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1 y 14%) in the calcium-sensing receptor gene (CASR).
2 nogen C (CTRC) and calcium-sensing receptor (CASR).
3  via activation of Ca(2+)-sensing receptors (CaSR).
4  CaSR) and/or anterior kidney (SORB and Sasa CaSR).
5 gland extracellular Ca(2+)-sensing receptor (CaSR).
6 tuents such as the calcium-sensing receptor (CaSR).
7 rypsin (CTR)C, and calcium-sensing receptor (CASR).
8 INK1, CFTR, and to a lesser extent, CTRC and CASR.
9 retention of a significant fraction of total CaSR.
10 d the modulation of synaptic transmission by CaSR.
11 sites within the extracellular domain of the CaSR.
12 nding sites in the sensing capability of the CaSR.
13 nhibited the calcium-dependent activation of CASR.
14 noma CBS cells, which possessed a functional CaSR.
15 lhex 231, a negative allosteric modulator of CaSR.
16 cancer may be mediated, in part, through the CaSR.
17 de agonist interaction site within the human CaSR.
18 evaluating the extraparathyroid functions of CasR.
19 to a direct action on the channel or via the CaSR.
20 or cysteine (Cys) at position 482 in the pig CaSR.
21 idues for entry and binding of Ca(2+) by the CaSR.
22 on in Ca(2+) binding and the function of the CaSR.
23   The extracellular Ca(++)-sensing receptor (CaSR), a G protein-coupled receptor that regulates renal
24  Activation of the calcium-sensing receptor (CaSR), a G-protein-coupled receptor present in nerve ter
25  expression of the calcium-sensing receptor (CaSR), a heterotrimeric G-protein-coupled receptor that
26 llular calcium ([Ca(2+)]o)-sensing receptor (CaSR), a member of the family C G protein-coupled recept
27                                              CASR activates the NLRP3 inflammasome through phospholip
28 ow that the murine calcium-sensing receptor (CASR) activates the NLRP3 inflammasome, mediated by incr
29 n explant cultures show that pharmacological CaSR activation by calcimimetics stimulates lung fluid s
30                                     Further, CaSR activation inhibited cell death triggered by high e
31                                              CaSR activation stimulated PTHrP production by breast ca
32 obilize intracellular calcium in response to CASR activation.
33       Cinacalcet and NPS-2143 are allosteric CaSR activators and inactivators, respectively, that ame
34                 The Ca(++) sensing receptor (CaSR) acts upstream of the microRNA-claudin-14 axis.
35 sR inhibitor Calhex 231 and augmented by the CasR agonist NPS-R568.
36                       KP-2067, a form of the CaSR agonist peptide, was included to establish the role
37                             In addition, the CaSR agonist spermidine reduced synaptic transmission an
38 -induced fluid secretion by a small-molecule CaSR agonist suggests that these compounds may provide a
39 ing extracellular Ca2+ or adding calindol, a CaSR agonist, produced concentration-dependent hyperpola
40                                              CaSR agonists (calcimimetics) and antagonists (calcilyti
41                              Ca(2+) or other CASR agonists activate the NLRP3 inflammasome in the abs
42  these neurons by varying [Ca(2+)](o), using CaSR agonists and antagonists, or expressing a dominant-
43 cellular cations, including aluminum and the CasR agonists gadolinium and calcium, stimulated DNA syn
44                         Thus, the absence of CasR alters neither the maturational profile of isolated
45 ssion of two other parathyroid marker genes, CasR and CCL21, although expression of these two genes w
46                                          (5) CaSR and IKCa proteins were restricted to caveolin-poor
47  region of the extracellular domain (ECD) of CaSR and its interaction with other Ca(2+)-binding sites
48 by which Ca(2+) and amino acids regulate the CaSR and may pave the way for exploration of the structu
49                                        Thus, CaSR and OGR1 activities can be regulated in a seesaw ma
50                                 We show that CaSR and OGR1 reciprocally inhibit signaling through eac
51  exploration of the structural properties of CaSR and other members of family C of the GPCR superfami
52 duction mechanism requires activation of the CaSR and signal mediation by the p38alpha MAP kinase pat
53 atic localization of prostate cancer via the CaSR and the Akt signaling pathway.
