Common mechanisms for the regulation of B cell differentiation and transformation by the transcriptional repressor protein BCL-6
Common mechanisms for the regulation of B cell differentiation and transformation by the transcriptional repressor protein BCL-6
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DOI：
10.1007/bf02697368
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发表时间：
2007-01-01
影响因子：
4.4
通讯作者：
Dent, Alexander
中科院分区：
文献类型：
--
作者：
Kusam, Saritha;Dent, Alexander
BCL-6转录抑制蛋白是正常B细胞分化的关键调节因子，并且BCL-6最近已被证明在几种小鼠模型系统中充当癌基因。BCL-6调节B细胞分化和促进原代B细胞转化的分子途径无疑是相关的;但是，在此情况下，这些途径知之甚少。BCL-6在B细胞中的功能的普遍接受的模型是BCL-6抑制活化的B细胞向浆细胞的终末分化，并且BCL-6的去调节作用是通过抑制活化的B细胞向浆细胞的终末分化来实现的。6的表达导致终末分化和持续增殖的抑制。BCL-6通过未知的机制在原代B细胞中诱导生殖中心表型，并且可以逆转浆细胞肿瘤系的终末分化。BCL-6能促进原代B细胞的永生化，并能增强端粒酶活性。大多数BCL-6靶基因和相互作用蛋白在正常B细胞分化和B细胞转化中的作用基本上是未解决的，并且是未来研究的重要领域。
The BCL-6 transcriptional repressor protein is a critical regulator of normal B cell differentiation and BCL-6 has recently been shown to act as an oncogene in several mouse model systems. The molecular pathways by which BCL-6 regulates B cell differentiation and also promotes the transformation of primary B cells are undoubtedly related; however, these pathways are poorly understood The commonly accepted model for BCL-6 function in B cells is that BCL-6 inhibits the terminal differentiation of activated B cells into plasma cells and that deregulation of BCL-6 expression leads to an inhibition of terminal differentiation and continued proliferation. BCL-6 induces a germinal-center phenotype in primary B cells by unknown mechanisms, and can reverse the terminal differentiation of plasma cell tumor lines. BCL-6 can promote the immortalization of primary B cells and can augment telomerase activity. The role of the vast majority of BCL-6 target genes and interacting proteins in normal B cell differentiation and B cell transformation is essentially unresolved and is an important area for future investigation.