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- W3145487422 abstract "Objective To investigate the mechanism of high transcription of the glial cell-line derived neurotrophic factor(gdnf)gene induced by hyperacetylation of histone H3 lysine 9(H3K9) at its promoter region II in rat C6 glioma cells. Methods The acetylation level of H3K9 at Egr-1 binding site in gdnf gene promoter region II and the binding capacity of Egr-1 to its binding site in gdnf promoter were examined by Ch IP-PCR in C6 astroglioma cells and normal rat astrocytes, and its changes were investigated in C6 astroglioma cells after treatment with histone acetyltransferase inhibitor curcumin or deacetylase inhibitor trichostatin A. Results Compared normal astrocytes, C6 astroglioma cells showed significantly increased acetylation level of H3K9 at Egr-1 binding site in gdnf gene promoter region II and Egr-1 binding capacity(P0.01). Curcumin treatment significantly reduced H3K9 acetylation level at Egr-1 binding site and decreased both the binding of Egr-1 to promoter region II and gdnf m RNA levels in C6 astroglioma cells(P0.05). Conversely, increased H3K9 acetylation at the Egr-1 binding site induced by trichostatin A significantly increased the binding of Egr-1 to promoter region II and gdnf m RNA expression levels(P0.05). Conclusion H3K9 hyperacetylation induces increased Egr-1 binding to gdnf gene promoter II, which might be the reason for the high transcription level of gdnf gene in rat C6 glioma cells." @default.
- W3145487422 created "2021-04-13" @default.
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- W3145487422 date "2015-01-01" @default.
- W3145487422 modified "2023-09-26" @default.
- W3145487422 title "Increased Egr-1 binding to promoter induced by histone hyperacetylation promotes gdnf gene transcription" @default.
- W3145487422 hasPublicationYear "2015" @default.
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