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Heartless worms hold clues to cardiac arrhythmias, sudden death

"We were really excited," Petersen said. "We already knew that KCR1 affected drug block of HERG in cells, and now we had data in vivo, in a living animal, that KCR1 was important for HERG function."

The investigators then turned to Ping Yang, Ph.D., research instructor and Dan M. Roden, M.D., director of the division of Clinical Pharmacology, both at Vanderbilt, to look for evidence that KCR1 impacts acquired long QT syndrome. Using a database of patients who developed acquired long QT syndrome after drug treatment, Yang was able to detect a variant in the KCR1 gene that occurred more often in control patients -- those who did not develop the syndrome.

"We suspect that this variant is protective, that patients who have it are somehow more protected against drug block of HERG compared to patients who don't have it," Petersen said. By engineering the variant into KCR1 and studying it in cells, the researchers confirmed that drugs do not block HERG as readily when the variant KCR1 is present.

"We're very encouraged because these studies demonstrate that you can identify a protein in the worm which seems totally unrelated to humans -- get a phenotype in vivo, and find evidence in humans that suggests this protein is relevant to cardiac potassium channel function," Petersen said. "We speculate that KCR1 might be useful in a therapeutic context to prevent HERG block." The investigators are now using the C. elegans tool to search for novel interacting proteins that modulate HERG drug block. Any new proteins they find may have therapeutic potential for preventing acquired long QT syndrome.

In addition to Petersen, Balser, Yang, and Roden, authors of the PNAS paper include Toni R. McFarland, Svetlana Z. Stepanovic, Kenshi Hayashi, M.D., Ph.D., and Alfred L. George, M.D., at Vanderbilt and David J. Reiner, Ph.D., and James H. Thomas, Ph.D., at the University of Washington. The research was supported by the National Institutes of
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19-Aug-2004


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