ライフサイエンスコーパス: cotransporter

1 d mediated by an electrogenic Na(+)/HCO3 (-) cotransporter.

2 nsight into the regulation of this essential cotransporter.

3 to modify the movement of Cl(-) through the cotransporter.

4 n turn, stimulates the activity of the Na-Cl cotransporter.

5 ncreased expression of the Na(+)-K(+)-2Cl(-) cotransporter.

6 lamus by enhancing the activity of the NKCC1 cotransporter.

7 two positions in the C termini of a dimeric cotransporter.

8 asis to glial cells with a Na(+)-K(+)-2Cl(-) cotransporter.

9 ture-function relationship of this important cotransporter.

10 usly, potassium inhibits the sodium chloride cotransporter.

11 extracellular potassium via kation chloride cotransporters.

12 ing during pharmacological blockage of these cotransporters.

13 ound); and (iii) water transport through the cotransporters.

14 Ste20 kinases and the Na(+)-driven chloride cotransporters.

15 ivation and promoting phosphorylation of the cotransporters.

16 he function and membrane localization of ion cotransporters.

17 oem loading by the SUT sucrose-H(+) (proton) cotransporters.

18 that the compounds function as 'strict' HCl cotransporters.

19 sterase 1 enzyme, sodium-dependent phosphate cotransporter 1 (encoded by the SLC20A1 gene), and osteo

20 ccompanied by down-regulation of the Na-K-Cl cotransporter 1 (Nkcc1) and the Ca(2+)-activated anion c

21 ted that the electroneutral Na(+)-K(+)-Cl(-) cotransporter 1 (NKCC1) can play a role in glioma cell m

22 onductance regulator (Cftr) and the Na-K-2Cl cotransporter 1 (Nkcc1) gene and protein expressions, le

23 The Na(+)-K(+)-Cl(-) cotransporter 1 (NKCC1) is particularly relevant in sett

24 natively, inhibition of the Na(+)-K(+)-Cl(-) cotransporter 1 (NKCC1), a Cl(-) importer expressed in m

25 The intestinal H(+)/peptide cotransporter 1 (PepT1) plays a major role in nitrogen s

26 nduce downregulation of the sodium-D-glucose cotransporter 1 (SGLT1) and of the concentrative nucleos

27 Na(+)-d-glucose cotransporter 1 (SGLT1) is rate-limiting for glucose abs

28 The sodium-glucose cotransporter 1 (SGLT1) substrate alpha-MG induced secre

29 Inhibition of the sodium-dependent glucose cotransporter 1 (SGLT1) with phloridzin partially inhibi

30 Na(+)-glucose cotransporter 1 (SGLT1)-mediated glucose uptake leads to

31 balanced expression of the Na(+)-K(+)-2Cl(-) cotransporter 1 and the K(+)-Cl(-) cotransporter 2 (KCC2

32 ation, do not display KCC2/Na(+)-K(+)-2Cl(-) cotransporter 1 imbalance when implanted in a wild-type

33 Na(+)/H(+) exchanger 3 and Na(+)/K(+)/2Cl(-) cotransporter 1 inhibition in undifferentiated and diffe

34 model showed that electrogenic Na(+)/HCO3(-) cotransporter 1 might be a target in the intestinal muco

35 tic varicosities, whereas gephyrin, Na-K-2Cl cotransporter 1, and GABA(A) receptor alpha1 subunit, bu

36 glucose transporter sodium-dependent glucose cotransporter 1, was evaluated in this study as a candid

37 nce regulator and electrogenic Na(+)/HCO3(-) cotransporter 1.

38 iflozin, an oral inhibitor of sodium-glucose cotransporters 1 and 2, in combination with insulin trea

39 de cotransporters, such as Na(+)-K(+)-2Cl(-) cotransporter-1 (NKCC1) and K(+)-Cl(-) cotransporter-2 (

40 Na(+)-K(+)-2Cl(-) cotransporter-1 (NKCC1) in the brain is critically invol

41 se effects may be signaled by sodium-glucose cotransporter-1 (SGLT1), sweet taste receptors, or both.

