ライフサイエンスコーパス: aquaporin 2

1 , including the AVP-regulated water channel, aquaporin 2.

2 odium potassium chloride cotransporter 2 and aquaporin 2.

3 chos biflorus lectin, EndoA cytokeratin, and aquaporin 2.

4 ker already exploited in clinical studies is aquaporin-2.

5 tion is required for exocytotic insertion of aquaporin-2.

6 codistributed with Tamm-Horsfall protein nor aquaporin-2.

7 the vasopressin-stimulated redistribution of aquaporin-2.

8 eraction involving the water channel protein aquaporin-2.

9 tors of the cAMP-dependent redistribution of aquaporin-2.

10 current multiplication and downregulation of aquaporins 2, 3, and 4 as contributors to the urinary co

11 mia can occur in the absence of increases in aquaporin-2 abundance.

12 idiuresis and increased urine osmolality and aquaporin-2 abundance.

13 e urea transporter-A1, and the water channel aquaporin 2, all of which are regulated by the transcrip

14 However, it remains a mystery how aquaporin-2 (an integral membrane protein) and other api

15 This effect decreased the abundance of aquaporin 2 and enhanced its intracellular retention, su

16 ry associated with increased urinary podocin:aquaporin 2 and nephrin:aquaporin 2 molar ratios.

17 The decline in aquaporin-2 and -3 was confirmed by immunocytochemistry.

18 binds to the cytoplasmic PDZ-ligand motif of aquaporin-2 and accelerates its endocytosis in the absen

19 d dedifferentiation of CD cells with loss of aquaporin-2 and epithelial-mesenchymal transition-like p

20 ant effect on the basal expression levels of aquaporin-2 and the bumetanide-sensitive Na-K-2Cl cotran

21 tes the urinary concentration by stimulating aquaporin-2 and urea transporters.

22 RT-PCR experiments demonstrated substantial aquaporin-2 and V2 receptor mRNA in microdissected arcad

23 n with greater renal medullary expression of aquaporin-2 and vasopressin-dependent renal cAMP formati

24 mma subunit of G proteins with that found in aquaporins 2 and 5, could explain the link with epinephr

25 ct to antibody specific for principal cells (aquaporin-2) and intercalated cells (band 3 and H(+)-ATP

26 contain both the AVP-elicited water channel, aquaporin 2, and a CaR.

27 ated potassium channel and the water channel aquaporin 2, and improved polyuria and hypokalemia in mu

28 allmark of vasopressin escape, a decrease in aquaporin-2, and demonstrated a decrease in the abundanc

29 calization with calbindin-D28k, H(+)-ATPase, aquaporin-2, and pendrin showed that distal convoluted t

30 d by a marked downregulation of whole kidney aquaporin-2 (AQP-2) protein and mRNA expression.

31 esicle-mediated insertion and removal of the aquaporin-2 (AQP-2) water channel.

32 Aquaporin-2 (AQP-2), a water channel located on the apic

33 To define the role of aquaporin-2 (AQP-2), the developmental expression of thi

34 with the vasopressin-sensitive water channel aquaporin-2 (AQP-2).

35 The vasopressin-sensitive water channel (aquaporin 2; AQP-2) mediates water transport across the

36 role of hyperosmolality in vivo to modulate aquaporin 2 (AQP2) and Na-K-2Cl co-transporter (NKCC2),

37 Total aquaporin 2 (AQP2) and phospho-S256-AQP2 (pAQP2) protein

38 inase A (PKA) activation, phosphorylation of aquaporin 2 (AQP2) at serine 256, and translocation of A

39 exosomal flotillin-1 or TSG101 but increased aquaporin 2 (AQP2) in a dose- and time-dependent manner

40 Human aquaporin 2 (AQP2) is a water channel found in the kidne

41 In collecting duct principal cells, aquaporin 2 (AQP2) is shuttled from intracellular vesicl

42 ctive, alternative strategies for modulating aquaporin 2 (AQP2) trafficking have been sought.

