ArticleJournal of molecular and cellular cardiology2018
Cardiac CaMKII activation promotes rapid translocation to its extra-dyadic targets.
Article in Journal of molecular and cellular cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Exploring the role of CaMKII in exercise-induced cardioprotection.Human cell · 2026Review
- High-throughput peptide-centric local stability assay extends protein-ligand identification to membrane proteins, tissues and bacteria.Nature structural & molecular biology · 2026Article
- Activated CaMKIIδ translocates to the RyR nanodomain in cardiomyocytes.Cardiovascular research · 2025Article
- Review
- Evaluating sex-specific responses to western diet across the lifespan: impact on cardiac function and transcriptomic signatures in C57BL/6J mice at 530 and 640/750 days of age.Cardiovascular diabetology · 2024Article
- Proteomic Analysis of Prehypertensive and Hypertensive Patients: Exploring the Role of the Actin Cytoskeleton.International journal of molecular sciences · 2024Article
- Near Infrared Responsive Gold Nanorods Attenuate Osteoarthritis Progression by Targeting TRPV1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Nuclear Calcium in Cardiac (Patho)Physiology: Small Compartment, Big Impact.Biomedicines · 2023Review
- AKAP18δ Anchors and Regulates CaMKII Activity at Phospholamban-SERCA2 and RYR.Circulation research · 2022Article
- The Oxidative Balance Orchestrates the Main Keystones of the Functional Activity of Cardiomyocytes.Oxidative medicine and cellular longevity · 2022Review
- CaMKIIδ post-translational modifications increase affinity for calmodulin inside cardiac ventricular myocytes.Journal of molecular and cellular cardiology · 2021Article
- Late NaPharmaceuticals (Basel, Switzerland) · 2021Article
- Abnormal Calcium Handling in Atrial Fibrillation Is Linked to Changes in Cyclic AMP Dependent Signaling.Cells · 2021Article
- Regulatory mechanism of calcium/calmodulin-dependent protein kinase II in the occurrence and development of ventricular arrhythmia (Review).Experimental and therapeutic medicine · 2021Review
- TRPV1 alleviates osteoarthritis by inhibiting M1 macrophage polarization via CaCell death & disease · 2021Article
- CaMKII and PKA-dependent phosphorylation co-regulate nuclear localization of HDAC4 in adult cardiomyocytes.Basic research in cardiology · 2021Article
- RIPK3-Mediated Necroptosis in Diabetic Cardiomyopathy Requires CaMKII Activation.Oxidative medicine and cellular longevity · 2021Article
- The CaMKII phosphorylation site Thr1604 in the CaChannels (Austin, Tex.) · 2020Article
- CaMKIIδC Drives Early Adaptive CaCirculation research · 2020Article
- CaMKII/calpain interaction mediates ischemia/reperfusion injury in isolated rat hearts.Cell death & disease · 2020Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Calcium-calmodulin dependent protein kinase IIδ (CaMKIIδ) is an important regulator of cardiac electrophysiology, calcium (Ca) balance, contraction, transcription, arrhythmias and progression to heart failure. CaMKII is readily activated at mouths of dyadic cleft Ca channels, but because of its low Ca-calmodulin affinity and presumed immobility it is less clear how CaMKII gets activated near other known, extra-dyad targets. CaMKII is typically considered to be anchored in cardiomyocytes, but while untested, mobility of active CaMKII could provide a mechanism for broader target phosphorylation in cardiomyocytes. We therefore tested CaMKII mobility and how this is affected by kinase activation in adult rabbit cardiomyocytes. We measured translocation of both endogenous and fluorescence-tagged CaMKII using immunocytochemistry, fluorescence recovery after photobleach (FRAP) and photoactivation of fluorescence. In contrast to the prevailing view that CaMKII is anchored near its myocyte targets, we found CaMKII to be highly mobile in resting myocytes, which was slowed by Ca chelation and accelerated by pacing. At low [Ca], CaMKII was concentrated at Z-lines near the dyad but spread throughout the sarcomere upon pacing. Nuclear exchange of CaMKII was also enhanced upon pacing- and heart failure-induced chronic activation. This mobilization of active CaMKII and its intrinsic memory may allow CaMKII to be activated in high [Ca] regions and then move towards more distant myocyte target sites.
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