{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T14:01:20Z","timestamp":1787752880742,"version":"build-2784847793"},"reference-count":49,"publisher":"American Society for Clinical Investigation","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,2,27]]},"abstract":"<jats:p>\n                    The mitochondrial calcium uniporter is widely accepted as the primary route of rapid calcium entry into mitochondria, where increases in matrix calcium contribute to bioenergetics but also mitochondrial permeability and cell death. Hence, regulation of uniporter activity is critical to mitochondrial homeostasis. The uniporter subunit EMRE is known to be an essential regulator of the channel-forming protein MCU in cell culture, but EMRE\u2019s impact on organismal physiology is less understood. Here we characterize a mouse model of EMRE deletion and show that EMRE is indeed required for mitochondrial calcium uniporter function in vivo.\n                    <jats:italic>\n                      EMRE\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    <\/jats:italic>\n                    mice are born less frequently; however, the mice that are born are viable, healthy, and do not manifest overt metabolic impairment, at rest or with exercise. Finally, to investigate the role of EMRE in disease processes, we examine the effects of EMRE deletion in a muscular dystrophy model associated with mitochondrial calcium overload.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.134063","type":"journal-article","created":{"date-parts":[[2020,2,4]],"date-time":"2020-02-04T12:25:06Z","timestamp":1580819106000},"source":"Crossref","is-referenced-by-count":63,"title":["EMRE is essential for mitochondrial calcium uniporter activity in a mouse model"],"prefix":"10.1172","volume":"5","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8604-1633","authenticated-orcid":true,"given":"Julia C.","family":"Liu","sequence":"first","affiliation":[{"name":"Cardiovascular Branch and"},{"name":"Center for Molecular Medicine, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, USA."},{"name":"Postdoctoral Research Associate Program, National Institute of General Medical Sciences, NIH, Bethesda, Maryland, 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