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| The first 150 words of the full text of this article appear below. |
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.22
We 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 enzyme
HinfI.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
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