Oxidative Bax dimerization promotes its translocation to mitochondria independently of apoptosis-Reference-Cited by-同舟云学术

Oxidative Bax dimerization promotes its translocation to mitochondria independently of apoptosis

Published:2005-06-21 Issue:11 Volume:19 Page:1504-1506
ISSN:0892-6638
Container-title:The FASEB Journal
language:en
Short-container-title:FASEB j.

Author:

D'Alessio M.¹,De Nicola M.¹,Coppola S.¹,Gualandi G.²,Pugliese L.³,Cerella C.¹,Cristofanon S.¹,Civitareale P.¹,Ciriolo M. R.¹,Bergamaschi A.⁴,Magrini A.⁴,Ghibelli L.¹

Affiliation:

1. Dipartimento di BiologiaUniversita' di Roma “Tor Vergata,” via Ricerca Scientifica Roma Italy

2. Universita' della Tuscia Viterbo

3. Safan Bionformatics Torino Italy

4. Cattedra di Medicina del LavoroUniversita' di Roma “Tor Vergata,” via Ricerca Scientifica Roma Italy

Funder

Ministero dell’Istruzione, dell’Università e della Ricerca

Publisher

Wiley

Subject

Genetics,Molecular Biology,Biochemistry,Biotechnology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1096/fj.04-3329fje

Reference73 articles.

1. Cell Death: The Significance of Apoptosis

2. GSH extrusion and the mitochondrial pathway of apoptotic signalling

3. Mechanisms of CD95 (APO-1/Fas)-mediated apoptosis

4. Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis

5. Damage-induced Bax N-terminal change, translocation to mitochondria and formation of Bax dimers/complexes occur regardless of cell fate

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