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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Nature Portfolio
2019
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oai:doaj.org-article:1894c8d823ab4177ab03857c322a339c2021-12-02T16:57:52ZHectd3 promotes pathogenic Th17 lineage through Stat3 activation and Malt1 signaling in neuroinflammation10.1038/s41467-019-08605-32041-1723https://doaj.org/article/1894c8d823ab4177ab03857c322a339c2019-02-01T00:00:00Zhttps://doi.org/10.1038/s41467-019-08605-3https://doaj.org/toc/2041-1723Ubiquitination 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.Jonathan J. ChoZhiwei XuUpasana ParthasarathyTheodore T. DrashanskyEric Y. HelmAshley N. ZunigaKyle J. LorentsenSamira MansouriJoshua Y. ChoMariola J. EdelmannDuc M. DuongTorben GehringThomas SeeholzerDaniel KrappmannMohammad N. UddinDanielle CalifanoRejean L. WangLei JinHongmin LiDongwen LvDaohong ZhouLiang ZhouDorina AvramNature PortfolioarticleScienceQENNature Communications, Vol 10, Iss 1, Pp 1-18 (2019) |
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Science Q 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 |
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. |
format |
article |
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 |
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 Portfolio |
publishDate |
2019 |
url |
https://doaj.org/article/1894c8d823ab4177ab03857c322a339c |
work_keys_str_mv |
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