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Editor—The aetiology of inflammatory bowel disease (IBD) is complex and shows clear evidence of familial clustering,1-3 and genetic linkage studies suggest a number of susceptibility genes.4-12 Changes in mucin expression are a feature of IBD.13-17 In ulcerative colitis there is a depletion of mucus, while the reverse is true for Crohn’s disease.18 Since the gene that encodes a major component of gel forming mucin of the large intestine,MUC2, located on 11p15.5, shows a high level of genetically determined polymorphism in length,19-21 it has been considered as a potential risk factor in IBD.22We have previously shown that the allele lengths range in size between approximately 45 and 200 repeats as judged by cutting genomic DNA samples with the restriction enzymeHinfI.19 This corresponds to apomucin sizes ranging from Mr 400-760 000. It is our hypothesis that these differences have a functional significance by changing the properties of the mucins in terms of the amount of apomucin backbone available for glycosylation or altering the spacing between the cysteine rich domains which are involved in cross linking or both. Here we report the work of …
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