Hectd3 promotes pathogenic Th17 lineage through Stat3 activation and Malt1 signaling in neuroinflammation

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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Autores principales: 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
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2019
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Science
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Acceso en línea:https://doaj.org/article/1894c8d823ab4177ab03857c322a339c
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Sumario: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.

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