کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9126851 | 1569963 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Transcriptional regulation of the mouse PNRC2 promoter by the nuclear factor Y (NFY) and E2F1
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
ژنتیک
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
To understand the molecular mechanisms that regulate the expression of PNRC2 gene, we have cloned and characterized the 5â²-flanking region of the gene. Potential transcriptional start sites were determined by 5â² RACE analysis. Functional analysis of the 5â² flanking region of the mPNRC2 gene by deletion mutagenesis, transient transfection and luciferase assays revealed that the â 67/+ 53 region is the minimal promoter of the mouse PNRC2 gene in HeLa cells. Within this sequence we identified two putative binding sites (inverted CCAAT box) for the transcription factor NFY (nuclear factor Y), a factor mediating cell type-specific and cell-cycle regulated expression of genes, and one binding site for E2F1, a founding member of the E2F family that displays the properties of both an oncogene and a tumor suppressor gene. Mutating each individual CCAAT site or changing the orientation of the CAATT box led to a 5-fold decrease in PNRC2 promoter activity in transient transfection experiments. Gel shift, supershift assay, and ChIP analysis demonstrated the specific binding of NFY and E2F1 proteins to the mouse PNRC2 promoter. Transient transfections and luciferase assays further revealed that overexpression of NFY enhanced-promoter activity of PNRC2 gene in a dose-dependent manner while overexpression of E2F1 strongly repressed the activity of the PNRC2 promoter. Since most genes regulated by E2F1 or NFY play a regulatory role in the cell cycle, the finding that the PNRC2 promoter is activated by NFY and repressed by E2F1 indicates that in addition to functioning as nuclear receptor coactivator, PNRC2 may also play a role in the cell cycle.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gene - Volume 361, 21 November 2005, Pages 89-100
Journal: Gene - Volume 361, 21 November 2005, Pages 89-100
نویسندگان
Dujin Zhou, Selma Masri, Jing Jing Ye, Shiuan Chen,