| Gene Name | GRSF1 |
| HF Protein Name | G-rich sequence factor 1 |
| HF Function | Essential for virus replication |
| Uniprot ID | Q12849 |
| Protein Sequence | View Fasta Sequence |
| NCBI Gene ID | 2926 |
| Host Factor (HF) Name in Paper | GRSF1 |
| Gene synonyms | N.A. |
| Ensemble Gene ID | ENSG00000132463 |
| Ensemble Transcript | ENST00000254799 [Q12849-1];ENST00000502323 [Q12849-5] |
| KEGG ID | Go to KEGG Database |
| Gene Ontology ID(s) | GO:0003723, GO:0003729, GO:0005737, GO:0005739, GO:0006378, GO:0008033, GO:0009952, GO:0016331, GO:0035770, GO:0042645, |
| MINT ID | N.A. |
| STRING | Click to see interaction map |
| GWAS Analysis | Click to see gwas analysis |
| OMIM ID | 604851 |
| PANTHER ID | PTHR13976:SF42 |
| PDB ID(s) | 2LMI, 4QU6, 4QU7, |
| pfam ID | PF00076, |
| 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 | ICP4-induced miR-101 attenuates HSV-1 replication |
| Author's Name | Xiangling Wang, Caifeng Diao, XiYang, ZhenYang, Min Liu, Xin Li & HuaTang |
| Journal Name | Scientific Reports |
| Pubmed ID | 26984403 |
| Abstract | Hepes simplex Virus type 1 (HSV-1) is an enveloped DNA virus that can cause lytic and latent infection. miRNAs post-transcriptionally regulate gene expression, and our previous work has indicated that HSV-1 infection induces miR-101 expression in HeLa cells. The present study demonstrates that HSV-1-induced miR-101 is mainly derived from its precursor hsa-mir-101-2, and the HSV-1 immediate early gene ICP4 (infected-cell polypeptide 4) directly binds to the hsa-mir-101-2 promoter to activate its expression. RNA-binding protein G-rich sequence factor 1 (GRSF1) was identified as a new target of miR-101 GRSF1 binds to HSV-1 p40 mRNA and enhances its expression, facilitating viral proliferation. Together, ICP4 induces miR-101 expression, which downregulates GRSF1 expression and attenuates the replication of HSV-1. This allows host cells to maintain a permissive environment for viral replication by preventing lytic cell death. These findings indicate that HSV-1 early gene expression modulates host miRNAs to regulate molecular defense mechanisms. This study provides novel insight into host-virus interactions in HSV-1 infection and may contribute to the development of antiviral therapeutics. |
| Used Model | HeLa cell |
| DOI | 10.1038/srep23205 |
