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. 2019 Aug 16;20(16):3986. doi: 10.3390/ijms20163986

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Molecular mechanisms associated with ACM pathogenesis. GPCR: G protein-coupled receptors, YAP: yes-associated protein, PG: Plakoglobin, TCF/LEF: T-cell factor/lymphoid enhancer-binding factor, Wnt: homologous wingless, APC: adenomatous polyposis coli, RYR2: type 2 ryanodine receptor, CASQ2: calsequestrin 2, CACNA1C: calcium voltage-gated channel subunit alpha1 C, SR: sarcoplasmic reticulum, SERCA: sarco-endoplasmic reticulum Ca²⁺ ATPase, PLN: phospholamban, LTCC: L-type calcium channel. ( Activation/Phosphorylation, Translocation, Inhibition).

Inline graphic — Molecular mechanisms associated with ACM pathogenesis. GPCR: G protein-coupled receptors, YAP: yes-associated protein, PG: Plakoglobin, TCF/LEF: T-cell factor/lymphoid enhancer-binding factor, Wnt: homologous wingless, APC: adenomatous polyposis coli, RYR2: type 2 ryanodine receptor, CASQ2: calsequestrin 2, CACNA1C: calcium voltage-gated channel subunit alpha1 C, SR: sarcoplasmic reticulum, SERCA: sarco-endoplasmic reticulum Ca²⁺ ATPase, PLN: phospholamban, LTCC: L-type calcium channel. ( Activation/Phosphorylation, Translocation, Inhibition).