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Titolo:
Embryonic neuronal death due to neurotrophin and neurotransmitter deprivation occurs independent of APAF-1
Autore:
Honarpour, N; Tabuchi, K; Stark, JM; Hammer, RE; Sudhof, TC; Parada, LF; Wang, X; Richardson, JA; Herz, J;
Indirizzi:
Univ Texas, SW Med Ctr, Dept Mol Genet, Dallas, TX 75390 USA Univ Texas Dallas TX USA 75390 Ctr, Dept Mol Genet, Dallas, TX 75390 USA Univ Texas, SW Med Ctr, Howard Hughes Med Inst, Dallas, TX 75390 USA Univ Texas Dallas TX USA 75390 ward Hughes Med Inst, Dallas, TX 75390 USA Univ Texas, SW Med Ctr, Dept Internal Med, Dallas, TX 75390 USA Univ Texas Dallas TX USA 75390 r, Dept Internal Med, Dallas, TX 75390 USA Univ Texas, SW Med Ctr, Dept Biochem, Dallas, TX 75390 USA Univ Texas Dallas TX USA 75390 ed Ctr, Dept Biochem, Dallas, TX 75390 USA Univ Texas, SW Med Ctr, Ctr Dev Biol, Dallas, TX 75390 USA Univ Texas Dallas TX USA 75390 ed Ctr, Ctr Dev Biol, Dallas, TX 75390 USA Univ Texas, SW Med Ctr, Dept Pathol, Dallas, TX 75390 USA Univ Texas Dallas TX USA 75390 Med Ctr, Dept Pathol, Dallas, TX 75390 USA
Titolo Testata:
NEUROSCIENCE
fascicolo: 2, volume: 106, anno: 2001,
pagine: 263 - 274
SICI:
0306-4522(2001)106:2<263:ENDDTN>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-DEATH; CYTOCHROME-C; SENSORY NEURONS; APOPTOTIC PATHWAYS; DISTINCT PATHWAYS; BAX DELETION; SPINAL-CORD; IN-VIVO; BCL-2; MICE;
Keywords:
caspase; cytochrome c; apoptosis; cell death; neuron; mouse;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Herz, J Univ Texas, SW Med Ctr, Dept Mol Genet, 5323 Harry Hines Blvd, Dallas, TX 75390 USA Univ Texas 5323 Harry Hines Blvd Dallas TX USA 75390 TX 75390 USA
Citazione:
N. Honarpour et al., "Embryonic neuronal death due to neurotrophin and neurotransmitter deprivation occurs independent of APAF-1", NEUROSCIENC, 106(2), 2001, pp. 263-274

Abstract

Apoptotic protease-activating factor-1 (Apaf-1), dATP, and procaspase-9 form a multimeric complex that triggers programmed cell death through the activation of caspases upon release of cytochrome e from the mitochondria intothe cytosol. Although cell death pathways exist that can bypass the requirement for cytochrome c release and caspase activation, several gene knockout studies have shown that the cytochrome c-mediated apoptotic pathway is critical for neural development. Specifically, the number of neuronal progenitor cells is abnormally increased in Apaf-1-, caspase-9-, caspase-3-deficient mice. However, the role of the cytochrome c cell death pathway for apoptosis of postmitotic, differentiated neurons in the developing brain has notbeen investigated in vivo. In this study we investigated embryonic neuronal cell death caused by trophic factor deprivation or lack of neurotransmitter release by analyzing Apaf-1/tyrosine kinase receptor A (TrkA) and Apaf-1/Munc-18 double mutant mice. Histological analysis of the double mutants' brains (including cell counting and terminal (TdT)-mediated dUTP-biotin nickend labeling (TUNEL) staining) reveals that neuronal cell death caused by these stimuli can proceed independent of Apaf-1. We propose that a switch between apoptotic programs (and their respective proteins) characterizes the transition of a neuronal precursor cell from the progenitor pool to the postmitotic population of differentiated neurons. (C) 2001 IBRO. Published by Elsevier Science Ltd. All rights reserved.

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Documento generato il 26/09/20 alle ore 22:51:17