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Titolo:
DNA damage-induced neural precursor cell apoptosis requires p53 and caspase 9 but neither Bax nor caspase 3
Autore:
DSa-Eipper, C; Leonard, JR; Putcha, G; Zheng, TS; Flavell, RA; Rakic, P; Kuida, K; Roth, KA;
Indirizzi:
Washington Univ, Sch Med, Dept Pathol, Div Neuropathol, St Louis, MO 63110USA Washington Univ St Louis MO USA 63110 Neuropathol, St Louis, MO 63110USA Biogen, Dept Inflammat Immunol & Cell Biol, Cambridge, MA 02139 USA Biogen Cambridge MA USA 02139 mmunol & Cell Biol, Cambridge, MA 02139 USA Yale Univ, Sch Med, Howard Hughes Med Inst, Immunobiol Sect, New Haven, CT06510 USA Yale Univ New Haven CT USA 06510 Immunobiol Sect, New Haven, CT06510 USA Yale Univ, Sch Med, Neurobiol Sect, New Haven, CT 06510 USA Yale Univ NewHaven CT USA 06510 Neurobiol Sect, New Haven, CT 06510 USA Vertex Pharmaceut, Cambridge, MA 02139 USA Vertex Pharmaceut Cambridge MAUSA 02139 rmaceut, Cambridge, MA 02139 USA
Titolo Testata:
DEVELOPMENT
fascicolo: 1, volume: 128, anno: 2001,
pagine: 137 - 146
SICI:
0950-1991(200101)128:1<137:DDNPCA>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL-NERVOUS-SYSTEM; X-DEFICIENT MICE; CYTOCHROME-C; STEM-CELLS; IN-VIVO; P53-DEPENDENT APOPTOSIS; TRANSGENIC MICE; DEATH; NEURONS; BCL-2;
Keywords:
apoptosis; neurodevelopment; caspase; Bcl2; p53; mouse;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Roth, KA Washington Univ, Sch Med, Dept Pathol, Div Neuropathol, St Louis,MO 63110USA Washington Univ St Louis MO USA 63110 hol, St Louis, MO 63110USA
Citazione:
C. D'Sa-Eipper et al., "DNA damage-induced neural precursor cell apoptosis requires p53 and caspase 9 but neither Bax nor caspase 3", DEVELOPMENT, 128(1), 2001, pp. 137-146

Abstract

Programmed cell death (apoptosis) is critical for normal brain morphogenesis and may be triggered by neurotrophic factor deprivation or irreparable DNA damage. Members of the Bcl2 and caspase families regulate neuronal responsiveness to trophic factor withdrawal; however, their involvement in DNA damage-induced neuronal apoptosis is less clear. To define the molecular pathway regulating DNA damage-induced neural precursor cell apoptosis, we haveexamined the effects of drug and gamma -irradiation-induced DNA damage on telencephalic neural precursor cells derived from wild-type embryos and mice with targeted disruptions of apoptosis-associated genes. We found that DNA damage-induced neural precursor cell apoptosis, both in vitro and in vivo, was critically dependent on p53 and caspase 9, but neither Pax nor caspase 3 expression. Neural precursor cell apoptosis was also unaffected by targeted disruptions of Bclx and Bcl2, and unlike neurotrophic factor-deprivation-induced neuronal apoptosis, was not associated with a detectable loss ofcytochrome c from mitochondria. The apoptotic pathway regulating DNA damage-induced neural precursor cell death is different from that required for normal brain morphogenesis, which involves both caspase 9 and caspase 3 but not p53, indicating that additional apoptotic stimuli regulate neural precursor cell numbers during telencephalic development.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 14:59:00