Activation of RyR2 by class I kinase inhibitors
Kinase inhibitors are a common treatment for cancer. Class I kinase inhibitors that target the ATP-binding pocket are particularly prevalent. Many of these compounds are cardiotoxic and can cause arrhythmias. Spontaneous release of Ca2+ via cardiac ryanodine receptors (RyR2), through a process terme...
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| Autores principales: | , , , , , , , , , |
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| Formato: | Articulo |
| Lenguaje: | Español |
| Publicado: |
2019
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| Materias: | |
| Acceso en línea: | http://sedici.unlp.edu.ar/handle/10915/108114 http://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC6393232&blobtype=pdf |
| Aporte de: |
| Sumario: | Kinase inhibitors are a common treatment for cancer. Class I kinase inhibitors that target the ATP-binding pocket are particularly prevalent. Many of these compounds are cardiotoxic and can cause arrhythmias. Spontaneous release of Ca2+ via cardiac ryanodine receptors (RyR2), through a process termed store overload-induced Ca2+ release (SOICR), is a common mechanism underlying arrhythmia. We explored whether class I kinase inhibitors could modify the activity of RyR2 and trigger SOICR to determine if this contributes to the cardiotoxic nature of these compounds. |
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