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原癌基因c-myb在巨核-红系造血发育中的研究进展
作者姓名:Liu XQ  Wang XX  Zhao L
作者单位:兰州大学第一医院中心实验室
摘    要:细胞核内原癌基因c-myb是造血系统的重要调控因子,参与造血细胞周期调控并调节造血细胞增殖和分化。近年来通过对不同细胞系及转基因鼠模型的研究发现,c-myb对巨核-红系祖细胞的定向分化起决定作用,该原癌基因的缺失导致红系定向严重受损,而对巨核系定向影响较小。瞬时转染及免疫沉淀实验已证实c-myb通过与造血调控的多个转录因子相互作用来实现其在造血系统的生理功能。对c-myb的结构、功能及相关分子调控机制的研究,有助于进一步阐明其在巨核-红系造血发育中的作用,并为血小板疾病、红细胞疾病的分子靶向治疗提供新的思路。本文就c-myb结构、功能、参与巨核红系造血调控的有关作用及相关分子机制作一综述。

关 键 词:原癌基因  c-myb  巨核-红系造血

Research progress of proto-oncogene c-myb in megakaryocyte-erythroid hematopoiesis
Liu XQ,Wang XX,Zhao L.Research progress of proto-oncogene c-myb in megakaryocyte-erythroid hematopoiesis[J].Journal of Experimental Hematology,2012,20(2):518-522.
Authors:Liu Xiao-Qin  Wang Xiao-Xia  Zhao Li
Institution:Central Laboratory, The First Hospital of Lanzhou University, Lanzhou, Gansu Province, China.
Abstract:The nuclear proto-oncogene c-myb is an essential regulator of hematopoiesis, it involves in the growth, survival, proliferation and differentiation of hematopoietic cells. More recently, different cell lines and transgenic mouse studies have suggested that c-myb plays a pivotal role in the megakaryocyte-erythroid progenitor cell lineage commitment. The deletion of the proto-oncogene c-myb would lead to profoundly impaired definitive erythropoiesis, but little influence in definitive megakaryopoiesis. Moreover, transient transfection and immunoprecipitation studies have demonstrated that c-myb exerts its physiological function in normal hematopoiesis by influencing a network of regulator molecules. Now therefore, insight into the structure, function and related molecular regulation mechanism of c-myb gene can help to further clarify its function in megakaryocyte-erythroid hematopoiesis and can provide new ideas for molecular target therapy of the platelet diseases and red blood cell diseases. In this article, c-myb structure, function and related effects involved in megakaryocyte-erythroid hematopoiesis as well as related molecular mechanisms are reviewed.
Keywords:proto-oncogene  c-myb  megakaryocyte-erythroid hematopoiesis
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