ライフサイエンスコーパス: AQP1

1 AQP1 deficiency is associated with a marked reduction of

2 AQP1 deficiency reduced plasma membrane water permeabili

3 AQP1 deletion did not affect choroid plexus size or stru

4 AQP1 deletion did not alter baseline lens morphology or

5 AQP1 expression also increased by 3-fold the number of l

6 AQP1 expression was also studied in extraocular microves

7 AQP1 expression was maximally induced under mild hyperto

8 AQP1 has no known specific interactions with cytoplasmic

9 AQP1 inhibited cyst development and promoted branching i

10 AQP1 intermediates containing the first three TM segment

11 AQP1 is a water channel, and under permissive conditions

12 AQP1 is expressed in the choroid plexus and participates

13 AQP1 is, thus, a novel target for pain management.

14 AQP1 knockout mice demonstrated reduced angiogenesis com

15 AQP1 overexpression decreased beta-catenin and cyclinD1

16 AQP1 protein, but not mRNA, was induced by hyperosmolali

17 AQP1 trafficking was mediated by the tonicity of the cel

18 AQP1 was overexpressed in 62% (13 of 21) and 75% (6 of 8

19 AQP1(+/+) MMTV-PyVT mice developed large breast tumors w

20 AQP1, CFTR, and AE2 were localized preferentially to the

21 AQP1, COL1A1 and CLEC3B were significantly differentiall

22 The water channel aquaporin 1 (AQP1) and certain Rh-family members are permeable to CO(

23 known mercury-sensitive site of aquaporin 1 (AQP1) and determined the X-ray crystal structures of the

24 However, abundantly expressed aquaporin 1 (AQP1) in erythrocytes is thought not to be part of band

25 identified clear expression of aquaporin 1 (AQP1) in seven cell lines.

26 Aquaporin 1 (AQP1) is a plasma membrane water-transporting protein ex

27 Further, our results identify aquaporin 1 (AQP1), a potent effector of fluid volume regulation and

28 Na+/glucose cotransporter, and aquaporin 1 (AQP1), a water channel, to the attachment site.

29 rats had increased abundance of aquaporin 1 (AQP1), AQP3, and Na-K-2Cl co-transporter proteins and a

30 t OEG express the water channel aquaporin 1 (AQP1), both in vivo and in vitro.

31 Expression of aquaporin-1 (AQP1) and -2 (AQP2) channels in the kidney are critical

32 ment epithelium (RPE) expresses aquaporin-1 (AQP1) and components of the natriuretic peptide signalin

33 ivity, and specificity of urine aquaporin-1 (AQP1) and perilipin-2 (PLIN2) concentrations as unique,

34 Aquaporin-1 (AQP1) enables greatly enhanced water flux across plasma

35 Aquaporin-1 (AQP1) expression is induced by hypertonicity in renal me

36 Aquaporin-1 (AQP1) facilitates the osmotic transport of water across

37 tivity, several studies suggest Aquaporin-1 (AQP1) functions as a nonselective monovalent cation chan

38 Aquaporin-1 (AQP1) is a major intrinsic protein that facilitates flux

39 Aquaporin-1 (AQP1) is a water channel expressed strongly at the ventr

40 Aquaporin-1 (AQP1) is a water channel protein expressed widely in vas

41 Aquaporin-1 (AQP1) is a water channel, overexpressed in cirrhosis, th

42 Aquaporin-1 (AQP1) is an integral membrane protein that facilitates o

43 cation permeation in wild-type aquaporin-1 (AQP1) is believed to be associated with the Asn-Pro-Ala

44 Water channel aquaporin-1 (AQP1) is expressed at epithelial cell plasma membranes i

45 Aquaporin-1 (AQP1) is the principal water-transporting protein in cel

46 The aquaporin-1 (AQP1) water channel is a potentially important drug targ

47 xample, in Xenopus oocytes, the aquaporin-1 (AQP1) water channel is cotranslationally directed into a

48 Aquaporin-1 (AQP1) water channels are expressed in the plasma membran

49 Aquaporin-1 (AQP1) water channels are expressed widely in organ and t

50 pe adenoviral vector to express aquaporin-1 (AQP1), presumably in the ductal cell layer and/or in sur

51 UT-B inhibitors did not reduce aquaporin-1 (AQP1)-facilitated water transport.

52 observed for several including aquaporin-1 (AQP1).

53 le is mediated predominantly by aquaporin-1 (AQP1).

