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Titolo:
COORDINATE ACTIVATION OF ACTIVATOR PROTEIN-1 AND INFLAMMATORY CYTOKINES IN RESPONSE TO NEISSERIA-GONORRHOEAE EPITHELIAL-CELL CONTACT INVOLVES STRESS-RESPONSE KINASES
Autore:
NAUMANN M; RUDEL T; WIELAND B; BARTSCH C; MEYER TE;
Indirizzi:
MAX PLANCK INST INFEKT BIOL,MOL BIOL ABT,MONBIJOUSTR 2 D-10117 BERLINGERMANY MAX PLANCK INST BIOL,INFEKT BIOL ABT D-72076 TUBINGEN GERMANY
Titolo Testata:
The Journal of experimental medicine
fascicolo: 7, volume: 188, anno: 1998,
pagine: 1277 - 1286
SICI:
0022-1007(1998)188:7<1277:CAOAPA>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
NF-KAPPA-B; SIGNAL-TRANSDUCTION PATHWAYS; JUN NH2-TERMINAL KINASE; C-JUN; TRANSCRIPTIONAL ACTIVITY; RHO-PROTEINS; BINDING; CDC42; P38; IDENTIFICATION;
Keywords:
NEISSERIA; INFLAMMATION; ACTIVATOR PROTEIN 1; C-JUN NH2-TERMINAL KINASE; P21-ACTIVATED KINASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
71
Recensione:
Indirizzi per estratti:
Citazione:
M. Naumann et al., "COORDINATE ACTIVATION OF ACTIVATOR PROTEIN-1 AND INFLAMMATORY CYTOKINES IN RESPONSE TO NEISSERIA-GONORRHOEAE EPITHELIAL-CELL CONTACT INVOLVES STRESS-RESPONSE KINASES", The Journal of experimental medicine, 188(7), 1998, pp. 1277-1286

Abstract

Neisseria gonorrhoeae (Ngo), the etiologic agent of gonorrhea, inducea number of proinflammatory cytokines by contact to epithelial cells. Cytokine genes and a variety of other immune response genes are activated as a result of the regulatory function of immediate early response transcription factors including activator protein 1 (AP-1). Since itis established that phosphorylation of c-Jun, the central component of AP-1, by the stress-activated c-Jun NH2-terminal kinase (JNK) increases the transcriptional activity of AP-1, we studied whether Ngo couldinduce stress response pathways involving JNK. We found that virulentNgo strains induce phosphorylation and activation of JNK but not of p38 kinase. Analysis of a nonpathogenic Ngo strain revealed only weak JNK activation. In respect to the molecular components upstream of the JNK signaling cascade, we show that a dominant negative mutant of MAP kinase kinase 4 (MKK4) represses transcription of an AP-1-dependent reporter gene. Regarding upstream stress response factors involved in Ngo-induced MKK4/JNK/AP-1 activation, we identified p21-accivated kinase(PAK) but not NIAPK/ERK kinase kinase (MEKK1). Inhibition of small GTPases including Rad and Cdc42 by Toxin B prevented JNK and AP-1 activation. Our results indicate that Ngo induce the activation of proinflammatory cytokines via a cascade of cellular stress response kinases involving PAK, which directs the signal from the Rho family of small GTPases to JNK/AP-1 activation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 11:14:03