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PMCA3: A Mysterious Isoform of Calcium Pump

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Regulation of Ca2+-ATPases,V-ATPases and F-ATPases

Part of the book series: Advances in Biochemistry in Health and Disease ((ABHD,volume 14))

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Abstract

Calcium ion as a powerful, universal extracellular and intracellular carrier of information involves precise controlling system to convey proper signals to the cells. The most sensitive for changes in cytosolic Ca2+ concentration is a family of plasma membrane calcium (PMCA) pump encoded by four independent genes (PMCA1–4). Differences in tissue-specific expression of the isoforms and splicing variants in excitable and non-excitable cells are considered to reflect a unique profile of calcium signaling in particular cells. Among PMCA isoforms, PMCA3 appears to be the least known, although it was cloned in 1989. Using different techniques, its developmental and cell- and tissue-dependent expression has been reported in a number of studies; nonetheless, our knowledge about PMCA3 role in the cells is still scarce. Low expression and restricted localization may indicate less important role of PMCA3 in comparison with other isoforms. However, its high Ca2+ and calmodulin affinity, low sensitivity to calpain degradation, and resistance to the stress conditions could offer some unique function. The present article focuses on the PMCA3 characteristics, especially in the light of new findings suggesting that this isoform could be critical for the maintenance of cytosolic Ca2+ concentration acting as a second line of defense against calcium overload.

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Acknowledgments

This work was supported by the Medical University of Lodz grant nos. 503/6-086-02/503-01 and 502-03/6-086-02/502-64-061 and, in part, by National Science Centre grant (to T. Boczek) based on decision UMO-2012/05/D/NZ4/02982.

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Correspondence to Ludmila Zylinska .

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Boczek, T., Zylinska, L. (2016). PMCA3: A Mysterious Isoform of Calcium Pump. In: Chakraborti, S., Dhalla, N. (eds) Regulation of Ca2+-ATPases,V-ATPases and F-ATPases. Advances in Biochemistry in Health and Disease, vol 14. Springer, Cham. https://doi.org/10.1007/978-3-319-24780-9_4

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