ライフサイエンスコーパス: AQP2

1 riptional regulation is highly selective for Aqp2.

2 interactions involved in cellular sorting of AQP2.

3 idney and in HEK-293 cells stably expressing AQP2.

4 th the translation rate and the half-life of AQP2.

5 cytosis and a 20% decrease in endocytosis of AQP2.

6 calcitonin-induced membrane accumulation of AQP2.

7 rane, but co-treatment with ATP internalized AQP2.

8 Ser269) in the carboxyl-terminal tail of rat AQP2.

9 enhances apical plasma membrane retention of AQP2.

10 phorylation and apical surface expression of AQP2.

11 in greater levels of AQP2 and phosphorylated AQP2.

12 an important role of EHD4 in trafficking of AQP2.

13 opressin-regulated genes (of 3659) including Aqp2.

14 o-IP) studies in mpkCCD14 cells uncovered an AQP2/14-3-3 interaction that was modulated by acute dDAV

15 lasmon resonance studies determined that the AQP2/14-3-3 interaction was modulated by phosphorylation

16 AQP2, a channel that appears to facilitate drug accumula

17 ut mice also expressed lower levels of pS256-AQP2, a phosphorylated form crucial for membrane traffic

18 without CHIP E3 ligase activity had greater AQP2 abundance and altered renal water handling, with de

19 It also led to an increased AQP2 abundance associated with alterations in phosphoryl

20 Whereas AQP2 abundance decreased after 3 h of hyperosmotic chall

21 vasopressin analog dDAVP increased Ser(P)269-AQP2 abundance more than 10-fold, but at a rate much slo

22 motic conditions and blunted the increase of AQP2 abundance that was induced after 24 h of hypertonic

23 tically modified mice revealed that RhoA and AQP2 accumulate at the apical surface of the collecting

24 2 trafficking and that hypertonicity-induced AQP2 accumulation at the cell surface depends on MAP kin

25 nt AQP2 trafficking or hypertonicity-induced AQP2 accumulation in the TGN.

26 t dDAVP increased mRNA and protein levels of AQP2 alongside 14-3-3beta and -zeta, whereas levels of 1

27 Confocal microscopy revealed that AQP2 also accumulated in the trans-Golgi network (TGN) f

28 periments, P2R activation decreased membrane AQP2 and AQP2-mediated water permeability in Xenopus ooc

29 separately heterozygous for floxed wild-type AQP2 and AQP2-T126M were bred to produce hemizygous mice

30 Both AQP2 and AQP3 gained access to the surface plasma membra

31 llary CD cells potentiated the expression of AQP2 and AQP3 mRNA, and cAMP production induced by dDAVP

32 oding two closely related aquaglyceroporins, AQP2 and AQP3, was linked to MPXR in a high-throughput l

33 t AQP2 reversed MPXR in cells lacking native AQP2 and AQP3.

34 sible role of cdks in the phosphorylation of AQP2 and identified a new PKA-independent pathway regula

35 In vitro, disturbing the interaction between AQP2 and integrin beta1 by mutating the RGD motif led to

36 We find that AQP2 and MAL are coexpressed in epithelial cells of the

37 to either glucose or NaCl, upregulated renal AQP2 and NKCC2 in vivo in BB rats.

38 d by increases in cell surface expression of AQP2 and osmotic water permeability in the absence of fo

39 Immunohistochemistry demonstrated increased AQP2 and p-AQP2 expression and trafficking to the apical

40 However, localization of both AQP2 and pAQP2 in the renal inner medullary principal ce

41 iquitylation, resulting in greater levels of AQP2 and phosphorylated AQP2.

42 TS family TRs in cell-specific expression of AQP2 and point to HOX, RXR, CREB and GATA family TRs as

43 ng cells results in membrane accumulation of AQP2 and reduced endocytosis of rhodamine-transferrin.

44 The relationship between AQP2 and S-glutathionylation is of potential interest be

45 rating co-localization of LC3 and Lamp1 with AQP2 and several other down-regulated proteins in IMCD c

46 y, these results suggest that CHIP regulates AQP2 and subsequently, renal water handling.

