{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T09:22:14Z","timestamp":1789982534042,"version":"4.0.1"},"reference-count":34,"publisher":"National Academy of Sciences","issue":"30","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2013,7,23]]},"abstract":"<jats:p>\n                    Endothelial dysfunction is associated with diverse cardiovascular pathologies. Here, we show a previously unappreciated role for the Abelson (Abl) family kinases (Abl and Arg) in endothelial function and the regulation of angiogenic factor pathways important for vascular homeostasis. Endothelial\n                    <jats:italic>Abl<\/jats:italic>\n                    deletion in\n                    <jats:italic>Arg<\/jats:italic>\n                    -null mice led to late-stage embryonic and perinatal lethality, with mutant mice displaying focal loss of vasculature and tissue necrosis. Loss of Abl kinases led to increased endothelial cell apoptosis both in vitro and in vivo, contributing to vascular dysfunction, infarction, and tissue damage. Mechanistically, we identify a unique dual role for Abl kinases in the regulation of angiopoietin\/Tie2 protein kinase signaling. Endothelial Abl kinases modulate Tie2 expression and angiopoietin-1\u2013mediated endothelial cell survival. These findings reveal a critical requirement for the Abl kinases in vascular development and function, which may have important implications for the clinical use of Abl kinase inhibitors.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1304188110","type":"journal-article","created":{"date-parts":[[2013,7,10]],"date-time":"2013-07-10T00:50:57Z","timestamp":1373417457000},"page":"12432-12437","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":64,"title":["Abl kinases are required for vascular function, Tie2 expression, and angiopoietin-1\u2013mediated survival"],"prefix":"10.1073","volume":"110","author":[{"given":"Elizabeth M.","family":"Chislock","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC 27710"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Colleen","family":"Ring","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC 27710"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ann Marie","family":"Pendergast","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC 27710"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2013,7,9]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/nm0603-653"},{"key":"e_1_3_3_2_2","first-page":"3527","article-title":"Endothelial cells in physiology and in the pathophysiology of vascular disorders","volume":"91","author":"Cines DB","year":"1998","unstructured":"DB Cines, et al., Endothelial cells in physiology and in the pathophysiology of vascular disorders. 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