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作 者:马彪[1] 逄越[1] 王旭[1] 刘庆平[1] 李文哲[1]
机构地区:[1]大连大学免疫学研究所,116622
出 处:《免疫学杂志》2012年第7期624-627,共4页Immunological Journal
基 金:国家自然科学基金(30972675);教育部留学回国基金;辽宁省大连市科技局计划启动项目(2010J21DW011)
摘 要:转录因子Pax5在B细胞定向分化发育过程中发挥重要调控作用。B细胞定向分化发育相关的转录因子如PU.1、干扰素调节因子4(Interferon regulatory factor 4,IRF4)、IRF8和NF-κB结合在Pax5基因5’上游增强子区,转录因子EBF、STAT5结合在Pax5基因5’上游启动子区,从而共同促进Pax5基因的表达。表达的Pax5蛋白不仅通过IgH的V(D)J片段染色质的甲基化和乙酰化修饰来调节IgH V(D)J重排,并且通过B细胞特异性基因(mb-1、VpreB、λ5、CD19、BLNK等)表达调控B细胞的定向分化发育。若Pax5基因缺失,影响组蛋白H3-K9的修饰,导致B细胞向非B细胞分化。总之,Pax5在B细胞定向分化发育中起到重要调控作用。Transcription factor Pax5 plays an important role in the B cell commitment. Firstly, the transcription factors such as PU.1, interferon regulatory factor (IRF) 4, IRF8, and NF-KB that interact with the Pax5 5" enhancer region, and the transcription factors EBF and STATS interact with the Pax5 5' promoter region, which together regulate Pax5 expression in early B cells during B cell commitment. Further, the expressed Pax5 protein not only control the H3-K9 methylation and the H3-K9 acetylation in the V(D)J locus of B cell, but also regulate B cell-specific gene expression, such as mb-1, VpreB, AS, D19, BLNK to facilitate B cell commitment. Inactivation of Pax5 will affect the H3-K9 histone modification, leading to differentiate B cells into non-B cells, suggesting that pax5 was crucial required for B cell commitment.
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