PXD066477 is an
original dataset announced via ProteomeXchange.
Dataset Summary
| Title | IFI35 suppresses the transcription of hepatitis B virus cccDNA minichromosome via promoting HNF4α proteasomal degradation |
| Description | Hepatitis B virus (HBV) infection is a major health problem with hundreds of millions of people still chronically infected worldwide. Although it is known that cytokines can inhibit HBV replication in infected hepatocytes, much is still unknown about the underlying mechanisms or mediators. In this study, we systematically analyzed tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ)induced proteins by proteomic analysis and identified interferon-inducible protein 35 (IFI35) as a novel host restriction factor for HBV replication. Overexpression of IFI35 suppressed HBV transcription, while its reduction showed the opposite effect. Mechanistically, IFI35 regulated the stability of hepatocyte nuclear factor 4α (HNF4α), which is essential for cccDNA transcription. IFI35 did not regulate the transcription of HNF4α but rather promoted its degradation. We found that IFI35 recruits tripartite motif-containing protein 21 (TRIM21), an E3 ubiquitin-protein ligase, for K48-linked ubiquitination of HNF4α. Results were further validated using patient-derived primary human hepatocytes (PHHs) and mouse model of HBV infection. Our results revealed that cytokines, especially IFN-γ, induced IFI35 in hepatocytes. IFI35 promoted the degradation of HNF4α via the TRIM21-mediated ubiquitination, which, in turn, leads to the suppression of cccDNA transcription and viral replication. Our findings demonstrate that IFI35-TRIM21-HNF4α axis may play a crucial role in TNF-α and IFN-γ induced suppression of HBV. Consequently, these results reveal a novel antiviral action of IFI35 against HBV. These findings may hold value in the development of alternative anti-HBV drugs. |
| HostingRepository | PRIDE |
| AnnounceDate | 2026-08-24 |
| AnnouncementXML | Submission_2026-08-23_16:56:41.698.xml |
| DigitalObjectIdentifier | |
| ReviewLevel | Peer-reviewed dataset |
| DatasetOrigin | Original dataset |
| RepositorySupport | Unsupported dataset by repository |
| PrimarySubmitter | Jaewon Oh |
| SpeciesList | scientific name: Homo sapiens (Human); NCBI TaxID: NEWT:9606; |
| ModificationList | TMT6plex-126 reporter+balance reagent acylated residue; monohydroxylated residue; iodoacetamide derivatized residue |
| Instrument | Orbitrap Exploris 480 |
Dataset History
| Revision | Datetime | Status | ChangeLog Entry |
|---|
| 0 | 2025-07-23 09:26:30 | ID requested | |
| ⏵ 1 | 2026-08-23 16:56:42 | announced | |
Publication List
| Kim N, Shin JJ, Oh JW, Won J, Lee AR, Dezhbord M, Park J, Lee KY, Kim DS, Kim KP, Kim KH, proteasomal degradation. J Biomed Sci, 33(1):(2026) [pubmed] |
| 10.1186/s12929-026-01239-w; |
Keyword List
| submitter keyword: Human, HBV, Proteomics |
Contact List
| Jae Won Oh |
|---|
| contact affiliation | Kyung Hee University |
| contact email | odinplate@naver.com |
| lab head | |
| Jaewon Oh |
|---|
| contact affiliation | Kyung Hee University |
| contact email | odinplate@naver.com |
| dataset submitter | |
Full Dataset Link List
Dataset FTP location
NOTE: Most web browsers have now discontinued native support for FTP access within the browser window. But you can usually install another FTP app (we recommend FileZilla) and configure your browser to launch the external application when you click on this FTP link. Or otherwise, launch an app that supports FTP (like FileZilla) and use this address: ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2026/08/PXD066477 |
| PRIDE project URI |
Repository Record List
[ + ]
[ - ]
- PRIDE
- PXD066477
- Label: PRIDE project
- Name: IFI35 suppresses the transcription of hepatitis B virus cccDNA minichromosome via promoting HNF4α proteasomal degradation
