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Novel MUC1 splice variants contribute to mucin overexpression in CFTR-deficient mice.

Journal article
Authors A Marina Hinojosa-Kurtzberg
Malin E V Johansson
Cathy S Madsen
Gunnar C. Hansson
Sandra J Gendler
Published in American journal of physiology. Gastrointestinal and liver physiology
Volume 284
Issue 5
Pages G853-62
ISSN 0193-1857
Publication year 2003
Published at Institute of Medical Biochemistry
Pages G853-62
Language en
Links dx.doi.org/10.1152/ajpgi.00326.2002
Keywords Alternative Splicing, Amino Acid Sequence, Animals, Cystic Fibrosis Transmembrane Conductance Regulator, deficiency, genetics, Intestines, metabolism, Mice, Mice, Inbred CFTR, Mucins, biosynthesis, genetics, metabolism, Mutation, Phenotype
Subject categories Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)

Abstract

A cystic fibrosis (CF) mouse expressing the human mucin MUC1 transgene (CFM) reverted the CF/Muc1(-/-) phenotype (little mucus accumulated in the intestine) to that of CF mice expressing mouse Muc1, which exhibited increased mucus accumulation. Western blots and immunohistochemical analysis showed that the MUC1 protein was markedly increased in CFM mice in which it was both membrane bound and secreted into the intestinal lumen. Studies to determine the reason for increased levels of the extracellular domain of MUC1 mucin identified mRNA and protein of two novel splice variants and the previously described secreted MUC1 lacking the cytoplasmic tail (MUC1/SEC). Novel MUC1 splice variants, CT80 and CT58, were both transmembrane proteins with cytoplasmic tails different from the normal MUC1. The MUC1-CT80 and MUC1/SEC forms are found expressed mainly in the CFM mice intestines. Thus MUC1 expression is increased, and it appears that alternate cytoplasmic tails may change its role in signaling. MUC1 could be an important contributor to the CF intestinal phenotype.

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