Paracellin-1, a renal tight junction protein required for paracellular Mg2+ resorption

David B. Simon, Yin Lu, Keith A. Choate, Heino Velazquez, Essam Al-Sabban, Manuel Praga, Giorgio Casari, Alberto Bettinelli, Giacomo Colussi, Juan Rodriguez-Soriano, David McCredie, David Milford, Sami Sanjad, Richard P. Lifton

Research output: Contribution to journalArticlepeer-review


Epithelia permit selective and regulated flux from apical to basolateral surfaces by transcellular passage through cells or paracellular flux between cells. Tight junctions constitute the barrier to paracellular conductance; however, little is known about the specific molecules that mediate paracellular permeabilities. Renal magnesium ion (Mg2+) resorption occurs predominantly through a paracellular conductance in the thick ascending limb of Henle (TAL). Here, positional cloning has identified a human gene, paracellin-1 (PCLN-1), mutations on which cause renal Mg2+ wasting. PCLN-1 is located in tight junctions of the TAL and is related to the claudin family of tight junction proteins. These finding provide insight into Mg2+ homeostasis, demonstrate the role of a tight junction protein in human disease, and identify an essential component of selective paracellular conductance.

Original languageEnglish
Pages (from-to)103-106
Number of pages4
Issue number5424
Publication statusPublished - Jul 2 1999

ASJC Scopus subject areas

  • General


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