47 CD spectroscopy indicated that wild-type AQP2 and the phospho-mimicking mutants had similar overa

48 ated forms of the water channel aquaporin-2 (AQP2) and modulate its function.

49 Total aquaporin 2 (AQP2) and phospho-S256-AQP2 (pAQP2) protein expression i

50 between the renal water channel aquaporin-2 (AQP2) and the lysosomal trafficking regulator-interactin

51 f aquaporin-2 (AQP2), phosphorylated AQP2 (p-AQP2), and AQP3 in the inner medulla and in the outer me

52 chloride co-transporter (NCC), aquaporin 2 (AQP2), and EGFR abundances using western blot.

53 AMP-promoted phosphorylation of aquaporin-2 (AQP2), and increased abundance of AQP2 on the apical mem

54 expression and apical trafficking of AQP2, p-AQP2, and increased AQP3 protein expression.

55 teraction is part of a process that controls AQP2 apical membrane abundance in a vasopressin-dependen

56 hout pS256, and pS269 alone is important for AQP2 apical membrane accumulation under some conditions.

57 otinib, a selective EGFR inhibitor, enhanced AQP2 apical membrane expression in collecting duct princ

58 The S256-phosphorylated form of AQP2 appears to interact more extensively with MAL than

59 ons of genes coding for the channel proteins Aqp2, Aqp3, Scnn1b (ENaCbeta), and Scnn1g (ENaCgamma), w

60 the effects of acute hypertonic challenge on AQP2 (aquaporin-2) water channel trafficking.

61 m targets PKA and phosphodiesterase PDE4D to AQP2 (aquaporin-2)-bearing vesicles to orchestrate the a

62 utations in the Trypanosoma brucei aquaporin AQP2 are associated with resistance to pentamidine and m

63 Here we present the X-ray structure of human AQP2 at 2.75 A resolution.

64 owever, AVP also causes dephosphorylation of AQP2 at S261.

65 Erlotinib increased phosphorylation of AQP2 at Ser-256 and Ser-269 and decreased phosphorylatio

66 Phosphorylation of AQP2 at Ser269 did not occur when Ser256 was replaced by

67 hich vasopressin-mediated phosphorylation of AQP2 at Ser269:(a) depends on prior PKA-mediated phospho

68 ctivating PKA and causing phosphorylation of AQP2 at serine 256, 264 and 269 residues and dephosphory

69 KCC2) and AQP2, with less phosphorylation of AQP2 at serine 256.

70 lished hypertonicity-induced accumulation of AQP2 at the cell surface but did not affect either vasop

71 eraction was modulated by phosphorylation of AQP2 at various sites in its carboxyl terminus, with Ser

72 ry cAMP, reduced abundance of phosphorylated AQP2 (at both serine-256 and serine-269), and lower urin

73 activation, phosphorylation of aquaporin 2 (AQP2) at serine 256, and translocation of AQP2 to the pl

74 sting conditions, maintains F-actin to block AQP2-bearing vesicles from reaching the plasma membrane)

75 gnaling module to membranes such as those of AQP2-bearing vesicles must be achieved by additional mec

76 Exosomes can transfer functional AQP2 between cells and this represents a novel physiolog

77 involved in controlling the distribution of AQP2 between intracellular vesicles and the apical plasm

78 plays a role in the regulated trafficking of AQP2 between intracellular vesicles and the apical surfa

79 interactions that govern the trafficking of AQP2 between these organelles.

80 d microscale thermophoresis to show that the AQP2 binds LIP5 in a phosphorylation-dependent manner.

81 cy of a critical PKA phosphorylation site on AQP2 both prevented calcitonin-induced membrane accumula

82 Non-phosphorylated AQP2 bound LIP5 with the highest affinity, whereas AQP2-

83 d inhibited clathrin-mediated endocytosis of AQP2, but exerted its effect in a cAMP, PKA and S256 pho

84 show that MAL induces surface expression of AQP2 by attenuating its internalization.

85 tes phosphorylation at four sites within the AQP2 C terminus (Ser(256), Ser(261), Ser(264), and Thr(2

86 bited by ATP, and the Ser-256 residue in the AQP2 C terminus is important for this direct interaction

87 from rat kidney papilla extract using a GST-AQP2 C-terminal fusion protein (GST-A2C) as a bait, by c

88 can phosphorylate different residues in the AQP2 C-terminus, and suggest new strategies to target di

89 phosphorylation of serine 261 residue on the AQP2 C-terminus.