43 The aquaporin 2 (AQP2) water channel, expressed in kidney co

44 ency led to a reduction in the percentage of aquaporin 2 (Aqp2)(+) principal cells (PCs) in the colle

45 Aquaporin 2 (AQP2), a putative substrate of calcineurin

46 KCC2), sodium chloride co-transporter (NCC), aquaporin 2 (AQP2), and EGFR abundances using western bl

47 odies against the exosomal proteins CD24 and aquaporin 2 (AQP2), conjugated to a fluorophore, we coul

48 The collecting duct water channel, aquaporin 2 (AQP2), plays a pivotal role in the renal wa

49 Taking advantage of the distribution of aquaporin 2 (Aqp2), which localizes to principal cells o

50 th phosphorylated forms of the water channel aquaporin-2 (AQP2) and modulate its function.

51 interaction between the renal water channel aquaporin-2 (AQP2) and the lysosomal trafficking regulat

52 There was also a decrease in inner medulla aquaporin-2 (AQP2) and urea transporter A1 (UT-A1) in GD

53 insipidus (NDI), we have analyzed the mouse aquaporin-2 (Aqp2) cDNA and gene and generated a mutated

54 me-dependent effect on vasopressin-inducible aquaporin-2 (AQP2) expression in immortalized mouse coll

55 Furthermore, aquaporin-2 (AQP2) expression in the inner medulla of th

56 r two novel recessive point mutations in the aquaporin-2 (AQP2) gene: L22V in exon 1 and C181W in exo

57 kidney, and immunolocalized its protein and aquaporin-2 (AQP2) in CD principal cells.

58 entification of a single base pair change in aquaporin-2 (Aqp2) in cph mutants through genetic linkag

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

60 The trafficking of aquaporin-2 (AQP2) involves multiple complex pathways, i

61 Aquaporin-2 (AQP2) is the vasopressin-regulated water ch

62 Aquaporin-2 (AQP2) mediates vasopressin-regulated collec

63 Five single-point aquaporin-2 (AQP2) mutations that cause non-X-linked nep

64 We reported that several aquaporin-2 (AQP2) point mutants that cause nephrogenic

65 trolling the abundances of the water channel aquaporin-2 (AQP2) protein and regulatory proteins in th

66 Mutations in aquaporin-2 (AQP2) that interfere with its cellular proc

67 ntrols water excretion through regulation of aquaporin-2 (AQP2) trafficking in renal collecting duct

68 nsipidus (NDI) is caused by mutations in the aquaporin-2 (AQP2) water channel.

69 y on the hormonally regulated trafficking of aquaporin-2 (AQP2) water channels in renal collecting du

70 sed diuresis paralleled by downregulation of aquaporin-2 (AQP2) water channels.

71 luminal fluid of the nephron occurs through aquaporin-2 (AQP2) water pores in principal cells that l

72 clase (AC), cAMP-promoted phosphorylation of aquaporin-2 (AQP2), and increased abundance of AQP2 on t

73 duct physiology, including eight sites among aquaporin-2 (AQP2), aquaporin-4, and urea transporter is

74 in abundance by vasopressin; interacts with aquaporin-2 (AQP2), Hsp70, and Hsc70; and can directly u

75 ignificantly increased the protein levels of aquaporin-2 (AQP2), phosphorylated AQP2 (p-AQP2), and AQ

76 e determined if the amount of immunoreactive aquaporin-2 (AQP2, the AVP-regulated water channel) or A

77 ets PKA and phosphodiesterase PDE4D to AQP2 (aquaporin-2)-bearing vesicles to orchestrate the acute r

78 inhibitor of cAMP-mediated redistribution of aquaporin-2, but its target in this pathway remains unkn

79 enes encoding the vasopressin 2 receptor and aquaporin 2 cause nephrogenic diabetes insipidus; howeve

80 ressin-regulated expression and insertion of aquaporin-2 channels in the luminal membrane of renal pr

81 of the vasopressin-responsive water channel aquaporin 2 compared with wild-type mice.

