ライフサイエンスコーパス: CaSR

1 rypsin (CTR)C, and calcium-sensing receptor (CASR).

2 y 14%) in the calcium-sensing receptor gene (CASR).

3 nogen C (CTRC) and calcium-sensing receptor (CASR).

4 via activation of Ca(2+)-sensing receptors (CaSR).

5 CaSR) and/or anterior kidney (SORB and Sasa CaSR).

6 the extracellular calcium-sensing receptor (CaSR).

7 monocytes through calcium-sensing receptor (CaSR).

8 tuents such as the calcium-sensing receptor (CaSR).

9 idues for entry and binding of Ca(2+) by the CaSR.

10 on in Ca(2+) binding and the function of the CaSR.

11 INK1, CFTR, and to a lesser extent, CTRC and CASR.

12 retention of a significant fraction of total CaSR.

13 d the modulation of synaptic transmission by CaSR.

14 sites within the extracellular domain of the CaSR.

15 nding sites in the sensing capability of the CaSR.

16 nhibited the calcium-dependent activation of CASR.

17 noma CBS cells, which possessed a functional CaSR.

18 lhex 231, a negative allosteric modulator of CaSR.

19 -1 abolishes phosphate-induced inhibition of CaSR.

20 ts into the internalization mechanism of the CaSR.

21 de agonist interaction site within the human CaSR.

22 or cysteine (Cys) at position 482 in the pig CaSR.

23 The extracellular Ca(++)-sensing receptor (CaSR), a G protein-coupled receptor that regulates renal

24 our data show that calcium-sensing receptor (CaSR), a G-protein-coupled receptor important for regula

25 Activation of the calcium-sensing receptor (CaSR), a G-protein-coupled receptor present in nerve ter

26 expression of the calcium-sensing receptor (CaSR), a heterotrimeric G-protein-coupled receptor that

27 llular calcium ([Ca(2+)]o)-sensing receptor (CaSR), a member of the family C G protein-coupled recept

28 CASR activates the NLRP3 inflammasome through phospholip

29 ow that the murine calcium-sensing receptor (CASR) activates the NLRP3 inflammasome, mediated by incr

30 n explant cultures show that pharmacological CaSR activation by calcimimetics stimulates lung fluid s

31 Further, CaSR activation inhibited cell death triggered by high e

32 CaSR activation stimulated PTHrP production by breast ca

33 obilize intracellular calcium in response to CASR activation.

34 Cinacalcet and NPS-2143 are allosteric CaSR activators and inactivators, respectively, that ame

35 iologic range for CKD significantly inhibits CaSR activity via non-competitive antagonism.

36 The Ca(++) sensing receptor (CaSR) acts upstream of the microRNA-claudin-14 axis.

37 sR inhibitor Calhex 231 and augmented by the CasR agonist NPS-R568.

38 KP-2067, a form of the CaSR agonist peptide, was included to establish the role

39 In addition, the CaSR agonist spermidine reduced synaptic transmission an

40 -induced fluid secretion by a small-molecule CaSR agonist suggests that these compounds may provide a

41 ing extracellular Ca2+ or adding calindol, a CaSR agonist, produced concentration-dependent hyperpola

42 CaSR agonists (calcimimetics) and antagonists (calcilyti

43 Ca(2+) or other CASR agonists activate the NLRP3 inflammasome in the abs

44 these neurons by varying [Ca(2+)](o), using CaSR agonists and antagonists, or expressing a dominant-

45 mer1c and CaSR, but neither with Homer1c nor CaSR alone, establishes sensitivity of AKT-Ser(473) phos

46 Depleting CaSR also suppressed keratinocyte proliferation by downr

47 ssion of two other parathyroid marker genes, CasR and CCL21, although expression of these two genes w

48 CaSR and E-cadherin were co-expressed at the cell-cell m

49 Here, we show that CaSR and Homer1 are co-expressed in mineralized mouse bo

50 with primary osteoblasts revealed that both CaSR and Homer1 are required for extracellular Ca(2+)-st

