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Biochim Biophys Acta Mol Cell Res. 2018 Nov;1865(11 Pt B):1660-1667. doi: 10.1016/j.bbamcr.2018.05.005. Epub 2018 May 8.

NCS-1 is a regulator of calcium signaling in health and disease.

Author information

1
Department of Pharmacology, Yale University, New Haven, CT, United States; Institut für Physiologie, Universität zu Lübeck, Ratzeburger Allee 160, D-23562 Lübeck, Germany.
2
Department of Pharmacology, Yale University, New Haven, CT, United States; Institut für Physiologie, Universität zu Lübeck, Ratzeburger Allee 160, D-23562 Lübeck, Germany. Electronic address: barbara.ehrlich@yale.edu.

Abstract

Neuronal Calcium Sensor-1 (NCS-1) is a highly conserved calcium binding protein which contributes to the maintenance of intracellular calcium homeostasis and regulation of calcium-dependent signaling pathways. It is involved in a variety of physiological cell functions, including exocytosis, regulation of calcium permeable channels, neuroplasticity and response to neuronal damage. Over the past 30 years, continuing investigation of cellular functions of NCS-1 and associated disease states have highlighted its function in the pathophysiology of several disorders and as a therapeutic target. Among the diseases that were found to be associated with NCS-1 are neurological disorders such as bipolar disease and non-neurological conditions such as breast cancer. Furthermore, alteration of NCS-1 expression is associated with substance abuse disorders and severe side effects of chemotherapeutic agents. The objective of this article is to summarize the current body of evidence describing NCS-1 and its interactions on a molecular and cellular scale, as well as describing macroscopic implications in physiology and medicine. Particular attention is paid to the role of NCS-1 in development and prevention of chemotherapy induced peripheral neuropathy (CIPN).

KEYWORDS:

CIPN; Calcium binding proteins; Calcium signaling; Cancer chemotherapy; Paclitaxel; Peripheral neuropathy

PMID:
29746899
PMCID:
PMC6224314
[Available on 2019-11-01]
DOI:
10.1016/j.bbamcr.2018.05.005
[Indexed for MEDLINE]

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