| Gene Name | TRIM11 |
| HF Protein Name | E3 ubiquitin-protein ligase TRIM11 |
| HF Function | TRIM11 inhibits IFNb-dependent antiviral response |
| Uniprot ID | Q96F44 |
| Protein Sequence | View Fasta Sequence |
| NCBI Gene ID | 81559 |
| Host Factor (HF) Name in Paper | TRIM11 |
| Gene synonyms | RNF92 |
| Ensemble Gene ID | ENSG00000154370 |
| Ensemble Transcript | ENST00000284551 [Q96F44-1];ENST00000366699 [Q96F44-2] |
| KEGG ID | Go to KEGG Database |
| Gene Ontology ID(s) | GO:0005634, GO:0005737, GO:0005829, GO:0008134, GO:0008270, GO:0019904, GO:0032897, GO:0045087, GO:0045892, GO:0046597, GO:0046598, GO:0050768, GO:0051607, GO:0061630, GO:1902187, |
| MINT ID | Q96F44 |
| STRING | Click to see interaction map |
| GWAS Analysis | Click to see gwas analysis |
| OMIM ID | 607868 |
| PANTHER ID | N.A. |
| PDB ID(s) | N.A., |
| pfam ID | PF13765, PF00622, PF00643, |
| Drug Bank ID | N.A., |
| ChEMBL ID | N.A. |
| Organism | Homo sapiens (Human) |
| Virus Name | Human herpesvirus 1 |
| Virus Short Name | HSV1 |
| Order | Herpesvirales |
| Virus Family | Herpesviridae |
| Virus Subfamily | Alphaherpesvirinae |
| Genus | Simplexvirus |
| Species | Herpes simplex virus 1 |
| Host | Human, mammals |
| Cell Tropism | Primary site of infection: epithelial mucosal cells , latency: remains latent in sensory neurons (ganglions) |
| Associated Disease | Skin vesicles or mucosal ulcers, rarely encephalitis and meningitis |
| Mode of Transmission | Contact, saliva |
| VIPR DB link | http://www.viprbrc.org/brc/vipr_allSpecies_search.do?method=SubmitForm&decorator=herpes |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/91/herpesviridae |
| Virus Host DB link | http://www.genome.jp/virushostdb/view/?virus_lineage=Herpesviridae |
| Paper Title | TRIM11 Negatively Regulates IFNb Production and Antiviral Activity by Targeting TBK1 |
| Author's Name | Younglang Lee, Byeongwoon Song, Chankyu Park, Ki-Sun Kwon |
| Journal Name | PLOS One |
| Pubmed ID | 23675467 |
| Abstract | The innate immune response is a host defense mechanism against infection by viruses and bacteria. Type I interferons (IFNalpha/beta) play a crucial role in innate immunity. If not tightly regulated under normal conditions and during immune responses, IFN production can become aberrant, leading to inflammatory and autoimmune diseases. In this study, we identified TRIM11 (tripartite motif containing 11) as a novel negative regulator of IFNbeta production. Ectopic expression of TRIM11 decreased IFNbeta promoter activity induced by poly (I:C) stimulation or overexpression of RIG-I (retinoic acid-inducible gene-I) signaling cascade components RIG-IN (constitutively active form of RIG-I), MAVS (mitochondrial antiviral signaling protein), or TBK1 (TANK-binding kinase-1). Conversely, TRIM11 knockdown enhanced IFNbeta promoter activity induced by these stimuli. Moreover, TRIM11 overexpression inhibited the phosphorylation and dimerization of IRF3 and expression of IFNbeta mRNA. By contrast, TRIM11 knockdown increased the IRF3 phosphorylation and IFNbeta mRNA expression. We also found that TRIM11 and TBK1, a key kinase that phosphorylates IRF3 in the RIG-I pathway, interacted with each other through CC and CC2 domain, respectively. This interaction was enhanced in the presence of the TBK1 adaptor proteins, NAP1 (NF-κB activating kinase-associated protein-1), SINTBAD (similar to NAP1 TBK1 adaptor) or TANK (TRAF family member-associated NF-κB activator). Consistent with its inhibitory role in RIG-I-mediated IFNbeta signaling, TRIM11 overexpression enhanced viral infectivity, whereas TRIM11 knockdown produced the opposite effect. Collectively, our results suggest that TRIM11 inhibits RIG-I-mediated IFNbeta production by targeting the TBK1 signaling complex. |
| Used Model | 293T and Vero cells |
| DOI | 10.1371/journal.pone.0063255 |