51 region of the extracellular domain (ECD) of CaSR and its interaction with other Ca(2+)-binding sites

52 by which Ca(2+) and amino acids regulate the CaSR and may pave the way for exploration of the structu

53 Thus, CaSR and OGR1 activities can be regulated in a seesaw ma

54 We show that CaSR and OGR1 reciprocally inhibit signaling through eac

55 exploration of the structural properties of CaSR and other members of family C of the GPCR superfami

56 llular protein, and cellular proteins, GAS1, CASR and OTOP2, and are promising biomarker candidates.

57 duction mechanism requires activation of the CaSR and signal mediation by the p38alpha MAP kinase pat

58 atic localization of prostate cancer via the CaSR and the Akt signaling pathway.

59 ply increasing calcium influx but stimulates CaSR and thereby promotes resting spontaneous glutamate

60 lect a rapidly mobilizable "storage form" of CaSR and/or may subserve distinct intracellular signalin

61 Extracellular calcium-sensing receptor (CaSR) and ovarian cancer gene receptor 1 (OGR1) are two

62 CaSR sequences), testis (SORB, SORD and Sasa CaSR) and/or anterior kidney (SORB and Sasa CaSR).

63 ter (SLC34A1), the calcium-sensing receptor (CASR), and fibroblast growth factor 23 (FGF23), proteins

64 (PTH), express the calcium-sensing receptor (CASR), and mobilize intracellular calcium in response to

65 reening as a novel calcium-sensing receptor (CaSR) antagonist.

66 Small molecule CaSR antagonists and/or negative allosteric modulators h

67 The actions of the CaSR appeared to be mediated by nuclear actions of PTHrP

68 ues, one from AMG 416 and the other from the CaSR at position 482 (Cys482), and correlate the degree

69 However, manipulation of CaSR at the systemic level causes promiscuous effects in

70 lt physiology and disease, with reference to CaSR-based therapeutics.

71 s linear over 60 min, and the rate of [(35)S]CaSR biosynthesis is significantly increased by the memb

72 ine was used to characterize early events in CaSR biosynthesis.

73 The [(35)S]CaSR biosynthetic rate also varies as a function of conf

74 Neither the Ca2+-sensing receptor (CaSR) blocker NPS2390 (0.1 and 10 mum) nor FK506 (10 mum

75 cells, co-transfection with both Homer1c and CaSR, but neither with Homer1c nor CaSR alone, establish

76 tivation of the endogenous CaR-encoding gene CASR by adenoviral expression of a CaR antisense cDNA in

77 g affinities of these predicted sites in the CaSR by monitoring aromatic-sensitized Tb(3+) fluorescen

78 responsible for the switching on and off the CaSR by the transition between its open inactive form an

79 of the parathyroid calcium-sensing receptor (Casr) by both hypercalcemia and a calcimimetic that decr

80 tro results indicate that stimulation of the CaSR, by Ca(2+) or by the calcimimetic R-568, produced a

81 ine-earth (M) spanning Ca, Sr, and Ba, MgSr, CaSr, CaBa, SrBa, and CaSrBa.

82 e with full-length CaSR, suggesting that the CaSR carboxyl terminus between residues Thr(868) and Arg

83 The CaSR carboxyl terminus is the chief determinant of intra

84 predicted ligand residues in the full-length CaSR caused abnormal responses to [Ca(2+)](o), similar t

85 A CaSR chimera containing the mGluR1alpha carboxyl terminu

86 TrkB and CaSR colocalize within late endosomes, cotraffic and coa

87 e that signaling pathways emanating from the CaSR control colonic epithelial cell proliferation in vi

88 d its receptor, the Ca(2+)-sensing receptor (CaSR), conveys the Ca(2+)(o) signals to promote keratino

89 m (CASR), serum calcium-related risk of CHD (CASR), coronary artery calcified plaque (PTPRN2), and ki

90 scular, extracellular Ca2+-sensing receptor (CaSR) could mediate these vasodilator actions was invest

91 ose sensor and the calcium-sensing receptor, CasR, could detect amino acids in the intestine to modif

92 mpathetic innervation density was reduced in CaSR-deficient mice in vivo.