54 emonstrate for the first time that the IL-10-AQP1 axis is a novel regulator of PCB-induced in utero e

55 With CO(2), AQP1 oocytes also have faster time constants for pH(S) r

56 Exposed to CO(2) or NH(3), AQP1 oocytes exhibit a greater maximal magnitude of pH(S

57 usly to facilitate rapid cell migration in a AQP1-expressing colon cancer cell line.

58 lowed frequency-dependent inactivation after AQP1 transfection.

59 logs in the presence of anantin, H-8, and an AQP1 inhibitor, AqB013.

60 ay involve inhibition of Wnt signaling by an AQP1-macromolecular signaling complex.

61 the time-dependent behavior of the AQP0 and AQP1 channels within lipid bilayers.

62 structures of water-selective AQPs AqpZ and AQP1, the asparagines of the 2 Asn-Pro-Ala motifs do not

63 ssays revealed close association of CAII and AQP1, an effect requiring the second acidic cluster of A

64 y a significant decrease in THP-, NKCC2- and AQP1-positive loop of Henle nephron segments in mutant D

65 f various cations through the AQP1-R195V and AQP1-R195S mutants are predicted computationally.

66 of proximal tubule cells from wild-type and AQP1 null mice.

67 acement of the glycine at this site in AQP0, AQP1, and AQP2 blocked expression of the mutants at the

68 ssion of AQP4, or of an unrelated aquaporin, AQP1, increased cytokine secretion in astrocyte and nona

69 mice and on knockout mice lacking aquaporins AQP1, AQP3, and AQP5.

70 l is a potentially important drug target, as AQP1 inhibition is predicted to have therapeutic action

71 ere we investigated the relationship between AQP1 and Wnt signaling in in vitro and in vivo models of

72 Both AQP1 mutants exhibit a surprising cooperative effect lea

73 tricular infusion rates, was not affected by AQP1 deletion.

74 n physiological salines were not affected by AQP1-siRNA treatment.

75 om wild-type mice and reduced by fivefold by AQP1 deletion.

76 ent of the net fluid flux in RPE mediated by AQP1 channels.

77 Moreover, functional inhibition of host-cell AQP1 and SGLT1 hampers C. parvum invasion of cholangiocy

78 idues in the high-permeability water channel AQP1 have additive effects and together increase the wat

79 ontain three proteins (ie, the water channel AQP1, the chloride channel CFTR, and the anion exchanger

80 duced by co-expression of a cognate channel, AQP1.

81 l events of AQP1 biogenesis reflect a common AQP1 folding pathway in diverse expression systems.

82 In conclusion, AQP1 promotes angiogenesis, fibrosis, and portal hyperte

83 creatinine) than in the 80 healthy controls (AQP1 median [95% CI], 1.1 [0.9-1.3] ng/mg urine creatini

84 transport in the choroid plexus; conversely, AQP1 block with 500 mum Cd2+ restores fluid transport.

85 In embryonic kidney cultures, AQP1 deletion increased cyst development by up to approx

86 nduced AQP1 expression, whereas it decreased AQP1 expression in N100.

87 By demonstrating AQP1 as a mobile component of the CO2 transport metabolo

88 sults are the first to identify differential AQP1 modulators isolated from a medicinal plant.

89 rogenesis in vivo and the mechanisms driving AQP1 expression during cirrhosis remain unclear.

90 t present, pharmacologic agents that enhance AQP1-mediated water transport, which would be expected t

91 de channel ClC-5 had constitutively enhanced AQP1 abundance in the proximal tubule brush border membr

92 the addition of cyclic nucleotides enhanced AQP1 surface expression and concomitantly diminished its

93 Here we re-examine AQP1 biogenesis and show that irrespective of the report

94 n and rat erythrocytes that natively express AQP1, in hemoglobin-free membrane vesicles from rat and

95 inal endothelia have the capacity to express AQP1, though intact retinal vessels chronically suppress

96 ithelial cells, which endogenously expressed AQP1, and of oocytes, which exogenously expressed AQP0.

97 e that secretes CSF and abundantly expresses AQP1, we confirmed the ion channel function of AQP1 and

98 The order of potency for AQP1 ion channel block matched the order for inhibition

99 n stability are the likely prerequisites for AQP1 activation by enhanced tubular fluid shear stress,

100 Here, a novel role for AQP1 in kidney involving the migration of proximal tubul

101 ound that the intracellular binding site for AQP1 involves loop D, a region associated with channel g

102 of aortic endothelia from wild-type and from AQP1-null mice, cell migration was greatly impaired in A

103 Cell cultures from AQP1 null mice were indistinguishable from those of wild

104 ts in the choroid plexus were dissected from AQP1 currents using Cs-methanesulfonate recording saline

105 nd in plasma membrane vesicles isolated from AQP1-transfected Chinese hamster ovary cell cultures.

