ライフサイエンスコーパス: PTH

1 PTH activates adenylyl cyclase (AC) through PTH 1 recept

2 PTH and 1,25D mutually upregulated 36 genes and mutually

3 PTH and FGF23 inhibited phosphate transport in a concent

4 PTH causes degradation of HDAC4, and this product appear

5 PTH markedly downregulated Galnt3 expression (2.7-fold)

6 PTH mediated the downregulation of DMP1 via the cAMP/pro

7 PTH regulates both HDAC4/5 and CRTC2 localization via ph

8 PTH secretion in explants increased in response to lepti

9 PTH stimulates expression of matrix metalloproteinase 13

10 PTH therapy promoted soft-tissue maturation by suppressi

11 PTH treatment enriched endosomal PTHR.

12 PTH was used as the bone anabolic control.

13 PTH-induced Mmp13 expression was significantly blocked b

14 PTH-induced Sost suppression was associated with specifi

15 Similar to 1,25D, PTH may modulate DMP1, but the underlying mechanism rema

16 were significantly more likely to achieve a PTH level of 300 pg/mL or lower: in trial A, 126 of 254

17 lular compartments and lysosomes alongside a PTH-induced dose-response relationship for fractional ph

18 eptor in the epidermis reveals an additional PTH family member that is expressed in the skin and may

19 L expression and secretion without affecting PTH inhibition of OPG expression, and it does so by bloc

20 expression systems and whether this affects PTH secretion.

21 ably, MCP-1(-/-) mice were protected against PTH-induced cortical and trabecular bone loss as well as

22 is and alkalosis are associated with altered PTH secretion in vivo, we examined whether pathophysiolo

23 therapeutic interventions aimed at altering PTH expression in diseases such as osteoporosis and seco

24 Treatment with anabolic PTH(1-34) (80 mug/kg/day) for 4 weeks failed to increase

25 ion wound healing between bisphosphonate and PTH therapies.

26 Circulating calcium and PTH levels were unchanged, but inorganic phosphate and 1

27 ic hyperparathyroidism (abnormal calcium and PTH) were referred to surgeons.

28 lopment, and elevations in serum calcium and PTH, were similar in males and females.

29 the prospective associations of 25-OH-D and PTH at 3 months postpartum with beta-cell function (Insu

30 pregnancy, and calculated free-25(OH)D3 and PTH were lower (P < 0.05).

31 postpartum had both vitamin D deficiency and PTH in the highest tertile at 3 months postpartum.

32 Plasma calcium levels fell and PTH levels increased within 10 minutes and remained low

33 Leptin, leptin receptor (long isoform), and PTH mRNA transcripts and protein were detected in an ove

34 Parathyroid hormone (PTH, 84 residues) and PTH-related protein (PTHrP, 141 residues) are natural ag

35 between 25(OH)D3 and free-25(OH)D3 (+ve) and PTH and 25(OH)D3 (-ve) (P < 0.0001).

36 ical and trabecular bone mass and attenuated PTH-induced trabecular bone anabolism, supporting the po

37 Significant associations between PTH and all 3 outcomes were found in univariate analyses

38 Our data support a link between PTH regulating HDAC4 phosphorylation by PKA, trafficking

39 PTH levels, whereas the relationship between PTH and trabecular bone decreases was bimodal.

40 m RANKL-treated WT, but not KO, BMMs blocked PTH-stimulated cAMP production in POBs.

41 Our results demonstrated that CFZ blocks PTH-induced osteoclast formation and bone resorption by

42 However, both PTH and FGF23-sensitive phosphate transport were abolish

43 first 3 months after transplantation in both PTH strata and remained less than 40 pg/mL thereafter.

44 We find that [d-Trp(12), Tyr(34)]bovine PTH(7-34) elicits a distinctive arrestin-signaling focus

45 id hormone analog [d-Trp(12), Tyr(34)]bovine PTH(7-34) in six different murine tissues after chronic

46 argeting genes/proteins mutually governed by PTH and 1,25D may be a viable approach for designing new

47 The induction of Saa3 by PTH may explain the suppression of bone formation when P

48 entify patterns of gene expression shared by PTH and 1,25D in regulating DMP1, as well as other facto

49 matched wild-type (Cdc73(+/+) and Cdc73(+/+)/PTH-Cre) littermates.

