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1 to the human colonic T84 epithelial cell Na-K-Cl cotransporter.
2 that it would be distantly related to the Na-K-Cl cotransporter.
3 nd increased gene expression of NKCC1--a Na+-K+-Cl- cotransporter.
4 o examine the effect on O2 dependency of the K+-Cl- cotransporter.
5 rter, and NKCC, the chloride accumulator Na+-K+-Cl- cotransporter.
6 ial homology to KCC2, the mammalian neuronal K(+)-Cl(-) cotransporter.
7 of spinal CSF-cNs (18.3%) express the Na(+)-K(+)-Cl(-) cotransporter 1 (NKCC1) allowing intracellula
8 been suggested that the electroneutral Na(+)-K(+)-Cl(-) cotransporter 1 (NKCC1) can play a role in gl
11 exhibited sustained expression of the Na(+)-K(+)-Cl(-) cotransporter 1 (NKCC1), whereas inhibitory n
12 is accompanied by down-regulation of the Na-K-Cl cotransporter 1 (Nkcc1) and the Ca(2+)-activated an
13 T(1A) receptor (encoded by Agtr1a) and Na(+)-K(+)-Cl(-) cotransporter-1 (NKCC1, encoded by Slc12a2) i
14 t colonic basolateral membrane suggests that K-Cl cotransporter: 1) is involved in transepithelial po
16 However, we did not find expression of the K(+)-Cl(-) cotransporter 2 (KCC2) responsible for Cl(-)
19 TAL, cisplatin-treated rats had higher Na(+)-K(+)-Cl(-) cotransporter 2 (NKCC2) abundance but lower p
20 pagliflozin reversed cisplatin-induced Na(+)-K(+)-Cl(-) cotransporter 2 inhibition and claudin-16 dow
21 (sodium-chloride symporter) and NKCC2 (Na(+)-K(+)-Cl(-) cotransporter 2) activation at residues Thr53
23 bundance and function of the neuron-specific K(+)/Cl(-) cotransporter 2 (KCC2), which maintains chlor
26 evidence indicates that the neuron-specific K-Cl cotransporter 2 (KCC2) is the major chloride extrus
27 and GABA(A) receptor alpha1 subunit, but not K-Cl cotransporter 2, are colocalized at the presumed po
29 a(+)-K(+)-2Cl(-) cotransporter-1 (NKCC1) and K(+)-Cl(-) cotransporter-2 (KCC2), critically influence
30 n the absence of water transport through the K(+)-Cl(-) cotransporter, a large osmotic gradient build
31 d with a monoclonal antibody to mammalian Na-K-Cl cotransporter and a fluorescent secondary antibody
32 mportant new insights into the regulation of K-Cl cotransporters and provides in vivo evidence that i
33 +)/Pi co-transporter 2, phosphorylated Na(+)/K(+)/Cl(-) cotransporter, and phosphorylated Na(+)/Cl(-)
34 sion patterns of KCC2, the chloride extruder K+-Cl- cotransporter, and NKCC, the chloride accumulator
35 P (sickle), Ca 2+ -sensitive K channel, and K:Cl cotransporter, and of therapies targeted at these t
36 in using bumetanide, a chloride importer Na-K-Cl cotransporter antagonist, for treatment of neurolog
39 n chloride cotransporters, e.g. Na-K-2Cl and K-Cl cotransporters, are activated to maintain fluid/ion
42 the expected functional characteristics of a K+Cl- cotransporter: Cl--dependent uptake of 86Rb+ which
43 Here we review what is known about the Na-(K)-Cl cotransporters cloned to date and what can be dedu
45 ing the chloride gradient by blocking the Na-K-Cl cotransporter eliminated responses to light moving
54 mutations that reduce the level of the sole K+/Cl- cotransporter in the fruitfly Drosophila melanoga
55 m tight junctions supports a role for the Na-K-Cl cotransporter in ciliary epithelium as a chloride e
57 assing a total of seven Na-Cl, Na-K-2Cl, and K-Cl cotransporters, in addition to two related transpor
59 t the behavior of the endogenous HEK cell Na-K-Cl cotransporter is unlike either of the two forms whi
60 that pharmacological inhibition of the Na(+)-K(+)-Cl(-) cotransporter isoform 1 (NKCC1) during ischem
61 , which inhibit Cl- influx through the Na(+)-K(+)-Cl- cotransporter isoform-1 (NKCC-1) and efflux thr
62 er isoform-1 (NKCC-1) and efflux through the K(+)-Cl- cotransporter isoform-2, were unable to inhibit
63 2 is 67% identical to the widely distributed K-Cl cotransporter isoform (KCC1) identified in rat brai
64 ary screening, we have identified a putative K-Cl cotransporter isoform (KCC2) in rat brain that is s
65 at cation-dependent Cl- transport protein Na-K-Cl cotransporter isoform 1 (NKCC1) plays a role in the
68 suggest that a novel mechanism involving Na-K-Cl cotransporter isoform 1 mediates the observed long-
72 ed K(+) channel (the Gardos channel) and the K(+)-Cl(-) cotransporter (KCC) - it would have a synergi
73 ent the structure of a CCC, the Mus musculus K(+)-Cl(-) cotransporter (KCC) KCC4, in lipid nanodiscs
74 a cryoelectron microscopy structure of human K(+)-Cl(-) cotransporter (KCC)1 bound with the VU0463271
76 ects of CDNB (1 mM) on the activities of the K+-Cl- cotransporter (KCC; measured as Cl--dependent K+
77 s among the polypeptide products of the four K-Cl cotransporter (KCC) genes are little understood.
