Technical Data
ARF, p14
The INK4a-ARF locus is comprised of two tumor suppressors, p16INK4a and p14ARF. These two proteins are encoded through differential splicing of alternative first exons. The p16INK4a (exon 1alpha) protein inhibits the cyclin D-dependent kinases (CDK) that control the phosphorylation of the Rb protein and cell proliferation. The p14ARF gene product complexes with the MDM2 protein within the nucleus, thus modulating the activity of the p53 protein. P14ARF is a potent tumor suppressor in the presence of wild-type p53, while mutant p53 substantially reduces growth inhibition by p14ARF. (1-3)

Positive control: BT549 cells
PabIgGAffinity Purified
100ul-20CBlue IceHumanRabbit
Synthetic peptide from the human sequence of p14ARF.
Purified by affinity chromatography.
Supplied as a liquid in PBS, pH 7.2, 0.05% sodium azide.
Specific for human p14ARF.
Intended for research use only. Not for use in human, therapeutic, or diagnostic applications.
1. Newcomb, E.W., et al. Incidence of p14ARF gene deletion in high-grade adult and pediatric astrocytomas. Human Pathology. 31(1): 115-9, 2000. 2. Taniguchi, T., et al. Expression of p16INK4a and p14ARF in hematological malignancies. Leukemia. 13(11): 1760-9, 1999. 3. Simon, M. et al. Functional evidence for a role of combined CDKN2A (p16-p14(ARF))/CDKN2A (p15) gene activation in malignant gliomas. Acta Neuropathol. 98(5): 444-52, 1999.