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A polymorphism upstream of\n                    <jats:italic>KCNE2<\/jats:italic>\n                    is associated with reduced lung function in human populations, but the pulmonary consequences of\n                    <jats:italic>KCNE2<\/jats:italic>\n                    gene disruption are unknown. Here, germline deletion of mouse\n                    <jats:italic>Kcne2<\/jats:italic>\n                    reduced pulmonary expression of potassium channel \u03b1 subunits\n                    <jats:italic>Kcnq1<\/jats:italic>\n                    and\n                    <jats:italic>Kcnb1<\/jats:italic>\n                    but did not alter expression of other\n                    <jats:italic>Kcne<\/jats:italic>\n                    genes. Kcne2 colocalized and coimmunoprecipitated with Kcnq1 in mouse lungs, suggesting the formation of pulmonary Kcnq1\u2010Kcne2 potassium channel complexes.\n                    <jats:italic>Kcne2<\/jats:italic>\n                    deletion reduced blood O\n                    <jats:sub>2<\/jats:sub>\n                    , increased CO\n                    <jats:sub>2<\/jats:sub>\n                    , increased pulmonary apoptosis, and increased inflammatory mediators TNF\u2010\u03b1, IL\u20106, and leukocytes in bronchoalveolar lavage (BAL) fluids. Consistent with increased pulmonary vascular leakage,\n                    <jats:italic>Kcne<\/jats:italic>\n                    2 deletion increased plasma, BAL albumin, and the BAL:plasma albumin concentration ratio.\n                    <jats:italic>\n                      Kcne2\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    mouse lungs exhibited baseline induction of the reperfusion injury salvage kinase pathway but were less able to respond\n                    <jats:italic>via<\/jats:italic>\n                    this pathway to imposed pulmonary ischemia\/reperfusion injury (IRI). We conclude that KCNE2 regulates KCNQ1 in the lungs and is required for normal lung function and resistance to pulmonary IRI. Our data support a causal relationship between\n                    <jats:italic>KCNE2<\/jats:italic>\n                    gene disruption and lung dysfunction.\u2014Zhou, L., K\u00f6hncke, C., Hu, Z., Roepke, T. K., Abbott, G. W. The KCNE2 potassium channel \u03b2 subunit is required for normal lung function and resilience to ischemia and reperfusion injury. FASEB J. 33, 9762\u20139774 (2019).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201802519r","type":"journal-article","created":{"date-parts":[[2019,6,4]],"date-time":"2019-06-04T16:31:54Z","timestamp":1559665914000},"page":"9762-9774","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["The KCNE2 potassium channel \u03b2 subunit is required for normal lung function and resilience to ischemia and reperfusion injury"],"prefix":"10.1096","volume":"33","author":[{"given":"Leng","family":"Zhou","sequence":"first","affiliation":[{"name":"Department of Anesthesiology Sichuan University  Chengdu China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Clemens","family":"K\u00f6hncke","sequence":"additional","affiliation":[{"name":"Experimental and Clinical Research Center Max Delbr\u00fcck Center for Molecular Medicine  Berlin Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhaoyang","family":"Hu","sequence":"additional","affiliation":[{"name":"Laboratory of Anesthesiology and Critical Care Medicine Translational Neuroscience Center West China Hospital Sichuan University  Chengdu China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Torsten K.","family":"Roepke","sequence":"additional","affiliation":[{"name":"Experimental and Clinical Research Center Max Delbr\u00fcck Center for Molecular Medicine  Berlin Germany"},{"name":"Clinic for Cardiology and Angiology Charit\u00e9\u2013Berlin University of Medicine Campus Mitte  Berlin Germany"},{"name":"Clinic for Internal Medicine and Cardiology Klinikum Niederlausitz  Senftenberg Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Geoffrey W.","family":"Abbott","sequence":"additional","affiliation":[{"name":"Bioelectricity Laboratory Department of Physiology and Biophysics School of Medicine University of California\u2010Irvine  Irvine California 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