54 ply increasing calcium influx but stimulates CaSR and thereby promotes resting spontaneous glutamate
55 lect a rapidly mobilizable "storage form" of CaSR and/or may subserve distinct intracellular signalin
56                        Osteoblasts from both CasR(+/+) and CasR(-/-) mice displayed an initial period
57 responses to these cations were identical in CasR(+/+) and CasR(-/-) osteoblasts.
58 ated osteoblastic cell lines from wild-type (CasR(+/+)) and receptor null (CasR(-/-)) mice to investi
59      Extracellular calcium-sensing receptor (CaSR) and ovarian cancer gene receptor 1 (OGR1) are two
60  human parathyroid calcium sensing receptor (CaSR) and that a function of extracellular Ca(2+) and th
61 CaSR sequences), testis (SORB, SORD and Sasa CaSR) and/or anterior kidney (SORB and Sasa CaSR).
62 ter (SLC34A1), the calcium-sensing receptor (CASR), and fibroblast growth factor 23 (FGF23), proteins
63 (PTH), express the calcium-sensing receptor (CASR), and mobilize intracellular calcium in response to
64 colonic crypt epithelial cells expressed the CaSR, and histologically differentiated carcinomas (i.e.
65 sis of the skeleton of 6-week-old homozygous CasR- and Gcm2-deficient mice also failed to identify an
66           In addition, the double homozygous CasR- and Gcm2-deficient mice demonstrated healing of th
67 (Gcm2-deficient) background by intercrossing CasR- and Gcm2-deficient mice.
68 reening as a novel calcium-sensing receptor (CaSR) antagonist.
69                               Small molecule CaSR antagonists and/or negative allosteric modulators h
70                           The actions of the CaSR appeared to be mediated by nuclear actions of PTHrP
71 pression in all cells in which TTF-1 and the CaSR are expressed, i.e., parathyroid cells, neural cell
72 ues, one from AMG 416 and the other from the CaSR at position 482 (Cys482), and correlate the degree
73                     However, manipulation of CaSR at the systemic level causes promiscuous effects in
74 lt physiology and disease, with reference to CaSR-based therapeutics.
75 s linear over 60 min, and the rate of [(35)S]CaSR biosynthesis is significantly increased by the memb
76 ine was used to characterize early events in CaSR biosynthesis.
77                                   The [(35)S]CaSR biosynthetic rate also varies as a function of conf
78           Neither the Ca2+-sensing receptor (CaSR) blocker NPS2390 (0.1 and 10 mum) nor FK506 (10 mum
79 tivation of the endogenous CaR-encoding gene CASR by adenoviral expression of a CaR antisense cDNA in
80  a phenylalkylamine, are thought to activate CaSR by allosterically increasing the affinity of the re
81 g affinities of these predicted sites in the CaSR by monitoring aromatic-sensitized Tb(3+) fluorescen
82 responsible for the switching on and off the CaSR by the transition between its open inactive form an
83 of the parathyroid calcium-sensing receptor (Casr) by both hypercalcemia and a calcimimetic that decr
84 tro results indicate that stimulation of the CaSR, by Ca(2+) or by the calcimimetic R-568, produced a
85 e with full-length CaSR, suggesting that the CaSR carboxyl terminus between residues Thr(868) and Arg
86                                          The CaSR carboxyl terminus is the chief determinant of intra
87 (+/-) and homozygous (-/-) disruption of the CaSR caused a further increase in the fetal calcium leve
88 predicted ligand residues in the full-length CaSR caused abnormal responses to [Ca(2+)](o), similar t
89                                            A CaSR chimera containing the mGluR1alpha carboxyl terminu
90 e that signaling pathways emanating from the CaSR control colonic epithelial cell proliferation in vi
91 scular, extracellular Ca2+-sensing receptor (CaSR) could mediate these vasodilator actions was invest
92 ose sensor and the calcium-sensing receptor, CasR, could detect amino acids in the intestine to modif
93            In contrast, concomitant Gcm2 and CasR deficiency failed to rescue the hypocalciuria in Ca
94                                              CasR deficiency was transferred onto the glial cells mis
95 zation of cartilage and bone associated with CasR deficiency, indicating that rickets and osteomalaci
96  indicating that rickets and osteomalacia in CasR-deficient mice are not due to an independent functi
97 eficiency rescued the perinatal lethality in CasR-deficient mice in association with ablation of the
98 mpathetic innervation density was reduced in CaSR-deficient mice in vivo.