106 ability in freshly isolated DRG neurons from AQP1(-/-) versus AQP1(+/+) mice.

107 the sequence was AQP4 congruent with AQP5 > AQP1 > AmtB > RhAG.

108 pH(S)(CO(2))*/P(f)*, the sequence was AQP5 > AQP1 congruent with AQP4.

109 er channel in maintaining fluid homeostasis, AQP1 also acts as a nonselective cation channel gated by

110 However, AQP1 was expressed in endothelial cells cultured from re

111 Human AQP1 was analyzed in the Xenopus laevis oocyte expressio

112 t point where the two helices cross in human AQP1.

113 Wild-type and mutant human AQP1 channels expressed in Xenopus laevis oocytes were c

114 26 potentiated the channel activity of human AQP1 by >20% but had no effect on channel activity of AQ

115 These results implicate AQP1 as a novel determinant in renal cyst development th

116 These results implicate AQP1 as an important determinant of tumor angiogenesis a

117 In AQP1-null erythrocytes, "chemical UT-B knockout" by UT-B

118 In AQP1-transfected, cultured proximal tubule cells, fluid

119 reated), and reduced by approximately 25% in AQP1 null mice.

120 te led to a 54 +/- 5% (p < 0.01) decrease in AQP1 luciferase-driven activity under hypertonic stress.

121 ion and increased beta-catenin expression in AQP1-null PKD mice, suggesting enhanced Wnt signaling.

122 ency was accelerated by more than 50-fold in AQP1-null lenses bathed in a 55-mM glucose solution for

123 nd cyst number were significantly greater in AQP1-null PKD mice than in AQP1-expressing PKD mice, wit

124 we show remarkably impaired tumour growth in AQP1-null mice after subcutaneous or intracranial tumour

125 in wild-type mice and 4.2 +/- 0.4 cm H2O in AQP1 null mice.

126 mice, cell migration was greatly impaired in AQP1-deficient cells, with abnormal vessel formation in

127 wer than control rats despite an increase in AQP1, AQP3, and Na-K-2Cl co-transporter expression.

128 o 5 d after ischemia-reperfusion, kidneys in AQP1 null mice showed remarkably greater tubular injury

129 uced thermal inflammatory pain perception in AQP1(-/-) mice evoked by bradykinin, prostaglandin E(2),

130 tched properties characterized previously in AQP1-expressing oocytes.

131 The reduced ICP and CSF production in AQP1 null mice provides direct functional evidence for t

132 [K(+)] was mildly reduced in AQP1 null mice.

133 /-15 mm(3), 12 mice) were greatly reduced in AQP1(-/-) MMTV-PyVT mice (P<0.005).

134 technology led to a substantial reduction in AQP1 expression under hypertonic conditions.

135 hat hypertonicity plays an important role in AQP1 induction, stability, and degradation.

136 astases (5+/-1/mouse) was much lower than in AQP1(+/+) MMTV-PyVT mice (31+/-8/mouse, P<0.005).

137 cantly greater in AQP1-null PKD mice than in AQP1-expressing PKD mice, with the difference mainly att

138 1alpha expression was increased in tumors in AQP1(-/-) MMTV-PyVT mice.

139 impaired angiogenesis in implanted tumors in AQP1-deficient mice and reduced migration of AQP1-defici

140 otif was also necessary for CAII to increase AQP1-mediated water flux.

141 microM significantly inhibited or increased AQP1 water permeability in these assays.

142 ock treatment promoted hypertonicity-induced AQP1 and heat shock protein 70 (HSP70) expression in bot

143 at shock that regulate hypertonicity-induced AQP1 expression are potentially important factors in uri

144 ntrary, urea inhibited hypertonicity-induced AQP1 expression in a dose-dependent manner.

145 ine, and heat shock on hypertonicity-induced AQP1 expression in cultured murine renal medullary-K2 (m

146 omoter are involved in hypertonicity-induced AQP1 expression in mIMCD-3 cells.

147 continuously to N100, hypertonicity-induced AQP1 expression was elevated, whereas the return to isot

148 taine in N150 enhanced hypertonicity-induced AQP1 expression, whereas it decreased AQP1 expression in

149 ct on the stability of hypertonicity-induced AQP1 expression.

