In contrast to neurodegerative diseases and cancer, the contribution of TG2 activity to celiac sprue pathogenesis has long been pretty well founded. The deamidation of distinct glutamine residues targeted by TG2 in gluten peptides has long been proven to reinforce peptide binding towards the sickness-linked proteins HLA-DQ2/eight, which might be https://juliev100iuf3.wikiexcerpt.com/user