{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang HT"],"funding":["NCI CCSG","NCATS NIH HHS","Purdue University Center for Cancer Research Small","NCI NIH HHS","U.S. Army Medical Research Acquisition Activity","Prostate Cancer Research Program"],"pagination":["1330-40"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4252817"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["1839(11)"],"pubmed_abstract":["Protein arginine methyltransferase 5 (PRMT5) symmetrically methylates arginine residues of histones and non-histone protein substrates and regulates a variety of cellular processes through epigenetic control of target gene expression or post-translational modification of signaling molecules. Recent evidence suggests that PRMT5 may function as an oncogene and its overexpression contributes to the development and progression of several human cancers. However, the mechanism underlying the regulation of PRMT5 expression in cancer cells remains largely unknown. In the present study, we have mapped the proximal promoter of PRMT5 to the -240bp region and identified nuclear transcription factor Y (NF-Y) as a critical transcription factor that binds to the two inverted CCAAT boxes and regulates PRM"],"journal":["Biochimica et biophysica acta"],"pubmed_title":["Transcriptional activation of PRMT5 by NF-Y is required for cell growth and negatively regulated by the PKC/c-Fos signaling in prostate cancer cells."],"pmcid":["PMC4252817"],"funding_grant_id":["CA23168","PC11190","P30 CA023168","PC120512","UL1 TR001108"],"pubmed_authors":["Zha ZG","Zhang D","Zhang HT","Hu CD"],"additional_accession":[]},"is_claimable":false,"name":"Transcriptional activation of PRMT5 by NF-Y is required for cell growth and negatively regulated by the PKC/c-Fos signaling in prostate cancer cells.","description":"Protein arginine methyltransferase 5 (PRMT5) symmetrically methylates arginine residues of histones and non-histone protein substrates and regulates a variety of cellular processes through epigenetic control of target gene expression or post-translational modification of signaling molecules. Recent evidence suggests that PRMT5 may function as an oncogene and its overexpression contributes to the development and progression of several human cancers. However, the mechanism underlying the regulation of PRMT5 expression in cancer cells remains largely unknown. In the present study, we have mapped the proximal promoter of PRMT5 to the -240bp region and identified nuclear transcription factor Y (NF-Y) as a critical transcription factor that binds to the two inverted CCAAT boxes and regulates PRM","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Nov","modification":"2025-04-29T10:39:43.649Z","creation":"2019-03-27T01:40:44Z"},"accession":"S-EPMC4252817","cross_references":{"pubmed":["25281873"],"doi":["10.1016/j.bbagrm.2014.09.015"]}}