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CDKN2A antibody
Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | P42771 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | polyclonal |
| Isotype | Rabbit Ig |
| Calculated MW | 16533 Da |
| Gene ID | 1029 |
|---|---|
| Other Names | Cyclin-dependent kinase inhibitor 2A {ECO:0000312|HGNC:HGNC:1787}, Cyclin-dependent kinase 4 inhibitor A, CDK4I, Multiple tumor suppressor 1, MTS-1, p16-INK4a, p16-INK4, p16INK4A, CDKN2A (HGNC:1787), CDKN2, MTS1 |
| Target/Specificity | This antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between amino acids from human. |
| Dilution | WB~~1:1000 |
| 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 | CDKN2A 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 |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Background
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.
References
Serrano M.,et al.Nature 366:704-707(1993).
Robertson K.D.,et al.Oncogene 18:3810-3820(1999).
Kitagawa Y.,et al.J. Biol. Chem. 277:46289-46297(2002).
Lin Y.C.,et al.Oncogene 26:7017-7027(2007).
Humphray S.J.,et al.Nature 429:369-374(2004).
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