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An overview of AVPR2 mutations in genetic forms of nephrogenic diabetes insipidus (review)
this case report describes a case of congenital nephrogenic diabetes insipidus with an AVPR2 gene I324M missense mutation; this is the first report of this mutation in patients with congenital nephrogenic diabetes insipidus
the canceling of the desensitization effect of OPC51803 by the pharmacochaperone effect after long-term treatment may produce sustainable signaling, and thus pharmacochaperone agonists such as OPC51803 may serve as promising therapeutics for NDI caused by misfolded V2R mutants.
AVPR2 missense mutation is associated with nephrogenic diabetes insipidus.
Data suggest that the congenital congenital nephrogenic diabetes insipidus (NDI) in the patient, his mother and grandmother was probably due to mutation of the arginine vasopressin receptor 2 (AVPR2) gene.
a splice site mutation in AVPR2 leads to partial X-linked NDI in two brothers.
A heterozygous deletion in exon 1 of the AVPR2 gene is associated with nephrogenic diabetes insipidus.
In this study, we identified and characterized a new gain-of function mutation of the V2R, which leads to nephrogenic syndrome of inappropriate diuresis.
We present a novel mutation in codon 137 within AVPR2 with substitution of glycine for arginine in male dizygotic twins.
Rescue of the N321K-V2R function by Val(4)-desmopressin action in nephrogenic diabetes insipidus.
AQP1 (show AQP1 ELISA Kits), AQP2 (show AQP2 ELISA Kits), and AQP3 (show AQP3 ELISA Kits), and V2R expression increased with gestation age in the fetal kidney, suggesting that this induction might contribute to the maturation of urinary concentrating capacity
Type 2 vasopressin (show AVP ELISA Kits) receptor (V2R) is in primary cilia of renal epithelial cells. There is also a functional cAMP-signaling pathway, which targets ciliary channel function and may help control the sensory function of the primary cilium.
Data show that upon heteromer formation with secretin receptor (SCTR (show SCTR ELISA Kits)), R137H, a nephrogenic diabetes insipidus (NDI)-causing vasopressin (show AVP ELISA Kits) receptor 2 (AVPR2) mutant that is defective in trafficking to cell surface, can functionally be rescued.
Conditional inactivation of Elf5 (show ELF5 ELISA Kits) in the developing collecting ducts results in a small but significant reduction in the expression levels of Aqp2 (show AQP2 ELISA Kits) and Avpr2 genes.
Data show that cryptochrome Cry1 (show CRY1 ELISA Kits) and Cry2 (show CRY2 ELISA Kits) expression must be circadian and appropriately phased to support rhythms, and arginine vasopressin (AVP (show AVP ELISA Kits)) receptor signaling is required to impose circuit-level circadian function.
In polycystic kidney disease, structural or functional loss of cilia leads to abnormal trafficking of AQP2 (show AQP2 ELISA Kits)/V2R leading to enhanced salt and water absorption.
AVPR2 expression levels in the kidneys of male TALLYHO/JngJ mice, independent of diabetes disease state, were significantly reduced compared with those of B6 mice.
V(2)R mRNA was expressed in medullary TAL (show TALDO1 ELISA Kits) (MTAL), macula densa, connecting tubule, and cortical and medullary collecting duct, and was weakly expressed in cortical TAL (show TALDO1 ELISA Kits) and distal convoluted tubule in rat, mouse, and human
The data support roles for multiple vasopressin V2-receptor-dependent signaling pathways in the vasopressin (show AVP ELISA Kits) signaling network of collecting duct cells, involving several kinases not generally accepted to regulate collecting duct function.
NF-kappaB (show NFKB1 ELISA Kits) activation is of importance for the downregulation of AQP2 (show AQP2 ELISA Kits) channel and vasopressin (show AVP ELISA Kits) V(2) receptor expression during sepsis. NF-kappaB (show NFKB1 ELISA Kits) inhibition ameliorates sepsis-induced acute renal failure.
RNA interference methodology can be used successfully in vivo to significantly reduce functional expression of the V2R in the mouse kidney.
Pax (show PXN ELISA Kits) transactivation domain-interacting protein is required for the urine concentration mechanism by modulating arginine vasopressin receptor 2 and AQP2 (show AQP2 ELISA Kits) expression in the inner medulla.
This gene encodes the vasopressin receptor, type 2, also known as the V2 receptor, which belongs to the seven-transmembrane-domain G protein-coupled receptor (GPCR) superfamily, and couples to Gs thus stimulating adenylate cyclase. The subfamily that includes the V2 receptor, the V1a and V1b vasopressin receptors, the oxytocin receptor, and isotocin and mesotocin receptors in non-mammals, is well conserved, though several members signal via other G proteins. All bind similar cyclic nonapeptide hormones. The V2 receptor is expressed in the kidney tubule, predominantly in the distal convoluted tubule and collecting ducts, where its primary property is to respond to the pituitary hormone arginine vasopressin (AVP) by stimulating mechanisms that concentrate the urine and maintain water homeostasis in the organism. When the function of this gene is lost, the disease Nephrogenic Diabetes Insipidus (NDI) results. The V2 receptor is also expressed outside the kidney although its tissue localization is uncertain. When these 'extrarenal receptors' are stimulated by infusion of a V2 selective agonist (dDAVP), a variety of clotting factors are released into the bloodstream. The physiologic importance of this property is not known - its absence does not appear to be detrimental in NDI patients. The gene expression has also been described in fetal lung tissue and lung cancer associated with alternative splicing.
vasopressin V2 receptor
, arginine vasopressin receptor 2
, AVPR V2
, antidiuretic hormone receptor
, renal-type arginine vasopressin receptor
, V-2 lysine vasopressin receptor
, arginine vasopressin receptor 2 (nephrogenic diabetes insipidus)
, nephrogenic diabetes insipidus
, Vasopressin receptor V2