RCAN (Regulator of Calcineurin): Beyond ‘Down Syndrome Critical Region (DSCR)’
Sun-Kyung Lee 1,2,* and Joohong Ahnn 1,2, *
1Department of Life Science, 2Research Institute for Natural Sciences, College of Natural Sciences, Hanyang University, Seoul 04763, Korea
Received March 6, 2020; Revised May 23, 2020; Accepted May 25, 2020.; Published online June 24, 2020.
© Korean Society for Molecular and Cellular Biology. All rights reserved.

ABSTRACT
The regulator of calcineurin (RCAN) was first reported as a novel gene called DSCR1, encoded in a region termed the Down syndrome critical region (DSCR) of human chromosome 21. Genome sequence comparisons across species using bioinformatics revealed three members of the RCAN gene family, RCAN1, RCAN2, and RCAN3, present in most jawed vertebrates, with one member observed in most invertebrates and fungi. RCAN is most highly expressed in brain and striated muscles, but expression has been reported in many other tissues, as well, including the heart and kidneys. Expression levels of RCAN homologs are responsive to external stressors such as reactive oxygen species, Ca2+, amyloid β and hormonal changes and upregulated in pathological conditions, including Alzheimer’s disease, cardiac hypertrophy, diabetes, and degenerative neuropathy. RCAN binding to calcineurin, a Ca2+/calmodulin-dependent phosphatase, inhibits calcineurin activity, thereby regulating different physiological events via dephosphorylation of important substrates. Novel functions of RCANs have recently emerged, indicating involvement in mitochondria homeostasis, RNA binding, circadian rhythms, obesity, and thermogenesis, some of which are calcineurin-independent. These developments suggest that besides significant contributions to DS pathologies and calcineurin regulation, RCAN is an important participant across physiological systems, suggesting it as a favorable therapeutic target.
Keywords: calcineurin, Down syndrome, RCAN1, RCAN2, RCAN3


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31 July 2020 Volume 43,
Number 7, pp. 591~670

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