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Cow (Bovine) Monoclonal CASR Primary Antibody for ELISA, FACS - ABIN266769
Goldsmith, Fan, Ray, Shiloach, McPhie, Rogers, Spiegel: Expression, purification, and biochemical characterization of the amino-terminal extracellular domain of the human calcium receptor. in The Journal of biological chemistry 1999
Show all 19 Pubmed References
Human Monoclonal CASR Primary Antibody for ELISA, FACS - ABIN250524
Handlogten, Shiraishi, Awata, Huang, Miller: Extracellular Ca(2+)-sensing receptor is a promiscuous divalent cation sensor that responds to lead. in American journal of physiology. Renal physiology 2001
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Monoclonal CASR Primary Antibody for WB - ABIN534080
Awata, Huang, Handlogten, Miller: Interaction of the calcium-sensing receptor and filamin, a potential scaffolding protein. in The Journal of biological chemistry 2001
Show all 2 Pubmed References
Human Polyclonal CASR Primary Antibody for IF (p), IHC (p) - ABIN1386858
Huang, Xiao, Tan, Xiao, Wang, Yin, Duan, Huang, Yang, Yin: Chitosan Oligosaccharide Reduces Intestinal Inflammation That Involves Calcium-Sensing Receptor (CaSR) Activation in Lipopolysaccharide (LPS)-Challenged Piglets. in Journal of agricultural and food chemistry 2016
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Human Polyclonal CASR Primary Antibody for WB - ABIN6137981
Zeng, Zhu, Xiao, Liu, Sun, Liu, Hao, Lu, Zhang, Li, Wang, Wei, Hu: Hypoxia-Induced Mitogenic Factor Acts as a Nonclassical Ligand of Calcium-Sensing Receptor, Therapeutically Exploitable for Intermittent Hypoxia-Induced Pulmonary Hypertension. in Hypertension (Dallas, Tex. : 1979) 2017
Human Polyclonal CASR Primary Antibody for IHC (p), WB - ABIN4886502
Yuan, Shi, Li, Yang, Tang, Hu, Du, Li, Gu, Wang, Xi, Tang: Evaluation of a TPTX model induced by ischemia. in Experimental animals 2018
Human Polyclonal CASR Primary Antibody for WB - ABIN1678994
Xiao, Su, Feng, Sun, Liu, Zhang, Lu, Li, Wang, Zhu, Hu: Monocrotaline Induces Endothelial Injury and Pulmonary Hypertension by Targeting the Extracellular Calcium-Sensing Receptor. in Journal of the American Heart Association 2017
data indicated that CaSR is expressed in human dental pulp and hDPCs and that it can negatively or positively regulate mineral trioxide aggregate-induced mineralization of hDPCs via the phosphoinositide 3-kinase/Akt pathway in a ligand-dependent manner
Results found that calcium-sensing receptor (CaSR) internalization is beta-arrestin-dependent and sensitive to modulation by allosteric ligands.
Study provides the evidence that serine-875 represents the missing inhibitory PKC phosphorlyation site in CaS that in tandem with threonine-888 controls receptor activity.
FIH interacts with the ankyrin repeat domain of HACE1.HACE1 is hydroxylated at asparagine 191 by FIH.FIH-dependent hydroxylation of HACE1 inhibits HACE1 ability to ubiquitinate Rac1.
Data show that CaSR activation increased cytosolic calcium, and reduced intracellular cAMP levels and mTOR activity thus improving the principal dysregulations of signaling molecules considered the most proximal events in the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD).
CaSR-dependent NLRP3 inflammasome activation in preadipocytes through ERK signaling.
Results indicate that calcium-sensing receptor (CaSR) signaling through beta-arrestin and the importance of the Arg(680)-Glu(767) salt bridge in mediating signaling bias.
In this study, we show that CaSR activation is associated with increased NCC activity.
CaSR rs7652589 polymorphism had a significant effect on the risk of developing calcium nephrolithiasis in the Yi population in Southwestern China.
A homozygous mutation of CASR gene is associated with Familial hypocalciuric hypercalcemia type 1.
5 'disease-switch' residues (Gln27, Asn178, Ser657, Ser820, Thr828) are affected by CaSR mutations in patients. 2 familial hypocalciuric hypercalcemia mutations (p.Asn178Asp, p.Ser820Ala) impaired Ca2+i signalling without altering ERK phosphorylation. Autosomal Dominant Hypoparathyroidism-associated p.Ser657Cys mutation uncoupled signalling by leading to increased Ca2+i mobilization while decreasing ERK phosphorylation
CaSR may modulate T lymphocytes to release cytokines through mitogenactivated protein kinase pathways and affect cardiomyocyte injury.
Genotype analysis in a cohort of aged males shows that Single nucleotide polymorphisms in CaSR increase the risk of osteoporosis in aging males.
Performed cytogenetic analysis in 23 patients with Sagliker syndrome; found base alterations and deletions in exons 2 and 3 of the calcium sensing receptor (CaSR) gene.
Based on these findings, ischemia/reperfusion-induced MCPIP1 expression regulates the migration and apoptosis of human vascular endothelial cells via HMGB1 and CaSR, respectively.
expressions of p27(Kip1) and CaSR were decreased in primary hyperparathyroidism patients
Study presents the novel concept that CaSR activation stimulates autophagy in preadipocytes, which in turn mediates the elevation of TNFalpha production.
The identification of the activation of CaSR-mediated protective pathway in renal cells sheds light on a possible cellular protective mechanism against Cd-induced kidney injury.
These findings suggest an inhibitory role for CaSR in endometrial cancer. Therefore, reduced CaSR expression may be a suitable explanation and valuable predictor for endometrial cancer progression.
