- 文献引用 : 1
|Application ||WB, IHC-P, E|
|Calculated MW||16533 Da|
|Other Names||Cyclin-dependent kinase inhibitor 2A, isoforms 1/2/3, Cyclin-dependent kinase 4 inhibitor A, CDK4I, Multiple tumor suppressor 1, MTS-1, p16-INK4a, p16-INK4, p16INK4A, CDKN2A, CDKN2, MTS1|
|Target/Specificity||This p16-INK4A Antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding S7 of human p16-INK4A.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Phospho-p16-INK4A(S7) Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||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.|
|Cellular Location||Cytoplasm. Nucleus|
|Tissue Location||Widely expressed but not detected in brain or skeletal muscle. Isoform 3 is pancreas-specific|
Provided below are standard protocols that you may find useful for product applications.
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.
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).