Nitric oxide synthase 1 modulates basal and beta-adrenergic-stimulated contractility by rapid and reversible redox-dependent s-nitrosylation of the heart
S-nitrosylation of several Ca2+ regulating proteins in response to beta-adrenergic stimulation was recently described in the heart; however the specific nitric oxide synthase (NOS) isoform and signaling pathways responsible for this modification have not
| Autores: | , , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2015 |
| País: | Chile |
| Idioma: | inglés |
| OAI Identifier: | oai:repositorio.anid.cl:10533/232575 |
| Acceso en línea: | https://hdl.handle.net/10533/232575 |
| Access Level: | acceso abierto |
| Sumario: | S-nitrosylation of several Ca2+ regulating proteins in response to beta-adrenergic stimulation was recently described in the heart; however the specific nitric oxide synthase (NOS) isoform and signaling pathways responsible for this modification have not |
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