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KI mice were born at the expected Mendelian ratio, and adult KI mice exhibited normal cardiac morphology and function at baseline. However, KI mice were protected from myocardial ischemia\/reperfusion (I\/R) injury and exhibited reduced cardiomyocyte apoptosis. Although suppression of endogenous Mst1 also reduced I\/R injury, there was no additive protective effect when Mst1 was inhibited in KI mice. The development of dilated cardiomyopathy induced by cardiac-specific overexpression of Mst1 was also ameliorated in KI mice. Lats2 and YAP, two other key components of the Hippo pathway, were not affected in KI mice. These results suggest that Ser14 phosphorylation of Bcl-xL plays an essential role in mediating both cardiomyocyte apoptosis and myocardial injury by acting as a key downstream mediator of Mst1 independently of the canonical Hippo pathway.<\/jats:p>","DOI":"10.1172\/jci.insight.86217","type":"journal-article","created":{"date-parts":[[2016,4,20]],"date-time":"2016-04-20T11:01:01Z","timestamp":1461150061000},"source":"Crossref","is-referenced-by-count":50,"title":["Mst1-mediated phosphorylation of Bcl-xL is required for myocardial reperfusion injury"],"prefix":"10.1172","volume":"1","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2005-3161","authenticated-orcid":true,"given":"Michinari","family":"Nakamura","sequence":"first","affiliation":[{"name":"Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey, 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