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Titolo:
Apaf1 in developmental apoptosis and cancer: how many ways to die?
Autore:
Cecconi, F; Gruss, P;
Indirizzi:
Univ Roma Tor Vergata, Dept Biol, I-00133 Rome, Italy Univ Roma Tor Vergata Rome Italy I-00133 Dept Biol, I-00133 Rome, Italy Max Planck Inst Biophys Chem, Dept Mol Cell Biol, D-37077 Gottingen, Germany Max Planck Inst Biophys Chem Gottingen Germany D-37077 ottingen, Germany
Titolo Testata:
CELLULAR AND MOLECULAR LIFE SCIENCES
fascicolo: 11, volume: 58, anno: 2001,
pagine: 1688 - 1697
SICI:
1420-682X(200110)58:11<1688:AIDAAC>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; CHROMOSOME ARM 12Q; CYTOCHROME-C; INNER-EAR; CASPASE ACTIVATION; DROSOPHILA HOMOLOG; ALLELIC LOSS; KAPPA-B; BCL-2; IDENTIFICATION;
Keywords:
Bcl-X; caspase; cell death; interdigital webs; neuronal founder cells; Nod; oncogenes;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Cecconi, F Univ Roma Tor Vergata, Dept Biol, Via Ric Sci, I-00133 Rome, Italy Univ Roma Tor Vergata Via Ric Sci Rome Italy I-00133 me, Italy
Citazione:
F. Cecconi e P. Gruss, "Apaf1 in developmental apoptosis and cancer: how many ways to die?", CELL MOL L, 58(11), 2001, pp. 1688-1697

Abstract

Apaf1 has been described as the core of the apoptosome. Deficiency in murine Apaf1 leads to embryonic lethality with a phenotype affecting many aspects of developmental apoptosis. In the developing brain, Apaf1 is a death regulator of the neuronal founder cells. Combined intercrosses of mouse linesmutant for members of the mitochondrial death pathway are providing us with some clues about the relative regulation existing among neuronal cell populations. Apaf1-deficient embryos dis-play an interesting phenotype in the inner ear and in limb development, which involves different caspase-dependent and -independent pathways. Moreover, APAF1 is mutated in human melanomas, and its depletion contributes to malignant transformation in a mouse model of cancer. This review has a double aim: the analysis of the alternativestaken by the embryo to bring into the suicidal program different cells at different stages, and the relevance of APAF1 in the onset and progression of cancer.

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Documento generato il 18/02/20 alle ore 14:59:05