top of page

Type 1 diabetes is a complex disease caused by a combination of genetic risk and environmental interaction. While rare single gene defects can trigger diabetes, it generally arises through a combination of synergistic defects that alter multiple immune programs. However, the study of genetic variants (eg SH2B3, PTPN22, IFIH1, TYK2, UBASH3A and others) that associate with diabetes can be used to help us understand how alterations in specific programs contribute to the development of disease. The James lab uses quantitative proteomics, gene editing and murine disease modeling to determine how coding changes in genes associated with diabetes impact protein function. Specifically, we aim to understand how these changes impact protein-protein interactions, cellular signaling and developmental outcome. Our end goal is to identify treatment strategies that are likely to be effective in patients expressing specific coding variants associated with diabetes.

PTPN22 UBASH3A James lab

*** Click to learn more

bottom of page