BOK controls apoptosis by Ca2+ transfer through ER-mitochondrial contact sites
Marcos A. Carpio, Robert E. Means, Allison L. Brill, Alva G. Sainz, Barbara E. Ehrlich, Samuel G. Katz
Abstract
cells is still insufficient to rescue thapsigargin-induced calcium transfer and apoptosis. Likewise, a BOK mutant unable to interact with IP3R restores ER-mitochondrial proximity, but not ER-mitochondrial calcium transfer, MAM protein composition, or apoptosis. This work identifies the dynamic coordination of ER-mitochondrial contact by BOK as an important control point for apoptosis.
Topics & Concepts
MitochondrionEndoplasmic reticulumCell biologyApoptosisCalciumThapsigarginCalcium signalingMitochondrial apoptosis-induced channelInositol trisphosphate receptorInositolBiologyUnfolded protein responseInner mitochondrial membraneChemistryReceptorSignal transductionBiochemistryOrganic chemistryMitochondrial Function and PathologyCell death mechanisms and regulationEndoplasmic Reticulum Stress and Disease