Researchers have discovered how a disease-associated protein gets inactivated, opening the door to possible new treatments. Professor Chaitan Khosla, the director of Stanford Chemistry, Engineering & Medicine for Human Health, oversaw the new study.
Celiac disease is an autoimmune disorder that affects by some estimates nearly 1 in 100 people. Celiac disease symptoms are triggered by gluten, a protein found in wheat and related plants, but gluten doesn't act alone to cause the digestive symptoms that patients suffer. Rather, gluten induces an overactive immune response when it's modified by the enzyme transglutaminase 2, or TG2, in the small intestine. New research published in the Feb. 23 issue of the Journal of Biological Chemistry identifies an enzyme that turns off TG2, potentially paving the way for new treatments for celiac disease.