50 Genetic causes of variation in circulating PTH concentrations are incompletely understood.

51 t associated with differences in circulating PTH concentrations.

52 At maximally effective concentrations, PTH and FGF23 equivalently decreased phosphate uptake an

53 etabolites, vitamin D binding protein (DBP), PTH and 25(OH)D3 half-life were measured in third-trimes

54 ercalcemia and a calcimimetic that decreases PTH secretion, demonstrating that they are dicer-indepen

55 vely blocked FGF23 action without disrupting PTH effects.

56 g men and suggest that endocrine disruption (PTH-FGF23) is a primary contributor to TDF-associated BM

57 is module in mice resulted in loss of either PTH induction or FGF23 and 1,25(OH)2D3 suppression of Cy

58 Elevated PTH (>/=55.6 pg/mL; top quarter) was associated with sig

59 Elevated PTH was significantly associated with N-terminal probrai

60 the proportion of patients with an elevated PTH.

61 , very low 25(OH)D (<12 ng/mL), and elevated PTH (>62 pg/mL) each had a small but significant associa

62 intake without elevated PTH or with elevated PTH alone were unaffected.

63 or very low calcium intake without elevated PTH or with elevated PTH alone were unaffected.

64 RT1 inhibitor, EX527, significantly enhanced PTH-induced Mmp13 expression.

65 w to an osteogenic environment with enhanced PTH anabolism.

66 WT mice responded to exogenous PTH with redistribution of Npt2a from proximal tubule mi

67 ugh an unidentified transcription factor for PTH and through ATF4 for the sympathetic tone.

68 1 site of the Mmp13 promoter is required for PTH stimulation of Mmp13 transcriptional activity.

69 pocalcemia and uremia, the major stimuli for PTH secretion.

70 Furthermore, PTH may modulate phosphate homeostasis by downregulating

71 To further highlight the utility of Gel-PTH, we achieved "AND" gating of controlled radical poly

72 With this "Gel-PTH", we demonstrate switching of controlled radical pol

73 by RAFT/iniferter and ATRP methods using Gel-PTH and a readily available compact fluorescent light (C

74 Logic-controlled polymerization with Gel-PTH offers a straightforward approach to achieve multipl

75 Only 3200 (31%) hypercalcemic patients had PTH levels measured, 2914 (28%) had a documented diagnos

76 High PTH levels independently associated with low sclerostin

77 PTH (>65 to </=300 pg/mL; n = 112), and high PTH (>300 pg/mL; n = 134) and underwent repeated, longit

78 sults did not differ across the low and high PTH strata, and rates of persistent hyperparathyroidism

79 calcemia peaked at 48% at week 8 in the high PTH stratum and then steadily decreased through month 12

80 higher than 40% when defined using a higher PTH threshold greater than 130 pg/mL.

81 h were most severe at the lowest and highest PTH levels.

82 ined as elevated intact parathyroid hormone (PTH) (>62 pg/mL) accompanied by a very low calcium intak

83 Parathyroid hormone (PTH) activates receptors on osteocytes to orchestrate bo

84 s that are regulated by parathyroid hormone (PTH) and 1alpha,25-dihydroxyvitamin D3 (1alpha,25[OH]2D3

85 Parathyroid hormone (PTH) and calcium levels, recurrent or persistent hyperpa

86 Parathyroid hormone (PTH) and FGF23 are the primary hormones regulating acute

87 ch Pi intake stimulates parathyroid hormone (PTH) and fibroblast growth factor-23 secretion, increasi

88 Parathyroid hormone (PTH) and the sympathetic tone promote Rankl expression i

89 ne catabolic actions of parathyroid hormone (PTH) are seen in patients with hyperparathyroidism, or w

90 Continuous parathyroid hormone (PTH) blocks its own osteogenic actions in marrow stromal

91 shown that intermittent parathyroid hormone (PTH) bone anabolic therapy involves SOST expression redu

92 hemodialysis with serum parathyroid hormone (PTH) concentrations higher than 500 pg/mL on active ther

93 etelcalcetide on serum parathyroid hormone (PTH) concentrations in patients receiving hemodialysis.