42 isoforms (SGLT1 to 6 and sodium-myoinositol cotransporter-1, SMIT1) are known, although their expres

43 K(+)/Cl(-) cotransporter 2 (KCC2) is selectively expressed in the a

44 y significant decrease in potassium chloride cotransporter 2 (Kcc2) mRNA expression in developing rat

45 neurons lacked expression of the K(+)-Cl(-) cotransporter 2 (KCC2), the predominant Cl(-) exporter i

46 +)-2Cl(-) cotransporter 1 and the K(+)-Cl(-) cotransporter 2 (KCC2).

47 e and activate the renal Na(+) -K(+) -2Cl(-) cotransporter 2 (NKCC2) and Na(+) Cl(-) cotransporter (N

48 The Na-K-2Cl cotransporter 2 (NKCC2) was thought to be kidney specifi

49 Inhibitors of sodium-glucose cotransporter 2 (SGLT2) are a novel class of antidiabete

50 on of the transporter protein sodium-glucose cotransporter 2 (SGLT2) has emerged as a promising way t

51 Sodium glucose cotransporter 2 (SGLT2) inhibition is a novel and promis

52 tion of plasma glucose with a sodium-glucose cotransporter 2 (SGLT2) inhibitor could improve insulin-

53 KO mice with the hypoglycemic sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin and the

54 ration of luseogliflozin, the sodium-glucose cotransporter 2 (SGLT2) inhibitor, on renal hemodynamics

55 cemic agent, empagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor.

56 Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a new class of an

57 pressure-lowering effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors are already establish

58 Carbasugar sodium-glucose cotransporter 2 (SGLT2) inhibitors are highly promising

59 Sodium-glucose cotransporter 2 (SGLT2) inhibitors improve glycaemia in

60 crements in glucagon release, sodium-glucose cotransporter 2 (SGLT2) inhibitors induce stimulation of

61 Sodium-glucose cotransporter 2 (SGLT2) inhibitors lower glycemia by enh

62 ss of glucose-lowering agents-sodium-glucose cotransporter 2 (SGLT2) inhibitors-has been reported to

63 sterol has been reported with sodium-glucose cotransporter 2 (SGLT2) inhibitors.

64 macological inhibition of the sodium-glucose cotransporter 2 (SGLT2) reduces plasma glucose by limiti

65 by inhibiting renal sodium-dependent glucose cotransporter 2 (SGLT2).

66 with depletion of sodium potassium chloride cotransporter 2 and aquaporin 2.

67 renal GLUT 2 (rGLUT2) but not sodium-glucose cotransporter 2 and was associated with reduced renal ca

68 Sodium-glucose cotransporter 2 inhibition with canagliflozin decreases

69 ermine the effect of 8 weeks' sodium glucose cotransporter 2 inhibition with empagliflozin 25 mg QD o

70 owering blood glucose using a sodium-glucose cotransporter 2 inhibitor (dapagliflozin), depleting neu

71 ycemia using treatment with a sodium-glucose cotransporter 2 inhibitor (SGLT2-I) for 7 days.

72 mbined use of metformin and a sodium glucose cotransporter 2 inhibitor (SGLT2I) is a promising treatm

73 ptide-1 receptor agonist, and sodium-glucose cotransporter 2 inhibitor classes of medications.

74 short-term treatment with the sodium glucose cotransporter 2 inhibitor empagliflozin attenuated renal

75 Background Canagliflozin is a sodium-glucose cotransporter 2 inhibitor that reduces glycemia as well

76 Canagliflozin is a sodium glucose cotransporter 2 inhibitor that significantly reduces the

77 The sodium-glucose cotransporter 2 inhibitor, empagliflozin, markedly and r

78 Empagliflozin, a sodium-glucose cotransporter 2 inhibitor, reduced cardiovascular morbid

79 TCOME trial, empagliflozin, a sodium-glucose cotransporter 2 inhibitor, reduced the risk of major adv

80 fits and potential risks from sodium glucose cotransporter 2 inhibitors (SGLT2i).

