Virus Details


VHFID6569

Host Factor Information

Gene Name NFIX
HF Protein Name Nuclear factor 1 X-type
HF Function Binding of NF-1X to JCV promoters is a critical mechanism supporting JCV propagation
Uniprot ID Q14938
Protein Sequence View Fasta Sequence
NCBI Gene ID 4784
Host Factor (HF) Name in Paper NF-1X
Gene synonyms N.A.
Ensemble Gene ID ENSG00000008441
Ensemble Transcript ENST00000397661 [Q14938-3];ENST00000585575 [Q14938-4];ENST00000587260 [Q14938-5];ENST00000587760 [Q14938-6];ENST00000592199 [Q14938-1]
KEGG ID Go to KEGG Database
Gene Ontology ID(s) GO:0000122, GO:0000981, GO:0003677, GO:0003700, GO:0003705, GO:0005634, GO:0006260, GO:0006366, GO:0045944,
MINT ID Q14938
STRING Click to see interaction map
GWAS Analysis Click to see gwas analysis
OMIM ID 164005
PANTHER ID PTHR11492
PDB ID(s) N.A.,
pfam ID PF00859, PF03165, PF10524,
Drug Bank ID N.A.,
ChEMBL ID N.A.
Organism Homo sapiens (Human)

Pathogen Information

Virus Name JC Virus
Virus Short Name JC
Order Unassigned
Virus Family Polyomaviridae
Virus Subfamily N.A.
Genus Polyomavirus
Species JC polyomavirus
Host Mammals, human
Cell Tropism Respiratory system, kidneys, or brain
Associated Disease Progressive multifocal leukoencephalopathy
Mode of Transmission N.A.
VIPR DB link N.A.
ICTV DB link https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/129/polyomaviridae
Virus Host DB link N.A.

Publication Information

Paper Title Interactions between c-Jun, nuclear factor 1, and JC virus promoter sequences: implications for viral tropism
Author's Name Veerasamy Ravichandran, Bruce F. Sabath, Peter N. Jensen, Sidney A. Houff, and Eugene O. Major
Journal Name Journal Of Virology
Pubmed ID 16928756
Abstract The infectious cycle of the human polyomavirus JC (JCV) is ultimately regulated in cellular nuclei at the level of viral protein expression and genomic replication. Such activity is prompted by interactions between variant nucleotide sequences within the JCV regulatory region (promoter) and cellular transcription factors that bind specific DNA consensus sites. In previous work we identified an NF-1 class member, NF-1X, as a critical transcription factor affecting the JCV cellular host range. Within variant JCV promoters, as well as other viral and cellular promoters, adjacently located NF-1 and AP-1 consensus sites are often found. The close proximity of these two binding sites suggests the opportunity for interaction between NF-1 and AP-1 proteins. Here, by electrophoretic mobility shift assays, we show temporal and dose-dependent interference by an AP-1 family member, c-Jun, upon NF-1 proteins binding an NF-1 consensus site derived from JCV promoter sequence. Moreover, as demonstrated by protein-protein interaction assays, we identify specific binding affinity independent of DNA binding between NF-1X and c-Jun. Finally, to compare the binding profiles of NF-1X and c-Jun on JCV promoter sequence in parallel with in vivo detection of viral activity levels, we developed an anchored transcriptional promoter (ATP) assay. With use of extracts from JCV-infected cells transfected to overexpress either NF-1X or c-Jun, ATP assays showed concurrent increases in NF-1X binding and viral protein expression. Conversely, increased c-Jun binding accompanied decreases in both NF-1X binding and viral protein expression. Therefore, inhibition of NF-1X binding by c-Jun appears to play a role in regulating levels of JCV activity.
Used Model Human primary tonsillar stromal cells
DOI 10.1128/JVI.01355-06