99                             Double Gcm2- and CasR-deficient mice provide an important model for evalu
100 ciency failed to rescue the hypocalciuria in CasR-deficient mice, consistent with direct regulation o
101 n responsiveness to extracellular calcium in CASR-deficient mice, consistent with the existence of an
102 cts of elevated parathyroid hormone (PTH) in CasR-deficient mice.
103 lease was well described by a combination of CaSR-dependent and CaSR-independent mechanisms.
104 us putative Ca(2+)-binding sites by grafting CaSR-derived, Ca(2+)-binding peptides to a scaffold prot
105 hrough loss of interaction with a C-terminal CaSR dileucine-based motif, whose disruption also decrea
106               Finally, receptors such as the CaSR do not interact with the cytoskeleton in any signif
107 gonist Ca(2+) (0.5 or 5 mm), suggesting that CaSR does not control its own release from the endoplasm
108 in (BSND), and the calcium-sensing receptor (CASR), each of which is important in sodium reabsorption
109  first time a direct interaction between the CaSR ECD and l-Phe.
110  l-Phe increases the binding affinity of the CaSR ECD for Ca(2+).
111               Both glycosylated forms of the CaSR ECD were purified as dimers and exhibit similar sec
112 re closely mimic the structure of the native CaSR ECD.
113 cellular domain of calcium-sensing receptor (CaSR) (ECD) (residues 20-612), containing either complex
114 g cells to extracellular calcium and reduced CaSR endocytosis, probably through loss of interaction w
115                   The Ca2+-sensing receptor (CaSR) expressed by parathyroid cells controls blood calc
116 AP2S1 mutations decreased the sensitivity of CaSR-expressing cells to extracellular calcium and reduc
117 utations were found to reduce the numbers of CaSR-expressing cells.
118 , ADH2 or uveal melanoma were transfected in CaSR-expressing HEK293 cells, and Ca(2+) i and ERK phosp
119                                 In contrast, CASR expression and localization are equivalent in the r
120 ow that the cells of the colon crypt acquire CaSR expression as they differentiate and migrate toward
121 in the CaSR gene, and murine models in which CaSR expression has been manipulated, have clearly demon
122  potential candidates involved in regulating CaSR expression in the colon and the chemopreventive act
123  human fetal lung at gestational stages when CaSR expression is maximal.
124  epithelial differentiation and that loss of CaSR expression may be associated with abnormal differen
125 mparison, whereas an almost complete loss of CaSR expression was observed in undifferentiated tumors.
126 e-differentiated histologic pattern, whereas CaSR expression was undetectable in less-differentiated
127                                              CaSR expression was weak in colon carcinomas with a more
128 channel TRPC6, and calcium sensing receptor (CaSR) expression.
129 r, G protein-linked Ca(2+)-sensing receptor (CaSR), first identified in the parathyroid gland, is exp
130                          In summary, reduced CaSR function enhanced synaptic transmission and CaSR st
131                                 Manipulating CaSR function in these neurons by varying [Ca(2+)](o), u
132 , strong intracellular acidification impairs CaSR function, but potentiates OGR1 function.
