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JCI table of contents, December 15 2004

niversity of Oxford, Oxford, United Kingdom.
Phone: 44-1865-222412; Fax: 44-1865-222502; E-mail: vincenzo.cerundolo@imm.ox.ac.uk.

A PDF of this article is available at: http://www.jci.org/cgi/content/full/114/12/1800.


Understanding acid sensing in the kidney

The normal daily diet generates volatile acid (carbon dioxide) and nonvolatile acid (hydrogen ions) from carbohydrate and protein metabolism, respectively, and the kidney is responsible for maintaining an acid-base balance by excreting these acids. In this issue of the Journal of Clinical Investigation, Patricia Preisig and colleagues from the University of Texas Southwestern Medical Center have identified the kidney's elusive acid sensor. The authors examined opossum kidney cells cultured under acidic conditions and found that a 24-hour exposure to acid activates the enzyme Pyk2, which then binds to the proto-oncogene c-Src, causing c-Src activation and subsequent activation of signaling pathways that increase production of NHE3, the molecule at the surface of renal proximal tubule cells in the kidney that release hydrogen ions from the cell.

In an accompanying commentary, Steven Gluck from the University of California San Francisco discusses the broader role of Pyk2 in acid-base balance in bone and other tissues beyond the kidney.

TITLE: Pyk2 activation is integral to acid stimulation of sodium/hydrogen exchanger 3

AUTHOR CONTACT:
Patricia Preisig
University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Phone: 214-648-8628; Fax: 214-648-2071; E-mail: Patricia.Preisig@UTSouthwestern.edu.

A PDF of this article will be available at:

A PDF of this article is available at:

Contact: Brooke Grindlinger
press_releases@the-jci.org
212-342-9006
Journal of Clinical Investigation
15-Dec-2004


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