The Role of RASGRF1 in Neurofibromatosis-Validating a Potential Therapeutic Target
Abstract
The goal of this research is to expand the knowledge of the genes that contribute to neurofibromatosis beyond the GAPi-related domain in NFl. It is hypothesized that the gene encoding RASGRFl, a GTP exchange factor (GEF), is one of these genes. Over-expression of Rasgrfl is predicted to exacerbate neurofibromatosis while Rasgrfl silencing will attenuate it. Two novel strains of mice ideally suited to test this hypothesis that were developed in my lab are being used to evaluate the role or Rasgrfl on the manifestations of neurofibromatosis type 1. One strain of mice over-express Rasgrfl, the other has diminished expression. These were crossed with a mouse model for NFl and the effects of the altered level of RASGRFl on tumorigenesis were monitored. The results indicate that over-expression of Rasgrfl significantly hastens the time of tumor onset and increase the overall frequency of tumor incidence. Tn contrast, diminished expression modestly delays the timing of tumor development, but overall frequency of tumor development is not changed.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2003
- Accession Number
- ADA421738
Entities
People
- Paul D. Soloway
Organizations
- Cornell University