|Applications||ELISA, ICC/IF, IHC-P, IP, WB, ChIP assay|
|Application Note||Recommended Starting Dilutions:|
For ELISA: Use at an assay dependent dilution.
For IHC-P: Use at a concentration of 1 μg/ml (see Sotillo et al. 2001)
For IF: Use at 1:250 dilution (see Abhishek Datta et al. 2004)
For IP: Use at an assay dependent dilution (see Abhishek Datta et at. 2005)
For WB: Use at 1:500-1:1,500. Optimal dilutions/concentrations should be determined by the end user.
Multiple bands with this antibody have frequently been reported. We believe that this is due to the different modification states of p19ARF. Nuclear extraction may be necessary in some samples.
|Positive Controls||The blocking peptide for this antibody is available as GTX22659|
(Please refer to the vial label for the specific concentration)|
|Purification||Immunogen affinity purified|
|Purification Note||The serum has been purified on a peptide-NHS-activated Sepharose column. Specific antibodies have been eluted with 100 mM glycine pH 2.5. The purified antibodies have been dialysed against PBS pH 7.4. |
|Full Name||cyclin-dependent kinase inhibitor 2A|
|Product Description||Rabbit polyclonal to CDKN2A |
|Background||The INK4a/ARF locus encodes two unrelated tumor suppressor proteins, p16INK4a and p19ARF that restrain cell growth by modifying the functions of the retinoblastoma protein and p53, respectively. It is among the most frequently mutated tumor suppressor loci in human cancer. Both p16INK4a and p19ARF act as cell proliferation inhibitors. The ARF gene, p19ARF in mouse and p14ARF in human, has become an important player in cell cycle regulation. In mice, tumor suppressor effects appear to be mediated by interactions between p19ARF and the p53 tumor-suppressor protein. p19ARF counters uncontrolled proliferation and oncogenic signals in p53-dependent pathways. Proteins encoded by the INK4a/ARF locus also play a role in Abelson virus transformation. Both p16INK4a and p19ARF are expressed in many cells as they emerge from the apoptotic crisis that characterizes the transformation process. Expression of p19ARF but not p16INK4a induces apoptosis in Ab-MLV-transformed pre-B cells. INK4a/ARF expression correlates with or precedes the emergence of cells expressing mutant p53. p19ARF is an important part in cellular defense against transforming signals from the Abl oncoprotein, providing direct evidence that the p19ARF-p53 regulatory loop plays an important role in lymphoma induction.|
|Synonyms||Cyclin dependent kinase inhibitor 2A, TP16, Cyclin dependent kinase 4 inhibitor A, MTS1, Cell cycle negative regulator beta, CMM2, CDKN2A, MLM, Cyclin dependent kinase inhibitor2A, Cyclin dependent kinase inhibitor P12, Cyclin dependent kinase4 inhibitor |
|Specificity||On Western blot the antibody reveals IVT murine p19ARF and a band of the same size in CTLL2 cells. It detects a specific band in WT mouse embryo fibroblasts which is not present in p19ARF-null MEFs.|
|Immunogen||Synthetic peptide conjugated to KLH, within amino acids 54-75 of Mouse p19ARF.|
|Species Reactivity||Human, Mouse|