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VDAC2 primes myeloma cells for BAK-dependent apoptosis and represents a novel therapeutic target.
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Nantes Université, CHU Nantes, CNRS, INSERM, CRCI2NA, Université d'Angers, Nantes, France.
SPATA33 functions as a mitophagy receptor in mammalian germline.
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Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, P. R. China.
Mitophagy is an essential mechanism in maintaining cellular homeostasis, in which damaged and superfluous mitochondria are selectively degraded by the autophagy-lysosome pathway. Our recent study revealed that SPATA33 functions as a novel receptor for mitophagy in the priming of mitochondria for degradation in male germline cells. SPATA33 directly mediates the interaction of the outer mitochondrial membrane protein VDAC2 with the autophagy machinery component ATG16L1 during mitophagy.
View Article and Find Full Text PDFBioID-based proteomic analysis of the Bid interactome identifies novel proteins involved in cell-cycle-dependent apoptotic priming.
Cell Death Dis
October 2020
Wellcome Centre for Cell-Matrix Research, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK.
Apoptotic priming controls the commitment of cells to apoptosis by determining how close they lie to mitochondrial permeabilisation. Variations in priming are important for how both healthy and cancer cells respond to chemotherapeutic agents, but how it is dynamically coordinated by Bcl-2 proteins remains unclear. The Bcl-2 family protein Bid is phosphorylated when cells enter mitosis, increasing apoptotic priming and sensitivity to antimitotic drugs.
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