Cleidocranial dysplasia Mutations in<unk>  are associated with the disease Cleidocranial dysostosis. One study proposes that this phenotype arises partly due to the<unk>  dosage insufficiencies. Because<unk>  promotes exit from the cell cycle, insufficient amounts of<unk>  are related to increased proliferation of osteoblasts observed in patients with cleodocranial disostosis. Osteosarcoma Variants of<unk>  have been associated with the osteosarcoma phenotype. Current research suggests that this is partly due to the role of<unk>  in mitigating the cell cycle.<unk>  plays a role as a tumor suppressor of osteoblasts by halting cell cycle progression at G1. Compared to normal osteoblast cell line MC3T3-E1, the oscillations of<unk>  in osteosarcoma ROS and SaOS cell lines are aberrant when compared to the oscillations of<unk>  levels in normal osteoblasts, suggesting that deregulation of<unk>  levels may contribute to abnormal cell proliferation by an inability to escape the cell cycle. Molecularly, It has been proposed that proteasome inhibition by MG132 can stabilize<unk>  protein levels in late G1 and S in MC3T3 cells, but not in osteosarcoma cells which consequently leads to a cancerous phenotype.
RUNX2
SOX2
BMPR1A
CDK13
SPATA16
KRAS
WRAP53
Kras