ライフサイエンスコーパス: cotransporter

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

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

3 ture-function relationship of this important cotransporter.

4 usly, potassium inhibits the sodium chloride cotransporter.

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

6 DPH oxidase (NOX) subunits, D(5) R, and NaCl cotransporter.

7 codes the thiazide-sensitive sodium-chloride cotransporter.

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

9 extracellular potassium via kation chloride cotransporters.

10 gene encodes electrogenic sodium bicarbonate cotransporter 1 (NBCe1).

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

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

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

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

15 We propose that sodium-glucose cotransporter 1 (SGLT1) senses increases in luminal gluc

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

17 cotransport (catalyzed by Na(+)/K(+)/2Cl(-) cotransporter 1 [NKCC1]) might similarly originate from

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

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

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

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

22 sport by the electrogenic sodium bicarbonate cotransporter 1, NBCe1.

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

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

25 2.7-fold increase; sodium-potassium-chloride cotransporter-1, 2.8-fold increase; aquaporin 4, 8.9-fol

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

27 e K(+)/Cl(-) transporters potassium-chloride cotransporter 2 (KCC2) and sodium-potassium-chloride tra

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

29 +)-2Cl(-) cotransporter 1 and the K(+)-Cl(-) cotransporter 2 (KCC2).

30 variation in the neuronal potassium-chloride cotransporter 2 (KCC2).

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

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

33 levels via inhibition of the sodium glucose cotransporter 2 (SGLT-2) in the kidney and has been show

34 etic treatment, we inhibited the Na+-glucose cotransporter 2 (SGLT2) along the proximal convoluted tu

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

36 Sodium-glucose cotransporter 2 (SGLT2) inhibition reduces cardiovascula

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

38 The sodium glucose cotransporter 2 (SGLT2) inhibitor empagliflozin promotes

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

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

41 Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a newer class of

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

43 Sodium-glucose cotransporter 2 (SGLT2) inhibitors are effective antidia

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

45 Sodium-glucose cotransporter 2 (SGLT2) inhibitors are the most recently

46 More recently, sodium-glucose cotransporter 2 (SGLT2) inhibitors have further improved

47 mellitus (T2DM) treated with sodium glucose cotransporter 2 (SGLT2) inhibitors have improved cardiov

48 Studies implicating sodium-glucose cotransporter 2 (SGLT2) inhibitors in glucagon secretion

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

50 Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of ho

51 Sodium/glucose cotransporter 2 (SGLT2) inhibitors were developed to low

52 -gamma/alpha/delta) agonists, sodium glucose cotransporter 2 (SGLT2) inhibitors, and farnesoid X rece

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

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

55 cular trials of inhibitors of sodium-glucose cotransporter 2 (SGLT2), exploratory results have sugges

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

57 e renal glucose cotransporter sodium glucose cotransporter 2 (SGLT2).

58 lysin inhibitors [ARNIs], and sodium/glucose cotransporter 2 [SGLT2] inhibitors) reduce mortality in

59 GLP-1] receptor agonists, and sodium-glucose cotransporter 2 [SGLT2] inhibitors) using routinely avai

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

61 alone or in combination with sodium/glucose cotransporter 2 inhibition (SGLT-2i).

62 Sodium-glucose cotransporter 2 inhibition with canagliflozin decreases

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

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

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

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

67 tcomes in Heart Failure), the sodium-glucose cotransporter 2 inhibitor dapagliflozin reduced the risk

68 The sodium-glucose cotransporter 2 inhibitor dapagliflozin reduces the risk

69 The sodium-glucose cotransporter 2 inhibitor empagliflozin reduced LV volum

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

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

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

73 targeted by Dapagliflozin, a sodium glucose cotransporter 2 inhibitor, in clinical trials for patien

74 Dapagliflozin (DAPA), a sodium-glucose cotransporter 2 inhibitor, is approved for treatments of

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

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

77 Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are a new class of g

78 Sodium-glucose cotransporter 2 inhibitors (SGLT2i) effectively lower pl

79 Sodium-glucose cotransporter 2 inhibitors (SGLT2i), a new drug class ap

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

81 cts on cardiovascular events, sodium glucose cotransporter 2 inhibitors and glucagon-like peptide 1 r

