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Titolo:
Bcl-X-L-Caspase-9 interactions in the developing nervous system: Evidence for multiple death pathways
Autore:
Zaidi, AU; DSa-Eipper, C; Brenner, J; Kuida, K; Zheng, TS; Flavell, RA; Rakic, P; Roth, KA;
Indirizzi:
Washington Univ, Sch Med, Dept Pathol & Immunol, Div Neuropathol, St Louis, MO USA Washington Univ St Louis MO USA munol, Div Neuropathol, St Louis, MO USA Vertex Pharmaceut, Cambridge, MA 02139 USA Vertex Pharmaceut Cambridge MAUSA 02139 rmaceut, Cambridge, MA 02139 USA Biogen, Dept Inflammat Immunol & Cell Biol, Cambridge, MA 02142 USA Biogen Cambridge MA USA 02142 mmunol & Cell Biol, Cambridge, MA 02142 USA Yale Univ, Sch Med, Dept Immunol, New Haven, CT 06520 USA Yale Univ New Haven CT USA 06520 d, Dept Immunol, New Haven, CT 06520 USA Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT 06520 USA Yale Univ NewHaven CT USA 06520 Dept Neurobiol, New Haven, CT 06520 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 1, volume: 21, anno: 2001,
pagine: 169 - 175
SICI:
0270-6474(20010101)21:1<169:BIITDN>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
X-DEFICIENT MICE; CELLS IN-VITRO; BCL-X; APOPTOSIS; NEURONS; CASPASE-14; PREVENTS; IDENTIFICATION; ACTIVATION; PROTEASE;
Keywords:
development; programmed cell death; p53; apoptosis; Bax; Caspase-3;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Roth, KA Washington Univ, Sch Med, Dept Pathol, 660 S Euclid Ave,Box 8118,St Louis, MO 63110 USA Washington Univ 660 S Euclid Ave,Box 8118 St Louis MO USA 63110 A
Citazione:
A.U. Zaidi et al., "Bcl-X-L-Caspase-9 interactions in the developing nervous system: Evidence for multiple death pathways", J NEUROSC, 21(1), 2001, pp. 169-175

Abstract

Programmed cell death is critical for normal nervous system development and is regulated by Bcl-2 and Caspase family members. Targeted disruption of bcl-x(L), an antiapoptotic bcl-2 gene family member, causes massive death of immature neurons in the developing nervous system whereas disruption of caspase-9, a proapoptotic caspase gene family member, leads to decreased neuronal apoptosis and neurodevelopmental abnormalities. To determine whether Bcl-X-L and Caspase-9 interact in an obligate pathway of neuronal apoptosis, bcl-x/caspase-9 double homozygous mutants were generated. The increased apoptosis of immature neurons observed in Bcl-X-L-eficient embryos was completely prevented by concomitant Caspase-9 deficiency. In contrast, bcl-x(-/-)/caspase-9(-/-) embryonic mice exhibited an expanded ventricular zone and neuronal malformations identical to that observed in mice lacking only Caspase-9. These results indicate both epistatic and independent actions of Bcl-X-L and Caspase-9 in neuronal programmed cell death. To examine Bcl-2 and Caspase family-dependent apoptotic pathways in telencephalic neurons, we compared the effects of cytosine arabinoside (AraC), a known neuronal apoptosis inducer, on wild-type, Bcl-X-L-, Bax-, Caspase-9-,Caspase-3-, and p53-deficient telencephalic neurons in vitro. AraC caused extensive apoptosis of wild-type and Bcl-X-L-deficient neurons. p53- and Bax- deficient neurons showed marked protection from AraC-induced death, whereas Caspase-9- and Caspase-3-deficient neurons showed minimal or no protection, respectively. These findings contrast with our previous investigation of AraC-induced apoptosis of telencephalic neural precursor cells in which death was completely blocked by p53 or Caspase-9 deficiency but not Bax deficiency. In total, these results indicate a transition from Caspase-9- to Bax- and Bcl-X-L-mediated neuronal apoptosis.

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Documento generato il 02/07/20 alle ore 23:18:39