93 These findings indicate that Homer1 mediates CaSR-dependent AKT activation via mTORC2 and thereby sta

94 lease was well described by a combination of CaSR-dependent and CaSR-independent mechanisms.

95 us putative Ca(2+)-binding sites by grafting CaSR-derived, Ca(2+)-binding peptides to a scaffold prot

96 hrough loss of interaction with a C-terminal CaSR dileucine-based motif, whose disruption also decrea

97 We demonstrate that the CaSR displays both constitutive and concentration-depend

98 Finally, receptors such as the CaSR do not interact with the cytoskeleton in any signif

99 gonist Ca(2+) (0.5 or 5 mm), suggesting that CaSR does not control its own release from the endoplasm

100 CaSR downstream signaling involves activation of protein

101 first time a direct interaction between the CaSR ECD and l-Phe.

102 l-Phe increases the binding affinity of the CaSR ECD for Ca(2+).

103 Both glycosylated forms of the CaSR ECD were purified as dimers and exhibit similar sec

104 re closely mimic the structure of the native CaSR ECD.

105 cellular domain of calcium-sensing receptor (CaSR) (ECD) (residues 20-612), containing either complex

106 g cells to extracellular calcium and reduced CaSR endocytosis, probably through loss of interaction w

107 At later developmental stages, CaSR enhances tropomyosin receptor kinase B (TrkB)/BDNF-

108 The Ca2+-sensing receptor (CaSR) expressed by parathyroid cells controls blood calc

109 AP2S1 mutations decreased the sensitivity of CaSR-expressing cells to extracellular calcium and reduc

110 utations were found to reduce the numbers of CaSR-expressing cells.

111 , ADH2 or uveal melanoma were transfected in CaSR-expressing HEK293 cells, and Ca(2+) i and ERK phosp

112 Cutaneous injury triggered a robust CaSR expression and a surge of Ca(2+)(i) in epidermis.

113 In contrast, CASR expression and localization are equivalent in the r

114 in the CaSR gene, and murine models in which CaSR expression has been manipulated, have clearly demon

115 CaSR expression in these monocytes and local [Ca(2+)] in

116 human fetal lung at gestational stages when CaSR expression is maximal.

117 epithelial differentiation and that loss of CaSR expression may be associated with abnormal differen

118 e-differentiated histologic pattern, whereas CaSR expression was undetectable in less-differentiated

119 CaSR expression was weak in colon carcinomas with a more

120 channel TRPC6, and calcium sensing receptor (CaSR) expression.

121 In summary, reduced CaSR function enhanced synaptic transmission and CaSR st

122 Manipulating CaSR function in these neurons by varying [Ca(2+)](o), u

123 , strong intracellular acidification impairs CaSR function, but potentiates OGR1 function.

124 nd in vivo Tissue-specific disruption of the casr gene in mammary epithelial cells in MMTV-PymT mice

125 onclude that common genetic variation in the CASR gene is associated with similar but milder features

126 In whites, CaSR gene SNP rs1801725 was associated with serum calciu

127 f the CaSR in 1993, genetic mutations in the CaSR gene, and murine models in which CaSR expression ha

128 sing from rare inactivating mutations in the CASR gene.

129 n mutations in the calcium-sensing receptor (Casr) gene lead to decreased urinary calcium excretion i

130 the association of calcium-sensing receptor (CaSR) gene single nucleotide polymorphism (SNP) rs180172

131 ith key roles in calcium regulation (ATP2B2, CASR, GUCA1B, HPCAL1), and genes identified in genome- a

132 Sympathetic neurons lacking CaSR had smaller neurite arbors in vitro, and sympatheti

133 campal pyramidal neurons, which also express CaSR, had smaller dendrites when transfected with domina

134 sorder, but recently milder mutations in the CASR have been shown to cause hypercalcemia when homozyg

135 h GG at rs7627468 (calcium-sensing receptor (CASR)) have lower pH level in urine (p = 0.0088).

