{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T21:10:07Z","timestamp":1791148207195,"version":"4.1.0"},"reference-count":49,"publisher":"The Company of Biologists","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2009,1,15]]},"abstract":"<jats:p>The arginine-glycine-aspartate (RGD)-binding integrins \u03b1v\u03b26 and \u03b1v\u03b28 activate latent TGF\u03b21 and TGF\u03b23 in vivo, but it is uncertain whether other RGD-binding integrins such as integrins \u03b1v\u03b25 and \u03b1v\u03b23 activate these TGF\u03b2 isoforms. To define the combined role of \u03b1v\u03b26- and \u03b1v\u03b28-integrin in TGF\u03b2 activation, we analyzed mice lacking function of both integrins by means of gene deletion and\/or pharmacologic inhibition. Most Itgb6\u2013\/\u2013;Itgb8\u2013\/\u2013 embryos die at mid-gestation; those that survive develop cleft palate\u2013as observed in Tgfb3\u2013\/\u2013 mice. Itgb8\u2013\/\u2013 mice treated with an anti-\u03b1v\u03b26-integrin antibody develop severe autoimmunity and lack Langerhans cells\u2013similar to Tgfb1-null mice. These results support a model in which TGF\u03b23-mediated palate fusion and TGF\u03b21-mediated suppression of autoimmunity and generation of Langerhans cells require integrins \u03b1v\u03b26 and \u03b1v\u03b28 but not other RGD-binding integrins as TGF\u03b2 activators.<\/jats:p>","DOI":"10.1242\/jcs.035246","type":"journal-article","created":{"date-parts":[[2008,12,31]],"date-time":"2008-12-31T13:24:22Z","timestamp":1230729862000},"page":"227-232","source":"Crossref","is-referenced-by-count":213,"title":["Mice that lack activity of \u03b1v\u03b26- and \u03b1v\u03b28-integrins reproduce the abnormalities of\n                    <i>Tgfb1<\/i>\n                    - and\n                    <i>Tgfb3<\/i>\n                    -null mice"],"prefix":"10.1242","volume":"122","author":[{"given":"Poshala","family":"Aluwihare","sequence":"first","affiliation":[{"name":"Department of Cell Biology, New York University School of Medicine, New York, NY 10016, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhenyu","family":"Mu","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, New York University School of Medicine, New York, NY 10016, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhicheng","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, New York University School of Medicine, New York, NY 10016, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dawen","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, New York University School of Medicine, New York, NY 10016, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul H.","family":"Weinreb","sequence":"additional","affiliation":[{"name":"Biogen Idec, Cambridge, MA 02142, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerald S.","family":"Horan","sequence":"additional","affiliation":[{"name":"Biogen Idec, Cambridge, MA 02142, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shelia M.","family":"Violette","sequence":"additional","affiliation":[{"name":"Biogen Idec, Cambridge, MA 02142, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John S.","family":"Munger","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, New York University School of Medicine, New York, NY 10016, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","reference":[{"key":"2021042520432226300_REF1","doi-asserted-by":"crossref","unstructured":"Annes, J. 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