90 framework for understanding why mutations in AQP2 cause NDI as well as structural insights into AQP2

91 Finally, increased AQP2 cell surface expression induced by hypertonicity la

92 lunted the hypertonicity-induced increase of AQP2 cell surface expression.

93 lated cell program from turning on in mature Aqp2(+) cell types.

94 These Aqp2(+) cell-derived intercalated cells were present in

95 In ex vivo kidney slices and MDCK-AQP2 cells, R-roscovitine, a specific inhibitor of cdks,

96 undetectable di-methyl K79, suggesting that Aqp2(+) cells give rise to intercalated cells.

97 ation, which are fundamental for controlling AQP2 cellular localization, stability, and function.

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

99 ls is physiologically regulated and exosomal AQP2 closely reflects cellular expression.

100 s was also able to track changes in exosomal AQP2 concentration that followed desmopressin treatment

101 the exosomal proteins CD24 and aquaporin 2 (AQP2), conjugated to a fluorophore, we could identify a

102 ol exosome treatment 52.8 +/- 11 mul cm(-2); AQP2-containing exosomes 77.4 +/- 4 mul cm(-2), P = 0.05

103 enes: ZBTB24, WFS1, HPSE2, ATRX, ASPH, AGXT, AQP2, CTNS, and PKHD1 Notably, when mutated, these genes

104 ound LIP5 with the highest affinity, whereas AQP2-DeltaP242 had 20-fold lower affinity as determined

105 tes characterized by an oxidative stress and AQP2-dependent water reabsorption disturbs.

106 The C terminus of AQP2 displays multiple conformations with the C-terminal

107 ed in the IMCD but not PT or MTAL (candidate AQP2 enhancer roles), and 5 TRs (including HoxA5, HoxA9

108 of 131 proteins, including the water channel AQP2, exhibited significant changes in abundance, most o

109 rough PKA activation, vasopressin stimulates AQP2 exocytosis by inhibiting MAP kinase signaling.

110 ner that was highly correlated with cellular AQP2 (exosomal AQP2 vs. cellular AQP2, Pearson correlati

111 o-IP with phosphorylation deficient forms of AQP2 expressed in HEK293 cells, or surface plasmon reson

112 Functional knockdown of hsc70 activity in AQP2 expressing cells results in membrane accumulation o

113 ing duct, we developed mice lacking Dot1l in Aqp2-expressing cells (Dot1l(AC)) and found that these m

114 rease AQP2 membrane accumulation in cultured AQP2-expressing cells and in kidney collecting duct prin

115 ch signaling was required for maintenance of Aqp2-expressing cells in distal nephron and collecting d

116 some alpha- and beta-intercalated cells from Aqp2-expressing progenitor cells or mature principal cel

117 ochemistry demonstrated increased AQP2 and p-AQP2 expression and trafficking to the apical plasma mem

118 m desmopressin-treated cells stimulated both AQP2 expression and water transport in untreated mCCDc11

119 dulating arginine vasopressin receptor 2 and AQP2 expression in the inner medulla.

120 AQP2 expression modulates the trafficking and internaliz

121 AQP2 expression was similar between the two groups, but

122 trol rats, but both groups exhibited similar AQP2 expression.

123 iagnosis of CN revealed loss of aquaporin 2 (AQP2) expression in collecting ducts in patients with el

124 Furthermore, aquaporin-2 (AQP2) expression in the inner medulla of the ptip knocko

125 olymerase II binding and mRNA abundances for Aqp2 far outstripped corresponding measurements for all

126 The ratio of AQP2/flotillin-1 in the urinary exosome was significantl

127 To test whether the ratio of exosomal AQP2/flotillin-1 is under physiological control in vivo,

128 stribution of the water channel aquaporin-2 (AQP2) from intracellular vesicles into the plasma membra

129 ntal insight into cell biological aspects of AQP2 function and may be relevant to better understand a

130 melarsoprol and pentamidine and that loss of AQP2 function could explain cases of innate and acquired

131 al analysis of the 5'-flanking region of the AQP2 gene (Genomatix) revealed 2 conserved clusters of p

132 e, which following excision of the wild-type AQP2 gene by tamoxifen-induced Cre-recombinase gave AQP2

133 vasopressin signaling selectively increases Aqp2 gene transcription or whether it triggers a broadly

134 ockdown of 14-3-3theta resulted in increased AQP2 half-life and increased AQP2 levels.

