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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 eraction involving the water channel protein aquaporin-2.
7 codistributed with Tamm-Horsfall protein nor aquaporin-2.
8 the vasopressin-stimulated redistribution of aquaporin-2.
9 ssin to regulate the molecular water channel aquaporin-2.
10 cells to regulate the water channel protein aquaporin-2.
11 tors of the cAMP-dependent redistribution of aquaporin-2.
12 current multiplication and downregulation of aquaporins 2, 3, and 4 as contributors to the urinary co
17 e urea transporter-A1, and the water channel aquaporin 2, all of which are regulated by the transcrip
21 stimulated abundance of phosphorylated pS256-aquaporin 2 and pT58-Na(+)-Cl(-) cotransporter and dimin
23 binds to the cytoplasmic PDZ-ligand motif of aquaporin-2 and accelerates its endocytosis in the absen
24 d dedifferentiation of CD cells with loss of aquaporin-2 and epithelial-mesenchymal transition-like p
25 ant effect on the basal expression levels of aquaporin-2 and the bumetanide-sensitive Na-K-2Cl cotran
27 RT-PCR experiments demonstrated substantial aquaporin-2 and V2 receptor mRNA in microdissected arcad
28 n with greater renal medullary expression of aquaporin-2 and vasopressin-dependent renal cAMP formati
29 mma subunit of G proteins with that found in aquaporins 2 and 5, could explain the link with epinephr
30 ct to antibody specific for principal cells (aquaporin-2) and intercalated cells (band 3 and H(+)-ATP
32 ated potassium channel and the water channel aquaporin 2, and improved polyuria and hypokalemia in mu
33 allmark of vasopressin escape, a decrease in aquaporin-2, and demonstrated a decrease in the abundanc
34 calization with calbindin-D28k, H(+)-ATPase, aquaporin-2, and pendrin showed that distal convoluted t
41 role of hyperosmolality in vivo to modulate aquaporin 2 (AQP2) and Na-K-2Cl co-transporter (NKCC2),
43 inase A (PKA) activation, phosphorylation of aquaporin 2 (AQP2) at serine 256, and translocation of A
44 in, and the diagnosis of CN revealed loss of aquaporin 2 (AQP2) expression in collecting ducts in pat
46 exosomal flotillin-1 or TSG101 but increased aquaporin 2 (AQP2) in a dose- and time-dependent manner
51 ency led to a reduction in the percentage of aquaporin 2 (Aqp2)(+) principal cells (PCs) in the colle
53 KCC2), sodium chloride co-transporter (NCC), aquaporin 2 (AQP2), and EGFR abundances using western bl
54 odies against the exosomal proteins CD24 and aquaporin 2 (AQP2), conjugated to a fluorophore, we coul
58 interaction between the renal water channel aquaporin-2 (AQP2) and the lysosomal trafficking regulat
59 There was also a decrease in inner medulla aquaporin-2 (AQP2) and urea transporter A1 (UT-A1) in GD
61 insipidus (NDI), we have analyzed the mouse aquaporin-2 (Aqp2) cDNA and gene and generated a mutated
62 me-dependent effect on vasopressin-inducible aquaporin-2 (AQP2) expression in immortalized mouse coll
64 such models are associated with the loss of aquaporin-2 (AQP2) from collecting duct principal cells,
65 promotes redistribution of the water channel aquaporin-2 (AQP2) from intracellular vesicles into the
67 r two novel recessive point mutations in the aquaporin-2 (AQP2) gene: L22V in exon 1 and C181W in exo
69 entification of a single base pair change in aquaporin-2 (Aqp2) in cph mutants through genetic linkag
70 e of the vasopressin-dependent water channel aquaporin-2 (AQP2) in the renal collecting duct and poly
79 trolling the abundances of the water channel aquaporin-2 (AQP2) protein and regulatory proteins in th
82 ntrols water excretion through regulation of aquaporin-2 (AQP2) trafficking in renal collecting duct
84 water permeability through regulation of the aquaporin-2 (AQP2) water channel. This action is widely
85 y on the hormonally regulated trafficking of aquaporin-2 (AQP2) water channels in renal collecting du
87 luminal fluid of the nephron occurs through aquaporin-2 (AQP2) water pores in principal cells that l
88 clase (AC), cAMP-promoted phosphorylation of aquaporin-2 (AQP2), and increased abundance of AQP2 on t
89 duct physiology, including eight sites among aquaporin-2 (AQP2), aquaporin-4, and urea transporter is
90 in abundance by vasopressin; interacts with aquaporin-2 (AQP2), Hsp70, and Hsc70; and can directly u
91 ignificantly increased the protein levels of aquaporin-2 (AQP2), phosphorylated AQP2 (p-AQP2), and AQ
93 e determined if the amount of immunoreactive aquaporin-2 (AQP2, the AVP-regulated water channel) or A
94 ets PKA and phosphodiesterase PDE4D to AQP2 (aquaporin-2)-bearing vesicles to orchestrate the acute r
96 inhibitor of cAMP-mediated redistribution of aquaporin-2, but its target in this pathway remains unkn
97 enes encoding the vasopressin 2 receptor and aquaporin 2 cause nephrogenic diabetes insipidus; howeve
