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The association of TSG101 with ALIX prevents predisposition to apoptosis, whereas ALIX\u2013ALG-2 interaction favors a death phenotype. Altered Ca<jats:sup>2+<\/jats:sup>homeostasis in cells and a simultaneous increase in the protein levels of ALIX and ALG-2 are required to elicit apoptosis by activating ER stress\u2013associated caspase 4\/12. We further demonstrate that in the presence of membrane-associated, disease-causing prion protein<jats:sup>Ctm<\/jats:sup>PrP, increased ALIX and ALG-2 levels are detected along with ER stress markers and associated caspases in transgenic brain lysates and cells. These effects were rescued by overexpression of TSG101. This is significant because MGRN1 deficiency is closely associated with neurodegeneration and prenatal and neonatal mortality, which could be due to excess cell death in selected brain regions or myocardial apoptosis during embryonic development.<\/jats:p>","DOI":"10.1091\/mbc.e16-12-0855","type":"journal-article","created":{"date-parts":[[2017,5,25]],"date-time":"2017-05-25T00:50:19Z","timestamp":1495673419000},"page":"2106-2122","source":"Crossref","is-referenced-by-count":20,"title":["Tumor susceptibility gene 101 regulates predisposition to apoptosis via ESCRT machinery accessory proteins"],"prefix":"10.1091","volume":"28","author":[{"given":"Zenia","family":"Kaul","sequence":"first","affiliation":[{"name":"Biophysics and Structural Genomics Division, Saha Institute of Nuclear Physics, Kolkata 700064, India"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Oishee","family":"Chakrabarti","sequence":"additional","affiliation":[{"name":"Biophysics and Structural 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