136 To confirm the role of the CaSR-Homer1 complex in AKT initiation, we show that in H

137 The CaSR-Homer1 protein complex, whose formation was increas

138 witch in the signaling cascade downstream of CaSR (i.e., from the PI3-kinase-Akt pathway to activatio

139 Since the identification of the CaSR in 1993, genetic mutations in the CaSR gene, and mu

140 dney, but the importance of extraparathyroid CaSR in calcium metabolism remains unknown.

141 indings demonstrated a critical role for the CaSR in epidermal regeneration and its therapeutic poten

142 e distribution pattern and expression of the CaSR in lower vertebrates strongly suggest that the CaSR

143 in [Ca(2+)](cyt), whereas overexpression of CaSR in normal PASMC conferred the nifedipine-induced ri

144 This review addresses the involvement of the CaSR in nutrient sensing; its putative and demonstrated

145 dipine) increase [Ca(2+)](cyt) by activating CaSR in PASMC from IPAH patients (in which CaSR is upreg

146 Ca(2+)](cyt) by potentiating the activity of CaSR in PASMC independently of their blocking (or activa

147 ine) to treat IPAH patients with upregulated CaSR in PASMC may exacerbate pulmonary hypertension.

148 We found large amounts of CaSR in perinatal mouse sympathetic neurons when their a

149 ites when transfected with dominant-negative CaSR in postnatal organotypic cultures.

150 iments confirmed that Homer1 associates with CaSR in primary human osteoblasts.

151 Our findings reveal a crucial role for CaSR in regulating the growth of neural processes in the

152 ositive homotropic cooperative activation of CaSR in response to [Ca(2+)]o signaling by positively im

153 oing developments concerning the role of the CaSR in stem cell differentiation are also reviewed.

154 TH)-dependent hypercalcemia, but the role of Casr in the kidney is unknown.

155 ion approaches to delineate the functions of CaSR in wound re-epithelialization.

156 the extracellular calcium-sensing receptor (CaSR) in 1993 in the laboratories of Brown and Hebert.

157 f the extracellular Ca(2+)-sensing receptor (CaSR) in the control of colonic epithelial cell prolifer

158 ribed by a combination of CaSR-dependent and CaSR-independent mechanisms.

159 CaSR inhibition increased blood calcium concentration in

160 d by the amino acids was also blocked by the CasR inhibitor Calhex 231 and augmented by the CasR agon

161 by in vitro microperfusion of cortical TAL, CaSR inhibitors increased calcium reabsorption and parac

162 These findings suggest that CaSR inhibitors may provide a new specific treatment for

163 ed internalization assay to directly measure CaSR internalization in real-time.

164 ddition, we provide compelling evidence that CaSR internalization is beta-arrestin-dependent while in

165 or the first time, we conclusively show that CaSR internalization is sensitive to immediate positive

166 the processes involved, and the mechanism of CaSR internalization remains poorly understood.

167 tization as indirect measures to investigate CaSR internalization.

168 assay to show that calcium-sensing receptor (CaSR) internalization is beta-arrestin-dependent and sen

169 The in vivo studies, using a novel Casr intestinal-specific knock-out mouse, indicate that

170 We dissect the intact CaSR into three globular subdomains, each of which conta

171 ge extracellular domain (ECD) of the dimeric CaSR, intracellular Ca(2+) responses are highly cooperat

