题 目:Dynamic regulation of menin-mediated histone methylation in neuroendocrine tumorigenesis
报告人:林文楚 (Research Scientist)
哈佛大学医学院Dana-Farber癌症研究所
邀请人:刘青松 研究员
时 间: 2012.12.14(周五). 上午 9:30
地 点: 强磁场中心 201 会议室
报告人介绍:1996年本科毕业于四川大学,后于2001在中科院上海生命科学研究院获得生化与分子生物学硕士学位。在美国于2006年获得生物医学博士学位。之后在哈佛大学医学院Dana-Farber癌症研究所博士后训练。现在哈佛大学医学院Dana-Farber癌症研究所以高级研究员身份工作。
报告摘要:Aberrations in epigenetic processes, such as histone methylation, can contribute to tumor initiation and progression. The menin tumor suppressor protein, deficient in hereditary and sporadic neuroendocrine tumors, forms an active complex with MLL family histone methyltransferases. Inactivation of the mouse Men1 gene leads to formation of neuroendocrine tumors mimicking the human MEN1 syndrome, making the mouse system an ideal model to further dissect the molecular mechanisms underlying neuroendocrine tumors. Loss of menin may be tumorigenic because it leads to decreased histone H3 lysine 4 trimethylation and therefore decreased expression of specific genes. Reversing the tumorigenesis caused by menin deficiency might therefore be achieved by inhibition of histone H3 lysine 4 demethylation. Retinoblastoma binding protein 2 (RBP2; also called JARID1A or KDM5A) can demethylate tri- and dimethylated lysine 4 in histone H3, which may antagonize the histone methyltransferase activity associated with menin.
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