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1 LC1A family members is a substrate-activated anion conductance.
2 agreement with the existence of an uncoupled anion conductance.
3 nly capable of mediating the substrate-gated anion conductance.
4  binding pocket during the activation of the anion conductance.
5 l polar and aliphatic residues essential for anion conductance.
6          These data reflect loss of the CFTR anion conductance.
7  rate of glutamate transport and an abnormal anion conductance.
8 r agonists to modulate the apical membrane's anion conductance.
9 rections without affecting activation of the anion conductance.
10 volume regulation through a volume-regulated anion conductance.
11 may involve activation of a volume-sensitive anion conductance.
12 ability of glutamate to further activate the anion conductance.
13  EAATs exhibit a sodium- and glutamate-gated anion conductance.
14 nsporters catalyzing substrate-gated or leak anion conductances.
15 We recorded the activities of three distinct anion conductances: (a) an inwardly rectifying anion cha
16          Interestingly, the amplitude of the anion conductance activated by the acidic amino acids do
17      Part of the current was generated by an anion conductance activated when uptake occurs.
18 including the kinetics of proton binding and anion conductance activation.
19 er, such as activation of the cation-induced anion conductance and creation of a substrate binding si
20  E111 and E113 may electrostatically control anion conductance and occupancy of the binding site with
21 ly slightly altered, and the relative cation/anion conductance and permeability ratios were unchanged
22 , as is well known, but it can also regulate anion conductance and selectivity of CFTR in native epit
23                 The model simulates both the anion conductance and the glutamate flux through the tra
24 he glutamate concentration dependence of the anion conductance and the kinetics of glutamate flux wer
25 DeltaF508/DeltaF508) airway epithelia lacked anion conductance, and they did not hyperabsorb Na(+).
26 rt the amplitudes of the substrate-activated anion conductances are not substantially affected indica
27  Most of these mutations lead to compromised anion conductance at the apical plasma membrane of secre
28 al cells, whereas stellate cells control the anion conductance, but by an as-yet-undefined route.
29                        The results show that anion conductance by ACRs has a fundamentally different
30                       Inhibition of the leak anion conductance by benzylserine requires the presence
31 aspartate was able to activate the uncoupled anion conductance by N451S, but with an almost 1000-fold
32  evidence for this co-binding state, and its anion conductance, by analyzing transient currents when
33 d that EAAT subtypes with particularly large anion conductances can directly influence the excitabili
34 otein and the appearance of a cAMP-activated anion conductance characteristic of CFTR function.
35                                     The leak anion conductance exhibits permeation properties that ar
36 ll numerous biological roles requiring gated anion conductance, from regulating skeletal muscle excit
37                          The glutamate-gated anion conductance in cones has a reversal potential of a
38 o the mechanism by which substrates gate the anion conductance in EAATs and suggest that in EAAT1, Ar
39 ontribute significantly to inward-rectifying anion conductance in mouse choroid plexus, which must th
40 d from decalcified cells revealed a dominant anion conductance in response to membrane hyperpolarizat
41 er, zinc reduced the current mediated by the anion conductance in the cone synaptic terminal glutamat
42 ransport, zinc potentiated activation of the anion conductance in the Muller cell glutamate transport
43                   Thus, the finding that the anion conductance is gated independently, rather than co
44 nsporters (EAATs), suggesting that this leak anion conductance is highly conserved within the EAAT pr
45                         At pH less than 5.5, anion conductance is rapidly and reversibly activated in
46 ubstrate uptake, but not substrate-activated anion conductance, is completely inhibited in these muta
47  not pTrial10, demonstrated a cAMP-dependent anion conductance, measured by fluorescence microscopy u
48 somes to identify a novel chloride-selective anion conductance mediated by OCA2 and required for mela
49       In addition, kainate blocked a resting anion conductance observed in the absence of glutamate.
50  that are similar to the substrate-activated anion conductance of ASCT2, preferring hydrophobic anion
51 We instead explored the role of the abnormal anion conductance of the EAAT1(P>R) mutation, and to do
52 a(++), but this effect resulted from reduced anion conductance, rather than from a direct effect on t
53 ddition, DeltaFRD elicited a cAMP-stimulated anion conductance response in primary human bronchial ep
54 not Rab11a, reduced by 50% the CFTR-mediated anion conductance response.
55                  Disruption of CFTR-mediated anion conductance results in defective fluid and electro
56       Glutamate transporters also display an anion conductance that is activated by the binding of Na
57 f glutamate, and they are associated with an anion conductance that is stoichiometrically uncoupled f
58  thermodynamically uncoupled substrate-gated anion conductance that may modulate cell excitability.
59    PepT1 did not display the substrate-gated anion conductances that have been found to be characteri
60            Our simulations show that without anion conductances the transmembrane movements of cation
61                                   Persistent anion conductances through GABA(A) receptors (GABA(A)Rs)
62                                     The leak anion conductance was increased by, but did not require
63                       We found that the leak anion conductance was inhibited by the binding of the ne
64  anhydrase was inhibited and transepithelial anion conductance was limited to HCO3- revealed a sharp
65                           A volume-sensitive anion conductance was observed when cell swelling was in
66 mbrane conductance regulator (Cftr)-mediated anion conductance was responsible.
67  The selectivity sequence of the SNAT2H-304A anion conductance was SCN->>NO3->I->Br->Cl->Mes-.
68                  The properties of this leak anion conductance were studied by electrophysiological r
69                             Volume-sensitive anion conductances were observed in both rat lacrimal gl
70  binding to the transporters induces a basal anion conductance, which is further activated by glutama
71        Interestingly, a Na(+)-dependent leak anion conductance with similar properties was previously
72 s the EC(50) for L-glutamate to activate the anion conductance, without affecting the EC(50) for the
73 to several seconds; (b) a quickly activating anion conductance (X-QUAC), important for anion efflux a
74 revailing anion; and (c) a slowly activating anion conductance (X-SLAC), activating above -100 mV.