Regulation of Tumor Progression by Mgat5-Dependent Glycosylation
Annual rept. 1 Jun 2001-1 Jun 2002
MOUNT SINAI HOSPITAL TORONTO (ONTARIO)SAMUEL LUNENFIELD RESEARCH INST
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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 34 was to location beta 1, 6G1cNAc-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.
- Genetic Engineering and Molecular Biology
- Medicine and Medical Research