133         The changes in TTF-1 inversely alter CaSR gene and calcitonin gene expression.
134 nd in vivo Tissue-specific disruption of the casr gene in mammary epithelial cells in MMTV-PymT mice
135 onclude that common genetic variation in the CASR gene is associated with similar but milder features
136                                      We used CaSR gene knockout mice to investigate the role of the C
137                                   In whites, CaSR gene SNP rs1801725 was associated with serum calciu
138 f the CaSR in 1993, genetic mutations in the CaSR gene, and murine models in which CaSR expression ha
139 identified gain-of-function mutations in the CASR gene, leading to a greater understanding of the pat
140  of expression and further functions for the CASR gene, which include a role in the epidermis, tooth
141 sing from rare inactivating mutations in the CASR gene.
142 n mutations in the calcium-sensing receptor (Casr) gene lead to decreased urinary calcium excretion i
143 the association of calcium-sensing receptor (CaSR) gene single nucleotide polymorphism (SNP) rs180172
144                  Sympathetic neurons lacking CaSR had smaller neurite arbors in vitro, and sympatheti
145 campal pyramidal neurons, which also express CaSR, had smaller dendrites when transfected with domina
146 sorder, but recently milder mutations in the CASR have been shown to cause hypercalcemia when homozyg
147              Since the identification of the CaSR in 1993, genetic mutations in the CaSR gene, and mu
148 ce are not due to an independent function of CasR in bone and cartilage but to the effect of severe h
149 dney, but the importance of extraparathyroid CaSR in calcium metabolism remains unknown.
150 e distribution pattern and expression of the CaSR in lower vertebrates strongly suggest that the CaSR
151  in [Ca(2+)](cyt), whereas overexpression of CaSR in normal PASMC conferred the nifedipine-induced ri
152 This review addresses the involvement of the CaSR in nutrient sensing; its putative and demonstrated
153 dipine) increase [Ca(2+)](cyt) by activating CaSR in PASMC from IPAH patients (in which CaSR is upreg
154 Ca(2+)](cyt) by potentiating the activity of CaSR in PASMC independently of their blocking (or activa
155 ine) to treat IPAH patients with upregulated CaSR in PASMC may exacerbate pulmonary hypertension.
156                    We found large amounts of CaSR in perinatal mouse sympathetic neurons when their a
157 ites when transfected with dominant-negative CaSR in postnatal organotypic cultures.
158 dentify any essential, nonredundant role for CasR in regulating chondrogenesis or osteogenesis, but f
159 knockout mice to investigate the role of the CaSR in regulating fetal calcium metabolism.
160       Our findings reveal a crucial role for CaSR in regulating the growth of neural processes in the
161 ositive homotropic cooperative activation of CaSR in response to [Ca(2+)]o signaling by positively im
162 oing developments concerning the role of the CaSR in stem cell differentiation are also reviewed.
163 TH)-dependent hypercalcemia, but the role of Casr in the kidney is unknown.
164 t regulation of urinary calcium excretion by CasR in the kidney.
165 dies are needed to establish the function of CasR in the skeleton.
166 t a function of extracellular Ca(2+) and the CaSR in these cells was the promotion of E-cadherin expr
167  the extracellular calcium-sensing receptor (CaSR) in 1993 in the laboratories of Brown and Hebert.
168 f the extracellular Ca(2+)-sensing receptor (CaSR) in the control of colonic epithelial cell prolifer
169 nd the role of the calcium-sensing receptor (CasR) in the skeleton, we used a genetic approach to abl
170 ribed by a combination of CaSR-dependent and CaSR-independent mechanisms.
