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Titolo:
Epistatic and independent functions of Caspase-3 and Bcl-X-L in developmental programmed cell death
Autore:
Roth, KA; Kuan, CY; Haydar, TF; DSa-Eipper, C; Shindler, KS; Zheng, TS; Kuida, K; Flavell, RA; Rakic, P;
Indirizzi:
Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Dept Pathol, St Louis, MO 63110 USA Howard Hughes Med Inst, Immunobiol Sect, New Haven, CT 06510 USA Howard Hughes Med Inst New Haven CT USA 06510 ct, New Haven, CT 06510 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 Inc, Cambridge, MA 02139 USA Vertex Pharmaceut Inc Cambridge MA USA 02139 Inc, Cambridge, MA 02139 USA
Titolo Testata:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
fascicolo: 1, volume: 97, anno: 2000,
pagine: 466 - 471
SICI:
0027-8424(20000104)97:1<466:EAIFOC>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
BAX-DEFICIENT MICE; NERVOUS-SYSTEM; IN-VIVO; APOPTOSIS; NEURONS; PATHWAYS; ELEGANS; APAF1; BRAIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Roth, KA Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 ol, St Louis, MO 63110 USA
Citazione:
K.A. Roth et al., "Epistatic and independent functions of Caspase-3 and Bcl-X-L in developmental programmed cell death", P NAS US, 97(1), 2000, pp. 466-471

Abstract

The number of neurons in the mammalian brain is determined by a balance between cell proliferation and programmed cell death. Recent studies indicated that Bcl-X-L prevents, whereas Caspase-3 mediates, cell death in the developing nervous system, but whether Bcl-X-L directly blocks the apoptotic function of Caspase-3 in vivo is not known. To examine this question. we generated bcl-x/caspase-3 double mutants and found that caspase-3 deficiency abrogated the increased apoptosis of postmitotic neurons but not the increased hematopoietic cell death and embryonic lethality caused by the bcl-x mutation. In contrast, caspase-3, but not bcl-x, deficiency changed the normal incidence of neuronal progenitor cell apoptosis, consistent with the lack of expression of Bcl-X-L in the proliferative population of the embryonic cortex. Thus, although Caspase-3 is epistatically downstream to Bcl-X-L in postmitotic neurons, it independently regulates apoptosis of neuronal foundercells. Taken together, these results establish a role of programmed cell death in regulating the size of progenitor population in the central nervoussystem, a function that is distinct from the classic role of cell death inmatching postmitotic neuronal population with postsynaptic targets.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/08/20 alle ore 00:27:16