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Titolo:
SM-20 is a novel mitochondrial protein that causes caspase-dependent cell death in nerve growth factor-dependent neurons
Autore:
Lipscomb, EA; Sarmiere, PD; Freemann, RS;
Indirizzi:
Univ Rochester, Sch Med & Dent, Dept Physiol & Pharmacol, Rochester, NY 14642 USA Univ Rochester Rochester NY USA 14642 Pharmacol, Rochester, NY 14642 USA Univ Rochester, Sch Med & Dent, Dept Environm Med, Rochester, NY 14642 USAUniv Rochester Rochester NY USA 14642 vironm Med, Rochester, NY 14642 USA
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 7, volume: 276, anno: 2001,
pagine: 5085 - 5092
SICI:
0021-9258(20010216)276:7<5085:SIANMP>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPRIVED SYMPATHETIC NEURONS; FACTOR-RESPONSIVE GENE; CYTOCHROME-C; CAENORHABDITIS-ELEGANS; POSTMITOTIC NEURONS; FACTOR DEPRIVATION; SMOOTH-MUSCLE; CYCLIN D1; EXPRESSION; APOPTOSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Freemann, RS Univ Rochester, Sch Med & Dent, Dept Physiol & Pharmacol, 601Elmwood Ave,Rochester, NY 14642 USA Univ Rochester 601 Elmwood Ave Rochester NY USA 14642 642 USA
Citazione:
E.A. Lipscomb et al., "SM-20 is a novel mitochondrial protein that causes caspase-dependent cell death in nerve growth factor-dependent neurons", J BIOL CHEM, 276(7), 2001, pp. 5085-5092

Abstract

Sympathetic neurons undergo protein synthesis-dependent apoptosis when deprived of nerve growth factor (NGF). Expression of SM-20 is up-regulated in NGF-deprived sympathetic neurons, and ectopic SM-20 is sufficient to promote neuronal death in the presence of NGF. We now report that SM-20 is a mitochondrial protein that promotes cell death through a caspase-dependent mechanism. SM-20 immunofluorescenee was present in the cytoplasm in a punctate pattern that colocalized with cytochrome oxidase I and with mitochondria-selective dyes. Analysis of SM-20/dihydrofolate reductase fusion proteins revealed that the first 25 amino acids of SM-20 contain a functional mitochondrial targeting sequence. An amino-terminal truncated form of SM-20 was not restricted to mitochondria but instead localized throughout the cytosol andnucleus. Nevertheless, the truncated SM-20 retained the ability to induce neuronal death, similar to the wild type protein, SM-20-induced death was accompanied by caspase-3 activation and was blocked by a general caspase inhibitor. Additionally, overexpression of SM-20, under conditions where cell death is blocked by a general caspase inhibitor, did not result in widespread release of cytochrome c from mitochondria, These results indicate that SM-20 is a novel mitochondrial protein that may be an important mediator of neurotrophin-withdrawal-mediated cell death.

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Documento generato il 04/12/20 alle ore 18:00:21