172 Direct CaSR involvement was demonstrated by using an si-RNA of

173 We conclude that CaSR is a direct determinant of blood calcium concentrat

174 The CaSR is a G protein-coupled cell surface receptor that b

175 The CaSR is a prototypical class C GPCR that maintains stabl

176 However, CaSR is also expressed in other organs, such as the kidn

177 However, CaSR is also expressed in the nervous system, where its

178 ssociation between CaM and the C terminus of CaSR is critical for maintaining proper responsiveness o

179 [(35)S]CaSR is relatively stable (half-life approximately 8 h),

180 Overall, these results suggest that CaSR is subject to cotranslational quality control, whic

181 t is thus necessary that the activity of the CaSR is tightly regulated, even while continuously being

182 g CaSR in PASMC from IPAH patients (in which CaSR is upregulated), but not in normal PASMC.

183 The calcium-sensing receptor (CaSR) is a G-protein-coupled receptor that has an extrac

184 The Ca(2+)-sensing receptor (CaSR) is a member of family C of the GPCRs responsible f

185 The calcium-sensing receptor (CaSR) is critical for skeletal development, but its mech

186 human parathyroid calcium sensing receptor (CaSR) is expressed in human colon epithelium and functio

187 The extracellular calcium-sensing receptor (CaSR) is the first identified G protein-coupled receptor

188 The calcium-sensing receptor (CaSR) is the main controller of PTH secretion and here w

189 g were observed in the keratinocyte-specific CaSR knockout ((Epid)Casr(-/-)) mice, whose shortened ne

190 d-type murine parathyroid glands, but not in CaSR knockout glands.

191 e, indicate that the genetic ablation of the Casr leads to hyperproliferation of colonic epithelial c

192 CASR loss- or gain-of-function mutations cause familial

193 y, Arg15Pro and Arg15Ser), which also caused CaSR loss-of-function, were not detected in FHH probands

194 tagonists, or expressing a dominant-negative CaSR markedly affected neurite growth in vitro.

195 In contrast, [(35)S]CaSR maturation to the plasma membrane was not significa

196 It is concluded that CaSR may function in the colon to regulate epithelial di

197 The endothelial cell CaSR may have a physiological role in the control of art

198 Intracellular CaSR may reflect a rapidly mobilizable "storage form" of

199 ity between [Ca(2+)]o and L-Phe in eliciting CaSR-mediated [Ca(2+)]i oscillations.

200 Inhibition of CaSR-mediated CPP uptake might be a therapeutic approach

201 K8644, had similar augmenting effects on the CaSR-mediated increase in [Ca(2+)](cyt) in IPAH-PASMC; h

202 We propose that CaSR-mediated NLRP3 inflammasome activation contributes

203 iltiazem and verapamil, had no effect on the CaSR-mediated rise in [Ca(2+)](cyt).

204 e keratinocyte-specific CaSR knockout ((Epid)Casr(-/-)) mice, whose shortened neo-epithelia exhibited

205 DR, GC, DHCR7, CYP2R1, CYP27B1, CYP24A1, and CASR) modify the effects of vitamin D3 or calcium supple

206 reated with MOFs crystals suggested that the CaSr-MOFs by themselves can upregulate osteogenic genes

207 The extracellular calcium-sensing receptor (CaSR) monitors the systemic, extracellular, free ionized

208 rossly normal but had undetectable levels of Casr mRNA and protein in the kidney.

209 (4) CaSR mRNA and protein were present in rat mesenteric art

210 lower vertebrates strongly suggest that the CaSR must play a role that is independent of mineral cat

211 neous synaptic transmission was decreased in CaSR mutant neurons.

212 reased on average by 88% in reduced affinity CaSR-mutant (CaSR(-/-)) neurons compared with wild-type.

213 nant hypocalcaemic hypercalciuria (ADHH) for CaSR mutations and performed in vitro functional express

214 Thus, these studies of disease-associated CaSR mutations have further elucidated the role of the V

215 ciated with a large proportion of truncating CaSR mutations that occurred in the homozygous or compou

216 A total of 70 different CaSR mutations were identified: 35 in FHH, 10 in NSHPT a

217 (CCCR) in comparison with FHH1 probands with CaSR mutations, and a calculated index of sCa x sMg/100

218 orate signaling disturbances associated with CaSR mutations, but their potential to modulate abnormal

219 patients with hypocalcemia who did not have CASR mutations.

