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) |
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. |
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 |