标题:Deletion of miRNAs in bone marrow prevents streptozotocin-induced murine autoimmune diabetes but deletion of miR-155 does not
作者:Chen,W.-B.;Gao,L.;Weiland,M.;Zhao,J.;Liu,M.;Zhou,L.;Mi,Q.-S.
作者机构:[Chen, W.-B] Institute of Pharmacology, Shandong University School of Medicine, Jinan, China, Henry Ford Immunology Program, Henry Ford Health System, 更多
通讯作者:Mi, QS
通讯作者地址:[Mi, QS]Henry Ford Hlth Syst, Henry Ford Immunol Program, Detroit, MI USA.
来源:Cell cycle
出版年:2013
卷:12
期:7
页码:1151-1152
DOI:10.4161/cc.24365
摘要:Recent studies have demonstrated that gene expression is regulated not only by protein-coding genes, but also by non-protein-coding RNA molecules, including microRNAs (miRNAs). miRNAs are a class of 21-25 nt single-stranded non-coding small RNAs dependent upon ribonuclease III enzyme Dicer for the processing of mature and functional miRNAs. Therefore, the deletion of the enzyme Dicer provides a genetic test for the relevance of miRNAs in mammalian development and function. We and others previously reported that loss of miRNAs in bone marrow induced by Tie2-Cre or in thymus by CD4-Cre, through tissue-specific deletion of miRNA-dependent Dicer, mainly regulated the development and function of CD4~+CD25~+Foxp3~+ regulatory T (Treg) cells and invariant natural killer T (iNKT) cells, but did not affect conventional CD4 and CD8 T cell development in the thymus.
收录类别:SCOPUS;SCIE
WOS核心被引频次:3
Scopus被引频次:3
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-84875887407&doi=10.4161%2fcc.24365&partnerID=40&md5=4b08ce866eae163e3a76a1abda866758
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