Mediator cyclin-dependent kinases upregulate transcription of inflammatory genes in cooperation with NF-[kappa]B and C/EBP[beta] on stimulation of Toll-like receptor 9
In eukaryotes, the Mediator complex has important roles in regulation of transcription by RNA polymerase II. Mediator is a large complex with more than 20 subunits that form head, middle, tail and CDK/cyclin modules. Among them, CDK8 and/or CDK19 (CDK8/19), and their counterpart cyclin C, form the C...
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Veröffentlicht in: | Genes to cells : devoted to molecular & cellular mechanisms 2017-03, Vol.22 (3), p.265 |
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creator | Yamamoto, Seiji Hagihara, Tomoko Horiuchi, Yoshiyuki Okui, Akira Wani, Shotaro Yoshida, Tokuyuki Inoue, Takao Tanaka, Aki Ito, Takashi Hirose, Yutaka Ohkuma, Yoshiaki |
description | In eukaryotes, the Mediator complex has important roles in regulation of transcription by RNA polymerase II. Mediator is a large complex with more than 20 subunits that form head, middle, tail and CDK/cyclin modules. Among them, CDK8 and/or CDK19 (CDK8/19), and their counterpart cyclin C, form the CDK/cyclin module together with Mediator subunits MED12 and MED13. Despite evidences of both activation and repression, the precise functional roles of CDK8/19 in transcription are still elusive. Our previous results indicate that CDK8/19 recruits epigenetic regulators to repress immunoresponse genes. Here, this study focused on Toll-like receptors (TLRs), which exert innate immune responses through recognition of pathogen-associated molecular patterns and examined the functional roles of CDK8/19. As a result, CDK8/19 regulated transcription of inflammatory genes on stimulation of TLR9 in myeloma-derived RPMI8226 cells, which led to expression of inflammation-associated genes such as IL8,IL10,PTX3 and CCL2. Mediator subunits CDK8/19 and MED1, inflammation-related transcriptional activator NF-[kappa]B and C/EBP[beta], and general transcription factors TFIIE and TFIIB colocalized at the promoter regions of these genes under this condition. Our results show that CDK8/19 positively regulates inflammatory gene transcription in cooperation with NF-[kappa]B and C/EBP[beta] on stimulation of TLR9. |
doi_str_mv | 10.1111/gtc.12475 |
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Mediator is a large complex with more than 20 subunits that form head, middle, tail and CDK/cyclin modules. Among them, CDK8 and/or CDK19 (CDK8/19), and their counterpart cyclin C, form the CDK/cyclin module together with Mediator subunits MED12 and MED13. Despite evidences of both activation and repression, the precise functional roles of CDK8/19 in transcription are still elusive. Our previous results indicate that CDK8/19 recruits epigenetic regulators to repress immunoresponse genes. Here, this study focused on Toll-like receptors (TLRs), which exert innate immune responses through recognition of pathogen-associated molecular patterns and examined the functional roles of CDK8/19. As a result, CDK8/19 regulated transcription of inflammatory genes on stimulation of TLR9 in myeloma-derived RPMI8226 cells, which led to expression of inflammation-associated genes such as IL8,IL10,PTX3 and CCL2. Mediator subunits CDK8/19 and MED1, inflammation-related transcriptional activator NF-[kappa]B and C/EBP[beta], and general transcription factors TFIIE and TFIIB colocalized at the promoter regions of these genes under this condition. Our results show that CDK8/19 positively regulates inflammatory gene transcription in cooperation with NF-[kappa]B and C/EBP[beta] on stimulation of TLR9.