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

Artikel i vetenskaplig tidskrift
Författare A Marina Hinojosa-Kurtzberg
Malin E V Johansson
Cathy S Madsen
Gunnar C. Hansson
Sandra J Gendler
Publicerad i American journal of physiology. Gastrointestinal and liver physiology
Volym 284
Nummer/häfte 5
Sidor G853-62
ISSN 0193-1857
Publiceringsår 2003
Publicerad vid Institutionen för medicinsk och fysiologisk kemi
Sidor G853-62
Språk en
Länkar dx.doi.org/10.1152/ajpgi.00326.2002
Ämnesord 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
Ämneskategorier Medicinsk bioteknologi (med inriktning mot cellbiologi (inklusive stamcellsbiologi), molekylärbiologi, mikrobiologi, biokemi eller biofarmaci)

Sammanfattning

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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