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Titolo:
Activation of nuclear factor kappa B and bcl-x survival gene expression bynerve growth factor requires tyrosine phosphorylation of I kappa B alpha
Autore:
Bui, NT; Livolsi, A; Peyron, JF; Prehn, JHM;
Indirizzi:
Univ Munster, Fac Med, Res Grp Apoptosis & Cell Death, Interdisciplinary Ctr Clin Res, D-48149 Munster, Germany Univ Munster Munster Germany D-48149 Clin Res, D-48149 Munster, Germany Univ Munster, Fac Med, Dept Pharmacol & Toxicol, D-48149 Munster, Germany Univ Munster Munster Germany D-48149 & Toxicol, D-48149 Munster, Germany Fac Med Pasteur, INSERM, Hematopoiet Cell Activat U526, F-06107 Nice, France Fac Med Pasteur Nice France F-06107 l Activat U526, F-06107 Nice, France
Titolo Testata:
JOURNAL OF CELL BIOLOGY
fascicolo: 4, volume: 152, anno: 2001,
pagine: 753 - 763
SICI:
0021-9525(20010219)152:4<753:AONFKB>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; RAT HIPPOCAMPAL-NEURONS; P75 NEUROTROPHIN RECEPTOR; SYMPATHETIC NEURONS; CELL-DEATH; PC12 CELLS; TRANSCRIPTION FACTOR; PROTEIN-KINASE; ENDOTHELIAL-CELLS; INDUCED APOPTOSIS;
Keywords:
nerve growth factor; nuclear factor-kappa B; Bcl-xL; tumor necrosis factor-alpha; I kappa B;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
65
Recensione:
Indirizzi per estratti:
Indirizzo: Prehn, JHM Univ Munster, Fac Med, Res Grp Apoptosis & Cell Death, Interdisciplinary Ctr Clin Res, Rontgenstr 21, D-48149 Munster, Germany Univ Munster Rontgenstr 21 Munster Germany D-48149 er, Germany
Citazione:
N.T. Bui et al., "Activation of nuclear factor kappa B and bcl-x survival gene expression bynerve growth factor requires tyrosine phosphorylation of I kappa B alpha", J CELL BIOL, 152(4), 2001, pp. 753-763

Abstract

NGF has been shown to support neuron survival by activating the transcription factor nuclear factor-kappaB (NF kappaB). We investigated the effect ofNGF on the expression of Bcl-xL, an anti-apoptotic Bcl-2 family protein. Treatment of rat pheochromocytoma PC12 cells, human neuroblastoma SH-SY5Y cells, or primary rat hippocampal neurons with NGF (0.1-10 ng/ml) increased the expression of bcl-xL mRNA and protein. Reporter gene analysis revealed asignificant increase in NF kappaB activity after treatment with NGF that was associated with increased nuclear translocation of the active NF kappaB p65 subunit. NGF-induced NF kappaB activity and Bcl-xL expression were inhibited in cells overexpressing the NF kappaB inhibitor, I kappaB alpha. Unlike tumor necrosis factor-alpha (TNF-alpha), however, NGF-induced NF kappaB activation occurred without significant degradation of I kappa Bs determined by Western blot analysis and time-lapse imaging of neurons expressing green fluorescent protein-tagged I kappaB alpha. Moreover, in contrast to TNF-alpha, NGF failed to phosphorylate I kappaB alpha at serine residue 32, butinstead caused significant tyrosine phosphorylation. Overexpression of a Y42F mutant of I kappaB alpha potently suppressed NFG-, but not TNF-alpha -induced NF kappaB activation. Conversely, overexpression of a dominant negative mutant of TNF receptor-associated factor-6 blocked TNF-alpha-, but not NGF-induced NF kappaB activation. We conclude that NGF and TNF-alpha inducedifferent signaling pathways in neurons to activate NF kappaB and bcl-x gene expression.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/11/20 alle ore 11:23:12