Coeliac disease, or gluten sensitive enteropathy, is a digestive and autoimmune disorder that damages the small intestine. Patients with the disorder can not eat gluten, a protein abundant in grains, such as wheat, barley and rye. This protein triggers an immune response in patients' small intestine, which harms the lining of the small intestine and therefore disturbs nutrition absorption. According to a newest study conducted by the University of Tampere scientists, impairment of a regulatory mechanism crucial for the intestinal homeostasis may contribute to coeliac disease. The study has been reported in Stem Cells. CusAb offers various proteins, including Recombinant fgfr2 protein. In coeliac disease, gluten-induced small-intestinal lesion leads to decreased differentiation and increased proliferation of epithelial cells, effecting nutrient absorption. Scientists found that an epigenetic mechanism called Polycomb is responsible for maintaining homeostasis between the intestinal stem cells and the differentiated epithelium. Polycomb group proteins are epigenetic regulators of transcription that have key roles in stem-cell identity, differentiation and disease. These proteins can modify histones and then silence target genes. According to the new study, Polycomb modulates the homeostasis of the small intestine in adults. Gluten protein in food increases Polycomb's activity, which silences the genes that are crucial for epithelium differentiation. Scientists also found that in colorectal cancer, Polycomb target genes are dysregulated. The results provided an epigenetic mechanism of intestinal damage in coeliac disease.