81 al mechanisms for benefits of sodium-glucose cotransporter 2 inhibitors and glucagon-like peptide-1 a

82 he case of a meta-analysis of sodium-glucose cotransporter 2 inhibitors for the treatment of type 2 d

83 Sodium-glucose cotransporter 2 inhibitors may improve short-term outcom

84 Sodium-glucose cotransporter 2 inhibitors were compared with placebo in

85 iagenic enzymes and Na(+)-K(+)/NH4(+)-2Cl(-) cotransporter 2 were higher, and transepithelial NH3 tra

86 pression of megalin, cubilin, sodium-glucose cotransporter 2, and type IIa sodium-dependent phosphate

87 ABA(A) receptor alpha1 subunit, but not K-Cl cotransporter 2, are colocalized at the presumed postsyn

88 li, and less abundant expression of Na(+)/Pi cotransporter 2, claudin-2, and aquaporin 1.

89 mpagliflozin, an inhibitor of sodium-glucose cotransporter 2, in addition to standard care, on cardio

90 zin, a selective inhibitor of sodium-glucose cotransporter 2, may improve glycemic control with a low

91 ion (c.265G>A; p.A89T) in the sodium/glucose cotransporter 2-encoding gene SGLT2 (also known as SLC5A

92 c acid and glycine due to potassium chloride cotransporter-2 (KCC2) down-regulation in the spinal cor

93 Cl(-) cotransporter-1 (NKCC1) and K(+)-Cl(-) cotransporter-2 (KCC2), critically influence spinal syna

94 ase-4 (DPP-4) inhibitors, and sodium-glucose cotransporter-2 (SGLT-2) inhibitors.

95 atients with type 2 diabetes, sodium-glucose cotransporter-2 (SGLT2) inhibitors are known to reduce g

96 Sodium-glucose cotransporter-2 (SGLT2) inhibitors, including empagliflo

97 as recently reported with the sodium-glucose cotransporter-2 inhibitor (SGLT-2i) empagliflozin in pat

98 Dapagliflozin is a sodium-glucose cotransporter-2 inhibitor approved for the treatment of

99 ene, SLC34A1 encoding renal sodium-phosphate cotransporter 2A (NaPi-IIa), revealed autosomal-recessiv

100 oding the sodium (Na(+))-dependent phosphate cotransporter 2c (NPT2c), cause hereditary hypophosphate

101 Disruption of the potassium/chloride cotransporter 3 (KCC3), encoded by the SLC12A6 gene, cau

102 ce of water transport through the K(+)-Cl(-) cotransporter, a large osmotic gradient builds at concen

103 een shown to colocalize with the Na(+)/Cl(-) cotransporter, a marker of the distal convoluted segment

104 he N-terminal domain of NKCC1 and to promote cotransporter activation.

105 ulations therefore suggest that reduced KCC2 cotransporter activity alone may underlie the generation

106 adjacent threonines required for inhibiting cotransporter activity.

107 ting and dehydration due to reduced Na-K-2Cl-cotransporter activity.

108 2, which encodes a sodium-potassium-chloride cotransporter and is also necessary for inner ear functi

109 he ERAD of a mammalian SLC12 cation chloride cotransporter and provide a framework for future studies

110 gradient maintained by the Na(+)-K(+)-2Cl(-) cotransporter and requires Ca(2+) entry through voltage-

111 1 protein, a well-described sodium/phosphate cotransporter and retrovirus receptor, has been identifi

112 ffects were mimicked by a chloride-extruding cotransporter and were rescued by restoring chloride hom

113 The cation/Cl(-) cotransporters and ECM metalloproteinases may be particu

114 ant new insights into the regulation of K-Cl cotransporters and provides in vivo evidence that increa

115 solute carrier 12 family of cation-chloride cotransporters and thereby modulate a range of processes

