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Biochem Biophys Res Commun. 2015 Apr 24;460(1):114-21. doi: 10.1016/j.bbrc.2015.02.004.

Ca(2+) homeostasis and endoplasmic reticulum (ER) stress: An integrated view of calcium signaling.

Author information

1
NMR-based Structural Biology, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany. Electronic address: jkrebs@nmr.mpibpc.mpg.de.
2
School of Dietetics and Human Nutrition, McGill University, Ste. Anne de Bellevue, Quebec H9X 3V9, Canada. Electronic address: luis.agellon@mcgill.ca.
3
Department of Biochemistry, University of Alberta, Edmonton, Alberta T6G 2H7, Canada. Electronic address: marek.michalak@ualberta.ca.

Abstract

Cellular Ca(2+) homeostasis is maintained through the integrated and coordinated function of Ca(2+) transport molecules, Ca(2+) buffers and sensors. These molecules are associated with the plasma membrane and different cellular compartments, such as the cytoplasm, nucleus, mitochondria, and cellular reticular network, including the endoplasmic reticulum (ER) to control free and bound Ca(2+) levels in all parts of the cell. Loss of nutrients/energy leads to the loss of cellular homeostasis and disruption of Ca(2+) signaling in both the reticular network and cytoplasmic compartments. As an integral part of cellular physiology and pathology, this leads to activation of ER stress coping responses, such as the unfolded protein response (UPR), and mobilization of pathways to regain ER homeostasis.

KEYWORDS:

Ca(2+) homeostasis; Ca(2+)-binding proteins; Calcium transport; ER stress; Membrane contact sites; MicroRNAs; Unfolded protein response (UPR)

PMID:
25998740
DOI:
10.1016/j.bbrc.2015.02.004
[Indexed for MEDLINE]

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