150 ess and thus attenuate hypertonicity-induced AQP1 expression.

151 uggest the potential for success by inducing AQP1 expression in human salivary ductal cells through e

152 s a positive control, 0.3 mM HgCl2 inhibited AQP1 water permeability by >95%.

153 In a model of focal brain injury, AQP1 null mice had remarkably reduced ICP and improved s

154 oliferation in oxygen-induced retinopathy is AQP1-independent.

155 gle-particle tracking of quantum dot-labeled AQP1.

156 nificantly impaired in neonatal mice lacking AQP1, as quantified in flat-mounted retinas and thin sec

157 Forced expression of full-length AQP1 cDNA in NIH-3T3 cells induced many phenotypic chang

158 Lens AQP1 does not have a similar domain and does not have ca

159 Lens AQP1 facilitates the maintenance of transparency and opp

160 Lens AQP1 lacks His40 and also lacks pH sensitivity.

161 mented with 150 mM NaCl (N150) caused little AQP1 induction.

162 s substratum-free pellets keratocyte markers AQP1, B3GNT7, PTDGS, and ALDH3A1 were upregulated.

163 ocytic function and expression of TM markers AQP1, CHI3L1, and TIMP3.

164 , OCT-3/4, AnkG, and MUC1 but not TM markers AQP1, MGP, CHI3L1, or TIMP3.

165 In mice, AQP1 expression increased tumor cell extravasation by >1

166 ition efficacy of 12 putative small-molecule AQP1 inhibitors reported in six recent studies, and one

167 Motile AQP1-expressing cells had prominent membrane ruffles at

168 at aquaporin isoforms AQP3 and AQP8, but not AQP1, can promote uptake of H(2)O(2) specifically throug

169 In MDCK cells, approximately 60% of AQP1 diffused freely, with D(1-3) approximately 3 x 10(-

170 In transfected COS-7 cells, >75% of AQP1 molecules diffused freely over approximately 7 mum

171 this finding, we found that the abundance of AQP1 in brush border apical and basolateral membranes wa

172 oviding evidence against the accumulation of AQP1 in lipid rafts.

173 (IC50 117 muM) and ion channel activities of AQP1 but did not alter AQP4 activity, whereas bacopaside

174 nnel, but not the water channel, activity of AQP1.

175 ffect requiring the second acidic cluster of AQP1.

176 Here, we investigated the consequences of AQP1 deficiency in mice that spontaneously develop well-

177 significantly reduced the protein content of AQP1.

178 lts establish the nature and determinants of AQP1 diffusion in cell plasma membranes and demonstrate

179 The determinants of AQP1 diffusion were investigated by measurements of AQP1

180 We tracked the membrane diffusion of AQP1 molecules labeled with quantum dots at an engineere

181 nstrate long-range nonanomalous diffusion of AQP1, challenging the prevailing view of universally ano

182 pose of this study was to test the effect of AQP1 deletion in cirrhosis and explore mechanisms regula

183 The effect of AQP1 on fibrogenesis in vivo and the mechanisms driving

184 proteins and (ii) cotranslational events of AQP1 biogenesis reflect a common AQP1 folding pathway in

185 was a reflection of endogenous expression of AQP1 and AQP8.

186 Adenoviral-mediated expression of AQP1 in the AQP1-deficient cells, which increased their

187 isplay marked decrement in the expression of AQP1 in the inner medulla.

188 ave shown that luminal surface expression of AQP1 in the proximal tubule brush border membrane is reg

189 hypothesized that the surface expression of AQP1 is regulated by fluid shear stress, contributing to

190 lutes, or the localization and expression of AQP1 on the plasma membrane.

191 Expression of AQP1 with CAII in Xenopus oocytes or mammalian cells inc

192 Although expression of AQP1, -3, -4, -5, -8, -9, and -11 has been reported in t

193 regulated the mRNA and protein expression of AQP1, suggesting that its activation occurs at a transcr

194 P1, we confirmed the ion channel function of AQP1 and assessed its functional relevance.

195 This suggests that the function of AQP1 in tonicity response could be coupled or correlated

196 further details on the molecular function of AQP1 related to tumorigenesis remain to be elucidated, o

197 Identification of AQP1 inhibitors remains an important priority.

198 Inhibition of AQP1 ionic conductance could be a useful adjunct therape

199 t functional evidence for the involvement of AQP1 in CSF dynamics, suggesting AQP1 inhibition as a no

200 Our results implicate the involvement of AQP1 in DRG neurons for the perception of inflammatory t

201 ults provide evidence for the involvement of AQP1 in migration of proximal tubule cells and possibly

202 id plexus is lost with targeted knockdown of AQP1 by small interfering RNA (siRNA), as confirmed by i

203 and contribute to the steady-state level of AQP1 expression.