135 Here, we show that AQP2 has an unconventional "selectivity filter." AQP2-sp

136 ng or having significantly reduced levels of AQP2, however, have not only urinary concentrating abnor

137 by vasopressin; interacts with aquaporin-2 (AQP2), Hsp70, and Hsc70; and can directly ubiquitylate t

138 Loss of AQP2 in AKI patients with elevated bilirubin and CN migh

139 In summary, the amount of AQP2 in exosomes released from collecting duct cells is

140 cells enhances the interaction of hsc70 with AQP2 in IP assays, and vasopressin stimulation in vivo i

141 t membrane association or apical delivery of AQP2 in LLC-PK(1) renal epithelial cells.

142 and stimulated the membrane accumulation of AQP2 in LLC-PK1 cells.

143 loss of expression of the water-channel gene Aqp2 in PKA knockout cells.

144 le increased plasma membrane localization of AQP2 in principal cells independent of AVP.

145 id (<10 min) plasma membrane accumulation of AQP2 in rat kidney collecting duct principal cells in si

146 n increased the plasma membrane abundance of AQP2 in these cells.

147 can directly ubiquitylate the water channel AQP2 in vitro shRNA knockdown of CHIP in CCD cells incre

148 illin-1 or TSG101 but increased aquaporin 2 (AQP2) in a dose- and time-dependent manner that was high

149 immunolocalized its protein and aquaporin-2 (AQP2) in CD principal cells.

150 expression of the water channel aquaporin-2 (AQP2) in the renal collecting duct.

151 identified the 70-kDa heat shock proteins as AQP2-interacting proteins.

152 ause NDI as well as structural insights into AQP2 interactions that may govern its trafficking.

153 entified the 70-kDa heat shock proteins as a AQP2 interactors and have shown for hsc70 that this inte

154 o-IP studies in HEK293 cells determined that AQP2 interacts selectively with 14-3-3zeta and -theta.

155 Our data also show that AQP2 interacts with hsp70 in multiple in vitro binding a

156 y, these data suggest that the water channel AQP2 interacts with integrins to promote renal epithelia

157 Finally, in addition to hsc70 and hsp70, AQP2 interacts with several other key components of the

158 The trafficking of aquaporin-2 (AQP2) involves multiple complex pathways, including regu

159 Here, we show that AQP2 is not only a water channel but also an integrin-bi

160 Upon stimulation by vasopressin, AQP2 is phosphorylated at serine 256 (S256), S264 and S2

161 Here, we show for the first time that AQP2 is subjected to S-glutathionylation in kidney and i

162 Human aquaporin 2 (AQP2) is a water channel found in the kidney collecting

163 Aquaporin-2 (AQP2) is crucial for water homeostasis, and vasopressin

164 Aquaporin-2 (AQP2) is essential for water homeostasis.

165 Aquaporin-2 (AQP2) is the vasopressin-regulated water channel that co

166 radation of proteins, most notably including AQP2, is an early event in hypokalemia-induced NDI.

167 r binding protein, a transcription factor of AQP2, is not altered in the mutant mice, but its nuclear

168 ecreased AQP2 protein half-life, and reduced AQP2 levels.

169 ed in increased AQP2 half-life and increased AQP2 levels.

170 ever, whether AQP2 phosphorylation modulates AQP2-LIP5 complex affinity is unknown.

171 We assessed the influence of fluconazole on AQP2 localization in vitro and in vivo as well as the dr

172 Basolateral exposure to dDAVP induced AQP2 localization to the apical membrane, but co-treatme

173 drug fluconazole as a potential modulator of AQP2 localization.

