In humans, the multiple tumor suppressor 1 locus (MTS1) encodes two unrelated genes, p16INK4a and p19ARF. Although both act as cell proliferation inhibitors, their mechanisms of action are different. p19ARF works as part of a p53-dependent pathway to counter uncontrolled proliferation and oncogenic signals. Mice lacking the p19ARF gene rapidly develop a broad spectrum of tumors. This result indicates that p19ARF is an important tumor suppressor. In addition, p19ARF helps prevent transforming signals from various oncoproteins via the p53 regulatory loop (3). These studies and others display the importance of p19ARF in cell cycle control and tumor suppression.
By Western blot, this antibody recognizes IVT murine p19ARF and a clear 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 (1). The antibody can be competed from recognizing p19ARF using the antigenic peptide at 10ug/ml.
Western Blot: 0.5-1ug/ml (ECL)
Immunohistochemistry: Not determined
ELISA (indirect): 1:5,000
|KLH coupled peptide containing amino acids 54-75 of mouse p19ARF.|
|Purified by affinity chromatography.|
|Antisera was eluted with 100 mM glycine, pH 2.5, and dialyzed against PBS, pH 7.4, 0.02% sodium azide.|
|Specific for p19ARF. Species crossreactivity: Reacts with mouse p19ARF. Does not react with rat and human.|
|Intended for research use only. Not for use in human, therapeutic, or diagnostic applications.|
1. Radfar, A., et al. P19ARF induces p53-dependent apoptosis during abelson virus-mediated pre-B cell transformation. Proc Natl Acad Sci USA. 95(22): 13194-99, 1998. 2. Larsen, C.J. Alternative protein p19ARF: a genuine tumor suppressor gene. Bull. Cancer. 85(4): 304-6, 1998. 3. de Stanchina, E., et al. E1A signaling to p53 involves the p19ARF tumor suppressor. Genes Dev. 12(15): 2434-42, 1998.|
4. Zindy, F., et al. Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization. Genes Dev. 12(15): 2424-33, 1998.
1.Grateful acknowledgments to M. Serrano and I. Palmero, National Center of Biotechnology, Madrid.