
IndraLab
Statements
CACNA1C increases the amount of calcium(2+). 8 / 9
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"Thus, only proteins in the junctional cleft, i.e., RyR2, exhibited higher PKA-dependent phosphorylation suggesting subcellularly restricted regulation of protein activity in Cacna1c myocytes possibly to promote Ca -induced SR Ca release in order to compensate for the reduced Cav1.2 protein levels."
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"EC coupling is initiated by Ca influx through the voltage-gated L-type Ca channels (Cav1.2) [1,2], which activate the opening of type-2 ryanodine receptors (RyR2s) of dyadic Ca stores of the sarcoplasmic reticulum (SR), triggering a much larger release of Ca via the Ca -induced Ca release (CICR) mechanism [1,2,3]."
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"Together, these results indicate that the higher spark density at the sarcolemma observed in patients with AF is neither caused by a higher SR calcium load nor by a lower NCX-1 activity.We then performed immunofluorescent labeling of the RyR2 clusters that give rise to calcium sparks and of the Cav1.2 that trigger calcium release through the RyR2s during excitation-contraction coupling."
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"As norepinephrine has low affinity for β1-AR, it would require high levels of norepinephrine release, as occurs with stress, to engage this mechanism, similar to the heart, where the fight or flight response involves β1-AR activation of Cav1.2 inducing calcium-mediated calcium release from the sarcoplasmic reticulum to increase muscle contraction."
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"In addition, we observe pathway hits in calcium signaling, specifically at RhoA, AKAP6, and calcium channels CACNA1C and CACNA2D3, all of which modulate calcium levels, which, in turn, through calcinuerin signaling, regulate the transcriptional activity of another associated gene in the calcium signaling pathway, NF-AT."