FGF8-mediated TRIM16 regulation promotes K48-linked ubiquitination and degradation of RIG-I to facilitate Influenza a virus immune evasion
Ran Wei, Huixia Zhang, Kaihui Cheng, Song Wang, Zhen Yuan, Sisi Ma, Zhijun Yu · 2026
Read FGF8-mediated TRIM16 regulation promotes K48-linked ubiquitination and degradation of RIG-I to facilitate Influenza a virus immune evasion by Ran Wei, Huixia Zhang, Kaihui Cheng, Song Wang, Zhen Yuan, Sisi Ma, Zhijun Yu (2026) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/pmc-13203027.txt.
Description
Influenza hides from the immune alarm by destroying its sensor, and a 2026 study headed by Ran Wei identifies the host accomplice. The research article shows how fibroblast growth factor 8 helps influenza A virus evade detection in human lung epithelial cells.
Infection raised FGF8 levels across several virus subtypes, and the factor boosted viral replication after entry by dampening interferon responses. Mechanistically, FGF8 acts as a scaffold that brings the enzyme TRIM16 to the viral sensor RIG-I, marking it for destruction at one specific lysine site. Silencing TRIM16 copied the effect of removing FGF8, so breaking this partnership is a candidate antiviral strategy.
Catalog record
| CREATOR | Ran Wei, Huixia Zhang, Kaihui Cheng, Song Wang, Zhen Yuan, Sisi Ma, Zhijun Yu |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 64 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |