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When separation means death: killing through the mitochondria, but starting from the endoplasmic reticulum
Author(s) -
Lamarca Violeta,
Scorrano Luca
Publication year - 2009
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/emboj.2009.135
Subject(s) - endoplasmic reticulum , medical school , biology , library science , microbiology and biotechnology , medicine , computer science , medical education
Proteins of the BCL‐2 family are key mitochondrial actors in the intrinsic pathway of apoptosis. However, they also exert housekeeping functions at the level of the endoplasmic reticulum (ER), controlling Ca 2+ homeostasis and the unfolded protein response (UPR). Klee et al (2009) in an article published in this issue, identified that proapoptotic proteins of the BCL‐2 family can activate the mitochondrial pathway of death also when restricted only at the ER, by engaging an atypical arm of the UPR requiring Ca 2+ . This paper elucidates how unconventional cascades overcome the spatial restriction of cellular signalling components and add a further layer of complexity to the regulation of cell death.