Chapter title |
Cholesterol and PIP2 Modulation of BKCa Channels.
|
---|---|
Chapter number | 8 |
Book title |
Cholesterol and PI(4,5)P2 in Vital Biological Functions
|
Published in |
Advances in experimental medicine and biology, January 2023
|
DOI | 10.1007/978-3-031-21547-6_8 |
Pubmed ID | |
Book ISBNs |
978-3-03-121546-9, 978-3-03-121547-6
|
Authors |
Vaithianathan, Thirumalini, Schneider, Elizabeth H, Bukiya, Anna N, Dopico, Alex M, Schneider, Elizabeth H., Bukiya, Anna N., Dopico, Alex M. |
Abstract |
Ca2+/voltage-gated, large conductance K+ channels (BKCa) are formed by homotetrameric association of α (slo1) subunits. Their activity, however, is suited to tissue-specific physiology largely due to their association with regulatory subunits (β and γ types), chaperone proteins, localized signaling, and the channel's lipid microenvironment. PIP2 and cholesterol can modulate BKCa activity independently of downstream signaling, yet activating Ca2+i levels and regulatory subunits control ligand action. At physiological Ca2+i and voltages, cholesterol and PIP2 reduce and increase slo1 channel activity, respectively. Moreover, slo1 proteins provide sites that seem to recognize cholesterol and PIP2: seven CRAC motifs in the slo1 cytosolic tail and a string of positively charged residues (Arg329, Lys330, Lys331) immediately after S6, respectively. A model that could explain the modulation of BKCa activity by cholesterol and/or PIP2 is hypothesized. The roles of additional sites, whether in slo1 or BKCa regulatory subunits, for PIP2 and/or cholesterol to modulate BKCa function are also discussed. |
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