Date published: 2025-11-1

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CLRN2 Activators

CLRN2 Activators encompass a group of compounds that facilitate the functional activity of CLRN2 through modulation of calcium signaling pathways. These activators include both direct and indirect mechanisms by which intracellular calcium dynamics and calcium-dependent processes are altered, resulting in the enhanced activation of CLRN2. For example, the calcium ionophore A23187 directly increases intracellular Ca2+ levels, which can lead to the activation of Ca2+-dependent signaling pathways and protein kinases. These kinases may then interact with and activate CLRN2. Similarly, thapsigargin and cyclopiazonic acid disrupt calcium homeostasis in the endoplasmic reticulum, leading to increased cytosolic calcium levels which then activate Ca2+-dependent pathways that can enhance the activity of CLRN2.

Furthermore, other compounds like BAPTA-AM and nimodipine work indirectly by modulating the cell's calcium buffering capacity or by blocking voltage-gated calcium channels, respectively. This modulation can result in compensatory cellular responses that ultimately lead to the activation of CLRN2. Inhibitors like SKF-96365, 2-APB, and Xestospongin C alter calcium entry or release within the cell, leading to the activation of compensatory pathways that enhance the activity of CLRN2. Additionally, compounds such as ML-9 and KN-93, which inhibit specific kinases like MLCK and CaMKII, may lead to the indirect activation of CLRN2 through the disruption of downstream calcium/calmodulin-dependent processes. Lastly, W-7's antagonism of calmodulin disrupts calmodulin-mediated signaling, which can in turn activate pathways leading to the enhancement of CLRN2 activity.

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