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Titolo:
Expression of the SM-20 gene promotes death in nerve growth factor-dependent sympathetic neurons
Autore:
Lipscomb, EA; Sarmiere, PD; Crowder, RJ; Freeman, RS;
Indirizzi:
Univ Rochester, Sch Med, Dept Pharmacol & Physiol, Rochester, NY 14642 USAUniv Rochester Rochester NY USA 14642 & Physiol, Rochester, NY 14642 USA Univ Rochester, Sch Med, Dept Environm Med, Rochester, NY 14642 USA Univ Rochester Rochester NY USA 14642 vironm Med, Rochester, NY 14642 USA
Titolo Testata:
JOURNAL OF NEUROCHEMISTRY
fascicolo: 1, volume: 73, anno: 1999,
pagine: 429 - 432
SICI:
0022-3042(199907)73:1<429:EOTSGP>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; C-JUN; POSTMITOTIC NEURONS; FACTOR DEPRIVATION; PROTEIN-SYNTHESIS; SMOOTH-MUSCLE; CYCLIN D1; APOPTOSIS; SURVIVAL; IDENTIFICATION;
Keywords:
nerve growth factor; apoptosis; sympathetic neuron; gene expression; cell death;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
21
Recensione:
Indirizzi per estratti:
Indirizzo: Freeman, RS Univer,chester, Sch Med, Dept Pharmacol & Physiol, 601 ElmwoodAve, Rochest Univ Rochester 601 Elmwood Ave Rochester NY USA 14642 Rochest
Citazione:
E.A. Lipscomb et al., "Expression of the SM-20 gene promotes death in nerve growth factor-dependent sympathetic neurons", J NEUROCHEM, 73(1), 1999, pp. 429-432

Abstract

Sympathetic neurons undergo apoptosis when deprived of nerve growth factor(NGF). Inhibitors of RNA or protein synthesis block this death, suggestingthat gene expression is important for apoptosis in this system. We have identified SM-20 as a new gene that increases in expression in sympathetic neurons after NGF withdrawal. Expression of SM-20 also increases during neuronal death caused by cytosine arabinoside or the phosphatidylinositol 3-kinase inhibitor LY294002. In addition, SM-20 protein synthesis is elevated in NGF-deprived neurons compared with neurons maintained with NGF. Importantly, expression of SM-20 in sympathetic neurons causes cell death in the presence of NGF. These results suggest that SM-20 may function to regulate cell death in neurons.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 18:09:23