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1 agreement with the existence of an uncoupled anion conductance.
2 nly capable of mediating the substrate-gated anion conductance.
3 binding pocket during the activation of the anion conductance.
4 rate of glutamate transport and an abnormal anion conductance.
5 These data reflect loss of the CFTR anion conductance.
6 ability of glutamate to further activate the anion conductance.
7 r agonists to modulate the apical membrane's anion conductance.
8 rections without affecting activation of the anion conductance.
9 EAATs exhibit a sodium- and glutamate-gated anion conductance.
10 volume regulation through a volume-regulated anion conductance.
11 may involve activation of a volume-sensitive anion conductance.
12 LC1A family members is a substrate-activated anion conductance.
13 nsporters catalyzing substrate-gated or leak anion conductances.
14 We recorded the activities of three distinct anion conductances: (a) an inwardly rectifying anion cha
18 er, such as activation of the cation-induced anion conductance and creation of a substrate binding si
19 E111 and E113 may electrostatically control anion conductance and occupancy of the binding site with
20 ly slightly altered, and the relative cation/anion conductance and permeability ratios were unchanged
21 , as is well known, but it can also regulate anion conductance and selectivity of CFTR in native epit
23 he glutamate concentration dependence of the anion conductance and the kinetics of glutamate flux wer
24 DeltaF508/DeltaF508) airway epithelia lacked anion conductance, and they did not hyperabsorb Na(+).
25 rt the amplitudes of the substrate-activated anion conductances are not substantially affected indica
26 Most of these mutations lead to compromised anion conductance at the apical plasma membrane of secre
27 al cells, whereas stellate cells control the anion conductance, but by an as-yet-undefined route.
30 aspartate was able to activate the uncoupled anion conductance by N451S, but with an almost 1000-fold
31 d that EAAT subtypes with particularly large anion conductances can directly influence the excitabili
34 ll numerous biological roles requiring gated anion conductance, from regulating skeletal muscle excit
36 o the mechanism by which substrates gate the anion conductance in EAATs and suggest that in EAAT1, Ar
37 ontribute significantly to inward-rectifying anion conductance in mouse choroid plexus, which must th
38 d from decalcified cells revealed a dominant anion conductance in response to membrane hyperpolarizat
39 er, zinc reduced the current mediated by the anion conductance in the cone synaptic terminal glutamat
40 ransport, zinc potentiated activation of the anion conductance in the Muller cell glutamate transport
42 nsporters (EAATs), suggesting that this leak anion conductance is highly conserved within the EAAT pr
44 ubstrate uptake, but not substrate-activated anion conductance, is completely inhibited in these muta
45 not pTrial10, demonstrated a cAMP-dependent anion conductance, measured by fluorescence microscopy u
46 somes to identify a novel chloride-selective anion conductance mediated by OCA2 and required for mela
48 that are similar to the substrate-activated anion conductance of ASCT2, preferring hydrophobic anion
49 We instead explored the role of the abnormal anion conductance of the EAAT1(P>R) mutation, and to do
50 a(++), but this effect resulted from reduced anion conductance, rather than from a direct effect on t
51 ddition, DeltaFRD elicited a cAMP-stimulated anion conductance response in primary human bronchial ep
55 f glutamate, and they are associated with an anion conductance that is stoichiometrically uncoupled f
56 thermodynamically uncoupled substrate-gated anion conductance that may modulate cell excitability.
57 thermodynamically uncoupled substrate-gated anion conductance that may modulate cell excitability.
58 PepT1 did not display the substrate-gated anion conductances that have been found to be characteri
61 anhydrase was inhibited and transepithelial anion conductance was limited to HCO3- revealed a sharp
67 binding to the transporters induces a basal anion conductance, which is further activated by glutama
69 s the EC(50) for L-glutamate to activate the anion conductance, without affecting the EC(50) for the
70 to several seconds; (b) a quickly activating anion conductance (X-QUAC), important for anion efflux a
71 revailing anion; and (c) a slowly activating anion conductance (X-SLAC), activating above -100 mV.
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