We found that subjects carrying the G allele of rs6776158 (AG and GG) had significantly higher risk of nephrolithiasis compared to the AA genotype.Our results indicate that rs6776158 polymorphism that might elevate the risk of nephrolithiasis in the Chinese population.
HNF1beta is a transcriptional activator of the CaSR.
CaSR signaling reduces AQP2 abundance both via AQP2-targeting miRNA-137 and the p38-MAPK/AQP2-pS261/ubiquitination/proteasomal axis.
In mouse strains with parathyroid-specific deletions of Klotho and CaSR and dual deletion of both genes, ablating CaSR in the parathyroid glandss increases PTH synthesis. CaSR together with Klotho regulates PTH biosynthesis and parathyroid growth.
These findings indicate that cardiac function could be enhanced significantly by combination therapy with CaSR inhibition and ESC transplantation; the effect was better than ESC transplantation alone, and the mechanism might be associated with a reduction in cell apoptosis via the inhibition of the MAPK pathway.
These studies indicate that the CaSR activation impairs glucose tolerance by a combination of alpha- and beta-cell defects and also influences pancreatic islet mass.
These findings suggest that trabecular bone formation can occur independently of the CaSR, and that the CaSR plays a collaborative role in the PTH anabolic effects on bone.
Vdr and Casr are required for beta-catenin-regulated cell proliferation and Adherens junction formation essential for re-epithelialization after wounding. Vitamin D and calcium signaling in keratinocytes are required for a normal regenerative response of the skin to wounding.
we suggest that decreased Ca2+ levels and increased CaSR expression might be involved in increased insulin secretion to compensate for insulin resistance in aged mice.
physiological fetal hypercalcemia, acting on the CaSR, promotes human fetal lung development via cAMP-dependent opening of CFTR.
CaSR was localized in the basolateral membrane of basolateral membrane of type-B intercalated cell and was more expressed during alkali-loading
Demonstrate a role for CaSR in cardiovascular system and suggest physiologically relevant changes in extracellular Ca(2+) concentrations could contribute to setting blood vessel tone levels and heart rate by directly acting on the cardiovascular CaSR.
Both vitamin D and calcium are needed for protection against malignant transformation of the colon and that their effect is modulated by the presence of a functional CaSR.
fluoride might be able to affect calcium homeostasis by regulating PTH, PTHrP, and CaSR
the activation of CaSR in the collecting duct prevents the cyclic AMP-dependent increase in AQP2-phosphorylation at S256 and water permeability, counteracting the short-term vasopressin response.
Deoxynivalenol induced cholecystokinin and glucagon-like peptide 1 release by enteroendocrine cells in mediated by casR/TRPA1 signaling.
Calcium-sensing receptor has a role in airway hyperresponsiveness and inflammation in allergic asthma
CaSR and OGR1 reciprocally inhibit signaling through each other in central neurons, and that this is lost in their transformed counterparts. Acidification impairs CaSR
results demonstrate a critical tumor suppressive role of CaSR in the colon. Restoration of CaSR expression and function is linked to regulation of the balance between proliferation, differentiation, and apoptosis
Studied the association of calcium-sensing receptor (CaSR) single nucleotide polymorphisms with growth traits in cattle.
CaSR activation may play a fundamental role in selecting specific differentiation checkpoints of neurogenesis and osteogenesis
The extracellular calcium-sensing receptor is expressed in the cumulus-oocyte complex in mammals and modulates oocyte meiotic maturation.
Calcium and the calcimimetic NPS R-467 reduce CaSR mRNA expression and stimulate cell growth/proliferation in equine size-sieved umbilical cord matrix mesenchymal stem cell.
CaSR is involved in inflammatory bowel disease and its signaling pathway that involves NF-kappaB and IkappaB is affected by dietary supplement NPS-2143
CASR, as the effector of extracellular calcium, modulates porcine fertilisation and early embryo development.
Long-term activation of CaSR with cinacalcet disrupted the cadherin-catenin complex, induced cytoskeletal remodeling, actin fiber formation, and redistribution of CaSR to the nuclear area. These changes indicate a significant and complex role of CaSR in epithelial remodeling and barrier function of esophageal cells.
Heteromeric TRPV4-TRPC1 channels mediate CaSR-induced vasorelaxation through NO production but not IKCa channel activation in rabbit mesenteric arteries.
The protein encoded by this gene is a G protein-coupled receptor that is expressed in the parathyroid hormone (PTH)-producing chief cells of the parathyroid gland, and the cells lining the kidney tubule. It senses small changes in circulating calcium concentration and couples this information to intracellular signaling pathways that modify PTH secretion or renal cation handling, thus this protein plays an essential role in maintaining mineral ion homeostasis. Mutations in this gene cause familial hypocalciuric hypercalcemia, familial, isolated hypoparathyroidism, and neonatal severe primary hyperparathyroidism.
extracellular calcium-sensing receptor
, parathyroid Ca(2+)-sensing receptor 1
, parathyroid cell calcium-sensing receptor
, G protein coupled receptor, family C, group 2, member A
, G protein-coupled receptor, family C, group 2, member A
, cation sensing receptor
, Calcium-sensing receptor (hypocalciuric hypercalcemia 1 severe neonatal hyperparathyroidism)
, Calcium-sensing receptor (hypocalciuric hypercalcemia 1, severe neonatal hyperparathyroidism)
, parathyroid Cell calcium-sensing receptor
, calcium-sensing receptor (hypocalciuric hypercalcemia 1, severe neonatal hyperparathyroidism)
, calcium-sensing receptor
, vomeronasal receptor F-1
, parathyroid gland calcium-sensing receptor
, extracellular calcium-sensing receptor-like