{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,7]],"date-time":"2026-11-07T10:30:14Z","timestamp":1794047414490,"version":"4.8.0"},"reference-count":41,"publisher":"Ferrata Storti Foundation (Haematologica)","issue":"2","license":[{"start":{"date-parts":[[2022,8,4]],"date-time":"2022-08-04T00:00:00Z","timestamp":1659571200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["haematol"],"abstract":"<jats:p>There is growing evidence for an inherited basis of susceptibility to childhood acute lymphoblastic leukemia. Genomewide association studies by us and others have identified non-coding acute lymphoblastic leukemia risk variants at the ARID5B gene locus, but the molecular mechanisms linking ARID5B to normal and malignant hematopoiesis remain largely unknown. Using a Vav1-driven transgenic mouse model, we characterized the role of Arid5b in hematopoiesis in vivo. Arid5b overexpression resulted in a dramatic reduction in the proportion of circulating B cells, immature, and mature Bcell fractions in the peripheral blood and the bone marrow, and also a decrease of follicular B cells in the spleen. There were significant defects in B-cell activation upon Arid5b overexpression in vitro with hyperactivation of B-cell receptor signaling at baseline. In addition, increased mitochondrial oxygen consumption rate of na\u00efve or stimulated B cells of Arid5b-overexpressing mice was observed, compared to the rate of wild-type counterparts. Taken together, our results indicate that ARID5B may play an important role in B-cell development and function.<\/jats:p>","DOI":"10.3324\/haematol.2022.281157","type":"journal-article","created":{"date-parts":[[2022,8,4]],"date-time":"2022-08-04T15:12:10Z","timestamp":1659625930000},"page":"502-512","source":"Crossref","is-referenced-by-count":14,"title":["&lt;i&gt;ARID5B&lt;\/i&gt; influences B-cell development and function in mouse"],"prefix":"10.3324","volume":"108","author":[{"given":"Charnise","family":"Goodings","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xujie","family":"Zhao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shannon","family":"McKinney-Freeman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun J.","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1856","published-online":{"date-parts":[[2022,8,4]]},"reference":[{"key":"44531","doi-asserted-by":"crossref","unstructured":"Pui CH, Robison LL, Look AT. Acute lymphoblastic leukaemia. Lancet. 2008; 371(9617):1030-1043.","DOI":"10.1016\/S0140-6736(08)60457-2"},{"key":"44532","doi-asserted-by":"crossref","unstructured":"Hunger SP, Mullighan CG. Acute lymphoblastic leukemia in children. N Engl J Med. 2015; 373(16):1541-1552.","DOI":"10.1056\/NEJMra1400972"},{"key":"44533","doi-asserted-by":"crossref","unstructured":"Moriyama T, Relling MV, Yang JJ. Inherited genetic variation in childhood acute lymphoblastic leukemia. Blood. 2015; 125(26):3988-3995.","DOI":"10.1182\/blood-2014-12-580001"},{"key":"44534","unstructured":"Garber JE, Goldstein AM, Kantor AF, Dreyfus MG, Fraumeni JF, Li FP. Follow-up study of twenty-four families with Li-Fraumeni syndrome. Cancer Res. 1991; 51(22):6094-6097."},{"key":"44535","doi-asserted-by":"crossref","unstructured":"Hemminki K, Jiang Y. Risks among siblings and twins for childhood acute lymphoid leukaemia: results from the Swedish Family-Cancer Database. 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ARID5B genetic polymorphisms contribute to racial disparities in the incidence and treatment outcome of childhood acute lymphoblastic leukemia. J Clin Oncol. 2012; 30(7):751-757.","DOI":"10.1200\/JCO.2011.38.0345"},{"key":"44543","doi-asserted-by":"crossref","unstructured":"Xu H, Yang WJ, Perez-Andreu V. Novel susceptibility variants at 10p12.31-12.2 for childhood acute lymphoblastic leukemia in ethnically diverse populations. J Natl Cancer Inst. 2013; 105(10):733-742.","DOI":"10.1093\/jnci\/djt042"},{"key":"44544","doi-asserted-by":"crossref","unstructured":"Vijayakrishnan J, Kumar R, Henrion MY. A genome-wide association study identifies risk loci for childhood acute lymphoblastic leukemia at 10q26.13 and 12q23.1. Leukemia. 2017; 31(3):573-579.","DOI":"10.1038\/leu.2016.271"},{"key":"44545","doi-asserted-by":"crossref","unstructured":"Prasad RB, Hosking FJ, Vijayakrishnan J. Verification of the susceptibility loci on 7p12.2, 10q21.2, and 14q11.2 in precursor B-cell acute lymphoblastic leukemia of childhood. Blood. 2010; 115(9):1765-1767.","DOI":"10.1182\/blood-2009-09-241513"},{"key":"44546","doi-asserted-by":"crossref","unstructured":"Healy J, Richer C, Bourgey M, Kritikou EA, Sinnett D. Replication analysis confirms the association of ARID5B with childhood B-cell acute lymphoblastic leukemia. Haematologica. 2010; 95(9):1608-1611.","DOI":"10.3324\/haematol.2010.022459"},{"key":"44547","doi-asserted-by":"crossref","unstructured":"Evans TJ, Milne E, Anderson D. Confirmation of childhood acute lymphoblastic leukemia variants, ARID5B and IKZF1, and interaction with parental environmental exposures. PloS One. 2014; 9(10)","DOI":"10.1371\/journal.pone.0110255"},{"key":"44548","doi-asserted-by":"crossref","unstructured":"Migliorini G, Fiege B, Hosking FJ. 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