80 Na(+)/K(+)/Cl(-) cotransporter NKCC1 and the K(+)/Cl(-) cotransporters KCC1, KCC2, KCC3 and KCC4 have
84 al disease, the regulatory mechanisms of the K(+)/Cl(-) cotransporter KCC2 (encoded by SLC12A5) durin
88 d postsynaptic activity acts on the neuronal K+/Cl- cotransporter KCC2 to shift the reversal potentia
89 larger in mature neurons, which express the K-Cl cotransporter KCC2 at high levels, and inhibition o
91 Targeted deletion of the neuronal-specific K-Cl cotransporter KCC2 generates mice with a profound s
96 /K(+) /2Cl(-) cotransporter type 1 (NKCC1), K(+) /Cl(-) cotransporter (KCC2), the water channel aqua
99 n caused a progressive downregulation of the K+-Cl- cotransporter (KCC2), which may have contributed
101 o test this, we immunostained retina for the K-Cl cotransporter (KCC2) that normally extrudes chlorid
104 ted that the protein product of Slc12a6, the K(+)-Cl(-) cotransporter Kcc3, was not detectable in gax
105 dates for Mendelian human disorders, and the K-Cl cotransporter KCC3, in particular, may be involved
106 EAAT1(P>R) mutation, the chloride-extruding K(+)-Cl(-) cotransporter KccB also caused astroglial mal
112 -sensitive K channel, and the electroneutral K:Cl cotransporter-leading to sickle cell dehydration.
113 s, particularly R(+)-butylindazone-sensitive K-Cl cotransporters, may have a synapse- and/or cell typ
115 tes this variation, presumably via an Na(+), K(+), Cl(-) cotransporter (NKCC) and the Shaw K(+) chann
116 mbrane conductance regulator (CFTR) or Na(+)-K(+)-Cl(-) cotransporters (NKCC) blocked alveolar fluid
117 tanide and furosemide, two blockers of Na(+)/K(+)/Cl(-) cotransporters (NKCC), inhibited all capacita
118 25% identity) to the bumetanide-sensitive Na-K-Cl cotransporter (NKCC or BSC) and the thiazide-sensit
122 at normally extrudes chloride and for the Na-K-Cl cotransporter (NKCC) that normally accumulates chlo
124 ovided by these new structures for the Na(+)/K(+)/Cl(-) cotransporter NKCC1 and the K(+)/Cl(-) cotran
127 cryo-electron microscopy structure of the Na-K-Cl cotransporter NKCC1, an extensively studied member
129 osphorylation-dependent activation of the Na-K-Cl cotransporter (NKCC1) has been previously well docu
133 re we report that a substrate of PP1, the Na-K-Cl cotransporter (NKCC1), bears this motif in its N te
134 at kidney, the "secretory" isoform of the Na-K-Cl cotransporter, NKCC1 (BSC-2), localizes to the baso
135 we show a key role for the bidirectional Na-K-Cl cotransporter, NKCC1, in the choroid plexus (ChP) t
136 examine the structure and function of the Na-K-Cl cotransporter, NKCC1, we tagged the transporter wit
138 ternatively spliced variants of the renal Na-K-Cl cotransporter (NKCC2) are found in distinct regions
141 esence of furosemide, an inhibitor of the Na,K,Cl-cotransporter, NMDA-induced edema were reduced by 6
142 ID cell formation, as did inhibitors of the K:Cl cotransporter, okadaic acid, and [(dihydroindenyl)
144 er BSC2, one of the two major isoforms of Na-K-Cl cotransporters present in mammalian cells, can be d
145 hat a time-dependent expression of the Na(+)-K(+)-Cl(-) cotransporter protein occurs not only in cort
146 vealed that an intense staining of the Na(+)-K(+)-Cl(-) cotransporter protein was observed in dendrit
148 dient by ion substitution or by blocking the K-Cl cotransporter resulted in the starburst cells respo
149 use line expressing an activated form of the K-Cl cotransporter Slc12a4 (Kcc1), which results in a se
152 al membrane transport systems, including the K+-Cl- cotransporter (termed KCC), cause HbS-containing
155 ch is mediated primarily by KCC2, a neuronal K+/Cl- cotransporter that determines the intracellular c
156 ility and the activities of the Na-K-2Cl and K-Cl cotransporters, the Na/H exchanger, and the Gardos
160 ty in unmyelinated C-fibres is coupled to Na-K-Cl cotransporter type 1 (NKCC1) loading of axonal chlo
161 double staining demonstrates that the Na(+)-K(+)-Cl(-) cotransporter was expressed in astrocytes wit
162 lyculin A, consistent with mediation via the K+-Cl- cotransporter, was revealed by depleting deoxygen
163 erogeneous; some cells that expressed the Na-K-Cl cotransporter were weakly stained with the anti-ROM
165 ctivity modulated the mRNA levels of KCC2, a K(+)-Cl(-) cotransporter whose expression correlates wit
167 hat the KCC1 cDNAs encode a widely expressed K-Cl cotransporter with the characteristics of the K-Cl