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1 ations, reduced K(+) affinity, and increased ion permeation.
2 and points to a role of the internal pore in ion permeation.
3 ergetics and electrostatics control membrane ion permeation.
4 of ligand-gating, allosteric modulation and ion permeation.
5 whether a mutation alters the energetics of ion permeation.
6 e charge and solvent philicity could enhance ion permeation.
7 ossibly be a temporary reservoir involved in ion permeation.
8 in channel gating in addition to its role in ion permeation.
9 states, consistent with its explicit role in ion permeation.
10 also be generated in more detailed models of ion permeation.
11 e central hydrated cavity, a crucial step in ion permeation.
12 e molecular mechanisms of channel gating and ion permeation.
13 the microscopic details of the mechanism of ion permeation.
14 uggesting that these residues have a role in ion permeation.
15 imer assembly, in addition to any effects on ion permeation.
16 pore loop are crucial for pore structure and ion permeation.
17 and pose intriguing mechanistic questions of ion permeation.
18 egatively charged residues in the process of ion permeation.
19 osolic G loop) may serve as gates to control ion permeation.
20 isms of channel gating, desensitization, and ion permeation.
21 esize that membrane interactions also affect ion permeation.
22 onductance; thus, the TARP C-tail influences ion permeation.
23 -helices is a key determinant of the rate of ion permeation.
24 a single gate into a position that occludes ion permeation.
25 y filter are critical for pain behaviour and ion permeation.
26 inhibited CRAC channel activity by blocking ion permeation.
27 ty to modulate RyR1 gating without affecting ion permeation.
28 es) into a position that physically occludes ion permeation.
29 an important role in channel activation and ion permeation.
30 h stabilizes a hydrated K(+) and facilitates ion permeation.
31 id interface and allosterically modulate the ion permeation.
32 hydrophobic gating mechanism for control of ion permeation.
33 nnels vary significantly among their rate of ion permeation.
34 ntribution of individual charged residues to ion permeation.
35 arallels to membranes deformed by unassisted ion permeation.
36 scanning to map the paracellular pathway of ion permeation across claudin-2-transfected Madin-Darby
37 c acid, significantly decreased paracellular ion permeation across I66C-transfected cells by a mechan
40 rchitecture explains the crucial features of ion permeation and blockade, and gives some strong hints
42 sidue determines single-channel conductance, ion permeation and channel block in the NMDA receptor, t
46 ning ligand recognition, heteromer assembly, ion permeation and desensitization in this prototypical
47 membrane channels both for basic studies of ion permeation and for applications in biotechnology.
48 e fundamental implications for understanding ion permeation and gating in P2X receptor channels, as w
50 ntributed profoundly to our understanding of ion permeation and gating, it remains unclear how much t
52 uch a wide inner pore may greatly facilitate ion permeation and high-affinity binding of multiple por
54 these results and describe the energetics of ion permeation and ionic fluxes, continuum approaches (P
61 els that underlie ligand binding, gating, or ion permeation, and have thus served as invaluable tools
62 ior (gating kinetics, modal transitions, and ion permeation) are interrelated and are modulated by th
63 that quantitatively relates the spontaneous ion permeation at equilibrium to the stationary ionic fl
66 ing medium is incorporated into the model of ion permeation by including the free energy of inserting
68 + channel subunits mediate rapid blockade of ion permeation by physical occlusion of the ion-conducti
69 Q747A) predicted to increase the size of its ion permeation cavity enhanced the sensor response and a
70 87 A resolution as a basis for understanding ion permeation, channel activation, the location of volt
71 (+) dynamics reveals a knock-on mechanism of ion permeation characterized by alternating occupancy of
74 eration and migration through both canonical ion permeation-dependent and noncanonical ion permeation
75 rporating intra- and extracellular geometry, ion permeation, diffusion, extrusion, and buffering sugg
77 te makes it feasible to simulate entire K(+) ion permeation events driven by a voltage bias and, ther
79 t the GYG motif is a critical determinant of ion permeation for HCN channels, and that HCN1 and HCN2
80 the potential of mean force (PMF) governing ion permeation from molecular dynamics simulations (MD)
81 ate dependence, suggesting the absence of an ion permeation gate at the cytosolic side of BK channel.