99 ressin-regulated expression and insertion of aquaporin-2 channels in the luminal membrane of renal pr
102 taxin-4's putative cognate receptor VAMP2 in aquaporin-2-containing vesicles, supports the view that
103 xP-flanked PKD1 gene and heterozygous for an aquaporin-2-Cre recombinase transgene to achieve collect
104 Pod:CR) and a tubular marker (Urinary pellet aquaporin 2:creatinine ratio) were measured in macro-alb
108 the interaction, in association with reduced aquaporin-2 endocytosis and prolonged plasma membrane aq
110 y, GSK3beta inactivation or deletion reduces aquaporin 2 expression by modulating adenylate cyclase a
112 f cirrhosis induced by carbon tetrachloride, aquaporin-2 expression in CBDL-induced cirrhosis was dec
113 of arginine vasopressin and upregulation of aquaporin 2 followed by trafficking of this water channe
114 s and prevented AVP-induced translocation of aquaporin 2, further suggesting the effects in SHR-A3 re
115 ive trafficking to the plasma membrane of an aquaporin 2-green fluorescent protein chimera, with rete
121 NK were able to phosphorylate residue S261of aquaporin-2 in vitro, a site showing a decrease in phosp
122 s) that also express the H(+)-ATPase but not aquaporin-2, indicating that pendrin is present in inter
124 ELISA in microdissected segments showed that aquaporin-2 is highly expressed in arcades and that the
125 ulated water channel of the collecting duct, aquaporin-2, is excreted in the urine, providing a means
127 tubular cells with ET but not PA, and urine aquaporin 2 levels were higher with ET (5.52 +/- 1.06 ng
128 lls of the collecting duct directly modulate aquaporin-2 levels and contribute to the concentration o
133 utant kidneys showed increased expression of aquaporin-2 mRNA but mislocalized expression of aquapori
137 ith type I PDZ sequences from the C-tails of aquaporin-2 or GluR1 recycled in a SAP97- and PKA-depend
138 gnificant change in serum vasopressin level, aquaporin 2, or Na(+)-K(+)-2Cl(-) co-transporter NKCC2/B
141 thelial injury predominantly at the level of aquaporin 2-positive collecting ducts with tubular epith
142 C-like cells selectively integrated into the aquaporin 2-positive medullary collecting duct when micr
143 d mCCDcl1 cells, and DHHC 3 was expressed in aquaporin 2-positive principal cells of mouse aldosteron
146 d temporally with a marked decrease in renal aquaporin-2 protein (measured by semiquantitative immuno
152 ing a peptide-derived polyclonal antibody to aquaporin-2, quantitative ELISA in microdissected segmen
153 Signaling events coupling PKA activation and aquaporin-2 regulation were largely unknown until the ad
154 nary concentrating ability, with a preserved aquaporin-2 response to desmopressin and an intact respo
158 es ClC-K1, Barttin, urea transporter-A1, and aquaporin 2 that are required for urinary concentration.
159 es are a site of expression of two proteins, aquaporin-2 (the vasopressin-regulated water channel) an
160 attenuated lithium-induced downregulation of aquaporin-2 through a mechanism different from that of a
161 cting duct (IMCD) by inducing trafficking of aquaporin-2 to the apical plasma membrane and that this
163 ked vasopressin-stimulated redistribution of aquaporin-2 to the plasma membrane domain in primary cul
164 ion studies demonstrated that trafficking of aquaporin-2 to the plasma membrane remained intact durin
167 mics that could explain regulation of apical aquaporin-2 trafficking and water permeability increase.
168 ys an essential role in vasopressin-mediated aquaporin-2 trafficking via a calmodulin-dependent mecha
170 expression of TonEBP target genes, including aquaporin-2, urea transporter, and aldose reductase.
171 iew that these proteins could play a role of aquaporin-2 vesicle targeting to the apical plasma membr
172 eability (P(f)) by triggering trafficking of aquaporin-2 vesicles to the apical plasma membrane.
174 s (NDI) that resulted from a mutation in the aquaporin-2 water channel (AQP2) was characterized, and
176 rt, to a vasopressin-independent decrease in aquaporin-2 water channel expression in the renal collec
177 echanisms that regulate the abundance of the aquaporin-2 water channel in renal collecting duct cells
178 caused phosphorylation and activation of the aquaporin-2 water channel present in the principal cells
179 n-4, in vasopressin-regulated trafficking of aquaporin-2 water channel vesicles to the apical plasma
180 nts that culminate in the phosphorylation of aquaporin-2 water channels and their redistribution from
184 g the collecting duct-specific water channel aquaporin 2, whereas autoantibodies of the two other pat
185 A-dependent phosphorylation at serine 256 of aquaporin-2, which triggers the redistribution to the pl
186 s and transgenic VvPIP2;4N and of four other aquaporins, (2) whole-plant, root, and leaf ecophysiolog