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Titolo:
NF-kappa B activation by N-CAM and cytokines in astrocytes is regulated bymultiple protein kinases and redox modulation
Autore:
Choi, J; Krushel, LA; Crossin, KL;
Indirizzi:
Scripps Clin & Res Inst, Dept Neurobiol, SBR14, La Jolla, CA 92037 USA Scripps Clin & Res Inst La Jolla CA USA 92037 R14, La Jolla, CA 92037 USA Inst Neurosci, San Diego, CA USA Inst Neurosci San Diego CA USAInst Neurosci, San Diego, CA USA
Titolo Testata:
GLIA
fascicolo: 1, volume: 33, anno: 2001,
pagine: 45 - 56
SICI:
0894-1491(200101)33:1<45:NBABNA>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-ADHESION MOLECULE; NECROSIS-FACTOR-ALPHA; NITRIC-OXIDE SYNTHASE; CREB-BINDING PROTEIN; TRANSCRIPTION FACTOR; NEURITE OUTGROWTH; C ISOZYMES; DEPENDENT TRANSCRIPTION; GLUCOCORTICOID RECEPTOR; GENE-TRANSCRIPTION;
Keywords:
interleukin-1 beta; tumor necrosis factor-alpha; protein tyrosine kinase; protein kinase C; calcium/calmodulin-dependent protein kinase II; oxidative stress; transcription;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
86
Recensione:
Indirizzi per estratti:
Indirizzo: Crossin, KL Scripps Clin & Res Inst, Dept Neurobiol, SBR14, 10550 N TorreyPines Rd, La Jolla, CA 92037 USA Scripps Clin & Res Inst 10550 N Torrey Pines Rd La Jolla CA USA 92037
Citazione:
J. Choi et al., "NF-kappa B activation by N-CAM and cytokines in astrocytes is regulated bymultiple protein kinases and redox modulation", GLIA, 33(1), 2001, pp. 45-56

Abstract

Interaction of the neural cell adhesion molecule (N-CAM) with astrocytes activates a transcription factor, NF-kappaB, that mediates inflammatory responses after neural injury. Here we describe intracellular signaling events that link N-CAM binding to NF-kappaB-mediated transcription. Addition of the third immunoglobulin domain of N-CAM (Ig III), which mimics the activity of intact N-CAM, or of cytokines (interleukin-1 beta or tumor necrosis factor-alpha), increased transcription from an NF-kappaB-responsive luciferase reporter gene construct that had been transiently transfected into neonatalrat forebrain astrocytes. NF-kappaB activity induced by Ig III or cytokines was decreased by inhibition of nonreceptor protein tyrosine kinases (PTKs), phospholipase C, protein kinase C (PKC), calcium/calmodulin-dependent protein kinase II (CaMKII), or oxidative stress. Inhibition of PKC blocked nuclear translocation of NF-kappaB protein while binding of NF-kappaB to DNA was decreased by modulation of redox homeostasis. In contrast, inhibition of CaMKII and nonreceptor PTKs altered neither nuclear translocation nor DNAbinding, suggesting that these kinases affect NF-kappaB transactivation. Anumber of agents that inhibit NF-kappaB activation in other cell types didnot affect activation in astrocytes. These findings suggest that activation of NF-kappaB by N-CAM and cytokines in astrocytes involves multiple signals that differentially affect NF-kappaB nuclear translocation, DNA binding,and transactivation. GLIA 33:45-56, 2001. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/01/20 alle ore 07:22:34