Cyclin-dependent Kinase Inhibitor p16INK4A Inhibits Phosphorylation of RNA Polymerase II by General Transcription Factor TFIIH
The cell cycle is regulated by various protein kinases, including cyclin-dependent kinases (CDKs). D-type CDKs, CDK4, and CDK6, phosphorylate retinoblastoma protein and are believed to regulate through the G1 phase of the cell cycle. CDK inhibitor p16INK4A has been characterized as binding CDK4 and...
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| Veröffentlicht in: | The Journal of biological chemistry 1998-03, Vol.273 (10), p.5427-5430 |
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| creator | Serizawa, Hiroaki |
| description | The cell cycle is regulated by various protein kinases, including cyclin-dependent kinases (CDKs). D-type CDKs, CDK4, and CDK6, phosphorylate retinoblastoma protein and are believed to regulate through the G1 phase of the cell cycle. CDK inhibitor p16INK4A has been characterized as binding CDK4 and CDK6 and as inhibiting phosphorylation of retinoblastoma protein by these CDKs. Thus p16INK4A is implicated in regulating the cell cycle at the G1 phase. The largest subunit of RNA polymerase II (pol II) contains an essential C-terminal domain (CTD). General transcription factor TFIIH, which contains CDK7, phosphorylates the CTD in vitro. The CTD phosphorylation is shown to be involved in transcriptional regulation in vivo and in vitro. Phosphorylation of RNA pol II CTD by TFIIH is thought to play an important role in transcriptional regulation. Here we report that p16INK4Aassociates with RNA pol II CTD and TFIIH. p16INK4Ainhibited the CTD phosphorylation by TFIIH. These findings suggest that p16INK4A may regulate transcription via CTD phosphorylation in the cell cycle. |
| doi_str_mv | 10.1074/jbc.273.10.5427 |
| format | Article |
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D-type CDKs, CDK4, and CDK6, phosphorylate retinoblastoma protein and are believed to regulate through the G1 phase of the cell cycle. CDK inhibitor p16INK4A has been characterized as binding CDK4 and CDK6 and as inhibiting phosphorylation of retinoblastoma protein by these CDKs. Thus p16INK4A is implicated in regulating the cell cycle at the G1 phase. The largest subunit of RNA polymerase II (pol II) contains an essential C-terminal domain (CTD). General transcription factor TFIIH, which contains CDK7, phosphorylates the CTD in vitro. The CTD phosphorylation is shown to be involved in transcriptional regulation in vivo and in vitro. Phosphorylation of RNA pol II CTD by TFIIH is thought to play an important role in transcriptional regulation. Here we report that p16INK4Aassociates with RNA pol II CTD and TFIIH. p16INK4Ainhibited the CTD phosphorylation by TFIIH. These findings suggest that p16INK4A may regulate transcription via CTD phosphorylation in the cell cycle.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.273.10.5427</identifier><identifier>PMID: 9488660</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Cattle ; Cyclin-Dependent Kinase Inhibitor p16 - metabolism ; Cyclin-Dependent Kinase Inhibitor p16 - pharmacology ; Cyclin-Dependent Kinases ; G1 Phase - physiology ; Gene Expression Regulation - genetics ; Phosphorylation ; Protein Kinase Inhibitors ; Protein-Serine-Threonine Kinases - metabolism ; Recombinant Proteins - genetics ; RNA Polymerase II - antagonists & inhibitors ; RNA Polymerase II - metabolism ; Thymus Gland - chemistry ; Transcription Factor TFIIH ; Transcription Factors - antagonists & inhibitors ; Transcription Factors, TFII ; Transcription, Genetic - genetics</subject><ispartof>The Journal of biological chemistry, 1998-03, Vol.273 (10), p.5427-5430</ispartof><rights>1998 © 1998 ASBMB. 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D-type CDKs, CDK4, and CDK6, phosphorylate retinoblastoma protein and are believed to regulate through the G1 phase of the cell cycle. CDK inhibitor p16INK4A has been characterized as binding CDK4 and CDK6 and as inhibiting phosphorylation of retinoblastoma protein by these CDKs. Thus p16INK4A is implicated in regulating the cell cycle at the G1 phase. The largest subunit of RNA polymerase II (pol II) contains an essential C-terminal domain (CTD). General transcription factor TFIIH, which contains CDK7, phosphorylates the CTD in vitro. The CTD phosphorylation is shown to be involved in transcriptional regulation in vivo and in vitro. Phosphorylation of RNA pol II CTD by TFIIH is thought to play an important role in transcriptional regulation. Here we report that p16INK4Aassociates with RNA pol II CTD and TFIIH. p16INK4Ainhibited the CTD phosphorylation by TFIIH. These findings suggest that p16INK4A may regulate transcription via CTD phosphorylation in the cell cycle.