174 More recently, aquaglyceroporin 2 (AQP2) loss of function was linked to melarsoprol-pentami

175 , P2R activation decreased membrane AQP2 and AQP2-mediated water permeability in Xenopus oocytes expr

176 athway that contributes to the regulation of AQP2-mediated water reabsorption and suggest new potenti

177 In summary, these data suggest that AQP2-mediated water transport is downregulated not only

178 of S269 independently of pS256, and induces AQP2 membrane accumulation by inhibiting clathrin-mediat

179 bitor dasatinib and siRNA, we could increase AQP2 membrane accumulation in cultured AQP2-expressing c

180 , and found that dasatinib no longer induced AQP2 membrane accumulation.

181 ells, resulting in a significant increase in AQP2 membrane accumulation.

182 269 is important for Src inhibition-induced AQP2 membrane accumulation; without serine 269, Src inhi

183 d design new strategies to induce or sustain AQP2 membrane expression when VP signalling is defective

184 Src inhibition causes serine 256-independent AQP2 membrane trafficking and induces phosphorylation of

185 er homeostasis, and vasopressin (VP) induces AQP2 membrane trafficking by increasing intracellular cA

186 ere polyuric (9-14 ml urine/day) compared to AQP2(+/+) mice (1.6 ml/day) and had reduced urine osmola

187 /-) mice by >300 mosmol but had no effect in AQP2(-/-) mice.

188 he cytoplasmic surface of a symmetry-related AQP2 molecule, suggesting potential protein-protein inte

189 In the presence of vasopressin, AQP2 monophosphorylated at S256 and diphosphorylated AQP

190 (pS256/261) increased in abundance, whereas AQP2 monophosphorylated at S261 decreased, raising the p

191 owed a significant positive correlation with AQP2 mRNA abundance among mpkCCD subclones (Ets1), and 2

192 n inhibitory form of TonEBP strongly reduced AQP2 mRNA and protein content under iso-osmotic conditio

193 orylatable amino acid, as seen in both S256L-AQP2 mutant mice and in Madin-Darby canine kidney cells

194 ney cells expressing an S269D "phosphomimic" AQP2 mutant showed constitutive localization at the plas

195 AQP2 mutants that mimic the Ser(256)-phosphorylated and

196 Prior gene knock-in of the human NDI-causing AQP2 mutation T126M produced mutant mice that died by ag

197 Similarly, in vivo, AQP2-null mice exhibited significant retention of integr

198 es an increased co-localization of hsc70 and AQP2 on the apical membrane of principal cells in rat ki

199 uaporin-2 (AQP2), and increased abundance of AQP2 on the apical membrane.

200 levels of aquaporin-2 (AQP2), phosphorylated AQP2 (p-AQP2), and AQP3 in the inner medulla and in the

201 creased expression and apical trafficking of AQP2, p-AQP2, and increased AQP3 protein expression.

202 Total aquaporin 2 (AQP2) and phospho-S256-AQP2 (pAQP2) protein expression in the inner medulla was

203 th cellular AQP2 (exosomal AQP2 vs. cellular AQP2, Pearson correlation coefficient r = 0.93).

204 n-dependent kinases (cdks) can phosphorylate AQP2 peptides at S261 in vitro.

205 increased the protein levels of aquaporin-2 (AQP2), phosphorylated AQP2 (p-AQP2), and AQP3 in the inn

206 Our data suggest that AQP2 phosphorylation allosterically controls its interac

207 and in vivo as well as the drug's effects on AQP2 phosphorylation and RhoA (a small GTPase, which und

208 etermines inner medullary cAMP formation and AQP2 phosphorylation and trafficking, the absence of whi

209 However, whether AQP2 phosphorylation modulates AQP2-LIP5 complex affinit

210 The changes in AQP2 phosphorylation status were paralleled by increases

211 mice, fluconazole increased collecting duct AQP2 plasma membrane localization and reduced urinary ou

212 Fluconazole promotes collecting duct AQP2 plasma membrane localization in the absence of AVP.

213 could identify a subpopulation of CD24- and AQP2-positive particles of characteristic exosomal size.

214 E had affinity similar to non-phosphorylated AQP2, possibly indicating a role in exosome excretion.

215 reduction in the percentage of aquaporin 2 (Aqp2)(+) principal cells (PCs) in the collecting ducts t

216 family TRs transactivated the mouse proximal AQP2 promoter.