171                                              CaSR inhibition increased blood calcium concentration in
172 d by the amino acids was also blocked by the CasR inhibitor Calhex 231 and augmented by the CasR agon
173  by in vitro microperfusion of cortical TAL, CaSR inhibitors increased calcium reabsorption and parac
174                  These findings suggest that CaSR inhibitors may provide a new specific treatment for
175           The in vivo studies, using a novel Casr intestinal-specific knock-out mouse, indicate that
176                        We dissect the intact CaSR into three globular subdomains, each of which conta
177 ge extracellular domain (ECD) of the dimeric CaSR, intracellular Ca(2+) responses are highly cooperat
178                                       Direct CaSR involvement was demonstrated by using an si-RNA of
179                             We conclude that CaSR is a direct determinant of blood calcium concentrat
180                                          The CaSR is a G protein-coupled cell surface receptor that b
181                                     However, CaSR is also expressed in other organs, such as the kidn
182                                     However, CaSR is also expressed in the nervous system, where its
183 ined in rats whether expression of the renal CaSR is altered in experimental chronic renal insufficie
184 ssociation between CaM and the C terminus of CaSR is critical for maintaining proper responsiveness o
185 null (CasR(-/-)) mice to investigate whether CasR is present in osteoblasts and accounts for their re
186                                       [(35)S]CaSR is relatively stable (half-life approximately 8 h),
187          Overall, these results suggest that CaSR is subject to cotranslational quality control, whic
188 g CaSR in PASMC from IPAH patients (in which CaSR is upregulated), but not in normal PASMC.
189                The calcium-sensing receptor (CaSR) is a G-protein-coupled receptor that has an extrac
190                 The Ca(2+)-sensing receptor (CaSR) is a member of family C of the GPCRs responsible f
191  receptor (CaR; alternate gene names, CaR or Casr) is a membrane-spanning G protein-coupled receptor.
192  human parathyroid calcium sensing receptor (CaSR) is expressed in human colon epithelium and functio
193  The extracellular calcium-sensing receptor (CaSR) is the first identified G protein-coupled receptor
194  cations, of which calcium-sensing receptor (CASR) is the prototypic extracellular calcium-sensing re
195 e, indicate that the genetic ablation of the Casr leads to hyperproliferation of colonic epithelial c
196 y, Arg15Pro and Arg15Ser), which also caused CaSR loss-of-function, were not detected in FHH probands
197 tagonists, or expressing a dominant-negative CaSR markedly affected neurite growth in vitro.
198                          In contrast, [(35)S]CaSR maturation to the plasma membrane was not significa
199                         It is concluded that CaSR may function in the colon to regulate epithelial di
200 ts suggest that extracellular Ca(2+) and the CaSR may function to regulate the differentiation of col
201                         The endothelial cell CaSR may have a physiological role in the control of art
202                                Intracellular CaSR may reflect a rapidly mobilizable "storage form" of
203 ity between [Ca(2+)]o and L-Phe in eliciting CaSR-mediated [Ca(2+)]i oscillations.
204 K8644, had similar augmenting effects on the CaSR-mediated increase in [Ca(2+)](cyt) in IPAH-PASMC; h
205 iltiazem and verapamil, had no effect on the CaSR-mediated rise in [Ca(2+)](cyt).
206          Osteoblasts from both CasR(+/+) and CasR(-/-) mice displayed an initial period of cell repli
207  cation-sensing response in osteoblasts from CasR(-/-) mice indicates the existence of a novel osteob
208 rom wild-type (CasR(+/+)) and receptor null (CasR(-/-)) mice to investigate whether CasR is present i
209 DR, GC, DHCR7, CYP2R1, CYP27B1, CYP24A1, and CASR) modify the effects of vitamin D3 or calcium supple
210  The extracellular calcium-sensing receptor (CaSR) monitors the systemic, extracellular, free ionized
211 rossly normal but had undetectable levels of Casr mRNA and protein in the kidney.
212                                          (4) CaSR mRNA and protein were present in rat mesenteric art
213                              In the Nx rats, CaSR mRNA expression and CaSR protein levels were found
214  lower vertebrates strongly suggest that the CaSR must play a role that is independent of mineral cat
215 neous synaptic transmission was decreased in CaSR mutant neurons.
216 reased on average by 88% in reduced affinity CaSR-mutant (CaSR(-/-)) neurons compared with wild-type.
