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http://purl.uniprot.org/citations/18086894http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18086894http://www.w3.org/2000/01/rdf-schema#comment"The positive elongation factor P-TEFb appears to function as a crucial C-terminal-domain (CTD) kinase for RNA polymerase II (Pol II) transcribing immediate early genes (IEGs) in neuroendocrine GH4C1 cells. Chromatin immunoprecipitation indicated that in resting cells Pol II occupied the promoter-proximal regions of the c-fos and junB genes, together with the negative elongation factors DSIF and NELF. Thyrotropin-releasing hormone (TRH)-induced recruitment of positive transcription elongation factor b (P-TEFb) abolished the pausing of Pol II and enhanced phosphorylation of CTD serine 2, resulting in transcription elongation. In addition, P-TEFb was essential for splicing and 3'-end processing of IEG transcripts. Importantly, the MEK1-extracellular signal-regulated kinase (ERK) signaling pathway activated by TRH up-regulated nuclear CDK9 and CDK9/cyclinT1 dimers (i.e., P-TEFb), facilitating the recruitment of P-TEFb to c-fos and other IEGs. Thus, in addition to established gene transcription control via promoter response elements, the MEK1-ERK signaling pathway controls transcription elongation by Pol II via the up-regulation of nuclear CDK9 integrated into P-TEFb."xsd:string
http://purl.uniprot.org/citations/18086894http://purl.org/dc/terms/identifier"doi:10.1128/mcb.01767-07"xsd:string
http://purl.uniprot.org/citations/18086894http://purl.uniprot.org/core/author"Fujita T."xsd:string
http://purl.uniprot.org/citations/18086894http://purl.uniprot.org/core/author"Ryser S."xsd:string
http://purl.uniprot.org/citations/18086894http://purl.uniprot.org/core/author"Schlegel W."xsd:string
http://purl.uniprot.org/citations/18086894http://purl.uniprot.org/core/author"Piuz I."xsd:string
http://purl.uniprot.org/citations/18086894http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18086894http://purl.uniprot.org/core/name"Mol Cell Biol"xsd:string
http://purl.uniprot.org/citations/18086894http://purl.uniprot.org/core/pages"1630-1643"xsd:string
http://purl.uniprot.org/citations/18086894http://purl.uniprot.org/core/title"Up-regulation of P-TEFb by the MEK1-extracellular signal-regulated kinase signaling pathway contributes to stimulated transcription elongation of immediate early genes in neuroendocrine cells."xsd:string
http://purl.uniprot.org/citations/18086894http://purl.uniprot.org/core/volume"28"xsd:string
http://purl.uniprot.org/citations/18086894http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/18086894
http://purl.uniprot.org/citations/18086894http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/18086894
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http://purl.uniprot.org/uniprot/#_A0A8I6A048-mappedCitation-18086894http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18086894
http://purl.uniprot.org/uniprot/#_A0A8I6A1J3-mappedCitation-18086894http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18086894
http://purl.uniprot.org/uniprot/#_A0A0H2UHI2-mappedCitation-18086894http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18086894
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http://purl.uniprot.org/uniprot/#_Q01986-mappedCitation-18086894http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18086894
http://purl.uniprot.org/uniprot/A0A0H2UHI2http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/18086894
http://purl.uniprot.org/uniprot/A0A8I6A048http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/18086894