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dc.contributor.authorZhentao Yang
dc.contributor.authorBin Jiang
dc.contributor.authorYan Wang
dc.contributor.authorHengxiao Ni
dc.contributor.authorJia Zhang
dc.contributor.author夏金梅
dc.contributor.author施铭岗
dc.contributor.author洪丽满
dc.contributor.authorJingsong Ruan
dc.contributor.authorTak Wah Mak
dc.contributor.author李勤喜
dc.contributor.author韩家淮
dc.date.accessioned2019-11-13T02:33:31Z
dc.date.available2019-11-13T02:33:31Z
dc.date.issued2018-04-25
dc.identifier.citation科学新闻,2018,(04):126
dc.identifier.issn1671-6582
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/172093
dc.description.abstract<正>文章简介在异柠檬酸脱氢酶1/2(IDH1/2)突变的细胞中,高浓度的2-羟基戊二酸(2-HG)通过抑制TET2的活性增强了DNA的甲基化。在本研究中,课题组发现2-HG可通过直接激活DNA甲基转移酶DNMT1的作用而促进RIP3启动子的
dc.description.sponsorship国家基础研究计划基金(973 Program;2015CB553800,2013CB944903,2014CB541804);;国家自然科学基金项目(91029304,31420103910,31330047,81630042,81372702,81402285,31571473);;中央高校基本科研专项资金(20720140552,10120100002);;国家基础科学人才培养基金(Grant No.J1310027)的资助
dc.language.isozh_CN
dc.subject细胞坏死
dc.subjectHG
dc.subject启动子
dc.subject甲基化
dc.title2-HG通过上调RIP3启动子的甲基化水平抑制细胞坏死
dc.typeArticle


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