204 orylation-dependent increase in the level of AQP1 trafficking resulting in membrane localization.

205 ncer cell lines, with high and low levels of AQP1 expression, respectively.

206 The half-life of AQP1 protein in isotonic conditions was approximately 4

207 e of overexpression and abnormal location of AQP1, CFTR, and AE2 in cystic cholangiocytes.

208 ed by either suppression of AQP1 by means of AQP1-small interfering RNA (siRNA) or inhibition of SGLT

209 ffusion were investigated by measurements of AQP1 diffusion following skeletal disruption (latrunculi

210 Comparable slowing of migration of AQP1-deficient cells was also found in an in vitro scrat

211 Migration of AQP1-deficient cells was reduced by >50% compared with w

212 AQP1-deficient mice and reduced migration of AQP1-deficient endothelial cells in vitro.

213 Here we report two new modulators of AQP1 channels, bacopaside I and bacopaside II, isolated

214 Interestingly, overexpression of AQP1 and AQP3 showed no differences in extracellular sig

215 calmodulin activation and phosphorylation of AQP1 at two threonine residues by protein kinase C.

216 les at the leading edge with polarization of AQP1 protein to lamellipodia, where rapid water fluxes o

217 007 significantly reduced migration rates of AQP1-positive HT29 cells without affecting viability.

218 The reduction of AQP1 expression in N150 was associated with reduced cell

219 ng of the miRs to the untranslated region of AQP1 was assessed using luciferase assays.

220 at TonEBP is necessary for the regulation of AQP1 expression in the inner medulla of the kidney under

221 In contrast, no up-regulation of AQP1 was observed when these cells were exposed to the s

222 a master switch regulating responsiveness of AQP1 ion channels to cGMP, and the tetrameric central po

223 ted, our results suggest a potential role of AQP1 as a novel therapeutic target for the management of

224 The role of AQP1 in endothelial cell function is unknown.

225 of this study was to investigate the role of AQP1 in retinal vessel proliferation.

226 ggested that pretranscriptional silencing of AQP1 in salivary glands is mediated by methylation of th

227 The atomic structure of AQP1 and amino acid sequence alignments of the mammalian

228 x that is inhibited by either suppression of AQP1 by means of AQP1-small interfering RNA (siRNA) or i

229 The cytosolic carboxy terminus of AQP1 has two acidic motifs homologous to known carbonic

230 QP0 40-fold to a level comparable to that of AQP1.

231 ible manipulation of cellular trafficking of AQP1.

232 abnormal microvascular anatomy in tumors of AQP1(-/-) MMTV-PyVT mice, with reduced vessel density.

233 controversy and expand our understanding of AQP1 as a multifunctional regulated channel.

234 hat cytoskeletal disruption had no effect on AQP1 diffusion in the plasma membrane, but that diffusio

235 tors reported in six recent studies, and one AQP1 activator.

236 le duct ligation, wild-type mice overexpress AQP1 that colocalizes with vascular markers and sites of

237 imilar to that of the highly water permeable AQP1.

238 e) and the 720 patient screening population (AQP1 median [95% CI], 0.5 [0.0-1.0] ng/mg urine creatini

239 AqF026 directly and specifically potentiates AQP1-mediated water transport, suggesting that it deserv

240 e of the three brain water-channel proteins (AQP1, AQP4, AQP9) in brain physiology.

241 P < .001) in the 19 patients with known RCC (AQP1 median [95% CI], 225.0 [121.0-450.0] ng/mg urine cr

242 Recently, AQP1 was reported to interact with beta-catenin.

243 hereas the return to isotonic medium reduced AQP1 expression in a time-dependent manner.

244 cirrhosis and explore mechanisms regulating AQP1.

245 l depletion in MDCK cells greatly restricted AQP1 diffusion, consistent with the formation of a netwo

246 ound that demethylation alone induced robust AQP1 expression.

247 signaling, and coimmunoprecipitation showed AQP1 interaction with beta-catenin, glycogen synthase ki

248 Immunofluorescence showed AQP1 expression in wild-type mice in epithelial cells co

249 Immunoprecipitation studies showed AQP1- Na(v)1.8 Na(+) interaction, which was verified in

250 of the six wild-type mice and in six of six AQP1-null mice.