220 rage by 88% in reduced affinity CaSR-mutant (CaSR(-/-)) neurons compared with wild-type.

221 Here, we describe a CaSR-NFATc1-microRNA-claudin-14 signaling pathway in the

222 alancing effects of solute activation of the CaSR on neuronal and hormonal secretagogue actions.

223 Blocking the expression of CaSR or E-cadherin in cultured keratinocytes markedly in

224 Silencing CaSR or TRPC6 expression in calcium-stimulated PC3 cells

225 gene encoding the calcium-sensing receptor (CASR) or AP2S1.

226 nt lysosomal Ca2+ release, activation of the CaSR, or displacement of FKBP12.6 from RyR2 for either p

227 RTDR1 (P=8.7 x 10(-9)), and rs73186030 near CASR (P=4.8 x 10(-8)).

228 ty of release (0.27 vs 0.46 for wild-type vs CaSR(-/-) pairs) with little change in quantal size (23

229 he dimeric extracellular domain (ECD) of the CaSR plays a crucial role in regulating Ca(2+) homeostas

230 hat Ca(2+) and/or 1,25(OH)(2)D(3) stimulated CaSR promoter activity and CaSR protein expression in th

231 First, when signaling in isolation, CaSR promotes growth through the PI3-kinase-Akt pathway.

232 iological fetal hypercalcemia, acting on the CaSR, promotes human fetal lung development via cAMP-dep

233 2)D(3) stimulated CaSR promoter activity and CaSR protein expression in the human colon carcinoma CBS

234 r tyrosine at position 482 in the native pig CaSR provided a complete gain of activity by the peptide

235 Thus CaSR provides a mechanism that may compensate for the fa

236 The calcium-sensing receptor (CaSR) provides a fundamental mechanism for diverse cells

237 in extracellular calcium, through studies of CaSR-PTHrP interactions in the MMTV-PymT transgenic mous

238 Taken together, our findings suggest that CaSR-PTHrP interactions might be a promising target for

239 sence of exogenous ATP, whereas knockdown of CASR reduces inflammasome activation in response to know

240 GLUT2 and CasR regulate K- and L-cell activity in response to nutr

241 aches showed that claudin-14 is required for CaSR-regulated renal Ca(++) metabolism.

242 aken together, these data suggest that renal Casr regulates calcium reabsorption in the thick ascendi

243 d other tissues, and the mechanisms by which CaSR regulates paracellular transport in the kidney rema

244 The calcium-sensing receptor (CaSR) regulates serum calcium concentrations.

245 g proteins form signaling complexes with two CaSR-related members of the G protein-coupled receptor (

246 n extracellular phosphate concentration, the CaSR represents a phosphate sensor in the parathyroid gl

247 ain (CaMBD) located within the C terminus of CaSR (residues 871-898).

248 Inactivity of AMG 416 on the pig CaSR resulted from a naturally occurring mutation encodi

249 Alignment of GPRC6A with CASR revealed conservation of both calcium and calcimime

250 8 x 10(-10)) and a suggestive association at CASR (rs7627468[A], OR=1.16, P=2.0 x 10(-8)).

251 Chronic inhibition of CaSR selectively increased renal tubular calcium absorpt

252 The CaSR senses the extracellular ionic activity of the diva

253 ory epithelium (SORB, SORF, all SVR and Sasa CaSR sequences), testis (SORB, SORD and Sasa CaSR) and/o

254 within a group of calcium sensing receptor (CaSR) sequences.

255 and epigenome-wide studies of serum calcium (CASR), serum calcium-related risk of CHD (CASR), coronar

256 ee FHH3-causing AP2sigma2 mutations impaired CaSR signal transduction in a dominant-negative manner.