217 nant hypocalcaemic hypercalciuria (ADHH) for CaSR mutations and performed in vitro functional express
218    Thus, these studies of disease-associated CaSR mutations have further elucidated the role of the V
219 ciated with a large proportion of truncating CaSR mutations that occurred in the homozygous or compou
220                      A total of 70 different CaSR mutations were identified: 35 in FHH, 10 in NSHPT a
221 (CCCR) in comparison with FHH1 probands with CaSR mutations, and a calculated index of sCa x sMg/100
222 orate signaling disturbances associated with CaSR mutations, but their potential to modulate abnormal
223  patients with hypocalcemia who did not have CASR mutations.
224 rage by 88% in reduced affinity CaSR-mutant (CaSR(-/-)) neurons compared with wild-type.
225                          Here, we describe a CaSR-NFATc1-microRNA-claudin-14 signaling pathway in the
226              These studies indicate that the CaSR normally suppresses PTH secretion in the presence o
227 alancing effects of solute activation of the CaSR on neuronal and hormonal secretagogue actions.
228                                    Silencing CaSR or TRPC6 expression in calcium-stimulated PC3 cells
229 action with mouse specific primers in either CasR(+/+) or CasR(-/-) osteoblasts, and immunoblot analy
230  gene encoding the calcium-sensing receptor (CASR) or AP2S1.
231 nt lysosomal Ca2+ release, activation of the CaSR, or displacement of FKBP12.6 from RyR2 for either p
232 ouse specific primers in either CasR(+/+) or CasR(-/-) osteoblasts, and immunoblot analysis with a Ca
233 hese cations were identical in CasR(+/+) and CasR(-/-) osteoblasts.
234 truct, and inhibited agonist-induced cAMP in CasR(-/-) osteoblasts.
235  RTDR1 (P=8.7 x 10(-9)), and rs73186030 near CASR (P=4.8 x 10(-8)).
236 ty of release (0.27 vs 0.46 for wild-type vs CaSR(-/-) pairs) with little change in quantal size (23
237 he dimeric extracellular domain (ECD) of the CaSR plays a crucial role in regulating Ca(2+) homeostas
238                The calcium-sensing receptor (CASR) plays a pivotal role in the regulation of calcium
239 hat Ca(2+) and/or 1,25(OH)(2)D(3) stimulated CaSR promoter activity and CaSR protein expression in th
240 iological fetal hypercalcemia, acting on the CaSR, promotes human fetal lung development via cAMP-dep
241 th a CasR-specific antibody was negative for CasR protein expression in osteoblasts.
242 2)D(3) stimulated CaSR promoter activity and CaSR protein expression in the human colon carcinoma CBS
243     In the Nx rats, CaSR mRNA expression and CaSR protein levels were found to be reduced by 35 and 3
244 r tyrosine at position 482 in the native pig CaSR provided a complete gain of activity by the peptide
245                                         Thus CaSR provides a mechanism that may compensate for the fa
246                The calcium-sensing receptor (CaSR) provides a fundamental mechanism for diverse cells
247 in extracellular calcium, through studies of CaSR-PTHrP interactions in the MMTV-PymT transgenic mous
248    Taken together, our findings suggest that CaSR-PTHrP interactions might be a promising target for
249 sence of exogenous ATP, whereas knockdown of CASR reduces inflammasome activation in response to know
250                                    GLUT2 and CasR regulate K- and L-cell activity in response to nutr
251 aches showed that claudin-14 is required for CaSR-regulated renal Ca(++) metabolism.
252 aken together, these data suggest that renal Casr regulates calcium reabsorption in the thick ascendi
253 d other tissues, and the mechanisms by which CaSR regulates paracellular transport in the kidney rema
254                The calcium-sensing receptor (CaSR) regulates PTH secretion to control the extracellul
255 ain (CaMBD) located within the C terminus of CaSR (residues 871-898).
256             Inactivity of AMG 416 on the pig CaSR resulted from a naturally occurring mutation encodi
257                     Alignment of GPRC6A with CASR revealed conservation of both calcium and calcimime
258 8 x 10(-10)) and a suggestive association at CASR (rs7627468[A], OR=1.16, P=2.0 x 10(-8)).
