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IRAK2 directs stimulus-dependent nuclear export of inflammatory mRNAs.
Zhou, Hao; Bulek, Katarzyna; Li, Xiao; Herjan, Tomasz; Yu, Minjia; Qian, Wen; Wang, Han; Zhou, Gao; Chen, Xing; Yang, Hui; Hong, Lingzi; Zhao, Junjie; Qin, Luke; Fukuda, Koichi; Flotho, Annette; Gao, Ji; Dongre, Ashok; Carman, Julie A; Kang, Zizhen; Su, Bing; Kern, Timothy S; Smith, Jonathan D; Hamilton, Thomas A; Melchior, Frauke; Fox, Paul L; Li, Xiaoxia.
Afiliación
  • Zhou H; Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
  • Bulek K; Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
  • Li X; Department of Immunology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland.
  • Herjan T; Department of Genetics, Stanford University School of Medicine, Stanford, United States.
  • Yu M; Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
  • Qian W; Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
  • Wang H; Department of Medicine, Mount Auburn Hospital, Harvard Medical School, Cambridge, United States.
  • Zhou G; Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
  • Chen X; Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
  • Yang H; Department of Genetics, Stanford University School of Medicine, Stanford, United States.
  • Hong L; Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
  • Zhao J; Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
  • Qin L; Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
  • Fukuda K; Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
  • Flotho A; Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
  • Gao J; Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
  • Dongre A; Zentrum für Molekulare Biologie der Universität Heidelberg, DKFZ-ZMBH Alliance, Heidelberg, Germany.
  • Carman JA; Discovery Biology, Bristol-Myers Squibb, Princeton, United States.
  • Kang Z; Discovery Biology, Bristol-Myers Squibb, Princeton, United States.
  • Su B; Discovery Biology, Bristol-Myers Squibb, Princeton, United States.
  • Kern TS; Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
  • Smith JD; Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Hamilton TA; Department of Immunobiology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Melchior F; Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Fox PL; Department of Immunobiology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
  • Li X; Department of Immunobiology, Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, United States.
Elife ; 62017 10 09.
Article en En | MEDLINE | ID: mdl-28990926
Expression of inflammatory genes is determined in part by post-transcriptional regulation of mRNA metabolism but how stimulus- and transcript-dependent nuclear export influence is poorly understood. Here, we report a novel pathway in which LPS/TLR4 engagement promotes nuclear localization of IRAK2 to facilitate nuclear export of a specific subset of inflammation-related mRNAs for translation in murine macrophages. IRAK2 kinase activity is required for LPS-induced RanBP2-mediated IRAK2 sumoylation and subsequent nuclear translocation. Array analysis showed that an SRSF1-binding motif is enriched in mRNAs dependent on IRAK2 for nuclear export. Nuclear IRAK2 phosphorylates SRSF1 to reduce its binding to target mRNAs, which promotes the RNA binding of the nuclear export adaptor ALYREF and nuclear export receptor Nxf1 loading for the export of the mRNAs. In summary, LPS activates a nuclear function of IRAK2 that facilitates the assembly of nuclear export machinery to export selected inflammatory mRNAs to the cytoplasm for translation.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: ARN Mensajero / Transporte Activo de Núcleo Celular / Quinasas Asociadas a Receptores de Interleucina-1 / Macrófagos Límite: Animals Idioma: En Revista: Elife Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: ARN Mensajero / Transporte Activo de Núcleo Celular / Quinasas Asociadas a Receptores de Interleucina-1 / Macrófagos Límite: Animals Idioma: En Revista: Elife Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido