Virus Details


VHFID6567

Host Factor Information

Gene Name NFIA
HF Protein Name Nuclear factor 1 A-type
HF Function Negatively regulates JC virus multiplication
Uniprot ID Q12857
Protein Sequence View Fasta Sequence
NCBI Gene ID 4774
Host Factor (HF) Name in Paper NF-1A
Gene synonyms KIAA1439
Ensemble Gene ID ENSG00000162599
Ensemble Transcript ENST00000371187 [Q12857-2];ENST00000371189 [Q12857-4];ENST00000403491 [Q12857-1];ENST00000407417 [Q12857-3]
KEGG ID Go to KEGG Database
Gene Ontology ID(s) GO:0000122, GO:0000978, GO:0000981, GO:0001077, GO:0003682, GO:0003700, GO:0005634, GO:0005654, GO:0006260, GO:0006355, GO:0008134, GO:0019079, GO:0030054, GO:0045944, GO:0060074, GO:0072189,
MINT ID Q12857
STRING Click to see interaction map
GWAS Analysis Click to see gwas analysis
OMIM ID 600727
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 DNA-binding transcription factor NF-1A negatively regulates JC virus multiplication
Author's Name Veerasamy Ravichandran and Eugene O. Major
Journal Name Journal Of General Virology
Pubmed ID 18474555
Abstract JC virus (JCV) DNA replication occurs in the nuclei of infected cells. The level of JCV genome expression depends on nucleotide sequences in the viral regulatory region and their interaction with host-cell nuclear transcription factors. Our previous studies showed a higher level of NF-1X in JCV-permissive cells compared with the other members of the NF-1 family, NF-1A, B and C, which suggests that NF-1X plays a positive role in JCV multiplication. It remained unclear whether a reduction in the level of NF-1A, which is expressed abundantly in JCV-non-permissive cell types, leads to an increase in JCV multiplication. In this study, we show that downregulation of NF-1A expression in JCV-non-susceptible progenitor and HeLa cells results in a reversion to susceptibility for JCV multiplication. These data demonstrate that a higher level of NF-1A protein in JCV-non-permissive cell types, compared with the level of NF-1X, may be acting as a negative regulator at the JCV promoter to control JCV multiplication.
Used Model HeLa cells
DOI 10.1099/vir.0.2008/000059-0