Different cellular pathways can lead to apoptosis. Apaf1 is the molecular core of the apoptosome, a multiproteic complex mediating the so-called mitochondrial pathway of cell death. The importance of this pathway during development has been clearly demonstrated by knocking out key genes. Also, the relevance of Apaf1 dosage during development has been recently underlined. Moreover, a growing body of evidences seems to point out a possible role of the mitochondria-dependent apoptosis in different pathologies. In particular, we discuss here some recent evidences regarding the putative role of the apoptosome in neurodegeneration and cancer.

Ferraro, E., Corvaro, M., Cecconi, F. (2003). Physiological and pathological roles of Apaf1 and the apoptosome. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 7(1), 21-34.

Physiological and pathological roles of Apaf1 and the apoptosome

CECCONI, FRANCESCO
2003-01-01

Abstract

Different cellular pathways can lead to apoptosis. Apaf1 is the molecular core of the apoptosome, a multiproteic complex mediating the so-called mitochondrial pathway of cell death. The importance of this pathway during development has been clearly demonstrated by knocking out key genes. Also, the relevance of Apaf1 dosage during development has been recently underlined. Moreover, a growing body of evidences seems to point out a possible role of the mitochondria-dependent apoptosis in different pathologies. In particular, we discuss here some recent evidences regarding the putative role of the apoptosome in neurodegeneration and cancer.
2003
Pubblicato
Rilevanza nazionale
Articolo
Sì, ma tipo non specificato
Settore BIO/06 - ANATOMIA COMPARATA E CITOLOGIA
English
Con Impact Factor ISI
Apaf1; Apoptosis; Apoptosome; Caspases; Cell death; Neurodegeneration
Ferraro, E., Corvaro, M., Cecconi, F. (2003). Physiological and pathological roles of Apaf1 and the apoptosome. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 7(1), 21-34.
Ferraro, E; Corvaro, M; Cecconi, F
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/53619
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