94 ad increased mean serum parathyroid hormone (PTH) concentrations.

95 min D [1,25(OH)2D], and parathyroid hormone (PTH) in maternal circulation and cord blood at delivery.

96 did not increase serum parathyroid hormone (PTH) in response to acute hypocalcemia compared with the

97 Parathyroid hormone (PTH) induces osteoclast formation and activity by increa

98 Genes related to the parathyroid hormone (PTH) influence cutaneous immune defense and development,

99 Parathyroid hormone (PTH) is a primary calcium regulatory hormone.

100 Parathyroid hormone (PTH) is an important regulator of osteoblast function an

101 Parathyroid hormone (PTH) is recognized to be an important suppressor.

102 Parathyroid hormone (PTH) is the only current anabolic treatment for osteopor

103 ized by increased serum parathyroid hormone (PTH) level and parathyroid cell proliferation.

104 defined as an elevated parathyroid hormone (PTH) level, after renal transplantation in a contemporar

105 inorganic phosphate and parathyroid hormone (PTH) levels and decreased bone formation indices and wer

106 iation between baseline parathyroid hormone (PTH) levels and major cardiovascular events, renal graft

107 ed tomography (HRpQCT), parathyroid hormone (PTH) levels, and bone turnover markers obtained at basel

108 OH-D with its regulator parathyroid hormone (PTH) may be required for optimal evaluation of the impac

109 dies, or elevated serum parathyroid hormone (PTH) or creatinine.

110 Parathyroid hormone (PTH) orchestrates the signaling of many pathways that di

111 ttent administration of parathyroid hormone (PTH) promotes new bone formation in patients with osteop

112 P-13) transcription and parathyroid hormone (PTH) regulates HDAC4 to control MMP-13 promoter activity

113 alcium reabsorption and parathyroid hormone (PTH) secretion and is involved in the etiology of second

114 let-7 family increased parathyroid hormone (PTH) secretion in normal and uremic rats, as well as in

115 y functional effects on parathyroid hormone (PTH) secretion in parathyroid neoplasms.

116 Upon parathyroid hormone (PTH) stimulation, the PTHR internalizes into early endos

117 dback mechanism between parathyroid hormone (PTH), 1,25(OH)2D3 (1,25D), and fibroblast growth factor

118 ome, and serum calcium, parathyroid hormone (PTH), 1,25-dihydroxyvitamin D [1,25(OH)(2)D], 24,25-dihy

119 MSCs were cultured with parathyroid hormone (PTH), 1,25-dihydroxyvitamin D3 (1,25D3), or PTH+1,25D3.

120 In response to parathyroid hormone (PTH), a bone anabolic hormone, LepR(+)Runx2-GFP(low) cel

121 Human parathyroid hormone (PTH), a member of class B GPCRs, binds to its receptor v

122 d oxyphil cells produce parathyroid hormone (PTH), express the calcium-sensing receptor (CASR), and m

123 nderwent measurement of parathyroid hormone (PTH), had documentation of hypercalcemia/hyperparathyroi

124 , a recombinant form of parathyroid hormone (PTH), is the only approved treatment for osteoporosis th

125 n (TSAT) concentration, parathyroid hormone (PTH), IV vitamin D dose, cinacalcet use, and phosphate b

126 pretransplant levels of parathyroid hormone (PTH), low PTH (>65 to </=300 pg/mL; n = 112), and high P

127 ALN, parathyroid hormone (PTH), or saline (vehicle control) was administered.

128 steoblast resistance to parathyroid hormone (PTH), which is indicated by decreased double-labeled sur

129 diates unique basal and parathyroid hormone (PTH)-, fibroblast growth factor 23 (FGF23)-, and 1,25(OH

130 macrophages in bone and parathyroid hormone (PTH)-dependent bone anabolism using murine models of tar

131 nd urine markers of the parathyroid hormone (PTH)-vitamin D-fibroblast growth factor 23 (FGF23) axis,

132 y regulated through the parathyroid hormone (PTH)/PTHrP receptor (PTH1R) signaling pathway.