82 In addition, aquaporin 2-containing endosomes also possess stimulator

83 taxin-4's putative cognate receptor VAMP2 in aquaporin-2-containing vesicles, supports the view that

84 xP-flanked PKD1 gene and heterozygous for an aquaporin-2-Cre recombinase transgene to achieve collect

85 despite normal effects on the transcellular aquaporin-2-dependent pathway.

86 Lithium-induced NDI is caused by aquaporin-2 downregulation and a reduced ratio of princi

87 the interaction, in association with reduced aquaporin-2 endocytosis and prolonged plasma membrane aq

88 Levels of cAMP, a major regulator of aquaporin 2 expression and trafficking, were also lower

89 y, GSK3beta inactivation or deletion reduces aquaporin 2 expression by modulating adenylate cyclase a

90 ase in water retention, urine osmolality and aquaporin-2 expression and phosphorylation.

91 f cirrhosis induced by carbon tetrachloride, aquaporin-2 expression in CBDL-induced cirrhosis was dec

92 of arginine vasopressin and upregulation of aquaporin 2 followed by trafficking of this water channe

93 s and prevented AVP-induced translocation of aquaporin 2, further suggesting the effects in SHR-A3 re

94 ive trafficking to the plasma membrane of an aquaporin 2-green fluorescent protein chimera, with rete

95 gp330, aquaporin-2, H+ ATPase, and the AE1 anion exchanger were

96 hrough actions to regulate the water channel aquaporin-2 in collecting duct principal cells.

97 ssessment of regulation and dysregulation of aquaporin-2 in humans.

98 cellular vesicles and causes accumulation of aquaporin-2 in the Golgi compartment.

99 NK were able to phosphorylate residue S261of aquaporin-2 in vitro, a site showing a decrease in phosp

100 s) that also express the H(+)-ATPase but not aquaporin-2, indicating that pendrin is present in inter

101 ing duct by inducing exocytotic insertion of aquaporin-2 into apical membrane.

102 ELISA in microdissected segments showed that aquaporin-2 is highly expressed in arcades and that the

103 ulated water channel of the collecting duct, aquaporin-2, is excreted in the urine, providing a means

104 Immunocytochemistry revealed abundant aquaporin-2 labeling of structures in the cortical labyr

105 tubular cells with ET but not PA, and urine aquaporin 2 levels were higher with ET (5.52 +/- 1.06 ng

106 lls of the collecting duct directly modulate aquaporin-2 levels and contribute to the concentration o

107 Aquaporin-2 mediates vasopressin-dependent renal collect

108 ased urinary podocin:aquaporin 2 and nephrin:aquaporin 2 molar ratios.

109 Aquaporin 2 mRNA served as a kidney reference gene to ac

110 utant kidneys showed increased expression of aquaporin-2 mRNA but mislocalized expression of aquapori

111 by a concomitant suppression of whole kidney aquaporin-2 mRNA levels.

112 Although the expression of aquaporin-2, NaPi-2, and paracellin-1 mRNAs tended to in

113 UT-A1/3(-/-) mice, there was no decrease in aquaporin 2 or aquaporin 3 expression.

114 ith type I PDZ sequences from the C-tails of aquaporin-2 or GluR1 recycled in a SAP97- and PKA-depend

115 gnificant change in serum vasopressin level, aquaporin 2, or Na(+)-K(+)-2Cl(-) co-transporter NKCC2/B

116 Vasopressin-induced aquaporin-2 phosphorylation within the type I PDZ-ligand

117 t populations, demarcated by the presence of aquaporin-2, polycystin-1, and podocin.

