ライフサイエンスコーパス: PTH

1 PTH and FGF23 inhibited phosphate transport in a concent

2 PTH forms a complex with the PTHR1 that is rapidly inter

3 PTH markedly downregulated Galnt3 expression (2.7-fold)

4 PTH reduced adipocyte numbers in CR + PTH mice, whereas

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

6 PTH secretion in explants increased in response to lepti

7 PTH significantly increased bone mass in all cohorts des

8 PTH treatment enriched endosomal PTHR.

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

10 Tgif1 is a PTH target gene and PTH treatment failed to increase bon

11 ate uptake, but S290A substitution abolished PTH-dependent phosphate transport.

12 tomycetin blocked PP1 activity and abrogated PTH-sensitive phosphate transport.

13 ucture of human PTH1R bound to a long-acting PTH analog and the stimulatory G protein.

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

15 help the establishment of vitamin D-adjusted PTH reference intervals. The study was approved by the U

16 y inhibits beta-arrestin-2 recruitment after PTH (1-34)-driven receptor activation and thus represent

17 dephosphorylated and rephosphorylated after PTH stimulation, and we found that protein phosphatase 1

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

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

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

21 The O-GlcNAcylated GLP-1 and PTH also displayed significantly improved in vivo activi

22 can improve the stability of both GLP-1 and PTH in serum despite the fact that the O-GlcNAc can be q

23 (Mettl1) and Mettl21b that mediate basal and PTH-induced expression of Cyp27b1 and FGF23- and 1,25(OH

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

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

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

27 nd that the joint association of 25(OH)D and PTH with beta-cell function, systemic inflammation, and

28 endent and joint associations of 25(OH)D and PTH with cardiometabolic biomarkers including high-sensi

29 endent and joint associations of 25(OH)D and PTH with each biomarker.

30 monstrate that the GR cooperates with D3 and PTH signaling, causing massive osteoclastogenesis, which

31 ences between primary headache disorders and PTH could uncover unique treatment targets for PTH.

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

33 a1 expression, total resistance to FGF23 and PTH regulation, and secondary suppression of renal Cyp27

34 nd changes in the plasma levels of FGF23 and PTH.

35 Tgif1 is a PTH target gene and PTH treatment failed to increase bone formation and bone

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

37 ated with reductions in plasma phosphate and PTH levels in normal mice and in a CKD mouse model.

38 Plasma phosphate and PTH significantly decreased after 3 hours, with both ret

39 tive agonists, parathyroid hormone (PTH) and PTH-related protein (PTHrP).

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

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

42 is revealed significant associations between PTH-CH and family history of CH (OR 3.32, 95% CI 1.31 to

43 Considerable overlap exists between PTH and common primary headache disorders.

44 there was an inverse linear relation between PTH and eGFR in white women after accounting for 25(OH)D

45 a cluster of sites, termed C24-DS1, binding PTH-sensitive cAMP-responsive element-binding protein (C

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

47 differences among groups in changes in BMD, PTH, serum or urine levels of minerals, or TFCA.

48 s in serum and urine levels of mineral, BMD, PTH (all subjects), and TFCA (n = 30).

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

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

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

52 t associated with differences in circulating PTH concentrations.

53 The most common PTH phenotypes are migraine-like headache and tension-ty

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

55 In contrast, PTH was nonlinearly associated with HOMA-B in black wome

56 PTH reduced adipocyte numbers in CR + PTH mice, whereas adipocyte size was reduced in CR/PTH-t

57 ts were CR and simultaneously injected (CR + PTH or CR + Veh) for 4 wk.

58 ce, whereas adipocyte size was reduced in CR/PTH-treated mice.

59 d Ctrl mice were injected daily with PTH (CR/PTH or Ctrl/PTH) or vehicle for 4 wk.

60 were injected daily with PTH (CR/PTH or Ctrl/PTH) or vehicle for 4 wk.

61 in white women after accounting for 25(OH)D, PTH and 25(OH)D were jointly and nonlinearly associated

62 ought to determine whether maternal 25(OH)D, PTH and calcium concentrations at 26 weeks gestation are

63 from examining the associations of 25(OH)D, PTH and calcium together with a range of perinatal outco

64 differences in the associations of 25(OH)D, PTH and calcium with important perinatal outcomes.

65 o explore the association between vitamin D, PTH and calcium with gestational hypertension (GH), pre-

66 termine whether differences in the vitamin D-PTH endocrine system contribute to racial disparities in

67 vides mechanistic insight into the vitamin D-PTH endocrine system, and further substantiates the role

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

69 ncrease in 25(OH)D concentrations, decreased PTH and no change in serum calcium.

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

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

72 SFB(+) microbiota enabled PTH to expand intestinal TNF(+) T and Th17 cells and inc

73 Butyrate was required for PTH to increase the number of bone marrow (BM) regulator

74 showed that the microbiota was required for PTH to stimulate bone formation and increase bone mass.

