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Journal Abstract Search

212 related items for PubMed ID: 24992280

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  • 23. Molecular basis of ranolazine block of LQT-3 mutant sodium channels: evidence for site of action.
    Fredj S, Sampson KJ, Liu H, Kass RS.
    Br J Pharmacol; 2006 May; 148(1):16-24. PubMed ID: 16520744
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  • 26. Mechanisms underlying age-associated manifestation of cardiac sodium channel gain-of-function.
    Nowak MB, Poelzing S, Weinberg SH.
    J Mol Cell Cardiol; 2021 Apr; 153():60-71. PubMed ID: 33373643
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  • 31. Na(+) channel mutation that causes both Brugada and long-QT syndrome phenotypes: a simulation study of mechanism.
    Clancy CE, Rudy Y.
    Circulation; 2002 Mar 12; 105(10):1208-13. PubMed ID: 11889015
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  • 33. GPD1L links redox state to cardiac excitability by PKC-dependent phosphorylation of the sodium channel SCN5A.
    Valdivia CR, Ueda K, Ackerman MJ, Makielski JC.
    Am J Physiol Heart Circ Physiol; 2009 Oct 12; 297(4):H1446-52. PubMed ID: 19666841
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  • 34. Analyses of a novel SCN5A mutation (C1850S): conduction vs. repolarization disorder hypotheses in the Brugada syndrome.
    Petitprez S, Jespersen T, Pruvot E, Keller DI, Corbaz C, Schläpfer J, Abriel H, Kucera JP.
    Cardiovasc Res; 2008 Jun 01; 78(3):494-504. PubMed ID: 18252757
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  • 35. A mutation in the human cardiac sodium channel (E161K) contributes to sick sinus syndrome, conduction disease and Brugada syndrome in two families.
    Smits JP, Koopmann TT, Wilders R, Veldkamp MW, Opthof T, Bhuiyan ZA, Mannens MM, Balser JR, Tan HL, Bezzina CR, Wilde AA.
    J Mol Cell Cardiol; 2005 Jun 01; 38(6):969-81. PubMed ID: 15910881
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  • 38. Cardiac sodium channel overlap syndromes: different faces of SCN5A mutations.
    Remme CA, Wilde AA, Bezzina CR.
    Trends Cardiovasc Med; 2008 Apr 01; 18(3):78-87. PubMed ID: 18436145
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  • 40. [HERG K+ channel, the target of anti-arrhythmias drugs].
    Guan FY, Yang SJ.
    Yao Xue Xue Bao; 2007 Jul 01; 42(7):687-91. PubMed ID: 17882949
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