ライフサイエンスコーパス: AQP2

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

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

3 in greater levels of AQP2 and phosphorylated AQP2.

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

5 calcitonin-induced membrane accumulation of AQP2.

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

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

8 enhances apical plasma membrane retention of AQP2.

9 an important role of EHD4 in trafficking of AQP2.

10 phorylation and apical surface expression of AQP2.

11 al glycosylation or membrane association, of Aqp2.

12 factor in vasopressin-mediated regulation of AQP2.

13 nhibiting calcineurin-mediated regulation of AQP2.

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

15 riptional regulation is highly selective for Aqp2.

16 interactions involved in cellular sorting of AQP2.

17 ed significantly the protein abundance of IM AQP2 (121+/-2 versus 100+/-5%; P<0.01), ISOM AQP2 (135+/

18 ), cortex plus outer stripe of outer medulla AQP2 (121+/-4 versus 100+/-1%; P<0.001), ISOM NKCC2 (133

19 AQP2 (121+/-2 versus 100+/-5%; P<0.01), ISOM AQP2 (135+/-6 versus 100+/-5%; P<0.001), cortex plus out

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

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

22 Aquaporin 2 (AQP2), a putative substrate of calcineurin phosphatase i

23 AQP2, a channel that appears to facilitate drug accumula

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

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

26 Whereas AQP2 abundance decreased after 3 h of hyperosmotic chall

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

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

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

30 2 trafficking and that hypertonicity-induced AQP2 accumulation at the cell surface depends on MAP kin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 tudies confirmed the decreased expression of AQP2 and UT-A1 in kidneys of GD rats as compared with co

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

56 rosmolality in vivo to modulate aquaporin 2 (AQP2) and Na-K-2Cl co-transporter (NKCC2), pivotal facto

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

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

59 lso a decrease in inner medulla aquaporin-2 (AQP2) and urea transporter A1 (UT-A1) in GD rats as comp

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

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

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

63 cation, diminished osmotic equilibration via AQP2, and diminished urea equilibration via UT-A1.

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

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

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

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

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

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

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

71 gy, including eight sites among aquaporin-2 (AQP2), aquaporin-4, and urea transporter isoforms A1 and

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

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

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

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

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

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

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

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

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

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

82 esponse to short-term vasopressin treatment: AQP2, Bclaf1, LRRC47, Rgl3, and SAFB2.

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

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

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

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

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

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

89 the glycine at this site in AQP0, AQP1, and AQP2 blocked expression of the mutants at the oocyte pla

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

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

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

93 The interference with normal trafficking of Aqp2 by this mutation resulted in a severe urine concent

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 s, TonEBP plays a central role in regulating AQP2 expression by enhancing AQP2 gene transcription.

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

125 AQP2 expression modulates the trafficking and internaliz

126 AQP2 expression was similar between the two groups, but

127 uli and CD and participates in regulation of AQP2 expression, phosphorylation, and function.

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

129 effect on vasopressin-inducible aquaporin-2 (AQP2) expression in immortalized mouse collecting duct p

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

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

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

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

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

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

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

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

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

139 e in regulating AQP2 expression by enhancing AQP2 gene transcription.

140 mal recessive missense V168M mutation in the AQP2 gene.

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

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

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

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

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

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

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

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

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

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

151 the predominant isoform that associates with AQP2 in the diabetic kidney.

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

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

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

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

156 of a single base pair change in aquaporin-2 (Aqp2) in cph mutants through genetic linkage mapping.

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

158 Protein abundance of AQP2 increased and was reversed by insulin in the inner

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

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

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

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

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

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

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

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

167 rovided direct genetic evidence that S256 in Aqp2 is indispensable for the apical accumulation, but n

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

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

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

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

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

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

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

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

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

177 calcineurin with cyclosporin A (CsA) alters AQP2 localization and phosphorylation in principal cells

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

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

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

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

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

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

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

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

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

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

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

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

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

191 ot significantly alter reduced expression of AQP2 mRNA that was induced by 3 h of hypertonic challeng

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

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

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

195 he population was heterozygous for the V168M AQP2 mutation and 1% was homozygous for the mutation.

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 n at S256 and the subsequent accumulation of Aqp2 on the apical membrane of the collecting duct princ

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

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

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

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

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

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

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

207 Our data suggest that AQP2 phosphorylation allosterically controls its interac

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

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

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

214 luciferase activity in cells that expressed AQP2 promoter-luciferase plasmid constructs, indicating

215 family TRs transactivated the mouse proximal AQP2 promoter.

216 at least partially by acting directly on the 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

221 256) by a Leu in the cytoplasmic tail of the Aqp2 protein, preventing its phosphorylation at S256 and

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

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

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 Co-localization of CnA isoforms with AQP2 revealed that CnA-alpha is the predominant isoform

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

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

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

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

238 17-AAG increased urine osmolality in AQP2(T126M/-) mice by >300 mosmol but had no effect in A

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

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

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

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

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

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

245 6M-transfected kidney cells showed increased AQP2-T126M plasma membrane expression with the Hsp90 inh

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

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

248 ane, and that its ER retention was less than AQP2-T126M, a functional mutant in severe recessive NDI.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

269 reabsorption, suggesting that it may affect AQP2 trafficking.

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

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

272 sites are involved in vasopressin-dependent AQP2 trafficking.

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

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

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

276 onstructs, indicating that TonEBP influences AQP2 transcriptional activity at least partially by acti

277 ancer element located 489 bp upstream of the AQP2 transcriptional start site abolished the hypertonic

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

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

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

281 AQP2 undergoes different regulated post-translational mo

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

283 None of the affected AQP2-V168M individuals had neurologic deficits, which al

284 siderable amount of the partially functional AQP2-V168M was expressed at the plasma membrane, and tha

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

286 AQP2 was also detected in autophagosomes in IMCD cells o

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

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

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

290 a mutation in the aquaporin-2 water channel (AQP2) was characterized, and the source of this rare mut

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

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

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

296 Alterations in subcellular localization of AQP2 were parallel with CnA-alpha.

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

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

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

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