Control of mitochondrial physiology and cell death by the Bcl-2 family proteins Bax and Bok
- 1 October 2017
- journal article
- review article
- Published by Elsevier in Neurochemistry International
- Vol. 109, 162-170
Abstract
No abstract availableKeywords
Funding Information
- Science Foundation Ireland (13/IA/1881, 14/JP-ND/B3077)
This publication has 168 references indexed in Scilit:
- Consequences of the combined loss of BOK and BAK or BOK and BAXCell Death & Disease, 2013
- A Novel Role for Bcl-2 in Regulation of Cellular Calcium ExtrusionCurrent Biology, 2012
- The permeability transition pore as a Ca2+ release channel: New answers to an old questionCell Calcium, 2012
- BCL-2 family member BOK is widely expressed but its loss has only minimal impact in miceCell Death & Differentiation, 2012
- New role of the BCL2 family of proteins in the regulation of mitochondrial dynamicsCurrent Opinion in Cell Biology, 2010
- The BCL-2 Family ReunionMolecular Cell, 2010
- Abnormal mitochondrial dynamics and neurodegenerative diseasesBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2010
- What is the mitochondrial permeability transition pore?Journal of Molecular and Cellular Cardiology, 2009
- Chemical Inhibition of the Mitochondrial Division Dynamin Reveals Its Role in Bax/Bak-Dependent Mitochondrial Outer Membrane PermeabilizationDevelopmental Cell, 2008
- Cell DeathCell, 2004