Nature Communications (Feb 2019)
Hectd3 promotes pathogenic Th17 lineage through Stat3 activation and Malt1 signaling in neuroinflammation
- 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
Affiliations
- Jonathan J. Cho
- Department of Anatomy and Cell Biology, College of Medicine, University of Florida
- Zhiwei Xu
- Department of Anatomy and Cell Biology, College of Medicine, University of Florida
- Upasana Parthasarathy
- Department of Anatomy and Cell Biology, College of Medicine, University of Florida
- Theodore T. Drashansky
- Department of Anatomy and Cell Biology, College of Medicine, University of Florida
- Eric Y. Helm
- Department of Anatomy and Cell Biology, College of Medicine, University of Florida
- Ashley N. Zuniga
- Department of Anatomy and Cell Biology, College of Medicine, University of Florida
- Kyle J. Lorentsen
- Department of Medicine, College of Medicine, University of Florida
- Samira Mansouri
- Department of Medicine, College of Medicine, University of Florida
- Joshua Y. Cho
- Department of Medicine, College of Medicine, University of Florida
- Mariola J. Edelmann
- Department of Microbiology and Cell Science, University of Florida
- Duc M. Duong
- Center for Neurodegenerative Diseases, Emory University School of Medicine
- Torben Gehring
- Research Unit Cellular Signal Integration, Institute of Molecular Toxicology and Pharmacology, Helmholtz Zentrum München - German Research Center for Environmental Health
- Thomas Seeholzer
- Research Unit Cellular Signal Integration, Institute of Molecular Toxicology and Pharmacology, Helmholtz Zentrum München - German Research Center for Environmental Health
- Daniel Krappmann
- Research Unit Cellular Signal Integration, Institute of Molecular Toxicology and Pharmacology, Helmholtz Zentrum München - German Research Center for Environmental Health
- Mohammad N. Uddin
- Department of Immunology and Microbial Disease, Albany Medical Center
- Danielle Califano
- Department of Immunology and Microbial Disease, Albany Medical Center
- Rejean L. Wang
- Department of Medicine, College of Medicine, University of Florida
- Lei Jin
- Department of Medicine, College of Medicine, University of Florida
- Hongmin Li
- Wadsworth Center, New York State Department of Health
- Dongwen Lv
- Department of Pharmacodynamics, College of Pharmacy, University of Florida
- Daohong Zhou
- UF Health Cancer Center, University of Florida
- Liang Zhou
- UF Health Cancer Center, University of Florida
- Dorina Avram
- Department of Anatomy and Cell Biology, College of Medicine, University of Florida
- DOI
- https://doi.org/10.1038/s41467-019-08605-3
- Journal volume & issue
-
Vol. 10,
no. 1
pp. 1 – 18
Abstract
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.
