Ash1l and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T cell autoimmunity.
第一作者:
Meng,Xia
第一单位:
National Key Laboratory of Medical Molecular Biology, Department of Immunology &Center for Immunotherapy, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005, China.
作者:
医学主题词
成年人(Adult);老年人(Aged);动物(Animals);自身免疫(Autoimmunity);细胞极性(Cell Polarity);DNA结合蛋白质类(DNA-Binding Proteins);后成说, 遗传(Epigenesis, Genetic);基因表达调控(Gene Expression Regulation);基因沉默(Gene Silencing);组蛋白脱乙酰基酶1(Histone Deacetylase 1);组蛋白赖氨酸N-甲基转移酶(Histone-Lysine N-Methyltransferase);组蛋白类(Histones);人类(Humans);甲基化(Methylation);小鼠(Mice);小鼠, 近交C57BL(Mice, Inbred C57BL);中年人(Middle Aged);启动区, 遗传(Promoter Regions, Genetic);Smad3蛋白质(Smad3 Protein);T淋巴细胞(T-Lymphocytes);T淋巴细胞, 调节性(T-Lymphocytes, Regulatory);转录因子(Transcription Factors);转化生长因子β(Transforming Growth Factor beta)
DOI
10.1038/ncomms15818
PMID
28598443
发布时间
2019-11-26
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Nature communications
15818页
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