116 are mediated by an electrogenic Na(+)/HCO3- cotransporter, and are more tightly coupled to network a

117 ansporter 2, phosphorylated Na(+)/K(+)/Cl(-) cotransporter, and phosphorylated Na(+)/Cl(-) cotranspor

118 volume-sensitive kinase" of the cation-Cl(-) cotransporters, and functions as a molecular rheostat of

119 otransporter, and phosphorylated Na(+)/Cl(-) cotransporter; and greater reductions in abundance and p

120 sing bumetanide, a chloride importer Na-K-Cl cotransporter antagonist, for treatment of neurological

121 e transportation into the cell through SGLT1 cotransporters can induce Ca(2+) influx and release of G

122 e relative expression of the cation-chloride cotransporters (CCC) NKCC1 (Slc12a2) and KCC2 (Slc12a5),

123 NKCC1 and KCC2, related cation-chloride cotransporters (CCC), regulate cell volume and gamma-ami

124 Plant cation-chloride cotransporters (CCCs) have been implicated in conferring

125 Equilibrative cation-chloride cotransporters (CCCs) move Cl(-) across the membrane, bu

126 ely by the expression of two cation-chloride cotransporters (CCCs), KCC2 and NKCC1, which serve as ch

127 like AtCCC) belongs to the Na(+)-K(+)-2Cl(-) cotransporter class of CCCs.

128 remodel the core chaperone systems to favor cotransporter degradation and biogenesis, respectively.

129 gulator (CFTR)-dependent and Na(+)K(+)2Cl(-) cotransporter-dependent fluid secretion, all requiring c

130 ependent HCO3 (-) efflux nor Na(+) /HCO3 (-) cotransporter-dependent HCO3 (-) influx were CO2 -sensit

131 ponsive kinase (OSR1), can phosphorylate the cotransporters directly.

132 dephosphorylated for full activation of the cotransporter during hypotonicity.

133 ngements of an electrogenic secondary-active cotransporter during its transport cycle, two measures o

134 4) of the thiazide-sensitive sodium chloride cotransporter encoded by SLC12A3, and those that regulat

135 KCC2 is a neuron-specific K(+)-Cl(-) cotransporter essential for establishing the Cl(-) gradi

136 educed dorsal spinal cord potassium chloride cotransporter expression and impaired spinal gamma-amino

137 of NCC immunoprecipitates revealed that the cotransporter formed complexes with the core chaperones

138 Sodium cotransporters from several different gene families belo

139 ride channels from the ClC family, or by KCl cotransporters from the SLC12 gene family.

140 effect on total KCC2 protein level and K-Cl cotransporter function.

141 The other members of this K(+)-Cl(-) cotransporter gene family are exclusively swelling-activ

142 neuron-specific member of the of K(+)-Cl(-) cotransporter gene family.

143 In contrast, cotransporters harboring disease-causing mutations that

144 Mammalian sodium-dependent Pi cotransporters have been grouped into three families NaP

145 m of HCO3 (-) uptake involves Na(+)/HCO3 (-) cotransporters, here we demonstrate that the C. elegans

146 In the human sodium glucose cotransporter (hSGLT1) cycle, the protein undergoes conf

147 thiazide diuretics, which inhibit the Na-Cl cotransporter in the distal nephron of the kidney; KLHL3

148 tation, and to do this we expressed chloride cotransporters in astrocytes.

149 ing and opposing the role of cation-chloride cotransporters in regulating Cl(-), we examine the parti

150 bstrate, the sodium, potassium, two chloride cotransporter, in HeLa cells.

151 emature alterations in the neuronal chloride cotransporters indicated by dysregulated NKCC1 and KCC2

152 o examine the effect of renal sodium-glucose cotransporter inhibition with empagliflozin on the fasti

153 are low, the electroneutral sodium chloride cotransporter is activated, leading to salt retention.

154 ion and overactivating the Na(+)-K(+)-2Cl(-) cotransporter isoform 1 (NKCC1) in neurons.

