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A unique zebrafish mutant with specific cardiac arrhythmia phenotypes was identified and mutation of the uncharacterized\n                    <jats:italic>tmem161b<\/jats:italic>\n                    gene shown to be causative. Tmem161b knockout mice are perinatal lethal and isolated embryonic cardiomyocytes exhibit arrhythmic Ca\n                    <jats:sup>2+<\/jats:sup>\n                    oscillations, suggesting functional conservation. Protein localization studies show Tmem161b is expressed in excitable cells and at cardiomyocyte plasma membranes. Imaging of in vivo action potentials shows\n                    <jats:italic>tmem161b<\/jats:italic>\n                    mutants have prolonged action potential repolarization. Patch-clamping of isolated cardiomyocytes confirms prolonged action potential repolarization and shows increased Ca\n                    <jats:sup>2+<\/jats:sup>\n                    and K\n                    <jats:sup>+<\/jats:sup>\n                    currents are likely the cause of altered action potential morphology. This suggests Tmem161b is a new conserved regulator of cardiac rhythm by inhibiting Ca\n                    <jats:sup>2+<\/jats:sup>\n                    and K\n                    <jats:sup>+<\/jats:sup>\n                    currents.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2018220118","type":"journal-article","created":{"date-parts":[[2021,2,17]],"date-time":"2021-02-17T16:06:32Z","timestamp":1613577992000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":21,"title":["The zebrafish\n                    <i>grime<\/i>\n                    mutant uncovers an evolutionarily conserved role for Tmem161b in the control of cardiac rhythm"],"prefix":"10.1073","volume":"118","author":[{"given":"Charlotte D.","family":"Koopman","sequence":"first","affiliation":[{"name":"Department of Cardiac Development and Genetics, Hubrecht Institute, University Medical Centre Utrecht, Utrecht 3584 CT, The Netherlands;"},{"name":"Department of 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