| General information | Literature | Expression | Regulation | Mutation | Homolog | Interaction |
Basic Information | |
|---|---|
Gene ID | 1030 |
Name | CDKN2B |
Synonymous | cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4);CDKN2B;cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) |
Definition | CDK inhibitory protein|CDK4B inhibitor|MTS-2|cyclin-dependent kinase 4 inhibitor B|cyclin-dependent kinases 4 and 6 binding protein|multiple tumor suppressor 2|p14-INK4b|p14_CDK inhibitor|p14_INK4B|p15 CDK inhibitor|p15-INK4b|p15_INK4B |
Position | 9p21 |
Gene type | protein-coding |
Title | Abstract |
| Oct-1 is involved in the transcriptional repression of the p15(INK4b) gene. | p15(INK4b) functions as a tumor suppressor and implicated in cellular senescence. Here, we show that the Oct-1 binding site in the human p15(INK4b) gene promoter functions as a silencer. Oct-1 specifically interacts with this binding site in vitro and in vivo and SMRT and HDAC1 are present in the p15(INK4b) proximal promoter region. Moreover, mouse embryo fibroblasts (MEFs) lacking Oct-1 have shown significantly increased levels of p15(INK4b) protein compared to their normal counterparts. Treatment with a histone deacetylase (HDAC) inhibitor has activated the expression of p15(INK4b) in wild-type MEFs but has no effect in MEFs lacking Oct-1, suggesting that Oct-1 represses p15(INK4b) gene expression in an HDAC-dependent manner. Finally, we show that the expression of Oct-1 protein significantly decreases, whereas p15(INK4b) protein significantly increases with the cellular aging process. Taken together, these results suggest that Oct-1 is an important transcriptional repressor for p15(INK4b) gene and the transcriptional repression of the p15(INK4b) gene by Oct-1 may be one of the regulatory mechanisms of cellular senescence. |