84 ew framework for understanding mechanisms of ion permeation, gating and channelopathy of cyclic-nucle
87 Understanding the mechanisms of gating and ion permeation in biological channels and receptors has
89 ism to lower the free energy barrier for the ion permeation in disagreement with predictions from the
91 y simulation studies on the understanding of ion permeation in selective and nonselective ion channel
92 lations capture the essential nature of K(+) ion permeation in the KcsA channel and provide a proof-o
93 and CRAC the general property of monovalent ion permeation in the nominal absence of extracellular d
94 o study and compare monovalent (Na(+), K(+)) ion permeation in the open-activated TRP vanniloid-1 (TR
96 rts of the subunits involved in ATP binding, ion permeation (including calcium permeability), and mem
99 eory indicated that the major barrier to Cl- ion permeation is at the intracellular side of the membr
104 nt implications for our understanding of how ion permeation may be controlled in similar ion channels
108 work, we employed a simulation strategy for ion permeation (molecular-dynamics simulations with bias
109 d the location of two binding sites for K(+) ion permeation near the channel entrance--i.e., an inner
110 important implications for understanding how ion permeation occurs, and further how it may be control
111 opening of Slo2.1 or Slo2.2, suggesting that ion permeation of Slo2 channels is not predominantly gat
115 late about their mechanistic consequences on ion permeation, pathological mutations, as well as funct
116 nner pore-forming domain, which contains the ion permeation pathway and elements of its gates, togeth
118 l is thought to decay nonlinearly across the ion permeation pathway because of the irregular three-di
119 ivation particle, which is stabilized in the ion permeation pathway by the N(153)VHNL(157) residues.
120 s (VSDs), one from each subunit, control one ion permeation pathway formed by four pore domains.
121 ve recently been shown to define part of the ion permeation pathway in several closely related member
123 ure of the C1C2 chimera demonstrate that the ion permeation pathway includes residues on one face of
125 cation of these mutations indicates that the ion permeation pathway lies between the core and gate ri
127 microscopy structure of chicken Slo2.2, the ion permeation pathway of the channel is closed by a con
129 oscopy structure of Slo2.2 suggests that the ion permeation pathway of these channels is closed by a
130 t 1 (TM1) is involved in forming part of the ion permeation pathway, and a missense mutation S427L in
131 potassium channels, a main component of the ion permeation pathway, configures a stack of binding si
132 ng an amino-acid residue thought to line the ion permeation pathway, identifying a region that govern
145 rdly rectifying K (Kir) channels control the ion-permeation pathway through diverse interactions with
147 its outward configuration with two potential ion permeation pathways exposed to the extracellular env
148 n the absence of PIP(2) show the cytoplasmic ion-permeation pathways occluded by four cytoplasmic loo
149 c-nucleotide binding site on these channels, ion permeation, pharmacological blockers, channel gating
152 e mechanisms of receptor desensitization and ion permeation, principles of antagonism, and complete s
153 ctric (continuum lipid), we found reasonable ion permeation profiles; cations bind and permeate, wher
155 eras between mPiezo1 and dPiezo to show that ion-permeation properties are conferred by C-terminal re
156 res as the dominant mechanism of uncatalyzed ion permeation, providing new understanding for the acti
158 actors give rise to energetic constraints on ion permeation that have important functional consequenc
162 ading to the opening of a gate that controls ion permeation through an integral transmembrane pore.
163 channels achieve highly selective and rapid ion permeation through an open pore, by restricting the
164 he context of electrostatics calculations of ion permeation through channels, and the effect of the l
166 arizes the postsynaptic afferent by altering ion permeation through hyperpolarization-activated cycli
167 olarized the postsynaptic neuron by altering ion permeation through hyperpolarization-activated cycli
170 racterized scorpion toxin Agitoxin2 inhibits ion permeation through Shaker K+ channels by binding to
171 and compared to refine our understanding of ion permeation through the channel formed by OmpF porin
172 However, the structural determinants of Cl- ion permeation through the channel pore are not known.
173 sed to compute current-voltage relations for ion permeation through the gramicidin A ion channel embe
175 aluminal loop contribute to determination of ion permeation through the intracellular Ca(2+) release
177 lished and molecular dynamics simulations of ion permeation through these channels are consistent wit
179 M2 "pore", Brownian dynamics simulations of ion permeation through this putative conducting open sta
182 els in the absence of ATP, or 2) coupling of ion permeation to gating, for which there is currently n
183 lored the mechanisms of uncatalyzed membrane ion permeation using atomistic simulations and electroph
184 th negatively charged amino acids facing the ion permeation vestibule of the channel in question.
186 the pore-lining helix in channel gating and ion permeation was probed by replacing them with amino a
187 olding, hydrogen bonding, ion solvation, and ion permeation, we replaced the peptide bond between Val
188 the peptide backbone and Trp side chains for ion permeation, we undertook an investigation of the two
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