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Background
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p16-INK4A functions as a stabilizer of the tumor suppressor protein p53 as it can interact with, and sequester, MDM1, a protein responsible for the degradation of p53. This protein acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein. The gene for this protein is frequently mutated or deleted in a wide variety of tumors, and is known to be an important tumor suppressor gene.
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Background
References
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- Ausserlechner, M.J., et al., Leukemia 19(6):1051-1057 (2005).
- Kawamata, N., et al., Eur. J. Haematol. 74(5):424-429 (2005).
- Wang, J.L., et al., Mod. Pathol. 18(5):629-637 (2005).
- Kuroda, H., et al., Cancer Genet. Cytogenet. 158(2):172-179 (2005).
- Fu, G.H., et al., FEBS Lett. 579(10):2105-2110 (2005).
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