{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T14:28:04Z","timestamp":1779114484675,"version":"3.51.4"},"reference-count":61,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>An effective immune system depends upon regulation of lymphocyte function and homeostasis. In recent years, members of the GTPases of the immunity associated protein (GIMAP) family were proposed to regulate T cell homeostasis. In contrast, little is known about their function and mode of action in B cells. We used a combination of transgenic mice and in vivo and in vitro techniques to conditionally and electively ablate GIMAP1 in resting and activated peripheral B cells. Our data suggest that GIMAP1 is absolutely essential for the survival of peripheral B cells, irrespective of their activation state. Together with recent data showing increased expression of GIMAP1 in B cell lymphomas, our work points to the possible potential of GIMAP1 as a target for manipulation in a variety of B cell\u2013mediated diseases.<\/jats:p>","DOI":"10.4049\/jimmunol.1501582","type":"journal-article","created":{"date-parts":[[2015,12,1]],"date-time":"2015-12-01T03:38:37Z","timestamp":1448941117000},"page":"207-216","source":"Crossref","is-referenced-by-count":29,"title":["GIMAP1 Is Essential for the Survival of Naive and Activated B Cells In Vivo"],"prefix":"10.1093","volume":"196","author":[{"given":"Louise M C","family":"Webb","sequence":"first","affiliation":[{"name":"Laboratory of Lymphocyte Signalling and Development, Babraham Institute , Cambridge CB22 3AT ,","place":["United Kingdom"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Preeta","family":"Datta","sequence":"additional","affiliation":[{"name":"Laboratory of Lymphocyte Signalling and Development, Babraham Institute , Cambridge CB22 3AT ,","place":["United Kingdom"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sarah E","family":"Bell","sequence":"additional","affiliation":[{"name":"Laboratory of Lymphocyte Signalling and Development, Babraham Institute , Cambridge CB22 3AT ,","place":["United Kingdom"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daisuke","family":"Kitamura","sequence":"additional","affiliation":[{"name":"Research Institute for Biomedical Sciences, Tokyo University of Science , Yamazaki 2669, Noda, Chiba 278-0022 ,","place":["Japan"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martin","family":"Turner","sequence":"additional","affiliation":[{"name":"Laboratory of Lymphocyte Signalling and Development, Babraham Institute , Cambridge CB22 3AT ,","place":["United Kingdom"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3423-7124","authenticated-orcid":false,"given":"Geoffrey W","family":"Butcher","sequence":"additional","affiliation":[{"name":"Laboratory of Lymphocyte Signalling and Development, Babraham Institute , Cambridge CB22 3AT ,","place":["United Kingdom"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2016,1,1]]},"reference":[{"key":"2025030702113538700_r1","doi-asserted-by":"crossref","first-page":"24383","DOI":"10.1074\/jbc.274.34.24383","article-title":"Spleen-specific expression of the malaria-inducible intronless mouse gene imap38","volume":"274","author":"Kr\u00fccken","year":"1999","journal-title":"J. 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