The LRRC26 auxiliary subunit fundamentally alters how BK potassium channels respond to voltage changes, enabling activation at resting membrane potentials rather than requiring depolarization. This regulatory protein modifies both the channel's intrinsic gating properties and the coupling between voltage sensors and pore opening, effectively rewiring the channel's electrical sensitivity. This mechanistic insight illuminates how secretory cells maintain potassium flux essential for hormone release and other secretory functions. BK channels are critical regulators of cellular excitability, influencing everything from smooth muscle contraction to neurotransmitter release. The discovery that LRRC26 can shift these channels' voltage dependence represents a significant advance in understanding ion channel regulation. For longevity research, this finding could inform therapeutic strategies targeting age-related dysfunction in secretory tissues, including pancreatic beta cells and adrenal glands. The work also suggests potential mechanisms underlying variability in cellular responses to electrical stimuli across different tissue types and aging states.
LRRC26 Subunit Rewires BK Channel Voltage Response Mechanisms
📄 Based on research published in PNAS
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