ライフサイエンスコーパス: CaSR

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