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Polycystin-L is a calcium-regulated cation channel permeable to calcium ions

Author

Listed:
  • Xing-Zhen Chen

    (Renal and)

  • Peter M. Vassilev

    (Brigham and Women's Hospital and Harvard Medical School)

  • Nuria Basora

    (Renal and)

  • Ji-Bin Peng

    (Renal and)

  • Hideki Nomura

    (Renal and)

  • Yoav Segal

    (Renal and)

  • Edward M. Brown

    (Brigham and Women's Hospital and Harvard Medical School)

  • Stephen T. Reeders

    (Renal and)

  • Matthias A. Hediger

    (Renal and)

  • Jing Zhou

    (Renal and)

Abstract

Polycystic kidney diseases are genetic disorders in which the renal parenchyma is progressively replaced by fluid-filled cysts1. Two members of the polycystin family (polycystin-1 and -2) are mutated in autosomal dominant polycystic kidney disease (ADPKD)2,3,4,5, and polycystin-L is deleted in mice with renal and retinal defects6. Polycystins are membrane proteins that share significant sequence homology6,7, especially polycystin-2 and -L (50% identity and 71% similarity). The functions of the polycystins remain unknown. Here we show that polycystin-L is a calcium-modulated nonselective cation channel that is permeable to sodium, potassium and calcium ions. Patch-clamp experiments revealed single-channel activity with a unitary conductance of 137 pS. Channel activity was substantially increased when either the extracellular or intracellular calcium-ion concentration was raised, indicating that polycystin-L may act as a transducer of calcium-mediated signalling in vivo. Its large single-channel conductance and regulation by calcium ions distinguish it from other structurally related cation channels.

Suggested Citation

  • Xing-Zhen Chen & Peter M. Vassilev & Nuria Basora & Ji-Bin Peng & Hideki Nomura & Yoav Segal & Edward M. Brown & Stephen T. Reeders & Matthias A. Hediger & Jing Zhou, 1999. "Polycystin-L is a calcium-regulated cation channel permeable to calcium ions," Nature, Nature, vol. 401(6751), pages 383-386, September.
    • Handle: RePEc:nat:nature:v:401:y:1999:i:6751:d:10.1038_43907
    DOI: 10.1038/43907
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