| Gene Name | ARID3A |
| HF Protein Name | AT-rich interactive domain-containing protein 3A |
| HF Function | E2FBP1 inhibits accumulation of ICP0 RNA |
| Uniprot ID | Q99856 |
| Protein Sequence | View Fasta Sequence |
| NCBI Gene ID | 1820 |
| Host Factor (HF) Name in Paper | E2FBP1 |
| Gene synonyms | DRIL1 DRIL3 DRX E2FBP1 |
| Ensemble Gene ID | ENSG00000116017 |
| Ensemble Transcript | ENST00000263620 |
| KEGG ID | Go to KEGG Database |
| Gene Ontology ID(s) | GO:0000977, GO:0001228, GO:0003682, GO:0005634, GO:0005654, GO:0005829, GO:0006977, GO:0042803, GO:0043231, GO:0045121, |
| MINT ID | Q99856 |
| STRING | Click to see interaction map |
| GWAS Analysis | Click to see gwas analysis |
| OMIM ID | 603265 |
| PANTHER ID | N.A. |
| PDB ID(s) | 2KK0, 4LJX, |
| pfam ID | PF01388, |
| 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 | The Herpes Simplex Virus Immediate-Early Ubiquitin Ligase ICP0 Induces Degradation of the ICP0 Repressor Protein E2FBP1 |
| Author's Name | Yayoi Fukuyo, Nobuo Horikoshi, Alexander M. Ishov, Saul J. Silverstein, and Takuma Nakajima |
| Journal Name | Journal Of Virology |
| Pubmed ID | 21248039 |
| Abstract | E2FBP1/hDRIL1, a DNA-binding A/T-rich interaction domain (ARID) family transcription factor, is expressed ubiquitously in human tissues and plays an essential role in maintaining the proliferation potential of passage-limited human fibroblasts by dissociating promyelocytic leukemia nuclear bodies (PML-NBs). This effect on PML-NBs is similar to that of viral immediate-early gene products, such as infected cellular protein 0 (ICP0) from human herpes simplex virus 1 (HSV-1), which also disrupts PML-NBs to override the intrinsic cellular defense. Here we report that E2FBP1 inhibits accumulation of ICP0 RNA and, at the same time, is degraded via ICP0s herpes ubiquitin ligase 2 (HUL-2) activity upon HSV-1 infection. These reciprocal regulatory roles of ICP0 and E2FBP1 are linked in an ARID-dependent fashion. Our results suggest that E2FBP1 functions as an intrinsic cellular defense factor in spite of its PML-NB dissociation function. |
| Used Model | TIG-3 and Hep-2 cells |
| DOI | 10.1128/JVI.02105-10 |
