Virus Details


VHFID3200

Host Factor Information

Gene Name CCND2
HF Protein Name G1/S-specific cyclin-D2
HF Function Important for viral replication
Uniprot ID P30279
Protein Sequence View Fasta Sequence
NCBI Gene ID 894
Host Factor (HF) Name in Paper CCND2
Gene synonyms N.A.
Ensemble Gene ID ENSG00000118971
Ensemble Transcript ENST00000261254 [P30279-1]
KEGG ID Go to KEGG Database
Gene Ontology ID(s) GO:0000307, GO:0000785, GO:0001934, GO:0005634, GO:0005654, GO:0005730, GO:0005829, GO:0007049, GO:0007616, GO:0008284, GO:0008344, GO:0019901, GO:0031965, GO:0043066, GO:0045737, GO:0051301, GO:0071481, GO:0097129, GO:1900087,
MINT ID P30279
STRING Click to see interaction map
GWAS Analysis Click to see gwas analysis
OMIM ID 123833
PANTHER ID PTHR10177:SF66
PDB ID(s) 6EI2,
pfam ID PF02984, PF00134,
Drug Bank ID N.A.,
ChEMBL ID CHEMBL3301386
Organism Homo sapiens (Human)

Pathogen Information

Virus Name Hepatitis B virus
Virus Short Name HBV
Order Unassigned
Virus Family Hepadnaviridae
Virus Subfamily N.A.
Genus Orthohepadnavirus
Species Hepatitis B virus
Host Human, mammals
Cell Tropism Hepatocytes
Associated Disease Hepatitis, hepatocellular carcinoma(chronic infections), cirrhosis
Mode of Transmission Sexual contact, blood, maternal-neonatal
VIPR DB link N.A.
ICTV DB link https://talk.ictvonline.org/ictv-reports/ictv_9th_report/reverse-transcribing-dna-and-rna-viruses-2011/w/rt_viruses/155/hepadnaviridae
Virus Host DB link N.A.

Publication Information

Paper Title Cyclin D2 plays a regulatory role in HBV replication
Author's Name Chun-li Song, Ji-hua Ren, Long-kuan Ran, Yong-guo Li, Xiao-song Li, Xiang Chen, Wan-yu Li, Ai-long Huang, Juan Chen
Journal Name Virology
Pubmed ID 24992041
Abstract Hepatitis B virus (HBV) infection is the leading cause of liver diseases. However, the molecular mechanisms of HBV infection and carcinogenesis have not been fully elucidated. In this study, we found that cyclin D2 was upregualted in HBV-expressing cells and liver tissues of HBV-transgenic mice. Gene silencing of cyclin D2 inhibited HBV DNA replicative intermediates, 3.5 kb mRNA, core protein level, as well as the secretions of HBsAg and HBeAg. On the contrary, overexpression of cyclin D2 promoted HBV replication. Furthermore, cyclin D2 regulated HBV replication by enhancing the activity of HBV core and Sp1 promoters by targeting transcription factor CREB2. Silencing of CREB2 abolished enhancement of HBV replication induced by cyclin D2. Together, our study has uncovered a positive role of cyclin D2 in HBV replication. It is conceivable that therapeutic application of cyclin D2 inhibitor in HBV infection therapy.
Used Model HepG2 and HepG2.2.15 cells
DOI 10.1016/j.virol.2014.05.027