara, T Kyoritsu Coll Pharm, Dept Biochem, 1-5-30 Shibakoen,Minato, Tokyo 1058512,Japan Kyoritsu Coll Pharm 1-5-30 Shibakoen,Minato Tokyo Japan 1058512
Citazione:
M. Funakoshi et al., "Differential involvement of p38 mitogen-activated protein kinase and phosphatidyl inositol 3-kinase in the IL-1-mediated NF-kappa B and AP-1 activation", INT IMMUNO, 1(3), 2001, pp. 595-604

Abstract

Interleukin-1 (IL-1) is a central regulator of the immune acid inflammatory responses by which various inflammatory genes are induced. Although IL-1 signaling is known to involve PI3-kinase. p38 mitogen-activated protein (MAP) kinase and extracellular signal-regulated kinase (ERK), the crosstalk oftheir kinases on the IL-1-mediated signal transduction is not clear. We used two specific inhibitors. SB203580 which selectively inhibits p38 MAP kinase and LY294002 which inhibits PI3-kinase. respectively, to explore the involvement of these kinases in the IL-1-induced NF-kappaB activation, using a human glioblastoma cell line, T98G. Two kinase inhibitors decreased IL-1-induced IL-8 mRNA and protein levels markedly. IL-1 caused phosphorylation of p38 MAP kinase with concomitant recruitment of PIS-kinase to IL-1 receptor I (IL-IRI) and its activation. In this content, pretreatment of LY294002, but not SB203580. inhibited IL-1-induced NF-kappaB activation significantly. While IL-1 induced-AP-1 activation was moderate. both LY294002 and S8103580 suppressed IL-1-induced AP-1 activation. These observations were prominent particularly in the TRAF6 transfection system, in which overexpressionof wild type TRAF6 augmented the IL-1 mediated NF-kappaB and AP-1 activation, while dominant negative TRAF6 construct (Delta TRAF6) suppressed these activation. Namely. LY294002, inhibited TRAF6-mediated IL-1-induced NF-kappaB and AP-1 activation markedly. while SB203580 inhibited TRAF6-induced AP-1 activation but not NF-kappaB activation. Above results indicated that both PI3-kinase and p38 MAP kinase: are differentially involved in IL-1-induced NF-kappaB and AP-1 activation. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 18:05:04