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Titolo:
The combination of Bcl-2 expression and NGF-deprivation facilitates the selective destruction of BAD protein in living sympathetic neurons
Autore:
Roberts, ML; Virdee, K; Sampson, CPB; Gordon, I; Parone, P; Tolkovsky, AM;
Indirizzi:
Univ Cambridge, Dept Biochem, Cambridge CB2 1QW, England Univ Cambridge Cambridge England CB2 1QW hem, Cambridge CB2 1QW, England Univ Oxford, Dept Human Anat & Genet, Oxford OX1 3QX, England Univ OxfordOxford England OX1 3QX Anat & Genet, Oxford OX1 3QX, England
Titolo Testata:
MOLECULAR AND CELLULAR NEUROSCIENCE
fascicolo: 2, volume: 16, anno: 2000,
pagine: 97 - 110
SICI:
1044-7431(200008)16:2<97:TCOBEA>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
NERVE GROWTH-FACTOR; PROGRAMMED CELL-DEATH; MICE OVEREXPRESSING BCL-2; CYTOCHROME-C; TRANSGENIC MICE; BH3 DOMAIN; SENSORY NEURONS; JNK ACTIVATION; PC12 CELLS; X-L;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Roberts, ML Univ London Royal Holloway & Bedford New Coll, Sch Biol Sci, Dept Biochem,Egham TW20 0EX, Surrey, England Univ London Royal Holloway & Bedford New Coll Egham Surrey England TW20 0EX
Citazione:
M.L. Roberts et al., "The combination of Bcl-2 expression and NGF-deprivation facilitates the selective destruction of BAD protein in living sympathetic neurons", MOL CELL NE, 16(2), 2000, pp. 97-110

Abstract

Bcl-2 overexpression prevents neuronal death after injury or neurotrophic factor-deprivation but the biochemical consequences of survival maintenanceby Bcl-2 have hardly been explored. We show that unlike NGF, adenovirally delivered hBcl-2 supports the survival of over 80% of the neurons without activating ERK and Akt phosphorylation, or suppressing JNK phosphorylation, or enhancing cell growth. However, the proapoptotic protein BAD, whose phosphorylation is induced by NGF, is degraded in NGF-deprived neurons expressing hBcl-2, while the level of Bcl-xL remains unaffected. Interestingly, degradation of BAD protein is prevented by the pan-caspase inhibitor Boc.Asp(OMe)fmk. We propose that NGF-deprivation promotes dephosphorylation of BAD while hBcl-2 facilitates its release into the cytoplasm where it is degradedby noncaspase, Boc.Asp(O-Me)fmk-inhibitable proteases. The potential importance of BAD degradation is suggested by our finding that overexpressed BADkills NGF- maintained sympathetic neurons by apoptosis, while hBcl-2 prevents BAD-induced death.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 05:28:11