Cbl promotes MyD88 ubiquitin-mediated degradation in macrophages via phosphorylation and calcium mobilization
findings establish Cbl as a novel suppressor of inflammation and direct-interacting E3 ligase of MyD88 in macrophages. Our study expands the knowledge of intrinsic immunoregulatory networks of TLR- MyD88 signaling and the regulatory mechanism of Cbl, suggesting new therapeutic strategies for inflammatory disorders.
Authors
- Zhengyu Jiang (ORCID: https://orcid.org/0000-0002-4788-9068)
- Jinren Zhu
- Juan Huang
- Yan Zhang
- Feihan Lyu
- Zhefan Wang
- Dan Wang
Institutions
- Naval Medical Research Command (US)
- Second Military Medical University (CN)
- Fudan University (CN)
- Shanghai Changzheng Hospital (CN)
- Changhai Hospital (CN)
- Shanghai Jinyuan Senior High School (CN)
- Yangpu Hospital of Tongji University (CN)
- East China Normal University (CN)
Publication Details
- Journal
- Frontiers in Immunology
- Published
- 2026-01-05
- DOI
- https://doi.org/10.3389/fimmu.2025.1679035
- Primary Topic
- Immune Response and Inflammation
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Natural Science Foundation of China
- Changhai Hospital of Shanghai