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Human Polyclonal AQP2 Primary Antibody for ICC, IHC (fro) - ABIN259116
Moeller, Knepper, Fenton: Serine 269 phosphorylated aquaporin-2 is targeted to the apical membrane of collecting duct principal cells. in Kidney international 2009
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Human Polyclonal AQP2 Primary Antibody for DB, IHC - ABIN253231
Trimpert, van den Berg, Fenton, Klussmann, Deen: Vasopressin increases S261 phosphorylation in AQP2-P262L, a mutant in recessive nephrogenic diabetes insipidus. in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2012
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Rat (Rattus) Polyclonal AQP2 Primary Antibody for WB - ABIN361469
Choi, Jung, Kwon: Extracellular pH affects phosphorylation and intracellular trafficking of AQP2 in inner medullary collecting duct cells. in American journal of physiology. Renal physiology 2015
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Human Polyclonal AQP2 Primary Antibody for ICC, IF - ABIN863207
Gonen, Walz: The structure of aquaporins. in Quarterly reviews of biophysics 2006
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Chicken Polyclonal AQP2 Primary Antibody for WB - ABIN2477484
Mummery, Feyen, Freund, Shen: Characteristics of embryonic stem cell differentiation: a comparison with two embryonal carcinoma cell lines. in Cell differentiation and development : the official journal of the International Society of Developmental Biologists 1990
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vasopressin (show AVP Antibodies)-mediated transcriptional regulation is highly selective for Aqp2
Data suggest that membrane-proximal signaling complexes constrained by AKAP220 (show AKAP11 Antibodies) impact the actin barrier dynamics and AQP2 trafficking to ensure water homeostasis.
These studies indicate that manipulation of the cholesterol content of the basolateral plasma membrane interferes with AQP2 posttranslational modification and subsequently regulated apical plasma membrane targeting of AQP2.
It was proposed that FXYD1 (show FXYD1 Antibodies) plays a role in regulating AQP2 retention in apical membrane, and that this involves transfers between raft-like membrane domains in endosomes and plasma membranes.
Both NFATc3 (show NFATC3 Antibodies) knock-out mice and ILK (show ILK Antibodies) conditional-knockdown mice (cKD-ILK (show ILK Antibodies)) display symptoms of NDI (show AVPR2 Antibodies) (polyuria and reduced AQP2 expression).
aquaporin-2 regulates serine/threonine phosphatases in renal collecting duct
Ativation of LXRbeta (show NR1H2 Antibodies) increases AQP2 protein levels in the renal collecting ducts via a posttranscriptional mechanism top regulate water electrolyte balance.
PDZ domain-containing protein (show USH1C Antibodies) Sipa1l1 (signal-induced proliferation-associated 1 like 1 (show SIPA1L1 Antibodies)) binds to the cytoplasmic PDZ (show INADL Antibodies)-ligand motif of aquaporin-2 and accelerates its endocytosis in the absence of vasopressin (show AVP Antibodies)
Conditional inactivation of Elf5 (show ELF5 Antibodies) in the developing collecting ducts results in a small but significant reduction in the expression levels of Aqp2 and Avpr2 (show AVPR2 Antibodies) genes.
These results provide the direct evidence that the Ser (show SIGLEC1 Antibodies)-261 dephosphorylation is involved in the pS256- and pS269-related AQP2 regulation.
Results indicate the functional recovery of recessive aquaporin 2 (AQP2) mutants through heteromerization.
AQP2 is associated with the pathogenesis of femalestress urinary incontinence.
Pretreatment with WRT also decreased the hypertonic stressinduced expression of AQP2, as with KT5720, a protein kinase A inhibitor. These results provided evidence of the beneficial effect of the traditional formula WRT in regulating water balance in hypertonic stress of the renal collecting ducts.
E3 ligases most likely to interact with AQP2.
The present study provides detailed insights into the transport properties of AQP2 with the use of microsecond-scale molecular dynamics simulations, and explains how these channels conduct water molecules while at the same time excluding other molecules.
Data suggest that AQP2 binds LIP5 (show VTA1 Antibodies) in a AQP2-phosphorylation-dependent manner; phospho-mimicking mutations and phosphorylation reduce thermal stability of AQP2; AQP2 phosphorylation allosterically controls its interaction with LIP5 (show VTA1 Antibodies). [AQP2 = aquaporin 2; LIP5 (show VTA1 Antibodies) = LYST-interacting protein 5; LYST (show LYST Antibodies) = lysosomal trafficking regulator (show LYST Antibodies) protein]
The genetic variant rs426496 in AQP2; rs591810 in AQP3 (show AQP3 Antibodies) and rs1805127, rs1805128, and rs17173510, in KCNE1 (show KCNE1 Antibodies) were found in patients with Meniere's disease
An overview ofAQP2 mutations in genetic forms of nephrogenic diabetes insipidus (show AVPR2 Antibodies) (review)
Impaired endometrial receptivity in patients who underwent controlled ovarian stimulation is correlated with a decreased expression of AQP2.
AQP1 (show AQP1 Antibodies), AQP2, and AQP3 (show AQP3 Antibodies), and V2R (show AVPR2 Antibodies) expression increased with gestation age in the fetal kidney, suggesting that this induction might contribute to the maturation of urinary concentrating capacity
Aquaporin 2 promotes cell migration and epithelial morphogenesis.
Data provide evidence supporting the role of S256 and S269 in the maintenance of AQP2 at the cell surface.
This gene encodes a water channel protein located in the kidney collecting tubule. It belongs to the MIP/aquaporin family, some members of which are clustered together on chromosome 12q13. Mutations in this gene have been linked to autosomal dominant and recessive forms of nephrogenic diabetes insipidus.
ADH water channel
, collecting duct water channel protein
, water channel protein for renal collecting duct
, water-channel aquaporin 2