75 nic enhancer with components responsible for PTH-mediated Cyp27b1 induction and 1,25(OH)(2)D(3)-media

76 H could uncover unique treatment targets for PTH.

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

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

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

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

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

82 Post-traumatic headache (PTH) is a highly disabling secondary headache disorder a

83 High PTH levels independently associated with low sclerostin

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

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

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

87 Lower 25(OH)D and higher PTH were each independently and jointly associated with

88 d lower concentrations of 25(OH)D and higher PTH, HOMA-IR, HOMA-B, hs-CRP, and eGFR than white women

89 25(OH)D (median 13.0 vs 36.0 nmol/L), higher PTH (median 7.7 vs 3.3 pmol/L) and similar calcium conce

90 ration of a fragment of Parathyroid hormone (PTH) activates osteoblast-mediated bone formation and is

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

92 sma phosphate, calcium, parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF-23) were studi

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

94 CRs) and natively binds parathyroid hormone (PTH) and parathyroid hormone related peptide (PTHrP).

95 as two native agonists, parathyroid hormone (PTH) and PTH-related protein (PTHrP).

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

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

98 r adding information on parathyroid hormone (PTH) can help explain the higher cardiometabolic risk am

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

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

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

102 Parathyroid hormone (PTH) has complex effects on bone, including stimulating

103 minerals, and levels of parathyroid hormone (PTH) in healthy postmenopausal women.

104 d the decrease in serum Parathyroid Hormone (PTH) induced by lactation, but amplified the increase in

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

106 Parathyroid hormone (PTH) is a critical regulator of skeletal development tha

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

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

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

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

111 Measuring the Parathyroid hormone (PTH) levels assists in the investigation and management

112 )-vitamin D(3) (D3) and parathyroid hormone (PTH) on osteoclastogenesis.

113 free mice, we show that parathyroid hormone (PTH) only caused bone loss in mice whose microbiota was

114 Vitamin D and parathyroid hormone (PTH) regulate mineral metabolism and are required to mai

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

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

117 ttent administration of parathyroid hormone (PTH) stimulates bone formation in vivo and also suppress

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

119 Circulating parathyroid hormone (PTH), 25(OH)D, calcium and peripheral white blood cells

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 Serum parathyroid hormone (PTH), calcium, phosphorus and alkaline phosphatase (ALP)

123 ing calcium, phosphate, parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), 25-hydroxyvit

124 se gene is regulated by parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), and 1,25(OH)(

125 ly reciprocal manner by parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), and 1,25(OH)(

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

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

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

129 ith decreased levels of parathyroid hormone (PTH), which is a key regulator of bone metabolism but al

130 ptide-1 (GLP-1) and the parathyroid hormone (PTH), which respectively help control glucose and calciu

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

132 racterized the sites of parathyroid hormone (PTH)-induced NHERF1 phosphorylation and identified 10 hi

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

134 FGF23) and reduction of parathyroid hormone (PTH).

135 -dependent secretion of parathyroid hormone (PTH).

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

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

138 However, PTH (1-34)-mediated G(s) activation is Undisturbed by EC

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

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

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

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

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

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

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

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

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

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

149 n 4,000 IU/d even without further changes in PTH levels.

150 ons elicit rapid and reversible increases in PTH secretion from freshly-isolated human parathyroid ce

151 A plateau in PTH levels was achieved at 16 weeks in the 4000 and 10,0

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

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

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

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

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

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

158 ed a significant association with increasing PTH concentration (p < 0.001).

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

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

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

162 In a multivariate Cox analysis, intact PTH (iPTH), phosphate, and 1,25D levels were associated

163 Cholecalciferol also suppressed intact PTH only among patients with severe vitamin D deficiency

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

165 ely balanced homeostatic mechanism involving PTH and FGF23 together with protection from 1,25(OH)(2)D

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

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

168 e which may partially overlap with the known PTH (1-34) binding site.

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 Like PTH, new small molecule SIK inhibitors cause decreased p

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

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

180 Mean PTH decreased in group 1 from 1865.18 +/- 828.93 pg/ml t

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

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

183 ratory method (Roche Diagnostics) to measure PTH concentrations with a turn-around time of less than

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

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

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

187 0% for high (942 pg/mL) and low (38.2 pg/mL) PTH concentration.

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

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

190 r, butyrate, is necessary for the ability of PTH to increase osteoblast numbers and stimulate bone fo

191 hich are critical for the anabolic action of PTH in bone.

192 In vivo activation of PTH signaling through the reestablished Jagged1 and oste

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

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

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

196 ng receptor (CaSR) is the main controller of PTH secretion and here we show that raising phosphate co

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

198 ts into the structural basis and dynamics of PTH binding and receptor activation.

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

200 The effects of PTH on bone marrow adiposity could enhance its anabolic

201 ividual and combined longitudinal effects of PTH(1-34) and loading on the bone morphometric and densi

202 therapeutically to mimic skeletal effects of PTH.

203 Simultaneous evaluation of PTH and phosphate levels may provide additional informat

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

205 oorly active N-terminal peptide fragments of PTH by conjugating them to nanobodies (VHHs) that recogn

206 bone metabolism and the anabolic function of PTH.

