| کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن | 
|---|---|---|---|---|
| 10753891 | 1050345 | 2014 | 8 صفحه PDF | دانلود رایگان | 
عنوان انگلیسی مقاله ISI
												MicroRNA-181 expression regulates specific post-transcriptional level of SAMHD1 expression in vitro
												
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																																												کلمات کلیدی
												
											موضوعات مرتبط
												
													علوم زیستی و بیوفناوری
													بیوشیمی، ژنتیک و زیست شناسی مولکولی
													 زیست شیمی
												
											پیش نمایش صفحه اول مقاله
												
												چکیده انگلیسی
												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.
											ناشر
												Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 452, Issue 3, 26 September 2014, Pages 760-767
											Journal: Biochemical and Biophysical Research Communications - Volume 452, Issue 3, 26 September 2014, Pages 760-767
نویسندگان
												Changzhong Jin, Xiaorong Peng, Fumin Liu, Linfang Cheng, Xiangyun Lu, Hangping Yao, Haibo Wu, Nanping Wu,