期刊
PLOS ONE
卷 14, 期 1, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0211111
关键词
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资金
- Israel Science Foundation (ISF) [1852/16]
- Israeli Ministry of Defense, Office of Assistant Minister of Defense for Chemical, Biological, Radiological and Nuclear (CBRN) Defense
- Foundation Fighting Blindness
- Edmond J. Safra Center for Bioinformatics at Tel Aviv University
- Zimin Institute for Engineering Solutions Advancing Better Lives
- Tel Aviv University Breakthrough Innovative Research Grants
- Tel Aviv University Richard Eimert Research Fund on Solid Tumors
- Djerassi-Elias Institute of Oncology
- Canada-Montreal Friends of Tel Aviv University
- Harold H. Marcus
- Amy Friedkin
- Garber Research Fund
HIV-1 is the causative agent of AIDS (Autoimmune Deficiency Syndrome). HIV-1 infection results in systemic CD4(+) T cell depletion, thereby impairing cell-mediated immunity. Micro-RNAs are short (similar to 22 nucleotides long), endogenous single-stranded RNA molecules that regulate gene expression by binding to the 3' untranslated regions (3' UTR) of mRNA transcripts. The relation between HIV-1 infection and human miRNA expression profile has been previously investigated, and studies have shown that the virus can alter miRNA expression and vice versa. Here, we broaden the understanding of the HIV-1 infection process, and show that miRNA-186, 210 and 222 are up-regulated following HIV-1 infection of human Sup-T1 cells. As a result, the host miRNA target genes: Dicer1 (Double-Stranded RNA-Specific Endoribonuclease), HRB (HIV-1 Rev-binding protein) and HIV-EP2 (Human Immunodeficiency Virus Type I Enhancer Binding Protein 2), are down-regulated. Moreover, testing the miRNA-gene anti-correlation on the Jurkat and the HeLa-MAGI cell lines demonstrated the ability of the miRNAs to down-regulate viral expression as well. To conclude, we found that human miR-186, 210 and 222 directly regulate the human genes Dicer1, HRB and HIV-EP2, thus may be filling key roles during HIV-1 replication and miRNA biogenesis. This finding may contribute to the development of new therapeutic strategies.
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