259                        Chronic inhibition of CaSR selectively increased renal tubular calcium absorpt
260                                          The CaSR senses the extracellular ionic activity of the diva
261 ory epithelium (SORB, SORF, all SVR and Sasa CaSR sequences), testis (SORB, SORD and Sasa CaSR) and/o
262  within a group of calcium sensing receptor (CaSR) sequences.
263 ee FHH3-causing AP2sigma2 mutations impaired CaSR signal transduction in a dominant-negative manner.
264                                              CaSR signaling in PC-3 cells was evaluated by measuring
265                                              CaSR signaling promoted the proliferation of human breas
266                   Here, we show that colonic CaSR signaling stimulates the degradation of cyclic nucl
267  osteoblasts, and immunoblot analysis with a CasR-specific antibody was negative for CasR protein exp
268                                         With CaSR-specific pharmacological reagents, we show that the
269                                              CASR stimulation also results in reduced intracellular c
270  function enhanced synaptic transmission and CaSR stimulation had the opposite effect.
271 ivo and changes in beta-catenin triggered by CaSR stimulation in human colonic epithelial cells in vi
272                                 Furthermore, CaSR stimulation promoted a down-regulation of beta-cate
273 K2 interaction network, including MKK2, HY5, CaSR, STN7 and kinesin-like protein, show a remarkable d
274  potential Ca(2+)-binding sites in a modeled CaSR structure using computational algorithms based on t
275 ibits maturation comparable with full-length CaSR, suggesting that the CaSR carboxyl terminus between
276              These findings demonstrate that CaSR-targeted compounds can rectify signaling disturbanc
277 mino acid residues and their location in the CaSR that accommodate AMG 416 binding and mode of action
278 ement was demonstrated by using an si-RNA of CaSR that impeded [Ca(2+)](e)-mediated induction of VDR.
279           The identification of variation in CASR that influences serum calcium concentration confirm
280 ide agonist of the calcium-sensing receptor (CaSR) that is being evaluated for the treatment of secon
281  which couples the calcium-sensing receptor (CaSR) to intracellular calcium (Ca(2+) i) signaling, lea
282  the extracellular calcium-sensing receptor, CaSR, to promote fluid-driven lung expansion through act
283                                 In addition, CasR transcripts could not be detected by reverse transc
284 ; type B), and the calcium-sensing receptor (CaSR; type C) using fluorescence recovery after photoble
285 we investigated the role of extraparathyroid CaSR using thyroparathyroidectomized, PTH-supplemented r
286                               Furthermore, a CaSR variant (Glu250Lys) was identified in FHH and ADHH
287                             Knockdown of the CaSR via RNA interference reduced cell proliferation in
288                                    Since the CaSR was cloned from rat and human kidney, this study ex
289                                       Kidney CaSR was expressed primarily in the thick ascending limb
290                                          The CaSR was never observed in bundles.
291                         The diffusion of the CaSR was unaffected by NHERF-1 or the addition of calciu
292 monstrated that the Ca(2+)-sensing receptor (CaSR) was upregulated and the extracellular Ca(2+)-induc
293   Thus, Insig1, Lss, Peci, Idi1, Hmgcs1, and Casr were subject to epigenetic regulation.
294         Novel ligands that interact with the CaSR were used in microelectrode recordings from rat iso
295  the extracellular calcium sensing receptor (CaSR) which in turn inhibits nonselective cation channel
296 H without mutations in calcium-sensing GPCR (CASR), which cause FHH1.
297 is process for the calcium-sensing receptor, CaSR, which enables cellular responses to changes in ext
298 erived from a location within the ECD of the CaSR, which would be anticipated to more closely mimic t
299                Replacing Cys482 in the human CaSR with serine or tyrosine ablated AMG 416 activity.
300                                 Knockdown of CaSR with siRNA in IPAH-PASMC significantly inhibited th

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