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

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

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

210 ks-old and treated either with injections of PTH(1-34); compressive loading of the right tibia; both

211 Although possible underlying mechanisms of PTH have been elucidated, a substantial void remains in

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

213 We show that backbone modification of PTH(1-34)-NH(2) and abaloparatide (a PTHrP derivative) w

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

215 anisms in the development and persistence of PTH.

216 ar remodeling, but also to the regulation of PTH, PTHrP, 1,25-Dyhydroxyvitamin D (1,25(OH)2D), osteoc

217 a(2+) homeostasis under direct regulation of PTH.

218 This largest series of PTH-CH defines it as a unique entity with specific evolu

219 es selectivity for PTHR1 superior to that of PTH(1-34).

220 ining the stimulatory effect of phosphate on PTH secretion.

221 n serum or urine levels of minerals, BMD, or PTH at week 26.

222 Cotreatment of DEX with D3 or PTH increased gene encoding calcitonin receptor (Calcr),

223 eoclasts when DEX was added to either D3- or PTH-treated mouse bone marrow cell (BMC) cultures.

224 statistically significant effect on FGF23 or PTH levels.

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

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

227 to 65 years and had a history of persistent PTH after mild TBI for at least 12 months.

228 lved in progression from acute to persistent PTH, and we identify potential drug targets to prevent a

229 drug targets to prevent and treat persistent PTH.

230 Patients with persistent PTH are hypersensitive to CGRP, which underscores its pa

231 reatment option for patients with persistent PTH.

232 res covalently bound 10-phenylphenothiazine (PTH).

233 dietary normalization of calcium, phosphate, PTH, and FGF23 rescued the skeletal phenotype of this mu

234 Rates of postoperative PTH < 10 (33.3% vs 24.1%, P = 0.57) and transient nerve

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

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

237 marrow adipocyte and osteoblast progenitors, PTH stimulated the transfer of fatty acids to osteoblast

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

239 The PTH1R (PTH [parathyroid hormone]/PTHrP [PTH-related protein] re

240 The PTH1R (PTH [parathyroid hormone]/PTHrP [PTH-related protein] receptor) is expressed in vascular

241 Rapid PTH monitoring is a valid tool for accurate assessment i

242 osphorylation status of NHERF1 and regulates PTH-sensitive, NPT2A-mediated phosphate uptake.

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

244 t of physiologic levels of butyrate restored PTH-induced anabolism.

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

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

247 Elevated serum PTH concentrations in primary and secondary hyperparathy

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

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

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

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

252 r serum calcium and markedly increased serum PTH levels.

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

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

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

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

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

258 d odds of GH, and a 37% reduced odds of SGA; PTH was associated with a 45% reduction in the odds of G

259 uct of the parathyroid glands and stimulates PTH release.

260 In summary, PTH administration to CR mice increased bone mass by shi

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

262 were significantly higher with loading than PTH.

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

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

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

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

267 ce lifetime imaging (FLIM), we observed that PTH paradoxically and transiently elevates intracellular

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

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

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

271 tween target and capture probe to assess the PTH concentration in undiluted patient plasma samples.

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

273 remodeling and an essential component of the PTH anabolic action.

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 Knockout of the PTH receptor, PTH1R, from the mouse kidney abrogates the

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

278 n at T303 in the DCT of mouse kidney via the PTH signaling cascade.

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

280 e models, a synergistic anabolic response to PTH(1-34) and tibia loading was shown.

281 d for increased bone turnover in response to PTH.

282 fically, whereas subclone 4 is responsive to PTH stimulation and capable of matrix mineralization, su

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

284 on and the biochemical mechanisms underlying PTH control of phosphate transport.

285 In an exploratory experiment in mice, a VHH-PTH peptide conjugate showed biological activity, wherea

286 .1 +/- 0.3 vs 2.1 +/- 0.2, P = 0.95) whereas PTH rose by time in the TPTX+AT group and was significan

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

288 We used the CR model to test whether PTH would reduce BMAT in mice by both altering cell fate

289 However, the mechanisms by which PTH elicits its anabolic effect are not fully elucidated

290 k, CR and Ctrl mice were injected daily with PTH (CR/PTH or Ctrl/PTH) or vehicle for 4 wk.

291 2017 in a headache centre and diagnosed with PTH-CH that developed within 7 days of head trauma.

292 steoblast number was increased 3-8-fold with PTH treatment.

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

294 tions for the treatment of osteoporosis with PTH analogs, this pathway may be part of a broader mecha

295 Patients with PTH-CH are more likely to suffer from the chronic varian

296 Patients with PTH-CH were at a higher risk of being intractable to acu

297 Twenty-six patients with PTH-CH were identified.

298 PTHR in endosomes from cells stimulated with PTH.

299 h co-treatment than in the mice treated with PTH alone.

300 erentiated into adipocytes and, treated with PTH, exhibited increased production of glycerol and fatt

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