251 olvement of AQP1 in CSF dynamics, suggesting AQP1 inhibition as a novel option for therapy of elevate

252 intact retinal vessels chronically suppress AQP1 expression.

253 Surprisingly, AQP1 immunoreactivity was detected in only a small perce

254 jection of a mixture of fluorescently tagged AQP1-expressing and control tumor cells.

255 miR-666 and miR-708 targeted AQP1 mRNA and were decreased in cirrhosis and in cells e

256 AQP1-R195S having a higher conductance than AQP1-R195V.

257 These results confirm that AQP1 can function as both a water channel and a gated io

258 We found that AQP1 expression was induced at a magnitude comparable to

259 We propose that AQP1 expression represents an important distinguishing c

260 olarized choroid plexus cultures showed that AQP1 current activation by 4.5 mum ANP decreases the nor

261 ble to adenoviral infection, suggesting that AQP1 is primarily silenced through pretranscriptional me

262 an artificial transcriptional complex at the AQP1 locus in A253 and hS/PCs.

263 hereas bacopaside II selectively blocked the AQP1 water channel (IC50 18 muM) without impairing the i

264 n AQP0 to be substantially lower than in the AQP1 pore.

265 nd the hypertonicity response element in the AQP1 promoter are involved in hypertonicity-induced AQP1

266 denoviral-mediated expression of AQP1 in the AQP1-deficient cells, which increased their water permea

267 Here, we measured the AQP1 inhibition efficacy of 12 putative small-molecule A

268 ve AqB011 was the most potent blocker of the AQP1 ion conductance (IC50 of 14 muM), with no effect on

269 rt the hypothesis that responsiveness of the AQP1 ionic conductance to cGMP is governed by tyrosine p

270 We next examined the distribution of the AQP1 protein in several types of primary lung tumors (16

271 This is confirmed by the distribution of the AQP1 water channel within endothelial membranes.

272 a 2- to 3-fold accelerated migration of the AQP1-expressing tumor cells compared to control cells.

273 The conclusion that the AQP1-associated cation current contributes to modulating

274 he permeation of various cations through the AQP1-R195V and AQP1-R195S mutants are predicted computat

275 th CAII increasing water conductance through AQP1 by a physical interaction between the two proteins.

276 e CAII failed to increase water flux through AQP1.

277 Thus, AQP1, but not the other proteins, conduct CO(2) and NH(3

278 alian cells increased water flux relative to AQP1 expression alone.

279 In addition to mediating fluid transport, AQP1 expression facilitates rapid cell migration in cell

280 t receptor potential channels, which trigger AQP1 translocation.

281 ns are experimentally confirmed in wild-type AQP1 and the mutants expressed in Xenopus oocytes.

282 hosphorylation, suggesting that AQP5, unlike AQP1, may be involved in signal transduction.

283 ducing metastasis in cancers that upregulate AQP1 expression.

284 Urine AQP1 and PLIN2 concentrations were measured by sensitive

285 Urine AQP1 and PLIN2 concentrations were significantly higher

286 ver operating characteristic curve for urine AQP1 and PLIN2 concentrations individually or in combina

287 ility, specificity, and sensitivity of urine AQP1 and PLIN2 to diagnose RCC.

288 Reduced uterine AQP1 levels were associated with defective spiral artery

289 y isolated DRG neurons from AQP1(-/-) versus AQP1(+/+) mice.

290 e studies were performed on wild-type versus AQP1-null mice.

291 that these miRs mediate osmolar changes via AQP1.

292 in isolated choroid plexus of wild-type vs. AQP1 null mice, as well as intracranial pressure (ICP) a

293 f newly formed retinal microvessels, whereas AQP1 was strongly expressed in all choroidal and hyaloid

294 s and epigenetic editing, to explore whether AQP1 expression could be achieved by activating the nati

295 P-gated cationic conductance associated with AQP1 is activated by an endogenous receptor guanylate cy

296 nsfection of B16F10 and 4T1 tumor cells with AQP1 did not affect their appearance, size, growth, or s

297 e transfection of non-endothelial cells with AQP1 or with a structurally different water-selective tr

298 CAII colocalizes with AQP1 in the renal proximal tubule.

299 es were performed on wild-type compared with AQP1 null mice using an established mouse model of oxyge

300 water configurations in the SF region, with AQP1-R195S having a higher conductance than AQP1-R195V.

301 s, with alveolar wall infiltration seen with AQP1-expressing tumor cells.