JCI table of contents, March 9, 2006

1 synthetic DNA molecules called "plasmids" which each contained a single mutant form of the claudin16 gene sequence, and put these plasmids into kidney cells in the laboratory. The cells were able to produce the mutant claudin16 protein. The authors made an antibody that recognized claudin16 protein and used it to determine where in the cells the various mutants were localized. Incubating the cells with this antibody revealed that most of the mutants, in contrast to the normal version of claudin16, were either degraded by the cell or they became trapped in various places inside the cell and thus could not function properly. In addition, when the researchers examined the movement of calcium and magnesium in and out of the cells, they found that cells that expressed the mutant claudin16 forms of the protein had defects in trafficking calcium and magnesium. The authors report that this study is important for the potential future therapeutic interventions that claudin16 corrective therapy may provide for patients with excess calcium loss due to these genetic mutations.

TITLE: Disease-associated mutations affect intracellular traffic and paracellular Mg2+ transport function of Claudin-16

AUTHOR CONTACT: Walter Hunziker
Institute of Molecular and Cell Biology, Singapore
Phone: 65-6586-9599; Fax: 65-6779-1117; E-mail: hunziker@imcb.a-star.edu.sg
View the PDF of this article at: https://www.the-jci.org/article.php?id=26323


New mechanism for allergic asthma identified

In a study appearing online on March 9 in advance of print publication in the April issue of the Journal of Clinical Investigation, Gesine Hansen and colleagues at Medizinische Hochschule Hannover in Germany have identified a potentially new target for treating asthma. The researchers examined a mouse model of asthma

Contact: Brooke Grindlinger
Journal of Clinical Investigation

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