Hectd3 promotes pathogenic Th17 lineage through Stat3 activation and Malt1 signaling in neuroinflammation
Ubiquitination may control protein stability or function. Here the authors show that an ubiquitination enzyme, Hectd3, ubiquitinates Stat3 and Malt1 to modulate their function but not degradation in T cells, and thereby promoting the differentiation of pathogenic Th17 cells and susceptibility to a m...
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| Language: | English |
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Nature Publishing Group
2019-02-01
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| Series: | Nature Communications |
| Online Access: | https://doi.org/10.1038/s41467-019-08605-3 |
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doaj-1894c8d823ab4177ab03857c322a339c2021-05-11T12:00:16ZengNature Publishing GroupNature Communications2041-17232019-02-0110111810.1038/s41467-019-08605-3Hectd3 promotes pathogenic Th17 lineage through Stat3 activation and Malt1 signaling in neuroinflammationJonathan J. Cho0Zhiwei Xu1Upasana Parthasarathy2Theodore T. Drashansky3Eric Y. Helm4Ashley N. Zuniga5Kyle J. Lorentsen6Samira Mansouri7Joshua Y. Cho8Mariola J. Edelmann9Duc M. Duong10Torben Gehring11Thomas Seeholzer12Daniel Krappmann13Mohammad N. Uddin14Danielle Califano15Rejean L. Wang16Lei Jin17Hongmin Li18Dongwen Lv19Daohong Zhou20Liang Zhou21Dorina Avram22Department of Anatomy and Cell Biology, College of Medicine, University of FloridaDepartment of Anatomy and Cell Biology, College of Medicine, University of FloridaDepartment of Anatomy and Cell Biology, College of Medicine, University of FloridaDepartment of Anatomy and Cell Biology, College of Medicine, University of FloridaDepartment of Anatomy and Cell Biology, College of Medicine, University of FloridaDepartment of Anatomy and Cell Biology, College of Medicine, University of FloridaDepartment of Medicine, College of Medicine, University of FloridaDepartment of Medicine, College of Medicine, University of FloridaDepartment of Medicine, College of Medicine, University of FloridaDepartment of Microbiology and Cell Science, University of FloridaCenter for Neurodegenerative Diseases, Emory University School of MedicineResearch Unit Cellular Signal Integration, Institute of Molecular Toxicology and Pharmacology, Helmholtz Zentrum München - German Research Center for Environmental HealthResearch Unit Cellular Signal Integration, Institute of Molecular Toxicology and Pharmacology, Helmholtz Zentrum München - German Research Center for Environmental HealthResearch Unit Cellular Signal Integration, Institute of Molecular Toxicology and Pharmacology, Helmholtz Zentrum München - German Research Center for Environmental HealthDepartment of Immunology and Microbial Disease, Albany Medical CenterDepartment of Immunology and Microbial Disease, Albany Medical CenterDepartment of Medicine, College of Medicine, University of FloridaDepartment of Medicine, College of Medicine, University of FloridaWadsworth Center, New York State Department of HealthDepartment of Pharmacodynamics, College of Pharmacy, University of FloridaUF Health Cancer Center, University of FloridaUF Health Cancer Center, University of FloridaDepartment of Anatomy and Cell Biology, College of Medicine, University of FloridaUbiquitination may control protein stability or function. Here the authors show that an ubiquitination enzyme, Hectd3, ubiquitinates Stat3 and Malt1 to modulate their function but not degradation in T cells, and thereby promoting the differentiation of pathogenic Th17 cells and susceptibility to a mouse model of multiple sclerosis.https://doi.org/10.1038/s41467-019-08605-3 |
| collection |
DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
Jonathan J. Cho Zhiwei Xu Upasana Parthasarathy Theodore T. Drashansky Eric Y. Helm Ashley N. Zuniga Kyle J. Lorentsen Samira Mansouri Joshua Y. Cho Mariola J. Edelmann Duc M. Duong Torben Gehring Thomas Seeholzer Daniel Krappmann Mohammad N. Uddin Danielle Califano Rejean L. Wang Lei Jin Hongmin Li Dongwen Lv Daohong Zhou Liang Zhou Dorina Avram |
| spellingShingle |
Jonathan J. Cho Zhiwei Xu Upasana Parthasarathy Theodore T. Drashansky Eric Y. Helm Ashley N. Zuniga Kyle J. Lorentsen Samira Mansouri Joshua Y. Cho Mariola J. Edelmann Duc M. Duong Torben Gehring Thomas Seeholzer Daniel Krappmann Mohammad N. Uddin Danielle Califano Rejean L. Wang Lei Jin Hongmin Li Dongwen Lv Daohong Zhou Liang Zhou Dorina Avram Hectd3 promotes pathogenic Th17 lineage through Stat3 activation and Malt1 signaling in neuroinflammation Nature Communications |
| author_facet |
Jonathan J. Cho Zhiwei Xu Upasana Parthasarathy Theodore T. Drashansky Eric Y. Helm Ashley N. Zuniga Kyle J. Lorentsen Samira Mansouri Joshua Y. Cho Mariola J. Edelmann Duc M. Duong Torben Gehring Thomas Seeholzer Daniel Krappmann Mohammad N. Uddin Danielle Califano Rejean L. Wang Lei Jin Hongmin Li Dongwen Lv Daohong Zhou Liang Zhou Dorina Avram |
| author_sort |
Jonathan J. Cho |
| title |
Hectd3 promotes pathogenic Th17 lineage through Stat3 activation and Malt1 signaling in neuroinflammation |
| title_short |
Hectd3 promotes pathogenic Th17 lineage through Stat3 activation and Malt1 signaling in neuroinflammation |
| title_full |
Hectd3 promotes pathogenic Th17 lineage through Stat3 activation and Malt1 signaling in neuroinflammation |
| title_fullStr |
Hectd3 promotes pathogenic Th17 lineage through Stat3 activation and Malt1 signaling in neuroinflammation |
| title_full_unstemmed |
Hectd3 promotes pathogenic Th17 lineage through Stat3 activation and Malt1 signaling in neuroinflammation |
| title_sort |
hectd3 promotes pathogenic th17 lineage through stat3 activation and malt1 signaling in neuroinflammation |
| publisher |
Nature Publishing Group |
| series |
Nature Communications |
| issn |
2041-1723 |
| publishDate |
2019-02-01 |
| description |
Ubiquitination may control protein stability or function. Here the authors show that an ubiquitination enzyme, Hectd3, ubiquitinates Stat3 and Malt1 to modulate their function but not degradation in T cells, and thereby promoting the differentiation of pathogenic Th17 cells and susceptibility to a mouse model of multiple sclerosis. |
| url |
https://doi.org/10.1038/s41467-019-08605-3 |
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