Key result
Structural analysis of the KefC-CTD/KefF complex reveals that KefF modulates the conformational flexibility of the KTN dimer hinge, stabilizing an open conformation essential for regulating ion flux.
The structural and functional analysis of the KefC-CTD/KefF complex demonstrates that KTN (RCK) domains regulate K+ flux by controlling the dimer-hinge conformation.
Preclinical bacterial findings offer no clinical guidance; extends KTN hinge models but leaves mammalian translation open.
KTN (RCK) domains are nucleotide-binding folds that form the cytoplasmic regulatory complexes of various K+ channels and transporters. The mechanisms these proteins use to control their transmembrane pore-forming counterparts remains unclear despite numerous electrophysiological and structural studies. KTN (RCK) domains consistently crystallize as dimers within the asymmetric unit, forming a pronounced hinge between two Rossmann folds. We have previously proposed that modification of the hinge angle plays an important role in activating the associated membrane-integrated components of the channel or transporter. Here we report the structure of the C-terminal, KTN-bearing domain of the E. coli KefC K+ efflux system in association with the ancillary subunit, KefF, which is known to stabilize the conductive state. The structure of the complex and functional analysis of KefC variants reveal that control of the conformational flexibility inherent in the KTN dimer hinge is modulated by KefF and essential for regulation of KefC ion flux.
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Roosild et al. (2009) studied this question. Structural analysis of the KefC-CTD/KefF complex reveals that KefF modulates the conformational flexibility of the KTN dimer hinge, stabilizing an open conformation essential for regulating ion flux.
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