Regulation of Tumor Progression by Mgat5-Dependent Glycosylation
Abstract
Task 1 was to further define the phenotype of Mgat5(-/-) cells regarding adhesion, signal transduction, and growth factor responsiveness. We have established immortalized embryonic fibroblast cell lines form Mgat5(-/-) mice, made Mgat5 retrovial vector for rescue of the mutant phenotypes, and established new technology (the Cellomics scan array system) to measure these parameters with precision. Task 2 was to use genetic methods to analysis Mgat5 dependent tumor progression in vivo. We have interbred Mgat5 mice with Pten mutant mice and preliminary results suggest the genes interaction, in the immune system and cancer. Task 3&4 was to location beta1, 6GlcNAc-branched N-glycans that mediate phenotype. We identified T cell receptor and a new mechanism of N-glycan action, and more will identified this year.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2001
- Accession Number
- ADA396502
Entities
People
- James W Dennis
Organizations
- Mount Sinai Hospital, Toronto