133 Parathyroid hormone (PTH, 84 residues) and PTH-related protein (PTHrP, 141 re

134 Synthetic parathyroid hormone [PTH(1-34)] has been investigated for its benefits on bon

135 Thus, the two major phosphaturic hormones, PTH and FGF23, have opposing effects on vitamin D produc

136 than that of the pluripotent agonist, human PTH(1-34).

137 ttransplant, persistent hyperparathyroidism (PTH >65 pg/mL) was 89.5%, 86.8%, 83.1%, and 86.2%, at mo

138 r length and condyle head length following I-PTH treatment.

139 Intermittent Parathyroid Hormone (I-PTH) is the only FDA approved anabolic drug therapy avai

140 The effects of I-PTH on the chondrogenic lineage of the mandibular condyl

141 To investigate the role of I-PTH on the MCC and subchondral bone, we carried out our

142 In conclusion, our study suggests that I-PTH plays a critical role in cellular proliferation, pro

143 Furthermore our microCT data showed that I-PTH treatment led to an increased bone volume fraction,

144 Our histology showed that the I-PTH treatment led to an increased number of cells expres

145 ylatable serines with alanines, had impaired PTH secretion after experimental uremia- or folic acid-i

146 articipants showed increase from baseline in PTH and decline in FGF23 by study week 4, with no differ

147 mpared with control mice with no increase in PTH mRNA levels and parathyroid cell proliferation compa

148 alcetide achieved more than 50% reduction in PTH concentrations compared with 138 patients (40.2%) ra

149 oportions of patients achieving reduction in PTH concentrations of more than 30% between the 198 of 3

150 mical end points (>50% and >30% reduction in PTH) and self-reported nausea or vomiting.

151 r work demonstrates that MCP-1 has a role in PTH's catabolic effects on bone including monocyte and m

152 To determine its role in PTH's catabolic effects, we continuously infused female

153 face and serum mineral parameters, including PTH, did not differ for subjects with normal ABix and PA

154 te was mutated, EX527 was unable to increase PTH-stimulated Mmp13 promoter activity, indicating a rol

155 increased trabecular bone mass and increased PTH-induced anabolism.

156 jected with mouse leptin exhibited increased PTH levels from baseline.

157 id cells, and acidosis transiently increased PTH secretion.

158 in D deficiency/insufficiency with increased PTH is an independent predictor of beta-cell dysfunction

159 ted BMMs with Saa3 knockdown did not inhibit PTH-stimulated responses in POBs.

160 aling pathways converge on NHERF1 to inhibit PTH- and FGF23-sensitive phosphate transport and down-re

161 SAA added to POBs inhibited PTH-stimulated cAMP responses, which was reversed by PTX

162 MMP13 expression, SIRT1 activation inhibits PTH stimulation of Mmp13 expression, and this regulation

163 We now report that CFZ inhibits PTH-induced RANKL expression and secretion without affec

164 y RANKL in a Cox2-dependent manner, inhibits PTH-stimulated cAMP signaling and osteoblast differentia

165 although the anabolic effect of intermittent PTH treatment on trabecular bone volume is blunted by de

166 ed with an impaired response to intermittent PTH treatment.

167 imes a week (n = 15); and group 3: 40 mug/kg PTH(1-34), three times a week (n = 15).

168 ree times a week (n = 15); group 2: 2 mug/kg PTH(1-34), three times a week (n = 15); and group 3: 40

169 Cdc73(+/-), Cdc73(+/L)/PTH-Cre and Cdc73(L/L)/PTH-Cre mice developed parathyroi

170 Cdc73(+/-), Cdc73(+/L)/PTH-Cre and Cdc73(L/L)/PTH-Cre mice had higher mean seru

171 arathyroid tumours in Cdc73(+/-), Cdc73(+/L)/PTH-Cre and Cdc73(L/L)/PTH-Cre mice had significantly in

172 conditional parathyroid-specific (Cdc73(+/L)/PTH-Cre and Cdc73(L/L)/PTH-Cre) mouse models.

