Gene Name | E2F6 |
HF Protein Name | Transcription factor E2F6 |
HF Function | Binds to silenced chromatin and critical for the maintenance of cell fate |
Uniprot ID | O75461 |
Protein Sequence | View Fasta Sequence |
NCBI Gene ID | 1876 |
Host Factor (HF) Name in Paper | E2F6 |
Gene synonyms | N.A. |
Ensemble Gene ID | ENSG00000169016 |
Ensemble Transcript | ENST00000307236 [O75461-3];ENST00000381525 [O75461-1];ENST00000542100 [O75461-2];ENST00000546212 [O75461-2] |
KEGG ID | Go to KEGG Database |
Gene Ontology ID(s) | GO:0000083, GO:0000122, GO:0000981, GO:0003677, GO:0003714, GO:0005634, GO:0005654, GO:0006351, GO:0046983, GO:0070317, GO:0071339, GO:0090575, |
MINT ID | O75461 |
STRING | Click to see interaction map |
GWAS Analysis | Click to see gwas analysis |
OMIM ID | 602944 |
PANTHER ID | PTHR12081;PTHR12081:SF19 |
PDB ID(s) | N.A., |
pfam ID | PF16421, PF02319, |
Drug Bank ID | N.A., |
ChEMBL ID | N.A. |
Organism | Homo sapiens (Human) |
Virus Name | Human papillomavirus type 16 |
Virus Short Name | HPV16 |
Order | Unassigned |
Virus Family | Papillomaviridae |
Virus Subfamily | N.A. |
Genus | Alphapapillomavirus |
Species | Human papillomavirus 16 |
Host | Human, monkeys |
Cell Tropism | Epithelial cells of skin, mucous membranes |
Associated Disease | Malignant tumours |
Mode of Transmission | Sexual, indirect and direct contact, auto-inoculation |
VIPR DB link | N.A. |
ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/121/papillomaviridae |
Virus Host DB link | http://www.genome.jp/virushostdb/view/?virus_lineage=Papillomaviridae |
Paper Title | Human papillomavirus type 16 E7 oncoprotein associates with E2F6 |
Author's Name | Margaret E. McLaughlin-Drubin, Kyung-Won Huh and Karl Munger |
Journal Name | Journal Of Virology |
Pubmed ID | 18579589 |
Abstract | The papillomavirus life cycle is intimately coupled to the differentiation state of the infected epithelium. Since papillomaviruses lack most of the rate-limiting enzymes required for genome synthesis, they need to uncouple keratinocyte differentiation from cell cycle arrest and maintain or reestablish a replication-competent state within terminally differentiated keratinocytes. The human papillomavirus (HPV) E7 protein appears to be a major determinant for this activity and induces aberrant S-phase entry through the inactivation of the retinoblastoma tumor suppressor and related pocket proteins. In addition, E7 can abrogate p21 and p27. Together, this leads to the activation of E2F1 to E2F5, enhanced expression of E2F-responsive genes, and increased cdk2 activity. E2F6 is a pRB-independent, noncanonical member of the E2F transcription factor family that acts as a transcriptional repressor. E2F6 expression is activated in S phase through an E2F-dependent mechanism and thus may provide a negative-feedback mechanism that slows down S-phase progression and/or exit in response to the activation of the other E2F transcription factors. Here, we show that low- and high-risk HPV E7 proteins, as well as simian virus 40 T antigen and adenovirus E1A, can associate with and inactivate the transcriptional repression activity of E2F6, thereby subverting a critical cellular defense mechanism. This may result in the extended S-phase competence of HPV-infected cells. E2F6 is a component of polycomb group complexes, which bind to silenced chromatin and are critical for the maintenance of cell fate. We show that E7-expressing cells show decreased staining for E2F6/polycomb complexes and that this is at least in part dependent on the association with E2F6. |
Used Model | HeLa S3 cells |
DOI | 10.1128/JVI.00579-08 |