</description><identifier>ISSN: 1356-9597</identifier><identifier>EISSN: 1365-2443</identifier><identifier>DOI: 10.1111/gtc.12475</identifier><identifier>CODEN: GECEFL</identifier><language>eng</language><publisher>Tokyo: Wiley Subscription Services, Inc</publisher><subject>Cooperation ; Cyclin-dependent kinases ; Genes ; Kinases</subject><ispartof>Genes to cells : devoted to molecular & cellular mechanisms, 2017-03, Vol.22 (3), p.265</ispartof><rights>Copyright © 2017 Molecular Biology Society of Japan and John Wiley & Sons Australia, Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27928,27929</link.rule.ids></links><search><creatorcontrib>Yamamoto, Seiji</creatorcontrib><creatorcontrib>Hagihara, Tomoko</creatorcontrib><creatorcontrib>Horiuchi, Yoshiyuki</creatorcontrib><creatorcontrib>Okui, Akira</creatorcontrib><creatorcontrib>Wani, Shotaro</creatorcontrib><creatorcontrib>Yoshida, Tokuyuki</creatorcontrib><creatorcontrib>Inoue, Takao</creatorcontrib><creatorcontrib>Tanaka, Aki</creatorcontrib><creatorcontrib>Ito, Takashi</creatorcontrib><creatorcontrib>Hirose, Yutaka</creatorcontrib><creatorcontrib>Ohkuma, Yoshiaki</creatorcontrib><title>Mediator cyclin-dependent kinases upregulate transcription of inflammatory genes in cooperation with NF-[kappa]B and C/EBP[beta] on stimulation of Toll-like receptor 9</title><title>Genes to cells : devoted to molecular & cellular mechanisms</title><description>In eukaryotes, the Mediator complex has important roles in regulation of transcription by RNA polymerase II. Mediator is a large complex with more than 20 subunits that form head, middle, tail and CDK/cyclin modules. Among them, CDK8 and/or CDK19 (CDK8/19), and their counterpart cyclin C, form the CDK/cyclin module together with Mediator subunits MED12 and MED13. Despite evidences of both activation and repression, the precise functional roles of CDK8/19 in transcription are still elusive. Our previous results indicate that CDK8/19 recruits epigenetic regulators to repress immunoresponse genes. Here, this study focused on Toll-like receptors (TLRs), which exert innate immune responses through recognition of pathogen-associated molecular patterns and examined the functional roles of CDK8/19. As a result, CDK8/19 regulated transcription of inflammatory genes on stimulation of TLR9 in myeloma-derived RPMI8226 cells, which led to expression of inflammation-associated genes such as IL8,IL10,PTX3 and CCL2. Mediator subunits CDK8/19 and MED1, inflammation-related transcriptional activator NF-[kappa]B and C/EBP[beta], and general transcription factors TFIIE and TFIIB colocalized at the promoter regions of these genes under this condition. 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Mediator is a large complex with more than 20 subunits that form head, middle, tail and CDK/cyclin modules. Among them, CDK8 and/or CDK19 (CDK8/19), and their counterpart cyclin C, form the CDK/cyclin module together with Mediator subunits MED12 and MED13. Despite evidences of both activation and repression, the precise functional roles of CDK8/19 in transcription are still elusive. Our previous results indicate that CDK8/19 recruits epigenetic regulators to repress immunoresponse genes. Here, this study focused on Toll-like receptors (TLRs), which exert innate immune responses through recognition of pathogen-associated molecular patterns and examined the functional roles of CDK8/19. As a result, CDK8/19 regulated transcription of inflammatory genes on stimulation of TLR9 in myeloma-derived RPMI8226 cells, which led to expression of inflammation-associated genes such as IL8,IL10,PTX3 and CCL2. Mediator subunits CDK8/19 and MED1, inflammation-related transcriptional activator NF-[kappa]B and C/EBP[beta], and general transcription factors TFIIE and TFIIB colocalized at the promoter regions of these genes under this condition. Our results show that CDK8/19 positively regulates inflammatory gene transcription in cooperation with NF-[kappa]B and C/EBP[beta] on stimulation of TLR9.</abstract><cop>Tokyo</cop><pub>Wiley Subscription Services, Inc</pub><doi>10.1111/gtc.12475</doi></addata></record> |
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title | Mediator cyclin-dependent kinases upregulate transcription of inflammatory genes in cooperation with NF-[kappa]B and C/EBP[beta] on stimulation of Toll-like receptor 9 |
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