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CFTR anion channel modulates expression of human transmembrane mucin MUC3 through the PDZ protein GOPC.

Artikel i vetenskaplig tidskrift
Författare Thaher Pelaseyed
Gunnar C. Hansson
Publicerad i Journal of cell science
Volym 124
Nummer/häfte Pt 18
Sidor 3074-83
ISSN 1477-9137
Publiceringsår 2011
Publicerad vid Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Sidor 3074-83
Språk en
Länkar dx.doi.org/10.1242/jcs.076943
Ämnesord Animals, Binding, Competitive, genetics, CHO Cells, Carrier Proteins, genetics, metabolism, Computational Biology, Cricetinae, Cystic Fibrosis, genetics, metabolism, pathology, physiopathology, Cystic Fibrosis Transmembrane Conductance Regulator, genetics, metabolism, Enterocytes, metabolism, pathology, Feedback, Physiological, Humans, Membrane Proteins, genetics, metabolism, Mucin-3, genetics, metabolism, PDZ Domains, genetics, Transgenes, genetics, Voltage-Dependent Anion Channels, genetics, metabolism
Ämneskategorier Cell- och molekylärbiologi

Sammanfattning

The transmembrane mucins in the enterocyte are type 1 transmembrane proteins with long and rigid mucin domains, rich in proline, threonine and serine residues that carry numerous O-glycans. Three of these mucins, MUC3, MUC12 and MUC17 are unique in harboring C-terminal class I PDZ motifs, making them suitable ligands for PDZ proteins. A screening of 123 different human PDZ domains for binding to MUC3 identified a strong interaction with the PDZ protein GOPC (Golgi-associated PDZ and coiled-coil motif-containing protein). This interaction was mediated by the C-terminal PDZ motif of MUC3, binding to the single GOPC PDZ domain. GOPC is also a binding partner for cystic fibrosis transmembrane conductance regulator (CFTR) that directs CFTR for degradation. Overexpression of GOPC downregulated the total levels of MUC3, an effect that was reversed by introducing CFTR. The results suggest that CFTR and MUC3 compete for binding to GOPC, which in turn can regulate levels of these two proteins. For the first time a direct coupling between mucins and the CFTR channel is demonstrated, a finding that will shed further light on the still poorly understood relationship between cystic fibrosis and the mucus phenotype of this disease.

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