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

83 new glucose-lowering agents - sodium-glucose cotransporter 2 inhibitors and incretin therapies - has

84 Sodium-glucose cotransporter 2 inhibitors improve outcomes in patients

85 s established the benefits of sodium-glucose cotransporter 2 inhibitors in patients with diabetes and

86 tment interventions including sodium glucose cotransporter 2 inhibitors in patients with type 2 diabe

87 urther support for the use of sodium-glucose cotransporter 2 inhibitors in primary and secondary prev

88 s strongly support a role for sodium-glucose cotransporter 2 inhibitors in the treatment of HFrEF pat

89 hese trials demonstrated that sodium-glucose cotransporter 2 inhibitors reduce adverse cardiovascular

90 g may be a mechanism by which sodium-glucose cotransporter 2 inhibitors reduce heart failure hospital

91 Sodium-glucose cotransporter 2 inhibitors reduce the risk of heart fail

92 ith type 2 diabetes mellitus, sodium-glucose cotransporter 2 inhibitors reduce the risk of hospitaliz

93 Sodium-glucose cotransporter 2 inhibitors reduce the risk of serious he

94 The efficacy and safety of sodium-glucose cotransporter 2 inhibitors such as sotagliflozin in prev

95 ation seen across 4 trials of sodium glucose cotransporter 2 inhibitors.

96 ce of ketosis associated with sodium-glucose cotransporter 2 inhibitors.

97 emic agents, including SGLT2 (sodium glucose cotransporter 2) inhibitors and GLP-1 (glucagon-like pep

98 SGLT2 (sodium-glucose cotransporter 2) inhibitors have been shown to lower blo

99 SGLT2 (sodium-glucose cotransporter 2) inhibitors lower cardiovascular events

100 oprotective effects of SGLT2 (sodium-glucose cotransporter 2) inhibitors may be related to their abil

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

102 rtugliflozin, an inhibitor of sodium-glucose cotransporter 2, have not been established.

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

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

105 Sodium-glucose cotransporter-2 (SGLT-2) inhibitors could increase the r

106 tract infections (UTIs) with sodium-glucose cotransporter-2 (SGLT-2) inhibitors have reported confli

107 Sodium-glucose cotransporter-2 (SGLT-2) inhibitors reduced heart failur

108 GLP-1 receptor agonists with sodium-glucose cotransporter-2 (SGLT-2) inhibitors.

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

110 transporter 2A (NaPi-IIa) and sodium-glucose cotransporter-2 (SGLT-2).

111 95% CI 0.79-0.95; p < 0.01), sodium-glucose cotransporter-2 (SGLT2) inhibitors (OR 0.68, 95% CI 0.58

112 (GLP-1) receptor agonists and sodium-glucose cotransporter-2 (SGLT2) inhibitors are increasingly used

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

114 warned that administration of sodium-glucose cotransporter-2 (SGLT2) inhibitors could lead to ketoaci

115 Use of sodium-glucose cotransporter-2 (SGLT2) inhibitors has been associated w

116 In contrast, the effects of sodium-glucose cotransporter-2 (SGLT2) inhibitors may be related primar

117 Sodium-glucose cotransporter-2 (SGLT2) inhibitors prevent glucose reabs

118 hropathy) have shown that the sodium-glucose cotransporter-2 (SGLT2) inhibitors, a newer generation o

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

120 renal glucose reabsorption is sodium-glucose cotransporter-2 (SGLT2).

121 Inhibition of the sodium-glucose cotransporter-2 (SGLT2i) improves outcomes in patients w

122 greater absolute benefit from sodium-glucose cotransporter-2 inhibition.

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

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

125 sk reductions in HHF with the sodium-glucose cotransporter-2 inhibitor dapagliflozin were assessed by

126 to investigate the effects of sodium-glucose cotransporter-2 inhibitor empagliflozin on central hemod

127 nhibitor class, and comparing sodium-glucose cotransporter-2 inhibitor versus dipeptidyl peptidase-4

128 showed that empagliflozin, a sodium-glucose cotransporter-2 inhibitor, reduces the risk of hospitali

129 uction in risk for HHF with a sodium-glucose cotransporter-2 inhibitor.

