NF-κB activation by depolarization of skeletal muscle cells depends on ryanodine and IP3 receptor-mediated calcium signals
Author
dc.contributor.author
Valdés, Juan Antonio
Author
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Segura Hidalgo, Jorge Antonio
Author
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Galaz, José Luis
Author
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Puentes, Natalia
Author
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Silva, Mónica
Author
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Jaimovich Pérez, Enrique
Author
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Carrasco, M. Angélica
Admission date
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2019-03-11T12:54:06Z
Available date
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2019-03-11T12:54:06Z
Publication date
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2007
Cita de ítem
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American Journal of Physiology - Cell Physiology, Volumen 292, Issue 5, 2018,
Identifier
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03636143
Identifier
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15221563
Identifier
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10.1152/ajpcell.00320.2006
Identifier
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https://repositorio.uchile.cl/handle/2250/164336
Abstract
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Depolarization of skeletal muscle cells by either high external K + or repetitive extracellular field potential pulses induces calcium release from internal stores. The two components of this release are mediated by either ryanodine receptors or inositol 1,4,5-trisphosphate (IP3) receptors and show differences in kinetics, amplitude, and subcellular localization. We have reported that the transcriptional regulators including ERKs, cAMP/Ca2+-response element binding protein, c-fos, c-jun, and egr-1 are activated by K+-induced depolarization and that their activation requires IP3-dependent calcium release. We presently describe the activation of the nuclear transcription factor NF-κB in response to depolarization by either high K+ (chronic) or electrical pulses (fluctuating). Calcium transients of relative short duration activate an NF-κB reporter gene to an intermediate level, whereas long-lasting calcium increases obtained by prolonged electrical stimulation protocols of various freque