Bax and Bak Promote Apoptosis by Modulating Endoplasmic Reticular and Mitochondrial Ca2+ Stores
Open Access
- 1 March 2002
- journal article
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 277 (11), 9219-9225
- https://doi.org/10.1074/jbc.m106817200
Abstract
No abstract availableKeywords
This publication has 53 references indexed in Scilit:
- Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and DeathScience, 2001
- Bax and Adenine Nucleotide Translocator Cooperate in the Mitochondrial Control of ApoptosisScience, 1998
- Close Contacts with the Endoplasmic Reticulum as Determinants of Mitochondrial Ca 2+ ResponsesScience, 1998
- Oxygen-bridged Dinuclear Ruthenium Amine Complex Specifically Inhibits Ca2+ Uptake into Mitochondria in Vitroand in Situ in Single Cardiac MyocytesJournal of Biological Chemistry, 1998
- The Role of Calcium in the Regulation of ApoptosisBiochemical and Biophysical Research Communications, 1997
- Inhibition of Bax Channel-Forming Activity by Bcl-2Science, 1997
- Mitochondrial control of apoptosisImmunology Today, 1997
- Bcl-xL forms an ion channel in synthetic lipid membranesNature, 1997
- Induction of Apoptotic Program in Cell-Free Extracts: Requirement for dATP and Cytochrome cCell, 1996
- Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell deathNature, 1990