130 ceptor agonists (GLP-1RA) and sodium-glucose cotransporter-2 inhibitors (SGLT2i) have demonstrated ca

131 The magnitude of effect of sodium-glucose cotransporter-2 inhibitors (SGLT2i) on specific cardiova

132 Sodium-glucose cotransporter-2 inhibitors and the risk for diabetic ket

133 Sodium-glucose cotransporter-2 inhibitors improve heart failure-related

134 tubular site of action of the sodium-glucose cotransporter-2 inhibitors may help circumvent these lim

135 Sodium-glucose cotransporter-2 inhibitors may reduce the risk for gout

136 Sodium-glucose cotransporter-2 inhibitors promote glycosuria, resulting

137 Sodium-glucose cotransporter-2 inhibitors reduce the risk of hospitaliz

138 SGLT2 (sodium-glucose cotransporter-2) inhibitors improve heart failure-associ

139 e major apical transporters sodium-phosphate cotransporter 2A (NaPi-IIa) and sodium-glucose cotranspo

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

141 des the plasma membrane Na(+) /dicarboxylate cotransporter 3, which imports inside the cell 4 to 6 ca

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

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

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

145 adjacent threonines required for inhibiting cotransporter activity.

146 th molecular dynamics simulations, of both a cotransporter and an exchanger.

147 2, which encodes a sodium-potassium-chloride cotransporter and is also necessary for inner ear functi

148 increased expression of the sodium chloride cotransporter and phosphorylation by the WNK-SPAK kinase

149 e with AtTMEM16 functioning as an anion/H(+) cotransporter and therefore, as a putative pH sensor.

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

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

152 a membrane transporters, which contains both cotransporters and exchangers.

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

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

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

156 eant poly-anions, the activity of cation-Cl- cotransporters, and the buildup of intra- and extracellu

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

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

159 The SLC12A cation-Cl(-) cotransporters (CCC), including NKCC1 and the KCCs, are

160 abidopsis thaliana) Na(+):K(+):2Cl(-) (NKCC) cotransporter CCC1 has a dual function in plant immunity

161 Cation-chloride-cotransporters (CCCs) catalyze transport of Cl(-) with K

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

163 Cation-chloride cotransporters (CCCs) mediate the coupled, electroneutra

164 Cation-chloride cotransporters (CCCs) mediate the electroneutral transpo

165 the expression ratio of the cation-chloride cotransporters (CCCs) NKCC1 and KCC2.

166 The secondary active cation-chloride cotransporters (CCCs) utilize the existing Na(+) and/or

167 order caused by dysfunction of the lysosomal cotransporter cystinosin, leads to cystine accumulation

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

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

170 Altered chloride cotransporter expression and changes in interneuron dens

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

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

173 Blockade of NKCC1 Cl(-) cotransporters further controlled interictal discharges

174 nknown, blocking known chloride channels and cotransporters had little effect on NaCl responses.

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

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

177 -Reg(S20E) and whether human Na(+)-d-glucose cotransporter hSGLT2 and the human glucose sensor hSGLT3

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

179 phaturia from downregulation of two key NaPi cotransporters in the kidney.

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

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

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

183 However, Na-K-Cl cotransporter isoform 1 (NKCC1) was significantly up-reg

184 est that a novel mechanism involving Na-K-Cl cotransporter isoform 1 mediates the observed long-term

185 Total kidney Na(+)/K(+)/2Cl(-) cotransporter isoform 2 (NKCC2) levels were greatly redu

186 included the electrogenic sodium-bicarbonate cotransporter isoforms 1 and 2 (NBCe1 and NBCe2), the el

187 ucture of a CCC, the Mus musculus K(+)-Cl(-) cotransporter (KCC) KCC4, in lipid nanodiscs determined

188 o-EM) structures of human potassium-chloride cotransporter KCC1 in potassium chloride or sodium chlor

189 the regulatory mechanisms of the K(+)/Cl(-) cotransporter KCC2 (encoded by SLC12A5) during maturatio

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

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

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

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

194 Immunostaining for chloride cotransporter KCC2 and interneurons were performed on re

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

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

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

198 tional enhancement of the potassium-chloride cotransporter KCC2.