217 ia, improved urine concentrating ability and AQP2 protein abundance, and reversed the lithium-induced

218 in increased AQP2 ubiquitylation, decreased AQP2 protein half-life, and reduced AQP2 levels.

219 nificantly increased urine concentration and AQP2 protein in the kidneys of Sprague-Dawley rats.

220 RNA knockdown of CHIP in CCD cells increased AQP2 protein t1/2 and reduced AQP2 ubiquitylation, resul

221 abundances of the water channel aquaporin-2 (AQP2) protein and regulatory proteins in the renal colle

222 ophosphorylated at S256 and diphosphorylated AQP2 (pS256/261) increased in abundance, whereas AQP2 mo

223 To confirm the importance of pS269 in AQP2 re-distribution, we expressed an AQP2 S269A mutant

224 proteins have been indirectly implicated in AQP2 recycling, the direct protein-protein interactions

225 de that the unconventional aquaglyceroporin, AQP2, renders cells sensitive to both melarsoprol and pe

226 ed in PT and MTAL but not in IMCD (candidate AQP2 repressor roles).

227 dependent pathways that can target different AQP2 residues, and design new strategies to induce or su

228 a lipophilic arsenical, whereas recombinant AQP2 reversed MPXR in cells lacking native AQP2 and AQP3

229 d that in fresh kidney slices, the increased AQP2 S-glutathionylation correlated with tert-butyl hydr

230 ; hCaSR-N124K) had a significant decrease in AQP2 S-glutathionylation secondary to reduced ROS levels

231 AQP2-S256E, S261E, T269E, and S256E/T269E all had reduce

232 This effect was most prominent for AQP2-S256E, which fits well with its role in apical memb

233 AQP2-S264E had affinity similar to non-phosphorylated AQ

234 269 in AQP2 re-distribution, we expressed an AQP2 S269A mutant in LLC-PK1 cells, and found that dasat

235 Conversely, EGF reduced VP-induced AQP2 Ser-256 phosphorylation, suggesting crosstalk betwe

236 nd suggest new strategies to target distinct AQP2 serine residues to induce membrane expression of th

237 gold electron microscopy localized Ser(P)269-AQP2 solely in the apical plasma membrane of rat collect

238 has an unconventional "selectivity filter." AQP2-specific gene knockout generated MPXR trypanosomes

239 NDI-causing mutations can be observed in the AQP2 structure, primarily situated within transmembrane

240 17-AAG increased urine osmolality in AQP2(T126M/-) mice by >300 mosmol but had no effect in A

241 Kidneys of AQP2(T126M/-) mice expressed core-glycosylated AQP2-T126

242 Kidneys of 17-AAG-treated AQP2(T126M/-) mice showed partial rescue of defective AQ

243 AQP2(T126M/-) mice were polyuric (9-14 ml urine/day) com

244 ne by tamoxifen-induced Cre-recombinase gave AQP2(T126M/-) mice.

245 M/-) mice showed partial rescue of defective AQP2-T126M cellular processing.

246 l gene knock-in" strategy to generate adult, AQP2-T126M mutant mice.

247 6M-transfected kidney cells showed increased AQP2-T126M plasma membrane expression with the Hsp90 inh

248 P2(T126M/-) mice expressed core-glycosylated AQP2-T126M protein in an endoplasmic reticulum pattern.

249 y heterozygous for floxed wild-type AQP2 and AQP2-T126M were bred to produce hemizygous mice, which f

250 of candidate protein folding "correctors" in AQP2-T126M-transfected kidney cells showed increased AQP

251 +)-ion binding sites are observed within the AQP2 tetramer, inducing a rearrangement of loop D, which

252 Mutations in aquaporin-2 (AQP2) that interfere with its cellular processing can pr

253 g regulator-interacting protein LIP5 targets AQP2 to multivesicular bodies and facilitates lysosomal

254 onin induced a significant redistribution of AQP2 to the apical membrane of principal cells in cortic

255 2 (AQP2) at serine 256, and translocation of AQP2 to the plasma membrane.

256 rrier" that obstructs the passive transit of AQP2 to the plasma membrane.

257 , suggesting crosstalk between VP and EGF in AQP2 trafficking and a role of EGF in water homeostasis.

