{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T10:29:20Z","timestamp":1791023360067,"version":"4.1.0"},"reference-count":74,"publisher":"Rockefeller University Press","issue":"5","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2005,9,5]]},"abstract":"<jats:p>B cell receptor (BCR) cross-linking induces B cell proliferation and sustains survival through the phosphorylation-dependent signals. We report that a loss of the protein phosphatase component G5PR increased the activation-induced cell death (AICD) and thus impaired B cell survival. G5PR associates with GANP, whose expression is up-regulated in mature B cells of the peripheral lymphoid organs. To study G5PR function, the G5pr gene was conditionally targeted with the CD19-Cre combination (G5pr\u2212\/\u2212 mice). The G5pr\u2212\/\u2212 mice had a decreased number of splenic B cells (60% of the controls). G5pr\u2212\/\u2212 B cells showed a normal proliferative response to lipopolysaccharide or anti-CD40 antibody stimulation but not to BCR cross-linking with or without IL-4 in vitro. G5pr\u2212\/\u2212 B cells did not show abnormalities in the BCR-mediated activation of Erks and NF-\u03baB, cyclin D2 induction, or Akt activation. However, G5pr\u2212\/\u2212 B cells were sensitive to AICD caused by BCR cross-linking. This was associated with an increased depolarization of the mitochondrial membrane and the enhanced activation of c-Jun NH2-terminal protein kinase and Bim. These results suggest that G5PR is required for the BCR-mediated proliferation associated with the prevention of AICD in mature B cells.<\/jats:p>","DOI":"10.1084\/jem.20050637","type":"journal-article","created":{"date-parts":[[2005,8,30]],"date-time":"2005-08-30T00:13:17Z","timestamp":1125360797000},"page":"707-719","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":28,"title":["Protein phosphatase subunit G5PR is needed for inhibition of B cell receptor\u2013induced apoptosis"],"prefix":"10.1084","volume":"202","author":[{"given":"Yan","family":"Xing","sequence":"first","affiliation":[{"name":"1Department of Immunology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan"},{"name":"2Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Honcho 4-1-8, Kawaguchi, Saitama 332-0012, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hideya","family":"Igarashi","sequence":"additional","affiliation":[{"name":"1Department of Immunology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan"},{"name":"2Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Honcho 4-1-8, Kawaguchi, Saitama 332-0012, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaodan","family":"Wang","sequence":"additional","affiliation":[{"name":"1Department of Immunology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan"},{"name":"2Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Honcho 4-1-8, Kawaguchi, Saitama 332-0012, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nobuo","family":"Sakaguchi","sequence":"additional","affiliation":[{"name":"1Department of Immunology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan"},{"name":"2Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Honcho 4-1-8, Kawaguchi, Saitama 332-0012, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2005,8,29]]},"reference":[{"key":"2023072513212273100_BIB1","doi-asserted-by":"crossref","first-page":"175","DOI":"10.1146\/annurev.iy.05.040187.001135","volume":"5","year":"1987","journal-title":"Annu. 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