P19 ARF-p53 Tumor Suppressor Pathway During Oncogene-Induced Apoptosis and Senescence

Abstract

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.

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Document Details

Document Type
Technical Report
Publication Date
Jun 01, 2001
Accession Number
ADB269109

Entities

People

  • Jianping Jin
  • Scott W. Lowe

Organizations

  • Cold Spring Harbor Laboratory

Tags

DTIC Thesaurus Topics

  • Antibodies
  • Apoptosis
  • Biological Aging
  • Biomedical Research
  • Breast Cancer
  • Cancer
  • Cell Physiological Processes
  • Computer Programs
  • Contractors
  • Government (Foreign)
  • Government Procurement
  • Governments
  • Inhibitors
  • Neoplasms
  • Proteins
  • Suppressors
  • Teamwork

Readers

  • Breast cancer cell signaling and growth regulation.
  • Immunology
  • Molecular and genetic basis of cancer.