Prosurvival AMBRA1 turns into a proapoptotic BH3-like protein during mitochondrial apoptosis
Published 2016 View Full Article
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Title
Prosurvival AMBRA1 turns into a proapoptotic BH3-like protein during mitochondrial apoptosis
Authors
Keywords
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Journal
Autophagy
Volume 12, Issue 6, Pages 963-975
Publisher
Informa UK Limited
Online
2016-04-29
DOI
10.1080/15548627.2016.1164359
References
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Related references
Note: Only part of the references are listed.- AMBRA1 and BECLIN 1 interplay in the crosstalk between autophagy and cell proliferation
- (2015) Valentina Cianfanelli et al. CELL CYCLE
- Ambra1 at a glance
- (2015) V. Cianfanelli et al. JOURNAL OF CELL SCIENCE
- AMBRA1 is able to induce mitophagy via LC3 binding, regardless of PARKIN and p62/SQSTM1
- (2014) F Strappazzon et al. CELL DEATH AND DIFFERENTIATION
- AMBRA1 Interplay with Cullin E3 Ubiquitin Ligases Regulates Autophagy Dynamics
- (2014) Manuela Antonioli et al. DEVELOPMENTAL CELL
- AMBRA1 links autophagy to cell proliferation and tumorigenesis by promoting c-Myc dephosphorylation and degradation
- (2014) Valentina Cianfanelli et al. NATURE CELL BIOLOGY
- mTOR inhibits autophagy by controlling ULK1 ubiquitylation, self-association and function through AMBRA1 and TRAF6
- (2013) Francesca Nazio et al. NATURE CELL BIOLOGY
- ATG5 is induced by DNA-damaging agents and promotes mitotic catastrophe independent of autophagy
- (2013) Dipak Maskey et al. Nature Communications
- Proteolysis of Ambra1 during apoptosis has a role in the inhibition of the autophagic pro-survival response
- (2012) V Pagliarini et al. CELL DEATH AND DIFFERENTIATION
- BH3 mimetics reveal the network properties of autophagy-regulatory signaling cascades
- (2011) Shoaib Ahmad Malik et al. Autophagy
- Mitochondrial BCL-2 inhibits AMBRA1-induced autophagy
- (2011) Flavie Strappazzon et al. EMBO JOURNAL
- Distinct regulation of nNOS and iNOS by CB2 receptor in remote delayed neurodegeneration
- (2011) S. Oddi et al. JOURNAL OF MOLECULAR MEDICINE-JMM
- The Autophagy Protein Atg12 Associates with Antiapoptotic Bcl-2 Family Members to Promote Mitochondrial Apoptosis
- (2011) Assaf D. Rubinstein et al. MOLECULAR CELL
- A systems level strategy for analyzing the cell death network: implication in exploring the apoptosis/autophagy connection
- (2010) E Zalckvar et al. CELL DEATH AND DIFFERENTIATION
- Chemosensitization of Prostate Cancer by Modulating Bcl-2 Family Proteins
- (2010) David Karnak et al. CURRENT DRUG TARGETS
- The Beclin 1 interactome
- (2010) Congcong He et al. CURRENT OPINION IN CELL BIOLOGY
- Crosstalk between apoptosis and autophagy within the Beclin 1 interactome
- (2010) Maria Chiara Maiuri et al. EMBO JOURNAL
- Disease-causing mutations in Parkin impair mitochondrial ubiquitination, aggregation, and HDAC6-dependent mitophagy
- (2010) Joo-Yong Lee et al. JOURNAL OF CELL BIOLOGY
- The dynamic interaction of AMBRA1 with the dynein motor complex regulates mammalian autophagy
- (2010) Sabrina Di Bartolomeo et al. JOURNAL OF CELL BIOLOGY
- Cross talk between apoptosis and autophagy by caspase-mediated cleavage of Beclin 1
- (2010) M Djavaheri-Mergny et al. ONCOGENE
- Beclin 1 cleavage by caspase-3 inactivates autophagy and promotes apoptosis
- (2010) Yushan Zhu et al. Protein & Cell
- Apoptosis blocks Beclin 1-dependent autophagosome synthesis: an effect rescued by Bcl-xL
- (2009) S Luo et al. CELL DEATH AND DIFFERENTIATION
- Antagonism of Beclin 1-dependent autophagy by BCL-2 at the endoplasmic reticulum requires NAF-1
- (2009) Natasha C Chang et al. EMBO JOURNAL
- Caspase-mediated cleavage of ATG6/Beclin-1 links apoptosis to autophagy in HeLa cells
- (2008) Dong-Hyung Cho et al. CANCER LETTERS
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