258 thought that S256 is the master regulator of AQP2 trafficking and membrane accumulation, and that its

259 her EGF receptor (EGFR) inhibitors stimulate AQP2 trafficking and reduce urine output.

260 e that acute hypertonicity profoundly alters AQP2 trafficking and that hypertonicity-induced AQP2 acc

261 Water reabsorption is regulated by AQP2 trafficking between intracellular storage vesicles

262 ng proteins form the basis for regulation of AQP2 trafficking by post-translational modifications.

263 show that calcitonin induces cAMP-dependent AQP2 trafficking in cortical collecting and connecting t

264 educed intracellular Ca(2+) levels, promotes AQP2 trafficking independent of the AVP-PKA axis.

265 Bidirectional control of AQP2 trafficking is managed by hormones and signaling en

266 did not affect either vasopressin-dependent AQP2 trafficking or hypertonicity-induced AQP2 accumulat

267 KAP220 impact the actin barrier dynamics and AQP2 trafficking to ensure water homeostasis.

268 t that serine 256 is the master regulator of AQP2 trafficking, and its phosphorylation has to precede

269 eractions play divergent roles in modulating AQP2 trafficking, phosphorylation, ubiquitylation, and d

270 ied a new PKA-independent pathway regulating AQP2 trafficking.

271 horylation of serine-256 and apical membrane AQP2 trafficking.

272 reabsorption, suggesting that it may affect AQP2 trafficking.

273 of AQP2, which is critical to regulation of AQP2 trafficking.

274 er269 and addressed the role of this site in AQP2 trafficking.

275 r hsc70 that this interaction is involved in AQP2 trafficking.

276 sites are involved in vasopressin-dependent AQP2 trafficking.

277 rine 269, Src inhibition exerts no effect on AQP2 trafficking.

278 ative strategies for modulating aquaporin 2 (AQP2) trafficking have been sought.

279 excretion through regulation of aquaporin-2 (AQP2) trafficking in renal collecting duct cells.

280 rough PKA activation, vasopressin stimulates Aqp2 transcription through induction of nuclear transloc

281 which Ser(256) is crucial and sufficient for AQP2 translocation from storage vesicles to the apical m

282 zeta in mpkCCD14 cells resulted in increased AQP2 ubiquitylation, decreased AQP2 protein half-life, a

283 ells increased AQP2 protein t1/2 and reduced AQP2 ubiquitylation, resulting in greater levels of AQP2

284 AQP2 undergoes different regulated post-translational mo

285 any sample processing, NTA tracked exosomal AQP2 upregulation induced by desmopressin stimulation of

286 ghly correlated with cellular AQP2 (exosomal AQP2 vs. cellular AQP2, Pearson correlation coefficient

287 AQP2 was also detected in autophagosomes in IMCD cells o

288 AQP2 was also shown to be disrupted in a laboratory-sele

289 he intensity of apical membrane staining for AQP2 was reduced significantly (by approximately 20%) in

290 fe-cycle-stage trypanosomes but, remarkably, AQP2 was specifically restricted to the flagellar pocket

291 ater restriction, and the abundance of renal AQP2 water channels was reduced, implying that vasopress

292 The aquaporin 2 (AQP2) water channel, expressed in kidney collecting duct

293 ility through regulation of the aquaporin-2 (AQP2) water channel. This action is widely accepted to b

294 onally regulated trafficking of aquaporin-2 (AQP2) water channels in renal collecting duct epithelial

295 paralleled by downregulation of aquaporin-2 (AQP2) water channels.

296 d of the nephron occurs through aquaporin-2 (AQP2) water pores in principal cells that line the kidne

297 dvantage of the distribution of aquaporin 2 (Aqp2), which localizes to principal cells of the collect

298 ed sites in PKA-null cells include Ser256 of AQP2, which is critical to regulation of AQP2 traffickin

299 es phosphorylation-dependent interactions of AQP2 with 14-3-3theta and -zeta.

300 The direct interaction of AQP2 with hsc70 is partially inhibited by ATP, and the S

301 Na(+)/K(+)/2Cl(-) cotransporter (NKCC2) and AQP2, with less phosphorylation of AQP2 at serine 256.