Molecular Mechanisms of Schwann Cell Proliferation in NF1
Abstract
Further studies documenting the molecular mechanisms responsible for Schwann cell proliferation in NFl- derived Schwann cell lines have been carried out. We have documented that the absence of neurofibromin leads to the presence of the tyrosine kinase receptors cKit and PDGF receptor in these Schwann cell lines. C-Kit is expressed early in normal Schwann cell development, where it does not play a role in proliferation, differentiation, or acting as a co-mitogen. Ongoing studies have shown that the c-Kit receptor acts to prevent apoptosis. Activation of cKit in normal Schwann cells leads to the activation of the transduction molecule Akt. In contrast, activation of NFl-derived Schwann cells leads to the activation of both Akt and MAP kinase. It was documented that transformed Schwann cells expressed additional isoforms of adenylyl cyclase and additional prostaglandin receptors relative to normal human Schwann cells. The cKit mediated pathways, which lead to the prevention of apoptosis in NF1-derived Schwann cells are under investigation.. In summary, these studies have further documented some of the molecular mechanisms responsible for the proliferation of Schwann cell NF1 tumors.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2000
- Accession Number
- ADA387668
Entities
People
- George H. Devries
Organizations
- Chicago Association for Research and Education in Science