| Literature DB >> 25944908 |
Jing Feng1, Weishan Yang1, Zili Xie1, Fang Xiang1, Zhijian Cao2, Wenxin Li2, Hongzhen Hu3, Zongyun Chen4, Yingliang Wu5.
Abstract
Among the three extracellular domains of the tetrameric voltage-gated K(+) (Kv) channels consisting of six membrane-spanning helical segments named S1-S6, the functional role of the S1-S2 linker still remains unclear because of the lack of a peptide ligand. In this study, the Kv1.3 channel S1-S2 linker was reported as a novel receptor site for human β-defensin 2 (hBD2). hBD2 shifts the conductance-voltage relationship curve of the human Kv1.3 channel in a positive direction by nearly 10.5 mV and increases the activation time constant for the channel. Unlike classical gating modifiers of toxin peptides from animal venoms, which generally bind to the Kv channel S3-S4 linker, hBD2 only targets residues in both the N and C termini of the S1-S2 linker to influence channel gating and inhibit channel currents. The increment and decrement of the basic residue number in a positively charged S4 sensor of Kv1.3 channel yields conductance-voltage relationship curves in the positive direction by ∼31.2 mV and 2-4 mV, which suggests that positively charged hBD2 is anchored in the channel S1-S2 linker and is modulating channel activation through electrostatic repulsion with an adjacent S4 helix. Together, these findings reveal a novel peptide ligand that binds with the Kv channel S1-S2 linker to modulate channel activation. These findings also highlight the functional importance of the Kv channel S1-S2 linker in ligand recognition and modification of channel activation.Entities:
Keywords: Kv channel, S1-S2 linker, human beta-defensin 2, electrostatic interaction, gating modifier; defensin; immunology; ligand-binding protein; toxin; voltage-dependent anion channel (VDAC)
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Year: 2015 PMID: 25944908 PMCID: PMC4505463 DOI: 10.1074/jbc.M115.639500
Source DB: PubMed Journal: J Biol Chem ISSN: 0021-9258 Impact factor: 5.157