期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 47, 期 7, 页码 1142-1152出版社
WILEY
DOI: 10.1002/eji.201746987
关键词
microRNAs; Posttranscriptional control; Thymocyte development
类别
资金
- Israeli Science Foundation
- Kekst Family Institute for Medical Genetics
- Deutsche Forschungsgemeinschaft Research Unit 1336
- ERC consolidator program (FP7)
- Minerva program
T-cell development is a spatially and temporally regulated process, orchestrated by well-defined contributions of transcription factors and cytokines. Here, we identify the noncoding RNA miR-142 as an additional regulatory layer within murine thymocyte development and proliferation. MiR-142 deficiency impairs the expression of cell cycle-promoting genes in mature mouse thymocytes and early progenitors, accompanied with increased levels of cyclin-dependent kinase inhibitor 1B (Cdkn1b, also known as p27(Kip1)). By using CRISPR/Cas9 technology to delete the miR-142-3p recognition element in the 3'UTR of cdkn1b, we confirm that this gene is a novel target of miR-142-3p in vivo. Increased Cdkn1b protein expression alone however was insufficient to cause proliferation defects in thymocytes, indicating the existence of additional critical miR-142 targets. Collectively, we establish a key role for miR-142 in the control of early and mature thymocyte proliferation, demonstrating the multifaceted role of a single miRNA on several target genes.
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