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Elevations of the intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    concentration and generation of reactive oxygen species induced by A\u03b2, and potentiated by mutant PS-1, were suppressed in calbindin-overexpressing cells. Impairment of mitochondrial function by A\u03b2 (which preceded apoptosis) was exacerbated by PS-1 mutations and was largely prevented by calbindin. These findings suggest that PS-1 mutations render neurons vulnerable to apoptosis by a mechanism involving destabilization of cellular calcium homeostasis, which leads to oxidative stress and mitochondrial dysfunction.\n                  <\/jats:p>","DOI":"10.1073\/pnas.95.6.3227","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:40:52Z","timestamp":1027680052000},"page":"3227-3232","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":183,"title":["Calbindin D28k blocks the proapoptotic actions of mutant presenilin 1: Reduced oxidative stress and preserved mitochondrial\u2009function"],"prefix":"10.1073","volume":"95","author":[{"given":"Qing","family":"Guo","sequence":"first","affiliation":[{"name":"Sanders\u2013Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536; and Department of Biochemistry and Molecular Biology, University 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