173 dc73(+/-), Cdc73(+/L)/PTH-Cre and Cdc73(L/L)/PTH-Cre mice developed parathyroid tumours, which had nu

174 dc73(+/-), Cdc73(+/L)/PTH-Cre and Cdc73(L/L)/PTH-Cre mice had higher mean serum calcium concentration

175 dc73(+/-), Cdc73(+/L)/PTH-Cre and Cdc73(L/L)/PTH-Cre mice had significantly increased proliferation,

176 -specific (Cdc73(+/L)/PTH-Cre and Cdc73(L/L)/PTH-Cre) mouse models.

177 d in low-calcium medium secreted 5-fold less PTH at 1.5 h than controls.

178 of renal function and serum mineral levels, PTH remained significantly associated with all-cause mor

179 Like PTH, new small molecule SIK inhibitors cause decreased p

180 ant levels of parathyroid hormone (PTH), low PTH (>65 to </=300 pg/mL; n = 112), and high PTH (>300 p

181 itamin D deficiency/insufficiency with lower PTH did not predict these outcomes.

182 ed Dietary Allowance) was unable to maintain PTH or to moderate the proportion of patients with an el

183 Mean PTH concentrations at baseline and during weeks 20-27 we

184 as the proportion of patients achieving mean PTH of 300 pg/mL or lower.

185 ter than 30% reduction from baseline in mean PTH during weeks 20-27.

186 role of the PDZ protein NHERF1 in mediating PTH and FGF23 effects.

187 ut not phospholipase C via Gq/11 (D/D mice), PTH significantly enhanced bone formation, indicating th

188 Surprisingly, in both male and female mice, PTH administration significantly increased osteoblast nu

189 cally, let-7 and miR-148 antagonism modified PTH secretion in vivo and in vitro, implying roles for t

190 Moreover, PTH treatment of HEK293 cells stably transfected with CL

191 ighty-eight (30.3%) patients achieved normal PTH within 1 year posttransplant.

192 Patients achieving normal PTH within 12 months of transplantation had a significan

193 hundred twenty-seven (26.6%) attained normal PTH between 1 and 2 years, with the remaining 694 (43.1%

194 urvival advantage for patients who normalize PTH within 24 months of transplantation (P = 0.038).

195 e identify a role for SIRT1 in the action of PTH in osteoblasts.

196 Systemic administration of PTH(1-34) augmented bone volume in autogenous grafts.

197 Therefore, a major arm of PTH signalling in osteocytes involves SIK inhibition, an

198 xamined is "...unlikely to arise in cases of PTH (Oenothera-like) meiosis since haplotypes are transf

199 However, the effect of combination of PTH and CFZ on osteoclastogenesis is unknown.

200 s beyond Gsalpha and Gq/11 act downstream of PTH on osteoblast differentiation.

201 s study therefore investigates the effect of PTH(1-34) on autogenous bone graft healing.

202 sulted in osteopenia with blunted effects of PTH anabolic actions, whereas depletion of differentiate

203 SIK inhibition mimics many of the effects of PTH in osteocytes as assessed by RNA-seq in cultured ost

204 therapeutically to mimic skeletal effects of PTH.

205 modified with an electropolymerized film of PTH followed by the assembly of IrO2 NPs on which the am

206 ists of PTHR1, and an N-terminal fragment of PTH, PTH(1-34), is used clinically to treat osteoporosis

207 Two h of PTH treatment augmented SIRT1 association with c-Jun, a

208 r(fl/fl) mice, emphasizing the importance of PTH in inhibiting Cldn14.

209 ith hyperparathyroidism, or with infusion of PTH in rodents.

210 tic lineage cells to secrete an inhibitor of PTH-stimulated osteoblast differentiation.

211 treated with a single dose (50 microg/kg) of PTH (1-34).

