{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T19:12:53Z","timestamp":1791573173976,"version":"4.3.4"},"reference-count":60,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2018,4]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>Endothelial upregulation of adhesion molecules serves to recruit leukocytes to inflammatory sites and appears to be promoted by NOTCH1; however, current models based on interactions between active NOTCH1 and NF-\u03baB components cannot explain the transcriptional selectivity exerted by NOTCH1 in this context.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results\u2014<\/jats:title>\n            <jats:p>Observing that Cre\/Lox-induced conditional mutations of endothelial Notch modulated inflammation in murine contact hypersensitivity, we found that IL (interleukin)-1\u03b2 stimulation induced rapid recruitment of RELA (v-rel avian reticuloendotheliosis viral oncogene homolog A) to genomic sites occupied by NOTCH1-RBPJ (recombination signal-binding protein for immunoglobulin kappa J region) and that NOTCH1 knockdown reduced histone H3K27 acetylation at a subset of NF-\u03baB\u2013directed inflammatory enhancers.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>Our findings reveal that NOTCH1 signaling supports the expression of a subset of inflammatory genes at the enhancer level and demonstrate how key signaling pathways converge on chromatin to coordinate the transition to an infla mmatory endothelial phenotype.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.117.310388","type":"journal-article","created":{"date-parts":[[2018,2,15]],"date-time":"2018-02-15T10:00:12Z","timestamp":1518688812000},"page":"854-869","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":44,"title":["Inhibition of Endothelial NOTCH1 Signaling Attenuates Inflammation by Reducing Cytokine-Mediated Histone Acetylation at Inflammatory Enhancers"],"prefix":"10.1161","volume":"38","author":[{"given":"Lars la Cour","family":"Poulsen","sequence":"first","affiliation":[{"name":"From the Department of Pathology, Oslo University Hospital Rikshospitalet (L.l.C.P., R.J.E., S.K., T.E.S.-N., A.R., M.S., J.W., M.K., E.B., O.S., H.S., G.H., E.S., J.H.), Department of Pathology, Institute for Clinical Medical Sciences (H.S., G.H.) and Department of Molecular Medicine, Institute for Basal Medical Sciences (A.S., P.C.), University of Oslo, Norway; Department of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, University of M\u00fcnster, Germany (R.D.-H., M.E., R.B., R..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Reidunn Jetne","family":"Edelmann","sequence":"additional","affiliation":[{"name":"From the Department of Pathology, Oslo University Hospital Rikshospitalet (L.l.C.P., R.J.E., S.K., T.E.S.-N., A.R., M.S., J.W., M.K., E.B., O.S., H.S., G.H., E.S., J.H.), Department of Pathology, Institute for Clinical Medical Sciences (H.S., G.H.) and Department of Molecular Medicine, Institute for Basal Medical Sciences (A.S., P.C.), University of Oslo, Norway; Department of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, University of M\u00fcnster, Germany (R.D.-H., M.E., R.B., R..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stig","family":"Kr\u00fcger","sequence":"additional","affiliation":[{"name":"From the Department of Pathology, Oslo University Hospital Rikshospitalet (L.l.C.P., R.J.E., S.K., T.E.S.-N., A.R., M.S., J.W., M.K., E.B., O.S., H.S., G.H., E.S., J.H.), Department of Pathology, Institute for Clinical Medical Sciences (H.S., G.H.) and Department of Molecular Medicine, Institute for Basal Medical Sciences (A.S., P.C.), University of Oslo, Norway; 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