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AVPR2 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. Additionally we are shipping AVPR2 Kits (3) and and many more products for this protein.
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Human Polyclonal AVPR2 Primary Antibody for 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 references for ABIN2801893
Human Polyclonal AVPR2 Primary Antibody for IF, ELISA - ABIN1536014
Birnbaumer, Seibold, Gilbert, Ishido, Barberis, Antaramian, Brabet, Rosenthal: Molecular cloning of the receptor for human antidiuretic hormone. in Nature 1992
Show all 2 references for ABIN1536014
Human Polyclonal AVPR2 Primary Antibody for ELISA - ABIN409117
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
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 (show AVP Antibodies) 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 (show AVP Antibodies) 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
Type 2 vasopressin (show AVP Antibodies) 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 cryptochrome Cry1 (show CRY1 Antibodies) and Cry2 (show CRY2 Antibodies) expression must be circadian and appropriately phased to support rhythms, and arginine vasopressin (AVP (show AVP Antibodies)) 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 Antibodies)/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 Antibodies) (MTAL), macula densa, connecting tubule, and cortical and medullary collecting duct, and was weakly expressed in cortical TAL (show TALDO1 Antibodies) 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 Antibodies) signaling network of collecting duct cells, involving several kinases not generally accepted to regulate collecting duct function.
NF-kappaB (show NFKB1 Antibodies) activation is of importance for the downregulation of AQP2 (show AQP2 Antibodies) channel and vasopressin (show AVP Antibodies) V(2) receptor expression during sepsis. NF-kappaB (show NFKB1 Antibodies) 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 Antibodies) transactivation domain-interacting protein is required for the urine concentration mechanism by modulating arginine vasopressin receptor 2 and AQP2 (show AQP2 Antibodies) expression in the inner medulla.
RGS2 (show RGS2 Antibodies) is involved in negative feedback regulation of V2R signaling
Determine expression of VR1 (show TRPV1 Antibodies)/VR2 receptors in early heart maturation.
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