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anti-Human AVPR2 Antikörper:
anti-Mouse (Murine) AVPR2 Antikörper:
anti-Rat (Rattus) 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 - 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
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 (zeige AQP2 Antikörper), or for bypassing defective AVPR2 signaling and restoring AQP2 (zeige AQP2 Antikörper) plasma membrane expression.
Data found Mutations of Vasopressin (zeige AVP Antikörper) 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.
AQP1 (zeige AQP1 Antikörper), AQP2 (zeige AQP2 Antikörper), and AQP3 (zeige AQP3 Antikörper), 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 (zeige AVP Antikörper) 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 (zeige AVP Antikörper) receptor in polycystic kidney disease is targeted by green mamba peptide
Data show that upon heteromer formation with secretin receptor (SCTR (zeige SCTR Antikörper)), R137H, a nephrogenic diabetes insipidus (NDI)-causing vasopressin (zeige AVP Antikörper) receptor 2 (AVPR2) mutant that is defective in trafficking to cell surface, can functionally be rescued.
Conditional inactivation of Elf5 (zeige ELF5 Antikörper) in the developing collecting ducts results in a small but significant reduction in the expression levels of Aqp2 (zeige AQP2 Antikörper) and Avpr2 genes.
Data show that cryptochrome Cry1 (zeige CRY1 Antikörper) and Cry2 (zeige CRY2 Antikörper) expression must be circadian and appropriately phased to support rhythms, and arginine vasopressin (AVP (zeige AVP Antikörper)) 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 (zeige AQP2 Antikörper)/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 (zeige TALDO1 Antikörper) (MTAL), macula densa, connecting tubule, and cortical and medullary collecting duct, and was weakly expressed in cortical TAL (zeige TALDO1 Antikörper) and distal convoluted tubule in rat, mouse, and human
The data support roles for multiple vasopressin V2-receptor-dependent signaling pathways in the vasopressin (zeige AVP Antikörper) signaling network of collecting duct cells, involving several kinases not generally accepted to regulate collecting duct function.
NF-kappaB (zeige NFKB1 Antikörper) activation is of importance for the downregulation of AQP2 (zeige AQP2 Antikörper) channel and vasopressin (zeige AVP Antikörper) V(2) receptor expression during sepsis. NF-kappaB (zeige NFKB1 Antikörper) 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.
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