Publication: Redox dependence of
endoplasmic reticulum (ER) Ca2+ signaling
Authors
Raturi, Arun ; Ortiz-Sandoval, Carolina ; Simmen, Thomas
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Publisher
F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The endoplasmic reticulum (ER) is a
multifunctional organelle that accommodates a large
array of functions. Recent publications have shown that
many of these functions are influenced by the ongoing
oxidative folding of secretory and membrane proteins.
Conversely, successful ER protein folding critically
depends on the cellular redox state, but also the
availability of Ca2+. These findings suggest the existence
of regulatory mechanisms that steer ER Ca2+
homeostasis according to the cellular redox state.
Indeed, accumulating evidence demonstrates that ER
Ca2+ uptake and release by sarco-endoplasmic reticulum
Ca2+ transport ATPases (SERCAs), stromal interaction
molecule 1 (STIM1), Orai1, inositol 1,4,5-trisphosphate
(IP3) receptors (IP3Rs) and ryanodine receptors (RyR)
depends on redox modifications of these channels and
pumps. In addition, ER chaperones and oxidoreductases
moonlight as regulators of ER Ca2+ channels and pumps.
Discrete redox conditions of channels, pumps and
oxidoreductases exist that allow for opening and closing.
Through these functions, redox regulation of ER Ca2+
influences signaling mechanisms governing cell growth
and migration, apoptosis and mitochondrial energy
production. Therefore, pharmacological intervention
based on ER redox or on ER redox-sensitive chaperones
and oxidoreductases is a promising strategy to influence
all metabolic syndromes including cancer and
neurodegeneration.
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Citation
Histology and Histopathology, vol. 29, nº 5, (2014)
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