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

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

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

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

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

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

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

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

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

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

209 lar transport requiring the Na(+) /phosphate cotransporter NaPi-IIb/Slc34a2, and a poorly characteriz

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

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

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

213 drases (CAs) with the electrogenic Na/HCO(3) cotransporter NBCe1-A speeds transport by regenerating/c

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

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

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

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

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

219 The Na/HCO(3) cotransporter NBCn1/SLC4A7 can affect glutamate neurotox

220 The roles of the Na(+) /HCO(3) (-) cotransporters NBCn1 and NBCn2 as well as their activato

221 BCe2), the electroneutral sodium-bicarbonate cotransporter (NBCn1), and the sodium-dependent chloride

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

223 The NaCl cotransporter NCC in the kidney distal convoluted tubule

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

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

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

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

228 NaCl cotransporter (NCC) expression was increased compared to

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

230 phorylation (and hence activity) of the NaCl cotransporter (NCC) in the distal convoluted tubule (DCT

231 ntake regulates the thiazide-sensitive Na-Cl cotransporter (NCC) in the distal convoluted tubule (DCT

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

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

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

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

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

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

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

239 (WNK) kinases regulate renal sodium-chloride cotransporter (NCC) to maintain body sodium and potassiu

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

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

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

243 additional sodium transporters (Na(+)-Cl(-) cotransporter (NCC), Na(+)-K(+)-2Cl(-) cotransporter (NK

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

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

246 assium intake on the thiazide-sensitive NaCl cotransporter (NCC).

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

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

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

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

251 he regulation of the thiazide-sensitive NaCl cotransporter (NCC).

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

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

254 phila Ncc69 gene encodes a Na(+)-K(+)-2Cl(-)-cotransporter (NKCC) that is critical for regulating int

255 Pharmacological antagonism of the cotransporter NKCC1 mitigated ethanol-induced potentiati

256 electron microscopy structure of the Na-K-Cl cotransporter NKCC1, an extensively studied member of th

257 Na(+)-K(+)-2Cl(-) Cotransporter (NKCC1) is a protein that aids in the acti

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

259 redicted to encode a Na+, K+, and Cl- (NKCC) cotransporter, NKCC1b.

260 t modulator of salt transport via the sodium cotransporter NKCC2 in the TAL.

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

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

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

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

265 Cl(-) cotransporter (NCC), Na(+)-K(+)-2Cl(-) cotransporter (NKCC2), and Na(+)-K(+)-ATPase (NKA)) and

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

267 The sodium-phosphate cotransporter NPT2a plays a key role in the reabsorption

268 The sodium-phosphate cotransporter Npt2a, which mediates a large proportion o

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

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

271 uctures are only available for a single DASS cotransporter protein in a substrate-bound, inward-facin

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

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

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

275 determining local levels of cation-chloride cotransporters remain elusive.

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

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

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

279 plasma membrane abundance of Na(+)-d-glucose cotransporter SGLT1 by blocking the exocytotic pathway a

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

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

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

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

284 of glucose and sodium by the sodium-glucose cotransporters SGLT2 and SGLT1 in the proximal tubule.

285 rs (GLUTs), not for sodium-dependent glucose cotransporters (SGLTs), which have recently been shown t

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

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

288 gliflozin, an inhibitor of the renal glucose cotransporter sodium glucose cotransporter 2 (SGLT2).

289 he Ste20 proline alanine-rich kinase-Na+-Cl- cotransporter (SPAK-NCC) phosphorylation cascade, associ

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

291 KCC2 is a vital neuronal K(+)/Cl(-) cotransporter that is implicated in the etiology of nume

292 mily encompasses transition metal and proton cotransporters that are present in many organisms from b

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

294 scular outcome trials for all sodium-glucose cotransporter type 2 inhibitors and the recent DAPA-HF t

295 ptide-1 receptor agonists and sodium-glucose cotransporter type 2 inhibitors as add-ons to lifestyle

296 tant, may not be critical for sodium-glucose cotransporter type 2 inhibitors in view of the consisten

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

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

299 Apical expression of the two cotransporters was also preserved.

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