Activation of RyR2 by class I kinase inhibitors
- Autores
- Chakraborty, A. D.; Gonano, Luis Alberto; Munro, M. L.; Smith, L. J,; Thekkedam, C.; Staudacher, V.; Gamble, A. B.; Macquaide, N.; Dulhunty, A. F.; Jones, P. P.
- Año de publicación
- 2019
- Idioma
- español castellano
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- 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.
Centro de Investigaciones Cardiovasculares - Materia
- Ciencias Médicas
- Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by-nc-sa/4.0/
- Repositorio
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- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/108114
Ver los metadatos del registro completo
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Activation of RyR2 by class I kinase inhibitorsChakraborty, A. D.Gonano, Luis AlbertoMunro, M. L.Smith, L. J,Thekkedam, C.Staudacher, V.Gamble, A. B.Macquaide, N.Dulhunty, A. F.Jones, P. P.Ciencias MédicasKinase 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.Centro de Investigaciones Cardiovasculares2019info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf773-786http://sedici.unlp.edu.ar/handle/10915/108114spainfo:eu-repo/semantics/altIdentifier/url/http://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC6393232&blobtype=pdfinfo:eu-repo/semantics/altIdentifier/issn/0007-1188info:eu-repo/semantics/altIdentifier/pmid/30588601info:eu-repo/semantics/altIdentifier/doi/10.1111/bph.14562info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-10-15T11:15:46Zoai:sedici.unlp.edu.ar:10915/108114Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-10-15 11:15:46.926SEDICI (UNLP) - Universidad Nacional de La Platafalse |
| dc.title.none.fl_str_mv |
Activation of RyR2 by class I kinase inhibitors |
| title |
Activation of RyR2 by class I kinase inhibitors |
| spellingShingle |
Activation of RyR2 by class I kinase inhibitors Chakraborty, A. D. Ciencias Médicas |
| title_short |
Activation of RyR2 by class I kinase inhibitors |
| title_full |
Activation of RyR2 by class I kinase inhibitors |
| title_fullStr |
Activation of RyR2 by class I kinase inhibitors |
| title_full_unstemmed |
Activation of RyR2 by class I kinase inhibitors |
| title_sort |
Activation of RyR2 by class I kinase inhibitors |
| dc.creator.none.fl_str_mv |
Chakraborty, A. D. Gonano, Luis Alberto Munro, M. L. Smith, L. J, Thekkedam, C. Staudacher, V. Gamble, A. B. Macquaide, N. Dulhunty, A. F. Jones, P. P. |
| author |
Chakraborty, A. D. |
| author_facet |
Chakraborty, A. D. Gonano, Luis Alberto Munro, M. L. Smith, L. J, Thekkedam, C. Staudacher, V. Gamble, A. B. Macquaide, N. Dulhunty, A. F. Jones, P. P. |
| author_role |
author |
| author2 |
Gonano, Luis Alberto Munro, M. L. Smith, L. J, Thekkedam, C. Staudacher, V. Gamble, A. B. Macquaide, N. Dulhunty, A. F. Jones, P. P. |
| author2_role |
author author author author author author author author author |
| dc.subject.none.fl_str_mv |
Ciencias Médicas |
| topic |
Ciencias Médicas |
| dc.description.none.fl_txt_mv |
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. Centro de Investigaciones Cardiovasculares |
| description |
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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2019 |
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2019 |
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