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[In previous studies, we showed that isolated eag (i-eag) domains rescued the dysfunction of long QT type-2 associated mutant hERG R56Q channels, by substituting for defective eag domains, when the channels were expressed in Xenopus oocytes or HEK 293 cells.Here, our goal was to determine whether the rescue of hERG R56Q channels by i-eag domains could be translated into the environment of cardiac myocytes.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
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Gene-disease associations inferred from text-mining the literature.
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