155 nnel (the Gardos channel) and the K(+)-Cl(-) cotransporter (KCC) - it would have a synergistic effect

156 The K(+):Cl(-) cotransporter (KCC) activity is modulated by phosphoryla

157 The K-Cl cotransporter (KCC) regulates red blood cell (RBC) volum

158 ow reduced expression of the cation-chloride cotransporter KCC2 (K(+)/Cl(-) exporter) and a reduced K

159 ng two specific markers: the cation-chloride cotransporter KCC2 (which determines the hyperpolarizing

160 Diminished levels of the K(+)/Cl(-) cotransporter KCC2 and a depolarizing GABAA receptor-med

161 kers of excitability, the potassium-chloride cotransporter KCC2 and GABAA receptors, undergo remarkab

162 midal cell model explicitly incorporated the cotransporter KCC2 and its effects on the internal/exter

163 The K-Cl cotransporter KCC2 establishes the low intraneuronal Cl-

164 ysfunction or loss of the potassium-chloride cotransporter KCC2 in a subset of pyramidal cells in the

165 ctional expression of the potassium-chloride cotransporter KCC2 in spinal cord dorsal horn neurons ar

166 al fall in [Cl(-)]i and the role of the K-Cl cotransporter KCC2 in this process.

167 The K(+)/Cl(-) cotransporter KCC2 is the main mechanism by which neuron

168 The neuronal K-Cl cotransporter KCC2 maintains the low intracellular chlor

169 The neuron-specific cation chloride cotransporter KCC2 plays a crucial role in hyperpolarizi

170 The K-Cl cotransporter KCC2 plays a crucial role in neuronal chlo

171 ed by the neuron-specific potassium-chloride cotransporter KCC2.

172 hich is maintained by the potassium-chloride cotransporter KCC2.

173 The K(+)/Cl(-) cotransporter (KCC2) allows adult neurons to maintain lo

174 sion by the neuron-specific type 2K(+)-Cl(-) cotransporter (KCC2).

175 functional downregulation of the K(+), Cl(-) cotransporter, KCC2.

176 mutation, the chloride-extruding K(+)-Cl(-) cotransporter KccB also caused astroglial malformation a

177 In healthy mature motoneurons (MNs), KCC2 cotransporters maintain the intracellular chloride conce

178 uced activity of the thiazide-sensitive NaCl cotransporter may support renal adaptation by activation

179 nd is mediated by three Na(+)-dependent P(i) cotransporters (members of the SLC34 and SLC20 families)

180 se kinase-1 (OSR1) activate the renal cation cotransporters Na(+) -K(+) -2Cl(-) cotransporter (NKCC2)

181 udes the mammalian SLC13 Na(+)/dicarboxylate cotransporters, NaDC1 and NaCT.

182 The human Na(+)/dicarboxylate cotransporter NaDC3 (SLC13A3) is found in various tissue

183 ed and synthesised a new class of H(+)/Cl(-) cotransporters named 'perenosins'.

184 NCKX4 and the Na(+)-dependent HPO4 (2-) (Pi) cotransporter NaPi-2b.

185 eral HCO3(-) entry through the Na(+)-HCO3(-) cotransporter (NBC) NBCe1-B, and luminal HCO3(-) exit me

186 activities of the basolateral Na(+) -HCO3(-) cotransporter (NBC1) and apical Cl(-) /HCO3(-) exchanger

187 The electrogenic sodium bicarbonate cotransporter NBCe1 (SLC4A4) is a robust regulator of in

188 Electrogenic Na(+)-bicarbonate cotransporter NBCe1 variants contribute to pH(i) regulat

189 encodes the electrogenic sodium bicarbonate cotransporter NBCe1, a membrane protein that acts to mai

190 nhydrases, the basolateral Na(+) bicarbonate cotransporter Nbce1, and the basolateral anion exchanger

191 ly-expressed electrogenic sodium bicarbonate cotransporter NBCe1, results in the bicarbonate-wasting

192 sly expressed electrogenic Na(+)/bicarbonate cotransporter NBCe1-A in an excised macropatch from the

193 In the electrogenic Na(+)-HCO3(-) cotransporter NBCe1-A, EL-3 is the largest extracellular

194 and shRNA specific to the 1Na(+):2HCO(3)(-) cotransporter NBCe1.

