{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T08:25:07Z","timestamp":1791188707375,"version":"4.1.0"},"reference-count":41,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2003,1,1]],"date-time":"2003-01-01T00:00:00Z","timestamp":1041379200000},"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":[[2003,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>We previously reported that the cross-linking of cluster of differentiation (CD)24 induces apoptosis in Burkitt\u2019s lymphoma cells and that this phenomenon can be enhanced by a B cell Ag receptor (BCR)-mediated signal. In this study, we extend our previous observation and report that CD24 also mediated apoptosis in human precursor-B acute lymphoblastic leukemia cell lines in the pro-B and pre-B stages accompanying activation of multiple caspases. Interestingly, simultaneous cross-linking of pre-BCR clearly inhibited CD24-mediated apoptosis in pre-B cells. We also observed that mitogen-activated protein kinases (MAPKs) were involved in the regulation of this apoptotic process. Pre-BCR cross-linking induced prompt and strong activation of extracellular signal-regulated kinase 1, whereas CD24 cross-linking induced the sustained activation of p38 MAPK, following weak extracellular signal-regulated kinase 1 activation. SC68376, a specific inhibitor of p38 MAPK, inhibited apoptosis induction by CD24 cross-linking, whereas anisomycin, an activator of p38 MAPK, enhanced the apoptosis. In addition, PD98059, a specific inhibitor of MEK-1, enhanced apoptosis induction by CD24 cross-linking and reduced the antiapoptotic effects of pre-BCR cross-linking. Collectively, whether pre-B cells survive or die may be determined by the magnitude of MAPK activation, which is regulated by cell surface molecules. Our findings should be important to understanding the role of CD24-mediated cell signaling in early B cell development.<\/jats:p>","DOI":"10.4049\/jimmunol.170.1.252","type":"journal-article","created":{"date-parts":[[2014,4,22]],"date-time":"2014-04-22T00:11:17Z","timestamp":1398125477000},"page":"252-260","source":"Crossref","is-referenced-by-count":49,"title":["Pre-B Cell Antigen Receptor-Mediated Signal Inhibits CD24-Induced Apoptosis in Human Pre-B Cells"],"prefix":"10.1093","volume":"170","author":[{"given":"Tomoko","family":"Taguchi","sequence":"first","affiliation":[{"name":"Department of Developmental Biology, National Research Institute for Child Health and Development , Tokyo ,","place":["Japan"]},{"name":"Department of Pediatrics, School of Medicine, Keio University , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nobutaka","family":"Kiyokawa","sequence":"additional","affiliation":[{"name":"Department of Developmental Biology, National Research Institute for Child Health and Development , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenichi","family":"Mimori","sequence":"additional","affiliation":[{"name":"Department of Developmental Biology, National Research Institute for Child Health and Development , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toyo","family":"Suzuki","sequence":"additional","affiliation":[{"name":"Department of Developmental Biology, National Research Institute for Child Health and Development , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takaomi","family":"Sekino","sequence":"additional","affiliation":[{"name":"Department of Developmental Biology, National Research Institute for Child Health and Development , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hideki","family":"Nakajima","sequence":"additional","affiliation":[{"name":"Department of Developmental Biology, National Research Institute for Child Health and Development , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masahiro","family":"Saito","sequence":"additional","affiliation":[{"name":"Department of Developmental Biology, National Research Institute for Child Health and Development , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yohko U","family":"Katagiri","sequence":"additional","affiliation":[{"name":"Department of Developmental Biology, National Research Institute for Child Health and Development , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nobutake","family":"Matsuo","sequence":"additional","affiliation":[{"name":"National Center for Child Health and Development , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshinobu","family":"Matsuo","sequence":"additional","affiliation":[{"name":"Fujisaki Cell Center, Hayashibara Biochemical Labs Inc. , Okayama ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hajime","family":"Karasuyama","sequence":"additional","affiliation":[{"name":"Department of Immune Regulation, Graduate School, Tokyo Medical and Dental University , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junichiro","family":"Fujimoto","sequence":"additional","affiliation":[{"name":"Department of Developmental Biology, National Research Institute for Child Health and Development , Tokyo ,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2003,1,1]]},"reference":[{"key":"2026020210105464100_R1","first-page":"751","volume-title":"Nature","year":"1990"},{"key":"2026020210105464100_R2","first-page":"2264","volume-title":"Proc. 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