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Phospho-p16-INK4A(S140) Antibody
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS: 1
- PROTOCOLS
- BACKGROUND
Application 
| IHC-P, WB, E |
|---|---|
| Primary Accession | P42771 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 16533 Da |
| Gene ID | 1029 |
|---|---|
| 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 S140 of human p16-INK4A. |
| Dilution | WB~~1:1000 IHC-P~~1:50~100 |
| 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(S140) Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | CDKN2A (HGNC:1787) |
|---|---|
| Synonyms | CDKN2, MTS1 |
| 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.
Background
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.
References
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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