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Cytosolic N-terminal segments of many K+ channel subunits mediate rapid blockade of ion permeation by physical occlusion of the ion-conducting pore. For some channels with large cytosolic structures, access to the channel pore by inactivation domains may occur through lateral entry pathways or "side portals" that separate the pore domain and associated cytosolic structures covering the axis of the permeation pathway. However, the extent to which side portals control access of molecules to the channel or influence channel gating is unknown. Here we use removal of inactivation by trypsin as a tool to examine basic residue accessibility in both the N terminus of the native auxiliary beta2 subunit of Ca2+-activated, BK-type K+ channels and beta2 subunits with artificial inactivating N termini. The results show that, for BK channels, side portals define a protected space that precedes the channel permeation pathway and excludes small proteins such as trypsin but allows inactivation domains to enter. When channels are closed, inactivation domains readily pass through side portals, with a central antechamber preceding the permeation pathway occupied by an inactivation domain approximately half of the time under resting conditions. The restricted volume of the pathway through side portals is likely to influence kinetic properties of inactivation mechanisms, blockade by large pharmacological probes, and accessibility of modulatory factors to surfaces of the channel within the protected space.
Bentrop,
NMR structure of the "ball-and-chain" domain of KCNMB2, the beta 2-subunit of large conductance Ca2+- and voltage-activated potassium channels.
2001, Pubmed,
Xenbase
Bentrop,
NMR structure of the "ball-and-chain" domain of KCNMB2, the beta 2-subunit of large conductance Ca2+- and voltage-activated potassium channels.
2001,
Pubmed
,
Xenbase
Benzinger,
Direct observation of a preinactivated, open state in BK channels with beta2 subunits.
2006,
Pubmed
,
Xenbase
Butler,
mSlo, a complex mouse gene encoding "maxi" calcium-activated potassium channels.
1993,
Pubmed
,
Xenbase
Ding,
Steady-state and closed-state inactivation properties of inactivating BK channels.
2002,
Pubmed
,
Xenbase
Ding,
Inactivating BK channels in rat chromaffin cells may arise from heteromultimeric assembly of distinct inactivation-competent and noninactivating subunits.
1998,
Pubmed
Gulbis,
Structure of the cytoplasmic beta subunit-T1 assembly of voltage-dependent K+ channels.
2000,
Pubmed
,
Xenbase
Hamill,
Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches.
1981,
Pubmed
Horrigan,
Coupling between voltage sensor activation, Ca2+ binding and channel opening in large conductance (BK) potassium channels.
2002,
Pubmed
,
Xenbase
Hoshi,
Biophysical and molecular mechanisms of Shaker potassium channel inactivation.
1990,
Pubmed
,
Xenbase
Jiang,
The open pore conformation of potassium channels.
2002,
Pubmed
Jiang,
Crystal structure and mechanism of a calcium-gated potassium channel.
2002,
Pubmed
Knaus,
Primary sequence and immunological characterization of beta-subunit of high conductance Ca(2+)-activated K+ channel from smooth muscle.
1994,
Pubmed
Kobertz,
Hanging gondola structure of the T1 domain in a voltage-gated K(+) channel.
2000,
Pubmed
,
Xenbase
Long,
Crystal structure of a mammalian voltage-dependent Shaker family K+ channel.
2005,
Pubmed
Masino,
Solution structure of polyglutamine tracts in GST-polyglutamine fusion proteins.
2002,
Pubmed
Orio,
New disguises for an old channel: MaxiK channel beta-subunits.
2002,
Pubmed
Rasmusson,
The beta subunit, Kv beta 1.2, acts as a rapid open channel blocker of NH2-terminal deleted Kv1.4 alpha-subunits.
1997,
Pubmed
Rettig,
Inactivation properties of voltage-gated K+ channels altered by presence of beta-subunit.
1994,
Pubmed
,
Xenbase
Ruppersberg,
Cloned neuronal IK(A) channels reopen during recovery from inactivation.
1991,
Pubmed
Sokolova,
Three-dimensional structure of a voltage-gated potassium channel at 2.5 nm resolution.
2001,
Pubmed
Solaro,
Trypsin-sensitive, rapid inactivation of a calcium-activated potassium channel.
1992,
Pubmed
Song,
Kunitz-type soybean trypsin inhibitor revisited: refined structure of its complex with porcine trypsin reveals an insight into the interaction between a homologous inhibitor from Erythrina caffra and tissue-type plasminogen activator.
1998,
Pubmed
Wallner,
Molecular basis of fast inactivation in voltage and Ca2+-activated K+ channels: a transmembrane beta-subunit homolog.
1999,
Pubmed
,
Xenbase
Wang,
Consequences of the stoichiometry of Slo1 alpha and auxiliary beta subunits on functional properties of large-conductance Ca2+-activated K+ channels.
2002,
Pubmed
,
Xenbase
Xia,
Ligand-dependent activation of Slo family channels is defined by interchangeable cytosolic domains.
2004,
Pubmed
,
Xenbase
Xia,
Rectification and rapid activation at low Ca2+ of Ca2+-activated, voltage-dependent BK currents: consequences of rapid inactivation by a novel beta subunit.
2000,
Pubmed
,
Xenbase
Xia,
Multiple regulatory sites in large-conductance calcium-activated potassium channels.
2002,
Pubmed
Xia,
Inactivation of BK channels by the NH2 terminus of the beta2 auxiliary subunit: an essential role of a terminal peptide segment of three hydrophobic residues.
2003,
Pubmed
,
Xenbase
Xia,
Molecular basis for the inactivation of Ca2+- and voltage-dependent BK channels in adrenal chromaffin cells and rat insulinoma tumor cells.
1999,
Pubmed
,
Xenbase
Zhang,
Allosteric regulation of BK channel gating by Ca(2+) and Mg(2+) through a nonselective, low affinity divalent cation site.
2001,
Pubmed
,
Xenbase
Zhou,
Potassium channel receptor site for the inactivation gate and quaternary amine inhibitors.
2001,
Pubmed
,
Xenbase
