Fibrocystin interacts with CAML, a protein involved in Ca2+ signaling

The predicted structure of the autosomal recessive polycystic kidney disease protein, fibrocystin, suggests that it may function as a receptor, but its function remains unknown. To understand its function, we searched for proteins that interact with the intracellular C-terminus of fibrocystin using...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2005-12, Vol.338 (2), p.880-889
Main Authors: Nagano, Junko, Kitamura, Kenichiro, Hujer, Kristine M, Ward, Christopher J, Bram, Richard J, Hopfer, Ulrich, Tomita, Kimio, Huang, Chunfa, Miller, R Tyler
Format: Article
Language:English
Subjects:
Adaptor Proteins, Signal Transducing - metabolism
Animals
Calcium - metabolism
Calcium Signaling - physiology
Cercopithecus aethiops
COS Cells
Humans
Polycystic Kidney Diseases - metabolism
Protein Binding
Receptors, Cell Surface - metabolism
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Summary:The predicted structure of the autosomal recessive polycystic kidney disease protein, fibrocystin, suggests that it may function as a receptor, but its function remains unknown. To understand its function, we searched for proteins that interact with the intracellular C-terminus of fibrocystin using the yeast two-hybrid system. From the screening, we found calcium modulating cyclophilin ligand (CAML), a protein involved in Ca(2+) signaling. Immunofluorescent analysis showed that both proteins are co-localized in the apical membrane, primary cilia, and the basal body of cells derived from the distal nephron Epitope-tagged expression constructs of both proteins were co-immunoprecipitated from COS7 cells. The intracellular C-terminus of fibrocystin interacts with CAML, a protein with an intracellular distribution that is similar to that of PKD2. Fibrocystin may participate in regulation of intracellular Ca(2+) in the distal nephron in a manner similar to PKD1 and PKD2 that are involved in autosomal dominant polycystic kidney disease.
ISSN:0006-291X
DOI:10.1016/j.bbrc.2005.10.022