212 tractant protein-1 (MCP-1), is a mediator of PTH's anabolic effects on bone.

213 Comparing normalization of PTH by 2 years to HPT patients, obesity (P < 0.001), mon

214 rize the mechanism and signaling pathways of PTH and FGF23 on phosphate transport and the role of the

215 performed on overall graft survival based on PTH normalization.

216 nsactivation, to assess the effect of CFZ on PTH action to induce osteoclastogenesis.

217 (PTH), 1,25-dihydroxyvitamin D3 (1,25D3), or PTH+1,25D3.

218 1,25D3- or PTH+1,25D3-treated LB BMSCs expressed significantly high

219 Modulation of TGF-beta or PTH signaling may reestablish coupled bone remodeling an

220 unted by deletion of Gsalpha in osteoblasts, PTH can stimulate osteoblast differentiation and bone fo

221 ules might help in the control of pathogenic PTH function such as hyperparathyroidism, where control

222 ation inhibits CaR activity, thus permitting PTH secretion, whereas alkalinization potentiates CaR ac

223 res covalently bound 10-phenylphenothiazine (PTH).

224 lacking AC6 (AC6(-/-)) have increased plasma PTH and FGF-23 levels compared with wild-type (WT) mice

225 ate diet almost completely suppressed plasma PTH levels in both AC6(-/-) and WT mice, indicating a se

226 electrode (SPCE) modified with polythionine (PTH) and iridium oxide nanoparticles (IrO2 NPs) is prese

227 A higher postoperative PTH also independently predicted disease recurrence.

228 ateral exploration whereas the postoperative PTH can guide follow-up after parathyroidectomy.

229 reduction from baseline in mean predialysis PTH concentrations during weeks 20-27 (noninferiority ma

230 Protein kinase A or C blockade prevented PTH but not FGF23 actions.

231 of PTHR1, and an N-terminal fragment of PTH, PTH(1-34), is used clinically to treat osteoporosis.

232 id phosphaturia through mechanisms requiring PTH and downregulation of renal Pi transporters but does

233 We concluded that endogenously secreted PTH and GHR signaling in bone are necessary to establish

234 uremic rats and decreased levels of secreted PTH in parathyroid cultures.

235 Mean EPO and vitamin D dose and serum PTH levels remained higher in blacks.

236 relation coefficients (slopes) between serum PTH and double-labeled surface (P=0.02) or osteoblast su

237 ate, 1,25(OH)2D and BUN, and decreased serum PTH and FGF23, relative to vehicle-treated CKD mice.

238 Elevated serum PTH concentrations in primary and secondary hyperparathy

239 Furthermore, mice with high serum PTH levels, regardless of high or low serum calcium, dem

240 at this SNP associated with 7% higher serum PTH concentration.

241 R-148 family prevented the increase in serum PTH level in uremic rats and decreased levels of secrete

242 acebo resulted in greater reduction in serum PTH over 26 weeks.

243 Chronic hypocalcemia increased serum PTH >4-fold less in PT-Dicer(-/-) mice compared with con

244 r, uremic PT-Dicer(-/-) mice increased serum PTH and FGF23 significantly less than uremic controls.

245 r serum calcium and markedly increased serum PTH levels.

246 M2.5 levels were associated with lower serum PTH (Estimate for baseline one interquartile increase in

247 506 to 14,777 U/wk (P<0.001), and mean serum PTH increased from 340 to 435 pg/ml (P<0.001).

248 ratified by timing of achieving normal serum PTH levels, and a multivariate logistic regression was c

249 med a genome-wide association study of serum PTH concentrations among 29,155 participants of European

250 The response of serum PTH, 1,25(OH)(2)D, 24,25(OH)(2)D, the ratio of 24,25(OH)

251 not inferior to cinacalcet in reducing serum PTH concentrations over 26 weeks; it also met superiorit

252 Recipient total serum PTH levels became detectable after 3 days from the proce

253 The other SNPs associated with serum PTH concentration included rs4074995 within RGS14 (P=6.6

254 NPs from five independent regions with serum PTH concentration, including the strongest association w

255 uct of the parathyroid glands and stimulates PTH release.

