2022  1,200
2021  1,540
2020  1,374
2019  1,023
2018  0,932
2017  0,977
2016  0,799
2015  0,662
2014  0,740
2013  0,739
2012  0,637
2011  0,658
2010  0,654
2009  0,570
2008  0,849
2007  0,805
2006  0,330
2005  0,435
2004  0,623
2003  0,567
2002  0,641
2001  0,490
2000  0,477
1999  0,762
1998  0,785
1997  0,507
1996  0,518
1995  0,502
Vol 57(2023) N 6 p. 1097-1124; DOI 10.1134/S002689332306002X Full Text

V.E. Baksheeva1, A.A. Zamyatnin, Jr.1,2,3,4, E.Yu. Zernii1*

Neuronal Calcium Sensor-1: A Zinc/Redox-Dependent Protein of Nervous System Signaling Pathways

1Belozersky Institute of Physicochemical Biology, Moscow State University, Moscow, 119992 Russia
2Faculty of Bioengineering and Bioinformatics, Moscow State University, Moscow, 119992 Russia
3Research Center for Translation Medicine, Sirius University of Science and Technology, Sirius, Krasnodar krai, 354340 Russia
4Institute of Molecular Medicine, Sechenov First Moscow State Medical University, Moscow, 119991 Russia

Received - 2023-04-17; Revised - 2023-06-08; Accepted - 2023-06-21

Intracellular calcium signaling is involved in regulating the key functional mechanisms of the nervous system. The control of neuronal excitability and plasticity by calcium ions underlies the mechanisms of higher nervous activity, and the mechanisms of this control are of particular interest to researchers. A family of highly specialized neuronal proteins described in recent decades can translate the information contained in calcium signals into the regulation of channels, enzymes, receptors, and transcription factors. Neuronal calcium sensor-1 (NCS-1) is the most common member of the family, which is intensely expressed in central nervous system (CNS) cells; and controls several vital processes, such as neuronal growth and survival, reception, neurotransmission, and synaptic plasticity. In addition to calcium ions, NCS-1 can bind the so-called mobile, or signaling intracellular zinc, an increased concentration of which is a characteristic feature of cells in oxidative stress. Zinc coordination under these conditions stimulates NCS-1 oxidation to form a disulfide dimer (dNCS-1) with altered functional properties. A combined effect of mobile zinc and an increased redox potential of the medium can thus induce aberrant NCS-1 activity, including signals that promote survival of neuronal cells or induce their apoptosis and, consequently, the development of neurodegenerative processes. The review details the localization, expression regulation, structure, and molecular properties of NCS-1 and considers the current data on its signaling activity in health and disease, including zinc-dependent redox regulation cascades.

neurons, calcium signals, neuronal calcium sensors, neuronal calcium sensor-1, zinc, oxidative stress, redox regulation, neurodegenerative disorders