Prosurvival AMBRA1 turns into a proapoptotic BH3-like protein during mitochondrial apoptosis

Collection with item attached
2016_04
Item details URL
http://open-repository.kisti.re.kr/cube/handle/open_repository/470623.do
Title
Prosurvival AMBRA1 turns into a proapoptotic BH3-like protein during mitochondrial apoptosis
Description
Autophagy and apoptosis are 2 stress-response mechanisms that are closely interconnected. However, the molecular interplays between these 2 pathways remain to be clarified. Here we report that the crucial proautophagic factor AMBRA1 can act as a positive mediator of mitochondrial apoptosis. Indeed, we show that, in a proapoptotic positive feedback loop, the C-terminal part of AMBRA1, generated by CASP/CASPASE cleavage upon apoptosis induction, inhibits the antiapoptotic factor BCL2 by a direct binding through its BH3-like domain. The mitochondrial AMBRA1-BCL2 complex is thus at the crossroad between autophagy and cell death and may represent a novel target in development of therapeutic approaches in clinical diseases.
provenance
Made available in Cube on 2016-08-06T06:59:57Z (GMT). No. of bitstreams: 0
language
en
creator
Strappazzon, Flavie
Di Rita, Anthea
Cianfanelli, Valentina
D'Orazio, Melania
Nazio, Francesca
Fimia, Gian Maria
Cecconi, Francesco
date
2016-04-28
accessioned
2016-08-06T06:59:57Z
available
2016-08-06T06:59:57Z
issued
2016-08-06
identifier
/pmc/articles/PMC4922440/
/pubmed/27123694
http://dx.doi.org/10.1080/15548627.2016.1164359
uri
http://open-repository.kisti.re.kr/cube/handle/open_repository/470623.do
publisher
Taylor & Francis
rights
http://creativecommons.org/licenses/by-nc/3.0/
? 2016 The Author(s). Published with license by Taylor & Francis Group, LLC
This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License http://creativecommons.org/licenses/by-nc/3.0/, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.
subject
Basic Research Papers
type
Text


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