118 thelial injury predominantly at the level of aquaporin 2-positive collecting ducts with tubular epith

119 C-like cells selectively integrated into the aquaporin 2-positive medullary collecting duct when micr

120 d mCCDcl1 cells, and DHHC 3 was expressed in aquaporin 2-positive principal cells of mouse aldosteron

121 We observed PON-2 expression in aquaporin 2-positive principal cells of the distal nephr

122 T5 transcription factors, which regulate the aquaporin 2 promoter.

123 d temporally with a marked decrease in renal aquaporin-2 protein (measured by semiquantitative immuno

124 Whole kidney aquaporin-2 protein abundance was 45% of controls at 18

125 Similarly, levels of aquaporin-2 protein in inner and outer medulla after wat

126 aporin-2 mRNA but mislocalized expression of aquaporin-2 protein in the cytoplasm of CD cells.

127 The marked suppression of whole kidney aquaporin-2 protein was accompanied by a concomitant sup

128 n in kidney inner medulla but did not change aquaporin-2 protein.

129 ing a peptide-derived polyclonal antibody to aquaporin-2, quantitative ELISA in microdissected segmen

130 nary concentrating ability, with a preserved aquaporin-2 response to desmopressin and an intact respo

131 -2 endocytosis and prolonged plasma membrane aquaporin-2 retention.

132 cotransporter, epithelial Na channel (ENaC), aquaporin-2, ROMK, and NaKATPase.

133 We also measured the expression of aquaporin-2, sodium/phosphate cotransporter (NaPi)-2, pa

134 es ClC-K1, Barttin, urea transporter-A1, and aquaporin 2 that are required for urinary concentration.

135 es are a site of expression of two proteins, aquaporin-2 (the vasopressin-regulated water channel) an

136 attenuated lithium-induced downregulation of aquaporin-2 through a mechanism different from that of a

137 cting duct (IMCD) by inducing trafficking of aquaporin-2 to the apical plasma membrane and that this

138 l step in vasopressin-induced trafficking of aquaporin-2 to the apical plasma membrane.

139 ked vasopressin-stimulated redistribution of aquaporin-2 to the plasma membrane domain in primary cul

140 ion studies demonstrated that trafficking of aquaporin-2 to the plasma membrane remained intact durin

141 Vasopressin-induced apical aquaporin-2 trafficking and forskolin-induced water perm

142 The molecular mechanisms that control aquaporin-2 trafficking and the consequent water reabsor

143 mics that could explain regulation of apical aquaporin-2 trafficking and water permeability increase.

144 ys an essential role in vasopressin-mediated aquaporin-2 trafficking via a calmodulin-dependent mecha

145 ation of 4-acetyldiphyllin as a modulator of aquaporin-2 trafficking.

146 expression of TonEBP target genes, including aquaporin-2, urea transporter, and aldose reductase.

147 iew that these proteins could play a role of aquaporin-2 vesicle targeting to the apical plasma membr

148 eability (P(f)) by triggering trafficking of aquaporin-2 vesicles to the apical plasma membrane.

149 Upon immunohistochemistry, aquaporin 2 was concentrated along the apical membrane o

150 s (NDI) that resulted from a mutation in the aquaporin-2 water channel (AQP2) was characterized, and

151 We hypothetized that upregulation of aquaporin-2 water channel could account for the water re

152 rt, to a vasopressin-independent decrease in aquaporin-2 water channel expression in the renal collec

153 echanisms that regulate the abundance of the aquaporin-2 water channel in renal collecting duct cells

154 caused phosphorylation and activation of the aquaporin-2 water channel present in the principal cells

155 n-4, in vasopressin-regulated trafficking of aquaporin-2 water channel vesicles to the apical plasma

156 nts that culminate in the phosphorylation of aquaporin-2 water channels and their redistribution from

157 The vasopressin-stimulated insertion of aquaporin-2 water channels into the apical membrane was

158 fects of acute hypertonic challenge on AQP2 (aquaporin-2) water channel trafficking.

159 of ClC-K1, Barttin, urea transporter-A1, and aquaporin 2 were significantly lower.

160 g the collecting duct-specific water channel aquaporin 2, whereas autoantibodies of the two other pat

161 A-dependent phosphorylation at serine 256 of aquaporin-2, which triggers the redistribution to the pl

162 s and transgenic VvPIP2;4N and of four other aquaporins, (2) whole-plant, root, and leaf ecophysiolog