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• W1502462023 endingPage "19033" @default.
• W1502462023 startingPage "19018" @default.
• W1502462023 abstract "The T-synthase (core 1 β3-galactosyltransferase) and its molecular chaperone Cosmc regulate the biosynthesis of mucin type O-glycans on glycoproteins, and evidence suggests that both T-synthase and Cosmc are transcriptionally suppressed in several human diseases, although the transcriptional regulation of these two genes is not understood. Here, we characterized the promoters essential for human Cosmc and T-synthase transcription. The upstream regions of the genes lack a conventional TATA box but contain CpG islands, cCpG-I and cCpG-II for Cosmc and tCpG for T-synthase. Using luciferase reporter assays, site-directed mutagenesis, ChIP assays, and mithramycin A treatment, we identified the core promoters within cCpG-II and tCpG, which contain two binding sites for Krüppel-like transcription factors, including SP1/SP3, respectively. Methylome analysis of Tn4 B cells, which harbor a silenced Cosmc, confirmed the hypermethylation of the Cosmc core promoter but not for T-synthase. These results demonstrate that Cosmc and T-synthase are transcriptionally regulated at a basal level by the specificity protein/Krüppel-like transcription factor family of members, which explains their ubiquitous and coordinated expression, and also indicate that they are differentially epigenetically regulated beyond X chromosome imprinting. These results are important in understanding the regulation of these genes that have roles in human diseases, such as IgA nephropathy and cancer. The T-synthase (core 1 β3-galactosyltransferase) and its molecular chaperone Cosmc regulate the biosynthesis of mucin type O-glycans on glycoproteins, and evidence suggests that both T-synthase and Cosmc are transcriptionally suppressed in several human diseases, although the transcriptional regulation of these two genes is not understood. Here, we characterized the promoters essential for human Cosmc and T-synthase transcription. The upstream regions of the genes lack a conventional TATA box but contain CpG islands, cCpG-I and cCpG-II for Cosmc and tCpG for T-synthase. Using luciferase reporter assays, site-directed mutagenesis, ChIP assays, and mithramycin A treatment, we identified the core promoters within cCpG-II and tCpG, which contain two binding sites for Krüppel-like transcription factors, including SP1/SP3, respectively. Methylome analysis of Tn4 B cells, which harbor a silenced Cosmc, confirmed the hypermethylation of the Cosmc core promoter but not for T-synthase. These results demonstrate that Cosmc and T-synthase are transcriptionally regulated at a basal level by the specificity protein/Krüppel-like transcription factor family of members, which explains their ubiquitous and coordinated expression, and also indicate that they are differentially epigenetically regulated beyond X chromosome imprinting. These results are important in understanding the regulation of these genes that have roles in human diseases, such as IgA nephropathy and cancer." @default.
• W1502462023 created "2016-06-24" @default.
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• W1502462023 date "2015-07-01" @default.
• W1502462023 modified "2023-10-13" @default.
• W1502462023 title "Promoters of Human Cosmc and T-synthase Genes Are Similar in Structure, Yet Different in Epigenetic Regulation" @default.
• W1502462023 cites W1482367616 @default.
• W1502462023 cites W1594048116 @default.
• W1502462023 cites W1964042784 @default.
• W1502462023 cites W1964263030 @default.
• W1502462023 cites W1965987734 @default.
• W1502462023 cites W1966649061 @default.
• W1502462023 cites W1973535960 @default.
• W1502462023 cites W1979666871 @default.
• W1502462023 cites W1983177609 @default.
• W1502462023 cites W1984505531 @default.
• W1502462023 cites W1986473194 @default.
• W1502462023 cites W1990353372 @default.
• W1502462023 cites W1990671435 @default.
• W1502462023 cites W1994018335 @default.
• W1502462023 cites W1995611890 @default.
• W1502462023 cites W2000721637 @default.
• W1502462023 cites W2003386539 @default.
• W1502462023 cites W2004181770 @default.
• W1502462023 cites W2004755955 @default.
• W1502462023 cites W2006044324 @default.
• W1502462023 cites W2006362317 @default.
• W1502462023 cites W2007058211 @default.
• W1502462023 cites W2007161309 @default.
• W1502462023 cites W2007731313 @default.
• W1502462023 cites W2011467292 @default.
• W1502462023 cites W2024523736 @default.
• W1502462023 cites W2025532285 @default.
• W1502462023 cites W2031291557 @default.
• W1502462023 cites W2036550192 @default.
• W1502462023 cites W2038976546 @default.
• W1502462023 cites W2041310039 @default.
• W1502462023 cites W2044088440 @default.
• W1502462023 cites W2047749014 @default.
• W1502462023 cites W2049499509 @default.
• W1502462023 cites W2055008180 @default.
• W1502462023 cites W2057071402 @default.
• W1502462023 cites W2059282001 @default.
• W1502462023 cites W2063124267 @default.
• W1502462023 cites W2067110717 @default.
• W1502462023 cites W2070269043 @default.
• W1502462023 cites W2072613524 @default.
• W1502462023 cites W2073865076 @default.
• W1502462023 cites W2074469807 @default.
• W1502462023 cites W2075253368 @default.
• W1502462023 cites W2077271194 @default.
• W1502462023 cites W2080620002 @default.
• W1502462023 cites W2087308464 @default.
• W1502462023 cites W2087471889 @default.
• W1502462023 cites W2089126365 @default.
• W1502462023 cites W2089542491 @default.
• W1502462023 cites W2089944349 @default.
• W1502462023 cites W2091512231 @default.
• W1502462023 cites W2094105923 @default.
• W1502462023 cites W2099343472 @default.
• W1502462023 cites W2100885850 @default.
• W1502462023 cites W2101366183 @default.
• W1502462023 cites W2106578889 @default.
• W1502462023 cites W2108206148 @default.
• W1502462023 cites W2108789237 @default.
• W1502462023 cites W2112689808 @default.
• W1502462023 cites W2120092055 @default.
• W1502462023 cites W2125256326 @default.
• W1502462023 cites W2131378508 @default.
• W1502462023 cites W2134076611 @default.
• W1502462023 cites W2140020627 @default.
• W1502462023 cites W2140449516 @default.
• W1502462023 cites W2144789664 @default.
• W1502462023 cites W2150630697 @default.
• W1502462023 cites W2159384610 @default.
• W1502462023 cites W225023543 @default.
• W1502462023 cites W2320296478 @default.
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• W1502462023 doi "https://doi.org/10.1074/jbc.m115.654244" @default.
• W1502462023 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4521027" @default.
• W1502462023 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26063800" @default.
• W1502462023 hasPublicationYear "2015" @default.
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