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Published ahead of print on December 21, 2005
J Am Soc Nephrol 17: 26-30, 2006
© 2006 American Society of Nephrology
doi: 10.1681/ASN.2005101025
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Fast Track

Identification of BSPRY as a Novel Auxiliary Protein Inhibiting TRPV5 Activity

Stan F.J. van de Graaf, Annemiete W.C.M. van der Kemp, Dennis van den Berg, Mijke van Oorschot, Joost G.J. Hoenderop and René J.M. Bindels

Department of Physiology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands

Address correspondence to: Dr. René J.M. Bindels, 286 Cell Physiology, Radboud University Nijmegen Medical Centre, PO Box 9101, NL-6500 HB Nijmegen, The Netherlands. Phone: +31-24-361-4211; Fax: +31-24-361-6413; E-mail: r.bindels{at}ncmls.ru.nl

Transient receptor potential vallinoid 5 (TRPV5) and TRPV6 are the most Ca2+-selective members of the TRP superfamily and are essential for active Ca2+ (re)absorption in epithelia. However, little is known about intracellular proteins that regulate the activity of these channels. This study identified BSPRY (B-box and SPRY-domain containing protein) as a novel factor involved in the control of TRPV5. The interaction between BSPRY and TRPV5 by GST pull-down and co-immunoprecipitation assays was demonstrated. BSPRY showed co-localization with TRPV5 in mouse kidney. Expression of BSPRY resulted in a significant reduction of the Ca2+ influx in Madin-Darby Canine Kidney cells that stably express TRPV5 without affecting channel cell-surface abundance. Finally, BSPRY expression in kidney was increased in 25-hydroxyvitamin D3-1{alpha}-hydroxylase knockout mice, suggesting an inverse regulation by vitamin D3. Together, these results demonstrate the physiologic role of the novel protein BSPRY in the regulation of epithelial Ca2+ transport via negative modulation of TRPV5 activity.




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J. G. J. Hoenderop and R. J. M. Bindels
Calciotropic and Magnesiotropic TRP Channels
Physiology, February 1, 2008; 23(1): 32 - 40.
[Abstract] [Full Text] [PDF]


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