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Virus Details


VHFID4966

Host Factor Information

Pathogen Information

Publication Information

Host Factor Information

Gene Name TGFB1
HF Protein Name Transforming growth factor beta-1
HF Function Downregulates human papillomavirus-16 oncogene expression
Uniprot ID P01137
Protein Sequence View Fasta Sequence
NCBI Gene ID 7040
Host Factor (HF) Name in Paper TGF- beta1
Gene synonyms TGFB
Ensemble Gene ID ENSG00000105329
Ensemble Transcript ENST00000221930
KEGG ID Go to KEGG Database
Gene Ontology ID(s) GO:0000060, GO:0000122, GO:0000165, GO:0001570, GO:0001657, GO:0001666, GO:0001837, GO:0001843, GO:0001933, GO:0001934, GO:0002028, GO:0002062, GO:0002244, GO:0002248, GO:0002460, GO:0002513, GO:0002576, GO:0003179, GO:0003823, GO:0005114, GO:0005125, GO:0005160, GO:0005576, GO:0005578, GO:0005615, GO:0005634, GO:0005737, GO:0005796, GO:0005886, GO:0006468, GO:0006611, GO:0006754, GO:0006796, GO:0006874, GO:0006954, GO:0007050, GO:0007093, GO:0007173, GO:0007179, GO:0007182, GO:0007183, GO:0007219, GO:0007406, GO:0007435, GO:0007492, GO:0007507, GO:0007565, GO:0007568, GO:0008083, GO:0008156, GO:0008284, GO:0008285, GO:0008354, GO:0009611, GO:0009749, GO:0009817, GO:0009986, GO:0010575, GO:0010628, GO:0010629, GO:0010716, GO:0010718, GO:0010742, GO:0010763, GO:0010800, GO:0010862, GO:0010936, GO:0014003, GO:0016202, GO:0016477, GO:0017015, GO:0019049, GO:0019221, GO:0019899, GO:0021915, GO:0022408, GO:0030214, GO:0030279, GO:0030308, GO:0030334, GO:0030335, GO:0030424, GO:0030501, GO:0,
MINT ID P01137
STRING Click to see interaction map
GWAS Analysis Click to see gwas analysis
OMIM ID 131300
PANTHER ID PTHR11848
PDB ID(s) 1KLA, 1KLC, 1KLD, 3KFD, 4KV5, 5FFO, 5VQP,
pfam ID PF00019, PF00688,
Drug Bank ID DB00070, DB06205,
ChEMBL ID CHEMBL1795178
Organism Homo sapiens (Human)

Pathogen Information

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

Publication Information

Paper Title TGF-beta1 and IL-4 downregulate human papillomavirus-16 oncogene expression but have differential effects on the malignant phenotype of cervical carcinoma cells
Author's Name Manuela Donalisio, Maura Cornaglia, Santo Landolfo, David Lembo
Journal Name Virus Research
Pubmed ID 18206261
Abstract Host immune response to human papillomavirus (HPV) is a crucial factor in viral clearance and control of persistent infections. The existence of an intercellular control mechanism mediated by cytokines to suppress HPV-gene transcription and to prevent malignant conversion of HPV-infected cells, has been postulated. In a previous study, we demonstrated the inhibitory activity of several cytokines on the HPV-16 long control region (LCR)-driven transcription among these, IL-4 was reported as a LCR inhibitor for the first time and proposed as a candidate for further studies. Here, we addressed the question of whether IL-4 represses HPV-16 oncogene transcription and exerts antitumor activity in HPV-16 positive cervical carcinoma cell lines. Results indicated that downregulation of E6 and E7 levels by IL-4 in CaSki cells is weaker than that exerted by TGF-beta1, a known LCR inhibitor, although both cytokines are equally active in suppressing LCR-driven transcriptional activity in a reporter cell line. Moreover, only TGF-beta rescued p53 expression, Rb response pathway, and induced cellular senescence. SiHa cells were unresponsive to both cytokines. These findings suggest that the two cytokines may play a role in the control of HPV infections, however, cervical carcinoma cells developed a partial or a total resistance to their inhibitory activity.
Used Model CaSki and SiHa cells
DOI 10.1016/j.virusres.2007.12.003