{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T16:07:27Z","timestamp":1790698047614,"version":"4.1.0"},"reference-count":38,"publisher":"American Physiological Society","issue":"6","funder":[{"name":"NIH","award":["R01 HL124319-01A1"],"award-info":[{"award-number":["R01 HL124319-01A1"]}]},{"name":"AHA","award":["14GRNT19710006"],"award-info":[{"award-number":["14GRNT19710006"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2020,6,1]]},"abstract":"<jats:p> The gene encoding SAP97 ( DLG1) joins a growing list of genes encoding ion channel interacting proteins (ChIPs) identified as potential channelopathy-susceptibility genes because of their ability to regulate the trafficking, targeting, and modulation of ion channels that are critical for the generation and propagation of the cardiac electrical impulse. In this study we provide the first data supporting DLG1-encoded SAP97\u2019s candidacy as a minor Brugada syndrome susceptibility gene. <\/jats:p>","DOI":"10.1152\/ajpheart.00481.2019","type":"journal-article","created":{"date-parts":[[2020,3,20]],"date-time":"2020-03-20T16:01:37Z","timestamp":1584720097000},"page":"H1357-H1370","source":"Crossref","is-referenced-by-count":21,"title":["Abnormal myocardial expression of SAP97 is associated with arrhythmogenic risk"],"prefix":"10.1152","volume":"318","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0734-9187","authenticated-orcid":false,"given":"Hassan","family":"Musa","sequence":"first","affiliation":[{"name":"Departments of Internal Medicine and of Physiology and Cell Biology, Dorothy M. 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