256 TPTX seems to suppress PTH more effectively and showed no recurrences after 3 y

257 ization potentiates CaR activity to suppress PTH secretion.

258 both osteoblasts and osteoclasts to suppress PTH-induced osteoclast differentiation and bone resorpti

259 siologic pHo elevation reversibly suppressed PTH secretion from perifused human parathyroid cells, an

260 increased bone mass significantly more than PTH did.

261 receptor in Sox9-cre cells demonstrated that PTH receptor expression is required for teriparatide-med

262 high or low serum calcium, demonstrated that PTH/PTH1R signaling exerts a suppressive effect on Cldn1

263 ne along with in vivo studies, we found that PTH sensitized the response of bone to GH by increasing

264 Our data support the notion that PTH is an important regulator of circulating sclerostin

265 eaction (PCR) and Western blot revealed that PTH decreased DMP1 gene transcription (85%) and protein

266 Here, we show that PTH induces the protein kinase A (PKA)-dependent phospho

267 Here we show that PTH inhibition of SOST (sclerostin), a WNT antagonist, r

268 Collectively, these results suggest that PTH and 1,25D share complementary effects in maintaining

269 These findings suggest that PTH-mediated Sost repression involves nuclear accumulati

270 The PTH concentration depended on circulating 25(OH)D and to

271 The PTH receptor (PTH1R) is a G protein-coupled receptor tha

272 r, alphaKlotho, FGFR1, FGFR3, FGFR4, and the PTH receptor.

273 compared with the vehicle-treated group, the PTH-treated WT mice had reduced trabecular thickness and

274 d development, but the full functions of the PTH family in cutaneous biology remain incompletely unde

275 Selective, inducible deletion of the PTH receptor in Sox9-cre cells demonstrated that PTH rec

276 he expression and potential functions of the PTH second receptor (PTH2R) and its ligand, the tuberoin

277 ghlighting the need for consideration of the PTH/25-OH-D axis when studying the impact of vitamin D s

278 PTH activates adenylyl cyclase (AC) through PTH 1 receptors and stimulates the cAMP/PKA signaling pa

279 The parathyroid glands acting through PTH play a critical role in the regulation of serum calc

280 Thus, PTH-induced phosphorylation of rHDAC4 at Ser-740 is cruc

281 Cortical decreases related directly to PTH levels, whereas the relationship between PTH and tra

282 Higher osteoblast resistance to PTH in patients with PAD was characterized by weaker cor

283 over and pronounced osteoblast resistance to PTH.

284 milar gene expression pattern in response to PTH and 1,25D treatment.

285 d for increased bone turnover in response to PTH.

286 orphisms (SNPs) with natural log-transformed PTH concentration adjusted for age, sex, season, study s

287 was significantly enhanced in the ALN versus PTH group.

288 plain the suppression of bone formation when PTH is applied continuously and may be a new therapeutic

289 .1 +/- 0.3 vs 2.1 +/- 0.2, P = 0.95) whereas PTH rose by time in the TPTX+AT group and was significan

290 ntagonist, requires HDAC4 and HDAC5, whereas PTH stimulation of RANKL, a stimulator of bone resorptio

291 When whole marrow was cultured with PTH+1,25D3, more TRAP(+) MNCs were seen in LB versus MB

292 Ultimately, rats were infused with PTH+1,25D3, and MB versus tibia MNCs were measured.

293 The experimental group was injected with PTH (80 mug/kg) daily for 2 weeks, while control group w

294 ses, vitamin D deficiency/insufficiency with PTH in the highest tertile at 3 months independently pre

295 ted FGF23 actions but did not interfere with PTH effects.

296 PTHR in endosomes from cells stimulated with PTH.

297 and known to express DMP1, were treated with PTH (1-34).

298 is to evaluate the effect of treatment with PTH on periodontal healing in rats.

299 Extended treatment with PTH or FGF23 down-regulated NPT2A without affecting NHER

300 d either bisphosphonate (zoledronate [Zol]), PTH, or saline (vehicle control [VC]) was administered f