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Electrophysiology

Channelosome and intracellular K+ channels in arrhythmia

Nature Cardiovascular Research volume 1, pages 874–875 (2022)Cite this article

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Mutations in Kir2.1 resulting in defects in trafficking to the cardiomyocyte sarcolemma promote arrhythmia in Anderson–Tawil syndrome. Macias and colleagues provide a dual mechanism underlying cardiac arrhythmia that involves chaperoning of voltage-gated Na+ channels and a unique population of intracellular Kir2.1 channels that regulate Ca2+ cycling at the sarcoplasmic reticulum.

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Fig. 1: Dual mechanisms of cardiac arrhythmia in the Kir2.1∆314–315 model of Anderson–Tawil syndrome.

References

  1. Katz, B. Arch. Sci. Physiol. (Paris) 3, 285–300 (1949).

    CAS  Google Scholar 

  2. Plaster, N. M. et al. Cell 105, 511–519 (2001).

    Article  CAS  Google Scholar 

  3. Bendahhou, S. et al. J. Biol. Chem. 278, 51779–51785 (2003).

    Article  CAS  Google Scholar 

  4. Tristani-Firouzi, M. et al. J. Clin. Invest. 110, 381–388 (2002).

    Article  CAS  Google Scholar 

  5. Macías, Á. et al. Nat. Cardiovasc. Res. https://doi.org/10.1038/s44161-022-00145-2 (2022).

  6. Milstein, M. L. et al. Proc. Natl Acad. Sci. USA 109, E2134–2143 (2012).

    Article  CAS  Google Scholar 

  7. Matamoros, M. et al. Cardiovasc. Res. 110, 279–290 (2016).

    Article  CAS  Google Scholar 

  8. Ponce-Balbuena, D. et al. Circ. Res. 122, 1501–1516 (2018).

    Article  CAS  Google Scholar 

  9. Paggio, A. et al. Nature 572, 609–613 (2019).

    Article  CAS  Google Scholar 

  10. Papanicolaou, K. N. et al. J. Mol. Cell. Cardiol. 139, 176–189 (2020).

    Article  CAS  Google Scholar 

  11. Costantin, L. L. & Podolsky, R. J. J. Gen. Physiol. 50, 1101–1124 (1967).

    Article  CAS  Google Scholar 

  12. Fink, R. H. A. & Veigel, C. Acta Physiol. Scand. 156, 387–396 (1996).

    Article  CAS  Google Scholar 

  13. Takeshima, H., Venturi, E. & Sitsapesan, R. J. Physiol. 593, 3241–3251 (2015).

    Article  CAS  Google Scholar 

  14. Fancher, I. S. et al. J. Am. Heart Assoc. 7, e007430 (2018).

    Article  Google Scholar 

  15. Fancher, I. S. et al. Arterioscler. Thromb. Vasc. Biol. 40, e240–e255 (2020).

    Article  CAS  Google Scholar 

Download references

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Authors and Affiliations

  1. Department of Kinesiology and Applied Physiology University of Delaware, Newark, DE, USA

    Ibra Fancher

  2. Department of Medicine, University of Illinois Chicago, Chicago, IL, USA

    Irena Levitan

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  1. Ibra Fancher
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  2. Irena Levitan
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Correspondence to Irena Levitan.

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The authors declare no competing interests.

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Fancher, I., Levitan, I. Channelosome and intracellular K+ channels in arrhythmia. Nat Cardiovasc Res 1, 874–875 (2022). https://doi.org/10.1038/s44161-022-00143-4

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