期刊
NATURE IMMUNOLOGY
卷 19, 期 10, 页码 1137-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41590-018-0208-x
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资金
- National Institutes of Health [Al034206, HG007893, CA164190, P30 CA008748]
- Hilton-Ludwig Cancer Prevention Initiative - Conrad N. Hilton Foundation
- Ludwig Cancer Research
- Irvington Fellowship of the Cancer Research Institute
- Howard Hughes Medical Institute
- NATIONAL CANCER INSTITUTE [U01CA164190, U54CA209975, P30CA008748] Funding Source: NIH RePORTER
- NATIONAL HUMAN GENOME RESEARCH INSTITUTE [U01HG007893] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R37AI034206] Funding Source: NIH RePORTER
Numerous microRNAs and their target mRNAs are coexpressed across diverse cell types. However, it is unknown whether they are regulated in a manner independent of or dependent on cellular context. Here, we explored transcriptome-wide targeting and gene regulation by miR-155, whose activation-induced expression plays important roles in innate and adaptive immunity. Through mapping of miR-155 targets through differential iCLIP, mRNA quantification with RNA-seq, and 3' untranslated region (UTR)-usage analysis with poly(A)-seq in macrophages, dendritic cells, and T and B lymphocytes either sufficient or deficient in activated miR-155, we identified numerous targets differentially bound by miR-155. Whereas alternative cleavage and polyadenylation (ApA) contributed to differential miR-155 binding to some transcripts, in most cases, identical 3'-UTR isoforms were differentially regulated across cell types, thus suggesting ApA-independent and cellular-context-dependent miR-155-mediated gene regulation. Our study provides comprehensive maps of miR-155 regulatory networks and offers a valuable resource for dissecting context-dependent and context-independent miRNA-mediated gene regulation in key immune cell types.
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