{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T03:22:47Z","timestamp":1792207367176,"version":"4.4.0"},"reference-count":37,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2014,7,29]],"date-time":"2014-07-29T00:00:00Z","timestamp":1406592000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2014,7,29]],"date-time":"2014-07-29T00:00:00Z","timestamp":1406592000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["P01 HL091799"],"award-info":[{"award-number":["P01 HL091799"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["1R01HL109209\u201001A1"],"award-info":[{"award-number":["1R01HL109209\u201001A1"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2014,11]]},"abstract":"<jats:sec>\n                    <jats:label\/>\n                    <jats:p>\n                      The most common cause of dilated cardiomyopathy and heart failure (HF) is ischemic heart disease; however, in a third of all patients the cause remains undefined and patients are diagnosed as having idiopathic dilated cardiomyopathy (IDC). Recent studies suggest that many patients with IDC have a family history of HF and rare genetic variants in over 35 genes have been shown to be causative of disease. We employed whole\u2010exome sequencing to identify the causative variant in a large family with autosomal dominant transmission of dilated cardiomyopathy. Sequencing and subsequent informatics revealed a novel 10\u2010nucleotide deletion in the BCL2\u2010associated athanogene 3 (\n                      <jats:italic>BAG3<\/jats:italic>\n                      ) gene (Ch10:del 121436332_12143641: del. 1266_1275 [NM 004281]) that segregated with all affected individuals. The deletion predicted a shift in the reading frame with the resultant deletion of 135 amino acids from the C\u2010terminal end of the protein. Consistent with genetic variants in genes encoding other sarcomeric proteins there was a considerable amount of genetic heterogeneity in the affected family members. Interestingly, we also found that the levels of BAG3 protein were significantly reduced in the hearts from unrelated patients with end\u2010stage HF undergoing cardiac transplantation when compared with non\u2010failing controls. Diminished levels of BAG3 protein may be associated with both familial and non\u2010familial forms of dilated cardiomyopathy. J. Cell. Physiol. 229: 1697\u20131702, 2014. \u00a9 2014 The Authors.\n                      <jats:italic>Journal of Cellular Physiology<\/jats:italic>\n                      Published by Wiley Periodicals, Inc.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/jcp.24615","type":"journal-article","created":{"date-parts":[[2014,3,13]],"date-time":"2014-03-13T02:21:02Z","timestamp":1394677262000},"page":"1697-1702","source":"Crossref","is-referenced-by-count":79,"title":["Decreased Levels of BAG3 in a Family With a Rare Variant and in Idiopathic Dilated Cardiomyopathy"],"prefix":"10.1002","volume":"229","author":[{"given":"Arthur M.","family":"Feldman","sequence":"first","affiliation":[{"name":"Departments of Medicine Neuroscience Physiology and Pharmacology Temple University School of Medicine Philadelphia Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rene 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