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Homo- and heterodimeric interactions between the gene products of PKD1 and PKD2.

http://www.ncbi.nlm.nih.gov/pubmed/9192675

PKD1 and PKD2 are two recently identified genes that are responsible for the vast majority of autosomal polycystic kidney disease, a common inherited disease that causes progressive renal failure. PKD1 encodes polycystin, a large glycoprotein that contains several extracellular motifs indicative of a role in cell-cell or cell-matrix interactions, and the PKD2 encodes a protein with homology to a voltage-activated calcium channel and to PKD1. It is currently unknown how mutations of either protein functionally cause autosomal polycystic kidney disease. We show that PKD1 and PKD2 interact through their C-terminal cytoplasmic tails. This interaction resulted in an up-regulation of PKD1 but not PKD2. Furthermore, the cytoplasmic tail of PKD2 but not PKD1 formed homodimers through a coiled-coil domain distinct from the region required for interaction with PKD1. These interactions suggest that PKD1 and PKD2 may function through a common signaling pathway that is necessary for normal tubulogenesis and that PKD1 may require the presence of PKD2 for stable expression.

Pubmed ID: 9192675 RIS Download

Mesh terms: Dimerization | Humans | Membrane Proteins | Protein Binding | Proteins | Recombinant Proteins | Signal Transduction | TRPP Cation Channels

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Associated grants

  • Agency: NIMH NIH HHS, Id: MH-01147
  • Agency: NIDDK NIH HHS, Id: R01-DK-51060

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