</description><subject>Animals</subject><subject>Cattle</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - pharmacology</subject><subject>Cyclin-Dependent Kinases</subject><subject>G1 Phase - physiology</subject><subject>Gene Expression Regulation - genetics</subject><subject>Phosphorylation</subject><subject>Protein Kinase Inhibitors</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Recombinant Proteins - genetics</subject><subject>RNA Polymerase II - antagonists & inhibitors</subject><subject>RNA Polymerase II - metabolism</subject><subject>Thymus Gland - chemistry</subject><subject>Transcription Factor TFIIH</subject><subject>Transcription Factors - antagonists & inhibitors</subject><subject>Transcription Factors, TFII</subject><subject>Transcription, Genetic - genetics</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kM-L1DAUx4Mo67h69iQEBG-dTdq0TY_D4OyWXdZFRvAW8uPVZmmTmnSUXvzbzeyMHgRzCd_3vt8vjw9CbylZU1Kzq0el13ldJLEuWV4_QytKeJEVJf36HK0IyWnW5CV_iV7F-EjSYw29QBcN47yqyAr92i56sC4zMIEz4GZ8a52MgFvXW2VnH_BEq_b-lm3-jCJ-6H2ceh-WQc7WO-w7_Pl-gx_8sIwQntItVgu-BpfkgPdBuqiDnZ7cO6mPtftd2968Ri86OUR4c_4v0Zfdx_32Jrv7dN1uN3eZTsfXWWMgzyWp8kZ1FWVESloyJjmjylSMV9qURnddVyhDmg6MIqQrdN0ozrhiGopL9OHUOwX__QBxFqONGoZBOvCHKOqmzklV8GS8Ohl18DEG6MQU7CjDIigRR-IiEReJ-FEfiafEu3P1QY1g_vrPiNP-_Wnf22_9TxtAKOt1D-M_Lc3JBYnCDwtBRG3BaTApoWdhvP3vBb8ByYKb9A</recordid><startdate>19980306</startdate><enddate>19980306</enddate><creator>Serizawa, Hiroaki</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19980306</creationdate><title>Cyclin-dependent Kinase Inhibitor p16INK4A Inhibits Phosphorylation of RNA Polymerase II by General Transcription Factor TFIIH</title><author>Serizawa, Hiroaki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2587-9de22a0629bf6140aa1544a841bd6486cd5dcfff3bd09fedb00f3c79b848b4ce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Cattle</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - pharmacology</topic><topic>Cyclin-Dependent Kinases</topic><topic>G1 Phase - physiology</topic><topic>Gene Expression Regulation - genetics</topic><topic>Phosphorylation</topic><topic>Protein Kinase Inhibitors</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Recombinant Proteins - genetics</topic><topic>RNA Polymerase II - antagonists & inhibitors</topic><topic>RNA Polymerase II - metabolism</topic><topic>Thymus Gland - chemistry</topic><topic>Transcription Factor TFIIH</topic><topic>Transcription Factors - antagonists & inhibitors</topic><topic>Transcription Factors, TFII</topic><topic>Transcription, Genetic - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Serizawa, Hiroaki</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Serizawa, Hiroaki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclin-dependent Kinase Inhibitor p16INK4A Inhibits Phosphorylation of RNA Polymerase II by General Transcription Factor TFIIH</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>1998-03-06</date><risdate>1998</risdate><volume>273</volume><issue>10</issue><spage>5427</spage><epage>5430</epage><pages>5427-5430</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>The cell cycle is regulated by various protein kinases, including cyclin-dependent kinases (CDKs). D-type CDKs, CDK4, and CDK6, phosphorylate retinoblastoma protein and are believed to regulate through the G1 phase of the cell cycle. CDK inhibitor p16INK4A has been characterized as binding CDK4 and CDK6 and as inhibiting phosphorylation of retinoblastoma protein by these CDKs. Thus p16INK4A is implicated in regulating the cell cycle at the G1 phase. The largest subunit of RNA polymerase II (pol II) contains an essential C-terminal domain (CTD). General transcription factor TFIIH, which contains CDK7, phosphorylates the CTD in vitro. The CTD phosphorylation is shown to be involved in transcriptional regulation in vivo and in vitro. Phosphorylation of RNA pol II CTD by TFIIH is thought to play an important role in transcriptional regulation. Here we report that p16INK4Aassociates with RNA pol II CTD and TFIIH. p16INK4Ainhibited the CTD phosphorylation by TFIIH. These findings suggest that p16INK4A may regulate transcription via CTD phosphorylation in the cell cycle.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>9488660</pmid><doi>10.1074/jbc.273.10.5427</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Cattle Cyclin-Dependent Kinase Inhibitor p16 - metabolism Cyclin-Dependent Kinase Inhibitor p16 - pharmacology Cyclin-Dependent Kinases G1 Phase - physiology Gene Expression Regulation - genetics Phosphorylation Protein Kinase Inhibitors Protein-Serine-Threonine Kinases - metabolism Recombinant Proteins - genetics RNA Polymerase II - antagonists & inhibitors RNA Polymerase II - metabolism Thymus Gland - chemistry Transcription Factor TFIIH Transcription Factors - antagonists & inhibitors Transcription Factors, TFII Transcription, Genetic - genetics |
| title | Cyclin-dependent Kinase Inhibitor p16INK4A Inhibits Phosphorylation of RNA Polymerase II by General Transcription Factor TFIIH |
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