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anti-Human AVPR2 Antikörper:
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Human Polyclonal AVPR2 Primary Antibody für WB - ABIN2801893
Seibold, Brabet, Rosenthal, Birnbaumer: Structure and chromosomal localization of the human antidiuretic hormone receptor gene. in American journal of human genetics 1992
Show all 5 Pubmed References
Human Polyclonal AVPR2 Primary Antibody für WB - ABIN929264
Canal, Wilkinson, Cooper, Wraith, Wynn, Bigger: Circadian rhythm and suprachiasmatic nucleus alterations in the mouse model of mucopolysaccharidosis IIIB. in Behavioural brain research 2010
Human Polyclonal AVPR2 Primary Antibody für ELISA - ABIN548129
Mutig, Paliege, Kahl, Jöns, Müller-Esterl, Bachmann: Vasopressin V2 receptor expression along rat, mouse, and human renal epithelia with focus on TAL. in American journal of physiology. Renal physiology 2007
Dog (Canine) Polyclonal AVPR2 Primary Antibody für ELISA - ABIN548157
Yirmiya, Rosenberg, Levi, Salomon, Shulman, Nemanov, Dina, Ebstein: Association between the arginine vasopressin 1a receptor (AVPR1a) gene and autism in a family-based study: mediation by socialization skills. in Molecular psychiatry 2006
Being a rapid diagnostic tool for congenital nephrogenic diabetes insipidus , direct sequencing of AVPR2 should be encouraged in newborns with familial predisposition to congenital nephrogenic diabetes insipidus.
A novel 22.1-kb deletion in AVPR2 was identified, leading to X-linked nephrogenic diabetes insipidus in a Chinese pedigree.
Here we provide an updated overview of the genetic defects causing NDI, the most recent strategies under investigation for rescuing the activity of mutated AVPR2 or AQP2, or for bypassing defective AVPR2 signaling and restoring AQP2 plasma membrane expression.
Data found Mutations of Vasopressin Receptor 2 Including Novel L312S Have Differential Effects on Trafficking
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.
X-linked nephrogenic diabetes insipidus and severity of illness in this family is caused by a novel deletion in the AVPR2 gene
AVP acting at V2R does not appear to regulate water losses from body fluids other than renal excretion during exercise.
This review summarizes some of the unexpected roles of V2R signaling and suggests that vasopressin signaling itself may contribute crucially to loss of polarity and enhanced proliferation in cystic kidney epithelium.
52 disease-causing mutations of AVPR2 were identified. missense mutations were most common (54%), followed by deletion mutations. 64 women who had monoallelic disease-causing AVPR2 mutations, 16 had NDI symptoms, including 4 complete NDI subjects
Three vasopressin receptor 2 variants: an apparent polymorphism (V266A) and two loss-of-function mutations (R181C and M311V) may be related to nephrogenic syndrome of inappropriate antidiuresis and to nephrogenic diabetes insipidus.
vasopressin receptor type 2 signaling is controlled by retromer and arrestin in a noncanonical regulatory pathway
AQP1, AQP2, and AQP3, 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 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.
type-2 vasopressin receptor in polycystic kidney disease is targeted by green mamba peptide
Data show that upon heteromer formation with secretin receptor (SCTR), R137H, a nephrogenic diabetes insipidus (NDI)-causing vasopressin receptor 2 (AVPR2) mutant that is defective in trafficking to cell surface, can functionally be rescued.
Conditional inactivation of Elf5 in the developing collecting ducts results in a small but significant reduction in the expression levels of Aqp2 and Avpr2 genes.
Data show that cryptochrome Cry1 and Cry2 expression must be circadian and appropriately phased to support rhythms, and arginine vasopressin (AVP) 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/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 (MTAL), macula densa, connecting tubule, and cortical and medullary collecting duct, and was weakly expressed in cortical TAL and distal convoluted tubule in rat, mouse, and human
The data support roles for multiple vasopressin V2-receptor-dependent signaling pathways in the vasopressin signaling network of collecting duct cells, involving several kinases not generally accepted to regulate collecting duct function.
NF-kappaB activation is of importance for the downregulation of AQP2 channel and vasopressin V(2) receptor expression during sepsis. NF-kappaB inhibition ameliorates sepsis-induced acute renal failure.
a single amino acid difference in the first extracellular loop determines the efficiency of cell surface expression
analysis of pharmacochaperone cell surface delivery with a three-dimensional homology model of the antagonist-bound hV2R
RNA interference methodology can be used successfully in vivo to significantly reduce functional expression of the V2R in the mouse kidney.
Pax transactivation domain-interacting protein is required for the urine concentration mechanism by modulating arginine vasopressin receptor 2 and AQP2 expression in the inner medulla.
RGS2 is involved in negative feedback regulation of V2R signaling
Determine expression of VR1/VR2 receptors in early heart maturation.
Nav and Cav conductances, along with a more positive inactivation voltage of the Nav current in the V2r1b vomeronasal sensory neurons, contributed to the larger spike amplitude and higher spike frequency induced by depolarizing current
Gene expression changes in nephrogenic diabetes insipidus V2 receptor deficient mice indicate increased proximal tubular sodium reabsorption
Describe VRQ397 (CRAVKY), a potent noncompetitive antagonist of V2R, which exhibits functional selectivity, in line with properties of a negative allosteric modulator.
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