IP3R-III 抑制因子

The class of IP3R-II inhibitors comprises a diverse array of chemical compounds strategically designed to modulate IP3R-II activity either directly or indirectly through intricate cellular pathways. These inhibitors play crucial roles in influencing cellular processes governed by IP3R-II-regulated calcium signaling, providing valuable tools for dissecting and manipulating intracellular calcium dynamics. 2-APB, as an indirect inhibitor, modulates the intracellular calcium signaling pathway by disrupting calcium release from the endoplasmic reticulum. Xestospongin C stands out as a direct inhibitor of IP3R-II, specifically targeting inositol trisphosphate receptors to hinder calcium release. 8-Bromo-cADPR acts as an indirect inhibitor by modulating the cADPR pathway, disrupting calcium release from intracellular stores and impacting IP3R-II activity. Ruthenium Red is a direct inhibitor that interferes with calcium release from the endoplasmic reticulum, binding to IP3Rs and blocking their calcium channel activity.

The indirect inhibitor 2-ABP modulates the intracellular calcium signaling pathway, inducing IP3R-II desensitization by acting as an IP3R agonist. U-73122 serves as an indirect inhibitor by targeting phospholipase C (PLC), disrupting IP3 production and downstream IP3R-II-mediated calcium release. Dantrolene, a direct inhibitor, interferes with calcium release from the endoplasmic reticulum, binding to the RyR1 receptor and inhibiting IP3R-II activity. MCI-186 acts as an indirect inhibitor by mitigating oxidative stress-induced calcium release, impacting IP3R-II activity. Carvedilol, an indirect inhibitor, modulates the beta-adrenergic signaling pathway, reducing IP3R-II-mediated calcium release. SKF 96365 is an indirect inhibitor that modulates calcium entry from the extracellular space by inhibiting receptor-operated calcium channels (ROCCs), impacting IP3R-II activity. Cytochalasin D, serving as an indirect inhibitor, modulates the actin cytoskeleton, influencing IP3R-II localization and activity. Heparin, an indirect inhibitor, competes with IP3 for binding to IP3R-II, reducing IP3R-II-mediated calcium release.