195 deficient in the electrogenic Na(+)/HCO3(-) cotransporter NBCe1.

196 The electrogenic Na(+)/bicarbonate cotransporter (NBCe1) of the Slc4 gene family is a power

197 cytes by the electrogenic sodium bicarbonate cotransporter (NBCe1) played a crucial role in causing c

198 The renal electrogenic Na(+)/HCO(3)(-) cotransporter (NBCe1-A) contributes to the basolateral s

199 ional interactions between the Na(+),HCO3(-) cotransporter NBCn1 (slc4a7) and the Ca(2+)/calmodulin-a

200 l variants of the electroneutral Na(+)/HCO3- cotransporter NBCn1, one full-length starting with "MIPL

201 mpensatory upregulation of the Na(+)/HCO3(-) cotransporter NBCn1.

202 ivate the thiazide-sensitive sodium chloride cotransporter NCC (encoded by Slc12a3).

203 Sodium chloride cotransporter (NCC) and alpha- and gamma-epithelial sodi

204 eins, the thiazide-sensitive sodium chloride cotransporter (NCC) and the epithelial sodium channel (E

205 e residue 126 (pS126 NKCC2) and of the Na-Cl cotransporter (NCC) at threonine 58 (pT58 NCC).

206 increased activity of the renal Na(+)-Cl(-) cotransporter (NCC) because of altered regulation by wit

207 -)-cotransporter (NKCC2) and the Na(+)-Cl(-)-cotransporter (NCC) by vasopressin includes their phosph

208 is and provide evidence that the Na(+)/Cl(-) cotransporter (NCC) compensated for the inactivation of

209 , and the thiazide-sensitive sodium-chloride cotransporter (NCC) has a key role in this process.

210 on of the thiazide-sensitive sodium-chloride cotransporter (NCC) in the distal convoluted tubule (DCT

211 tubule (DCT) by the thiazide-sensitive NaCl cotransporter (NCC) is a major determinant of total body

212 The thiazide-sensitive Na(+)/Cl(-) cotransporter (NCC) is activated by low potassium intake

213 on in the thiazide-sensitive sodium chloride cotransporter (NCC) is common in patients with Gitelman'

214 The thiazide-sensitive NaCl cotransporter (NCC) is important for renal salt handling

215 The thiazide-sensitive Na-Cl cotransporter (NCC) is the major pathway for salt reabso

216 The thiazide-sensitive NaCl cotransporter (NCC) is the primary mediator of salt reab

217 and phosphorylated thiazide-sensitive Na+Cl- cotransporter (NCC) levels were increased in KO kidneys.

218 uble knockout of pendrin and the Na(+)/Cl(-) cotransporter (NCC) manifest profound salt wasting.

219 -wnk1 kinase complex to regulate Na(+)/Cl(-) cotransporter (NCC) mediated salt reabsorption in the di

220 The thiazide-sensitive NaCl cotransporter (NCC) of the renal distal convoluted tubul

221 Cl(-) cotransporter (NKCC2) and Na(+) -Cl(-) cotransporter (NCC) via phosphorylation.

222 pithelial sodium channel (ENaC), Na(+)/Cl(-) cotransporter (NCC), and with no-lysine-kinase 1 (WNK1).

223 ance of total and phosphorylated Na(+)/Cl(-) cotransporter (NCC), claudin-7, and cleaved forms of epi

224 NKs regulate the activity of the Na(+):Cl(-) cotransporter (NCC), the epithelial sodium channel (ENaC

225 the renal thiazide-sensitive sodium chloride cotransporter (NCC), which is necessary for the developm

226 The Na-Cl cotransporter (NCC), which is the target of inhibition b

227 l(-) cotransporter 2 (NKCC2) and Na(+) Cl(-) cotransporter (NCC).

