دورية أكاديمية
LUBAC assembles a ubiquitin signaling platform at mitochondria for signal amplification and transport of NF-κB to the nucleus.
العنوان: | LUBAC assembles a ubiquitin signaling platform at mitochondria for signal amplification and transport of NF-κB to the nucleus. |
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المؤلفون: | Wu Z; Department Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Bochum, Germany., Berlemann LA; Department Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Bochum, Germany., Bader V; Department Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Bochum, Germany.; Department Biochemistry of Neurodegenerative Diseases, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Bochum, Germany., Sehr DA; Department Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Bochum, Germany., Dawin E; Department Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Bochum, Germany.; Leibniz-Institut für Analytische Wissenschaften-ISAS-e.V, Dortmund, Germany., Covallero A; Department of Biomedical Sciences, University of Padua, Padua, Italy., Meschede J; Department Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Bochum, Germany., Angersbach L; Department Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Bochum, Germany., Showkat C; Department Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Bochum, Germany., Michaelis JB; Faculty of Medicine, Institute of Biochemistry II, Goethe University Frankfurt, Frankfurt am Main, Germany., Münch C; Faculty of Medicine, Institute of Biochemistry II, Goethe University Frankfurt, Frankfurt am Main, Germany., Rieger B; Institute for Integrative Cell Biology and Physiology, Faculty of Biology, University of Münster, Münster, Germany., Namgaladze D; Institute of Biochemistry I, Faculty of Medicine, Goethe-University Frankfurt, Frankfurt, Germany., Herrera MG; Department Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Bochum, Germany., Fiesel FC; Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.; Neuroscience PhD Program, Mayo Clinic Graduate School of Biomedical Sciences, Jacksonville, FL, USA., Springer W; Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.; Neuroscience PhD Program, Mayo Clinic Graduate School of Biomedical Sciences, Jacksonville, FL, USA., Mendes M; Proteomics of Cellular Signaling, Department of Infection and Immunity, Luxembourg Institute of Health, Strassen, Luxembourg., Stepien J; Medizinisches Proteom-Center, Ruhr-Universität Bochum, Bochum, Germany.; Medical Proteome Analysis, Center for Protein Diagnostics (PRODI), Ruhr-University Bochum, Bochum, Germany., Barkovits K; Medizinisches Proteom-Center, Ruhr-Universität Bochum, Bochum, Germany.; Medical Proteome Analysis, Center for Protein Diagnostics (PRODI), Ruhr-University Bochum, Bochum, Germany., Marcus K; Medizinisches Proteom-Center, Ruhr-Universität Bochum, Bochum, Germany.; Medical Proteome Analysis, Center for Protein Diagnostics (PRODI), Ruhr-University Bochum, Bochum, Germany., Sickmann A; Leibniz-Institut für Analytische Wissenschaften-ISAS-e.V, Dortmund, Germany., Dittmar G; Proteomics of Cellular Signaling, Department of Infection and Immunity, Luxembourg Institute of Health, Strassen, Luxembourg.; Department of Life Sciences and Medicine, University of Luxembourg, Belvaux, Luxembourg., Busch KB; Institute for Integrative Cell Biology and Physiology, Faculty of Biology, University of Münster, Münster, Germany., Riedel D; Laboratory for Electron Microscopy, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany., Brini M; Department of Biology, University of Padua, Padua, Italy.; Centro Studi per la Neurodegenerazione (CESNE), University of Padova, Padua, Italy., Tatzelt J; Department Biochemistry of Neurodegenerative Diseases, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Bochum, Germany.; RESOLV Cluster of Excellence, Ruhr University Bochum, Bochum, Germany., Cali T; Department of Biomedical Sciences, University of Padua, Padua, Italy.; Centro Studi per la Neurodegenerazione (CESNE), University of Padova, Padua, Italy.; Padua Neuroscience Center (PNC), University of Padua, Padua, Italy., Winklhofer KF; Department Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Bochum, Germany.; RESOLV Cluster of Excellence, Ruhr University Bochum, Bochum, Germany. |
المصدر: | The EMBO journal [EMBO J] 2022 Dec 15; Vol. 41 (24), pp. e112006. Date of Electronic Publication: 2022 Nov 18. |
نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't; Research Support, N.I.H., Extramural |
اللغة: | English |
بيانات الدورية: | Publisher: Nature Publishing Group Country of Publication: England NLM ID: 8208664 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1460-2075 (Electronic) Linking ISSN: 02614189 NLM ISO Abbreviation: EMBO J Subsets: MEDLINE |
أسماء مطبوعة: | Publication: 2024- : [London] : Nature Publishing Group Original Publication: Eynsham, Oxford, England : Published for the European Molecular Biology Organization by IRL Press, [c1982- |
مواضيع طبية MeSH: | NF-kappa B*/genetics , NF-kappa B*/metabolism , Ubiquitin*/metabolism, Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Signal Transduction/physiology ; Mitochondria/metabolism ; Ubiquitination |
مستخلص: | Mitochondria are increasingly recognized as cellular hubs to orchestrate signaling pathways that regulate metabolism, redox homeostasis, and cell fate decisions. Recent research revealed a role of mitochondria also in innate immune signaling; however, the mechanisms of how mitochondria affect signal transduction are poorly understood. Here, we show that the NF-κB pathway activated by TNF employs mitochondria as a platform for signal amplification and shuttling of activated NF-κB to the nucleus. TNF treatment induces the recruitment of HOIP, the catalytic component of the linear ubiquitin chain assembly complex (LUBAC), and its substrate NEMO to the outer mitochondrial membrane, where M1- and K63-linked ubiquitin chains are generated. NF-κB is locally activated and transported to the nucleus by mitochondria, leading to an increase in mitochondria-nucleus contact sites in a HOIP-dependent manner. Notably, TNF-induced stabilization of the mitochondrial kinase PINK1 furthermore contributes to signal amplification by antagonizing the M1-ubiquitin-specific deubiquitinase OTULIN. Overall, our study reveals a role for mitochondria in amplifying TNF-mediated NF-κB activation, both serving as a signaling platform, as well as a transport mode for activated NF-κB to the nuclear. (© 2022 The Authors. Published under the terms of the CC BY NC ND 4.0 license.) |
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معلومات مُعتمدة: | R01 NS085070 United States NS NINDS NIH HHS; R01 NS110085 United States NS NINDS NIH HHS; RF1 NS085070 United States NS NINDS NIH HHS; U54 NS110435 United States NS NINDS NIH HHS |
فهرسة مساهمة: | Keywords: HOIP; NEMO; OTULIN; PINK1; ubiquitin |
المشرفين على المادة: | 0 (NF-kappa B) 0 (Ubiquitin) EC 2.3.2.27 (Ubiquitin-Protein Ligases) |
تواريخ الأحداث: | Date Created: 20221118 Date Completed: 20221216 Latest Revision: 20240707 |
رمز التحديث: | 20240707 |
مُعرف محوري في PubMed: | PMC9753471 |
DOI: | 10.15252/embj.2022112006 |
PMID: | 36398858 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1460-2075 |
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DOI: | 10.15252/embj.2022112006 |