Critical Determinants of Ca2+-Dependent Inactivation within an EF-Hand Motif of L-Type Ca2+ Channels
By B. Peterson, Joanna S. Lee, J. Mulle, Yan Wang, Marita de Leon, D. T. Yue. 2000
197 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine, Cellular and Molecular Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/dbf045bbbe96a57798686ea7e6ff470673f4fb47
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In Cardiology and Cardiovascular Medicine
In Cellular and Molecular Neuroscience
In Molecular Biology
Citations in the corpus
- Computer model of action potential of mouse ventricular myocytes. (2004, methodology): “In Ca(2) channels, the Ca(2) dependence of inactivation is mediated by the highly localized increase of [Ca(2) ] that binds to calmodulin, which is constitutively bound to the Ca(2) channel (74, 75).”
- A computational model of the human left-ventricular epicardial myocyte. (2004, background): “Recent experimental data from both isolated myocytes (Linz and Meyer, 1998; Sipido et al., 1995) as well as recombinant channels expressed in HEK293 cells ( Peterson et al., 1999, 2000 ) show that voltage-dependent inactivation of ICaL is slow and incomplete whereas Ca21-mediated inactivation is”
- Neuronal voltage-gated calcium channels: structure, function, and dysfunction. (2014, background): “Upon a rise in intracellular calcium, channelanchored CaM binds calcium, which in turn promotes a conformational change in the C terminus/CaM complex and gives rise to CDI (Ben Johny et al., 2013; Erickson et al., 2001, 2003; Peterson et al., 2000) (Figure 2).”