IndraLab

Statements

BBR activates KCNH2. 13 / 13
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"Our study demonstrates that BBR induces hERG channel deficiency by inhibiting channel trafficking after incubation for 24h."
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"The result surprisingly manifested that binding to the two residues accounts for BBR induced hERG defect."
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"Mature hERG (155 kDa) was reduced, whereas ER located hERG (135 kDa) was increased by BBR."
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"Together, these data illustrate that resveratrol and fexofenadine showed functional rescue of hERG channel deficiency triggered by BBR, while astemizole only recovered protein expression."
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"Moreover, we first investigated the pharmacological rescue of BBR triggered hERG defect and provided reference for clinical safety of BBR."
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"In this study, we tested three drugs that have previously been reported to rescue trafficking deficient hERG channel for restoration of BBR induced hERG defect."
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"To seek rescue strategies for BBR induced hERG channel deficiency, we chose three drugs (resveratrol, astemizole, and fexofenadine, which were previously used to correct trafficking of hERG channel) to test whether the misprocessed hERG channel by BBR could be transported to the cell surface."
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"To clarify whether hERG channel deficiency caused by BBR incubation was also on account of Phe656 and Tyr652 binding similar to acute application of BBR."
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"Pharmacological rescue of BBR induced hERG channel deficiency."
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"Additional studies would be necessary to define the mechanisms by which BBR induces hERG1 channel blocking and by which hERG1 inhibition mediates phenotypic alterations in OC."
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"Phe656 and Tyr652 binding accounts for BBR induced hERG channel deficiency."
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"These results suggest that BBR induced hERG channel deficiency was on account of Phe656 and Tyr652 binding."
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"In this study, we demonstrated that 1) cav-1 participates in BBR induced hERG deficiency on cell surface; 2) residues Tyr652 and Phe656, essential components of hERG binding sites, mediate hERG surface expression inhibition by BBR incubation; and 3) fexofenadine and resveratrol can shorten APD of ventricular cardiomyocytes prolonged by BBR."
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