228 phosphorylation of the renal sodium chloride cotransporter (NCC).

229 ls and the abundance of phosphorylated Na-Cl cotransporter (NCC).

230 n phosphorylate and activate the renal Na-Cl cotransporter (NCC).

231 stimulate the thiazide-sensitive Na(+)-Cl(-) cotransporter (NCC).

232 ption, respectively, through the Na(+)/Cl(-) cotransporter (NCC).

233 KCC2, and thiazide-sensitive sodium-chloride cotransporter, NCC, in vitro, and both co-localize with

234 The thiazide-sensitive sodium chloride cotransporter, NCC, is the major NaCl transport protein

235 dulates the activity of the renal Na(+)Cl(-) cotransporter, NCC.

236 In contrast, the Na(+)-K(+)-Cl(-) cotransporter Ncc69, which normally allows chloride into

237 iation, presumably via an Na(+), K(+), Cl(-) cotransporter (NKCC) and the Shaw K(+) channel (dKV3.1).

238 The Na-K-Cl cotransporter (NKCC) plays central roles in cellular chl

239 r Ncc69, the fly sodium-potassium-2-chloride cotransporter (NKCC), in tubule K(+) secretion.

240 uctance regulator (CFTR) or Na(+)-K(+)-Cl(-) cotransporters (NKCC) blocked alveolar fluid secretion,

241 short-hairpin (sh) RNA against the Na-K-2Cl cotransporter NKCC1 (shNKCC1) in NPCs of the neonatal su

242 n in the expression of the neuronal chloride cotransporter NKCC1 that promotes the accumulation of in

243 eparation, AqF026 did not affect the Na-K-Cl cotransporter NKCC1.

244 (-) is outward because the Na(+)-K(+)-2Cl(-) cotransporter (NKCC1) elevates the Cl(-) concentration i

245 The Na-K-Cl cotransporter (NKCC1) is expressed in most vertebrate ce

246 ddition of a basolateral Na(+) -K(+) -2Cl(-) cotransporter (NKCC1), assumed to be present in rat and

247 ransporter activity of the Na(+)-K(+)-2Cl(-) cotransporters (NKCC1) and anion exchangers (AE), the 2

248 Na(+)-dependent chloride cotransporters (NKCC1, NKCC2, and NCC) are activated by

249 egulation of the medullary Na(+)-K(+)-2Cl(-) cotransporter NKCC2 in these mice compared with wild-typ

250 -state surface levels of the apical Na/K/2Cl cotransporter NKCC2 regulate NaCl reabsorption by epithe

251 pression and function of the sodium chloride cotransporters NKCC2 and NCC (key components of salt rea

252 the downregulation of the Na(+)/K(+)/2Cl(-) cotransporter (NKCC2) and AQP2, with less phosphorylatio

253 al cation cotransporters Na(+) -K(+) -2Cl(-) cotransporter (NKCC2) and Na(+) -Cl(-) cotransporter (NC

254 Activation of the Na(+)-K(+)-2Cl(-)-cotransporter (NKCC2) and the Na(+)-Cl(-)-cotransporter

255 enhance the phosphorylation of the Na-K-2Cl cotransporter (NKCC2) at serine residue 126 (pS126 NKCC2

256 The furosemide-sensitive Na(+)-K(+)-2Cl(-)-cotransporter (NKCC2) is crucial for NaCl reabsorption i

257 The furosemide-sensitive Na(+)-K(+)-2Cl(-) cotransporter (NKCC2) is responsible for urine concentra

258 fold increase in activated Na(+)-K(+)-2Cl(-) cotransporter (NKCC2).

259 hibitory action toward the Na(+)-K(+)-2Cl(-) cotransporter, NKCC2.

260 abundant expression of the sodium-phosphate cotransporter Npt2a at the brush border membrane.

