Tescalcin (TESC, also known as calcineurin-homologous protein 3, CHP3) is a 24-kDa EF-hand Ca2+-binding protein that has recently emerged as a regulator of cell differentiation and growth. The TESC gene has also been linked to human brain abnormalities, and high expression of tescalcin has been found in several cancers. The expression level of tescalcin changes dramatically during development and upon signal-induced cell differentiation. Recent studies have shown that tescalcin is not only subjected to up- or down-regulation, but also has an active role in pathways that drive cell growth and differentiation programs. At the molecular level, there is compelling experimental evidence showing that tescalcin can directly interact with and regulate the activities of the Na+/H+ exchanger NHE1, subunit 4 of the COP9 signalosome (CSN4) and protein kinase glycogen-synthase kinase 3 (GSK3). In hematopoetic precursor cells, tescalcin has been shown to couple activation of the extracellular signal-regulated kinase (ERK) cascade to the expression of transcription factors that control cell differentiation. The purpose of this Commentary is to summarize recent efforts that have served to characterize the biochemical, genetic and physiological attributes of tescalcin, and its unique role in the regulation of various cellular functions.
Incorrect language was used in the Commentary that concerns the apparent controversy between the results of tescalcin knockdown in hematopoietic precursor cell lines and its gene knockout in mice reported by Ukarapong et al. (2012). In the Commentary, the wording is as follows: "To explain the conflicting data, the authors [Ukarapong et al.] speculate that CHP1 and/or CHP2 could compensate for the lack of tescalcin, or that their genetic knockout was incomplete and allowed for the expression of a partial protein (Ukarapong et al., 2012)". This gives the impression that Ukarapong et al. themselves argued about the incomplete knockout. The wording should read: "To explain the conflicting data, the authors [Ukarapong et al.] speculate that CHP1 and/or CHP2 could compensate for the lack of tescalcin (Ukarapong et al., 2012). Another possibility can be associated with the presence of a transcript corresponding to exons 1, 2, 7 and 8 of the TESC gene in the knockout mouse tissues detected by Ukarapong et al. Although unlikely, this finding leaves a formal possibility for this mRNA to be translated into a product with residual functional activity".
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