https://orcid.org/0000-0002-1643-5805
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ABSTRACT
The mitochondrial BKCa channel (mitoBKCa) is a splice variant of plasma membrane BKCa (Maxi-K, BKCa, Slo1, KCa1.1). While a high-resolution structure of mitoBKCa is not available yet, functional and structural studies of the plasma membrane BKCa have provided important clues on the gating of the channel by voltage and Ca2+, as well as the interaction with auxiliary subunits. To date, we know that the control of expression of mitoBKCa, targeting and voltage-sensitivity strongly depends on its association with its regulatory β1-subunit, which overall participate in the control of mitochondrial Ca2+-overload in cardiac myocytes. Moreover, novel regulatory mechanisms of mitoBKCa such as β-subunits and amyloid-β have recently been proposed. However, major basic questions including how the regulatory BKCa-β1-subunit reaches mitochondria and the mechanism through which amyloid-β impairs mitoBKCa channel function remain to be addressed.
Acknowledgments
The authors thank the enormous support of Professor Riccardo Olcese, PhD, for all the important contributions to this paper. This work was supported by the doctoral fellowship from Fundação para a Ciência e a Tecnologia (FCT; SFRH/BD/146484/2019) (CSC), the CONACyT postdoctoral fellowship EPE-2016291121 and EPE-2017291231 (ALGC), and by UC MEXUS-CONACyT Postdoctoral Fellowship FE-13-248 (EB) and AHA-WSA 15POST22490015 (EB).
Disclosure statement
No potential conflict of interest was reported by the authors.