261 cKL downregulated the renal sodium-phosphate cotransporter Npt2a in alphaKL-null mice supporting dire

262 r (PTHR), type II sodium-dependent phosphate cotransporter (Npt2a), and beta2-adrenergic receptor (be

263 transporter high-affinity Na+ /taurocholate cotransporter (NTCP) and the BA synthesizing enzyme chol

264 oltage-dependence of Na(+)-coupled phosphate cotransporters of the SLC34 family arises from displacem

265 ssed water-translocating Na(+) /K(+) /2Cl(-) cotransporter promoted TRPV4 activation despite the abse

266 ically associate with the potassium-chloride cotransporter protein, KCC2, which sets the driving forc

267 the presence of the neuronal cation-chloride-cotransporter protein, KCC2.

268 etween the GABABR and the potassium-chloride cotransporter protein, KCC2.

269 ression and activity of distal renal tubular cotransporter proteins and to discuss the gene mutations

270 1 expression, increased NKCC1/KCC2b chloride cotransporter ratio, altered dendritic development, and

271 Activities of the Na(+)/glucose cotransporter SGLT-1 and GLUT2 were unaffected in LEPR-B

272 nhibiting glucose reuptake by sodium/glucose cotransporter (SGLT) 2 in the kidney, without affecting

273 Analogs selective for sodium-glucose cotransporter (SGLT) family members and the sweet taste

274 Inhibitors of the sodium-dependent glucose cotransporters (SGLT) have appeared as viable therapeuti

275 ucose metabolism but requires sodium/glucose cotransporters (SGLT).

276 Implications of the sodium glucose cotransporter SGLT1 in either pumping water or passively

277 fy the physiological role of Na(+)-D-glucose cotransporter SGLT1 in small intestine and kidney, Sglt1

278 ty either by the electrogenic sodium-glucose cotransporter SGLT1, or by closure of ATP-sensitive pota

279 d urea through the intestinal sodium/glucose cotransporter SGLT1.

280 The sodium glucose cotransporter SGLT2 in the early proximal tubule is the

281 large extent mediated by the sodium/glucose cotransporters (Sglts) because the Sglt inhibitor phlori

282 The two main sodium-glucose cotransporters (SGLTs), SGLT1 and SGLT2, provide new the

283 aromatic residues in sodium-dependent sugar cotransporters (SGLTs).

284 e in the proximal tubules via sodium-glucose cotransporters (SGLTs).

285 ine expressing an activated form of the K-Cl cotransporter Slc12a4 (Kcc1), which results in a semi-do

286 The neuron-specific K(+)-Cl(-) cotransporter SLC12A5, also known as KCC2, helps mediate

287 e type IIb Na(+)-coupled inorganic phosphate cotransporter (SLC34A2 flounder isoform) that were predi

288 hat overexpression of the Na(+)/myo-inositol cotransporter (SMIT1) and myo-inositol supplementation e

289 levels of two kinases upstream of the NKCC1 cotransporter, SPAK (STE20/SPS1-related proline alanine

290 Cation-chloride cotransporters, such as Na(+)-K(+)-2Cl(-) cotransporter-

291 r 2, and type IIa sodium-dependent phosphate cotransporter, suggesting apical dedifferentiation accou

292 lithium-NDI mice lacking the sodium-chloride cotransporter, suggesting that inhibition of carbonic an

293 KCC2 is a neuron-specific K(+)-Cl(-) cotransporter that is essential for Cl(-) homeostasis an

294 ated the contribution of the cation chloride cotransporters to setting [Cl(-)]i in these SCN neurons

295 tive, reversible inhibitor of sodium-glucose cotransporter type 2 (SGLT2) that is marketed in United

296 osphorylation of the thiazide-sensitive NaCl cotransporter was consistently lower in AS(-/-) mice tha

297 Expression of the KCC2 cotransporter was elevated in interneurons of denervated

298 3-S96A) had no effect on the activity of the cotransporter when compared with wild type KCC3.

299 d driving forces and thus activity for these cotransporters, which by transport of water during their

300 ed in Xenopus oocytes, functions as an Na-Cl cotransporter with two major characteristics, making it