P19 ARF-p53 Tumor Suppressor Pathway During Oncogene-Induced Apoptosis and Senescence
Annual summary rept. 15 May 2000-15 May 2001
COLD SPRING HARBOR LAB OF QUANTITATIVE BIOLOGY NY
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The primary objective of this study is to provide new insights into the role of the p53 and ARF tumor suppressors in cancer development and therapy. During the second year of this project, we found that E1A oncogene can increase mRNA levels of tumor suppressor ARF. The region of E1A responsible for ARF induction is also important for apoptosis function of E1A. We also found that oncogene E1A can reduce apoptosis inhibitor gene, A20, expression, which can inhibit E1A-induced apoptosis once overexpressed. In collaboration with C. Sher, we tried to produce different monoclonal antibodies to p19ARF. Right now, we are doing the intensive screens to determine the antibodies specificity.
- Medicine and Medical Research