A systematic approach for assessing Ca²⁺ handling in cardiac myocytes.
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[1] N. Macquaide,et al. Measuring Ca²⁺ sparks in cardiac myocytes. , 2015, Cold Spring Harbor protocols.
[2] N. Macquaide,et al. Assessing Ca²⁺-removal pathways in cardiac myocytes. , 2015, Cold Spring Harbor protocols.
[3] N. Macquaide,et al. Basic methods for monitoring intracellular Ca2+ in cardiac myocytes using Fluo-3. , 2015, Cold Spring Harbor protocols.
[4] N. Macquaide,et al. Measuring sarcoplasmic reticulum Ca2+ content, fractional release, and Ca2+ buffering in cardiac myocytes. , 2015, Cold Spring Harbor protocols.
[5] N. Macquaide,et al. Characterizing the trigger for sarcoplasmic reticulum Ca2+ release in cardiac myocytes. , 2015, Cold Spring Harbor protocols.
[6] K. Mikoshiba,et al. The IP3 Receptor Regulates Cardiac Hypertrophy in Response to Select Stimuli , 2010, Circulation research.
[7] S. Huke,et al. IP3 receptor-dependent Ca2+ release modulates excitation-contraction coupling in rabbit ventricular myocytes. , 2008, American journal of physiology. Heart and circulatory physiology.
[8] A. Zima,et al. IP3‐dependent nuclear Ca2+ signalling in the mammalian heart , 2007, The Journal of physiology.
[9] M. Berridge,et al. Inositol 1,4,5-trisphosphate supports the arrhythmogenic action of endothelin-1 on ventricular cardiac myocytes , 2006, Journal of Cell Science.
[10] Z. Kubalová,et al. Modulation of cytosolic and intra‐sarcoplasmic reticulum calcium waves by calsequestrin in rat cardiac myocytes , 2004, The Journal of physiology.
[11] D. Bers. Cardiac excitation–contraction coupling , 2002, Nature.
[12] W. Wier,et al. Flux of Ca2+ across the sarcoplasmic reticulum of guinea‐pig cardiac cells during excitation‐contraction coupling. , 1991, The Journal of physiology.