257 In vitro, DGKD knockdown impairs CaSR-signal transduction, an effect rectified with the c

258 CaSR signaling in PC-3 cells was evaluated by measuring

259 CaSR signaling promoted the proliferation of human breas

260 Here, we show that colonic CaSR signaling stimulates the degradation of cyclic nucl

261 s, and this process is strictly dependent on CaSR signaling triggered by increases in [Ca(2+)](ex).

262 P uptake and IL-1beta release in response to CaSR signaling.

263 icted to influence calcium-sensing receptor (CaSR) signaling.

264 tation and targeting vitamin D activation or CaSR-signaling pathways in patients with recurrent kidne

265 iate positive and negative modulation by the CaSR-specific allosteric modulators N-(3-[2-chlorophenyl

266 With CaSR-specific pharmacological reagents, we show that the

267 CASR stimulation also results in reduced intracellular c

268 function enhanced synaptic transmission and CaSR stimulation had the opposite effect.

269 ivo and changes in beta-catenin triggered by CaSR stimulation in human colonic epithelial cells in vi

270 Furthermore, CaSR stimulation promoted a down-regulation of beta-cate

271 K2 interaction network, including MKK2, HY5, CaSR, STN7 and kinesin-like protein, show a remarkable d

272 potential Ca(2+)-binding sites in a modeled CaSR structure using computational algorithms based on t

273 ibits maturation comparable with full-length CaSR, suggesting that the CaSR carboxyl terminus between

274 These findings demonstrate that CaSR-targeted compounds can rectify signaling disturbanc

275 mino acid residues and their location in the CaSR that accommodate AMG 416 binding and mode of action

276 ement was demonstrated by using an si-RNA of CaSR that impeded [Ca(2+)](e)-mediated induction of VDR.

277 The identification of variation in CASR that influences serum calcium concentration confirm

278 ide agonist of the calcium-sensing receptor (CaSR) that is being evaluated for the treatment of secon

279 which couples the calcium-sensing receptor (CaSR) to intracellular calcium (Ca(2+) i) signaling, lea

280 the extracellular calcium-sensing receptor, CaSR, to promote fluid-driven lung expansion through act

281 ; type B), and the calcium-sensing receptor (CaSR; type C) using fluorescence recovery after photoble

282 we investigated the role of extraparathyroid CaSR using thyroparathyroidectomized, PTH-supplemented r

283 Furthermore, a CaSR variant (Glu250Lys) was identified in FHH and ADHH

284 fied predicted heterozygous loss-of-function CASR variants (6 different nonsense/frameshift variants

285 Missense CASR variants were identified in two unrelated hypocalce

286 Rare CASR variants were identified in whole-exome sequences f

287 Knockdown of the CaSR via RNA interference reduced cell proliferation in

288 Kidney CaSR was expressed primarily in the thick ascending limb

289 The CaSR was never observed in bundles.

290 The diffusion of the CaSR was unaffected by NHERF-1 or the addition of calciu

291 monstrated that the Ca(2+)-sensing receptor (CaSR) was upregulated and the extracellular Ca(2+)-induc

292 Thus, Insig1, Lss, Peci, Idi1, Hmgcs1, and Casr were subject to epigenetic regulation.

293 Novel ligands that interact with the CaSR were used in microelectrode recordings from rat iso

294 the extracellular calcium sensing receptor (CaSR) which in turn inhibits nonselective cation channel

295 H without mutations in calcium-sensing GPCR (CASR), which cause FHH1.

296 is process for the calcium-sensing receptor, CaSR, which enables cellular responses to changes in ext

297 erived from a location within the ECD of the CaSR, which would be anticipated to more closely mimic t

298 Conversely, stimulating endogenous CaSR with calcimimetic NPS-R568 accelerated wound re-epi

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

301 t activation of the Ca(2+) sensing receptor (CaSR) with Gd(3+) triggers the appearance of ZO-2 at the