Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10753891 | Biochemical and Biophysical Research Communications | 2014 | 8 Pages |
Abstract
SAM domain and HD domain 1 (SAMHD1) is a newly discovered human immunodeficiency virus (HIV)-1 host restriction factor with high expression in HIV-1-non-permissive cells and low expression in HIV-1-permissive cells. The regulatory mechanism of SAMHD1 expression is still unclear. We examined the relationship between the expression levels of SAMHD1 mRNA and protein and microRNA-181 (miR-181) level in different cell lines. MiR-181 level was negatively correlated with SAMHD1 expression level. By examining the impact of miR-181 on SAMHD1 3â² untranslated region (UTR) reporter luciferase activity and on SAMHD1 mRNA and argonaute RISC catalytic component 2 (AGO2) binding, we found that miR-181 acted directly on the SAMHD1 3â² UTR and regulated SAMHD1 mRNA levels after transcription. MiR-181 over-expression significantly reduced the level of SAMHD1 expression in THP-1 cells; miR-181 inhibition up-regulated SAMHD1 expression in THP-1 and Jurkat cells. Our results suggest that miR-181 regulates the level of post-transcriptional SAMHD1 expression negatively by directly binding to the 3â² UTR in SAMHD1.
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Authors
Changzhong Jin, Xiaorong Peng, Fumin Liu, Linfang Cheng, Xiangyun Lu, Hangping Yao, Haibo Wu, Nanping Wu,