MHC class II regulation by epigenetic agents and microRNAs

被引:8
作者
Tomasi, Thomas B. [1 ,2 ,3 ]
Magner, William J. [1 ]
Wiesen, Jennifer L. [1 ]
Oshlag, Julian Z. [1 ]
Cao, Felicia [1 ]
Pontikos, Alex N. [1 ]
Gregorie, Christopher J. [1 ]
机构
[1] Roswell Pk Canc Inst, Dept Immunol, Mol Med Lab, Buffalo, NY 14263 USA
[2] SUNY Buffalo, Dept Med, Sch Med & Biomed Sci, Buffalo, NY 14214 USA
[3] SUNY Buffalo, Dept Microbiol & Immunol, Sch Med & Biomed Sci, Buffalo, NY 14214 USA
基金
美国国家卫生研究院;
关键词
MHC; Epigenetic; MicroRNA; Stress; Senescence; Immunity; Gene regulation; HISTONE DEACETYLASE INHIBITORS; NF-KAPPA-B; TARGET MESSENGER-RNAS; SENESCENCE-LIKE STATE; GENE-EXPRESSION; TUMOR-CELLS; TRANSLATIONAL REPRESSION; ANTIGEN PRESENTATION; TROPHOBLAST CELLS; INDUCED APOPTOSIS;
D O I
10.1007/s12026-009-8128-3
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
MicroRNAs have been shown to regulate gene expression both transcriptionally and translationally. Here, we examine evidence that various stresses regulate miRNAs which, in turn, regulate immune gene levels. Multiple studies are reviewed showing altered microRNA levels in normal cells under stress and in various disease states, including cancer. Unexpected was the finding that Dicer expression is altered by treatments with several agents, such as interferons and cortisone, employed in the treatment of immune disorders. Potential signal transduction pathways, including JAK/Stat, PI3K and PKR, that may regulate Dicer and microRNA levels in normal and stressed mammalian cells are discussed.
引用
收藏
页码:45 / 58
页数:14
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