ライフサイエンスコーパス: PTHrP

1 PTHrP failed to upregulate Cyclin D1 and to antagonize R

2 PTHrP inhibition can prevent tumor-induced bone destruct

3 PTHrP may regulate articular chondrocyte maintenance in

4 PTHrP normally functions in a feedback loop with Indian

5 PTHrP upregulates BMP receptor 1A expression in the mamm

6 PTHrP was also expressed by the 3 mycobacterial granulom

7 PTHrP was expressed by all biopsied lesions of patients

8 PTHrP(1-36) peptide enhances human beta-cell proliferati

9 PTHrP-induced accumulation of AR depended on the activit

10 PTHrP-induced tyrosine phosphorylation of AR resulted in

11 PTHrP/forskolin induces dephosphorylation of histone dea

12 cells up-regulated CCL2 and was blocked by a PTHrP antagonist, suggesting that prostate cancer-derive

13 Consequently, a PTHrP-Ihh feedback loop is established, but over a short

14 To understand whether there is a PTHrP-independent role of Ihh signaling in regulating ch

15 (iii) blockage of ADAMTS-7 almost abolishes PTHrP-mediated inhibition of chondrocyte hypertrophy and

16 enesis, as blockage of ECM1 nearly abolishes PTHrP regulation of chondrocyte hypertrophy, and overexp

17 ls, and Gli2 partners with Smads to activate PTHrP and promote TGF-beta-induced bone metastasis.

18 d in human islets transduced with adenoviral PTHrP constructs or treated with PTHrP peptides.

19 essed IHH and PTHrP expression in an allelic PTHrP-LacZ-knockin mouse and several versions of PTHrP-n

20 omoting Runx2 target genes IL11, MMP-13, and PTHrP.

21 ytes, such as those derived by WNT, BMP, and PTHrP/IHH molecules, suggesting that the FAM20B-catalyze

22 of phosphorylated VASP were diminished, and PTHrP levels were dysregulated.

23 his study is to determine 1) whether HGF and PTHrP have additive/synergistic effects on beta-cell gro

24 tracellular target activated by both HGF and PTHrP in beta-cells.

25 Combined overexpression of HGF and PTHrP in the beta-cell of doubly transgenic mice did not

26 accompanied by marked reductions in Ihh and PTHrP as well as sFRP-1, an endogenous Wnt signaling ant

27 We assessed IHH and PTHrP expression in an allelic PTHrP-LacZ-knockin mouse

28 x2 knockdown in MDA-MB-231 inhibited IHH and PTHrP expression in the presence of TGFbeta.

29 xpression, and putative functions of IHH and PTHrP in articular cartilage in the mouse.

30 Indian hedgehog (Ihh) and PTHrP signaling play crucial roles in regulating the ons

31 PTHrP-induced chondrocyte proliferation and PTHrP-delayed maturation.

32 th recombinant FGF2/FGF9 decreased Ptch1 and PTHrP expression in superficial/polymorphic layers and p

33 PTH and PTHrP display different selectivity for two distinct PTH

34 ns and enabled the design of altered PTH and PTHrP peptides that adopt the ECD-binding mode of the op

35 n of osteoclast-promoting factors, RANKL and PTHrP, even after the osteoblast differentiation ceases

36 of the osteoclastogenesis factors, RANKL and PTHrP.

37 NL) compared to PTHrP+/+ (wild-type; WT) and PTHrP+/- (heterozygous; HZ) littermates.

38 (TUBTS) - were used to immobilize whole anti-PTHrP antibodies and Fab' fragments to surfaces as biore

39 und with IRMA (n = 57); r(2) = 0.99 assaying PTHrP 1-86 equiv fragments.

40 Because PTHrP contributes to hypercalcemia and bone metastases,

41 emonstrate a novel signaling linkage between PTHrP and Wnt signaling pathways that results in downreg

42 Normal osteoblasts survive depletion of both PTHrP and CREB1.

43 onds potently to PTH, it is not activated by PTHrP.

44 pression of ERK activation in these cells by PTHrP or a MEK inhibitor coincided with a delay in chond

45 es (INKs), are not appreciably influenced by PTHrP.

46 ADAMTS-7 is an important target of canonical PTHrP signaling, since (i) PTHrP induces ADAMTS-7, (ii)

47 tracellular calcium, through studies of CaSR-PTHrP interactions in the MMTV-PymT transgenic mouse mod

48 ken together, our findings suggest that CaSR-PTHrP interactions might be a promising target for the d

49 lcium transients, while endoproteases cleave PTHrP, resulting in fragments with different cellular fu

50 lates chondrocyte hypertrophy by controlling PTHrP expression.

51 vidence that Ihh signaling directly controls PTHrP expression and chondrocyte morphology in the growt

52 Conventional PTHrP detection methods like immunoradiometric assay (IR

53 differentially regulate genes such as CXCR4, PTHrP, RUNX2, and TGFbeta1 that are associated with homi

54 bone metastatic breast cancer would decrease PTHrP expression and therefore osteolytic bone destructi

55 differentiation factor 5 were used to delete PTHrP from articular chondrocytes in the mid-region of m

56 results showed that prostate cancer-derived PTHrP acts in the bone marrow to potentiate CD11b(+)Gr1(

57 ist, suggesting that prostate cancer-derived PTHrP plays an important role in elevation of osteoblast

58 of prostate cancer, levels of tumor-derived PTHrP correlated with CD11b(+)Gr1(+) cell recruitment an

59 Tumor-derived PTHrP has emerged as a key molecule playing multiple rol

60 Tumor-derived PTHrP has emerged as a key molecule playing multiple rol

61 tial, suggesting that prostate tumor-derived PTHrP potentiates this activity of CD11b(+)Gr1(+) cells.

62 ive cascade is driven by tumor cell-derived, PTHrP-mediated induction of CCL2, which facilitates tumo

63 ensating in response to a partial Cre-driven PTHrP deletion, a finding that underscores the need to s

64 Co-stimulation with ATP and either PTHrP (43-52) or PTHrP (70-77) increased proliferation,

65 rced expression of either retroviral-encoded PTHrP or Nkx3.2 inhibits chondrocyte maturation.

66 rrounding tissues in skin biopsies expressed PTHrP.

67 pontin) and secreted bone-resorbing factors (PTHrP, IL8) promoting osteolytic disease.

68 Finally, PTHrP fragments potentiated bradykinin-induced calcium t

69 is new ultrasensitive, multiplexed assay for PTHrP and fragments is promising for clinical diagnosis,

70 Of importance, ECM1 seems to be critical for PTHrP action in chondrogenesis, as blockage of ECM1 near

71 ocytes, indicating that PP2A is critical for PTHrP-mediated regulation of chondrocyte hypertrophy.

72 First, the absence of efficacy for PTHrP at PTH-2R is due to the presence of His-5 in PTHrP

73 PKC zeta is essential for PTHrP- and HGF-induced beta-cell proliferation.

74 tibiae and femurs from littermates null for PTHrP, Runx2, or both genes.

75 mozygous for the deletion of the PTHrP gene (PTHrP-/- null; NL) compared to PTHrP+/+ (wild-type; WT)

76 expression of the osteoclast inducing genes PTHrP and RANKL.

77 and expression of the TGF-beta target genes PTHrP, IL-11, CTGF, and RUNX2.

78 rentiation partially through regulating Gli2/PTHrP during endochondral bone development.

79 peptide (PTHrP) and the parathyroid hormone-PTHrP receptor increase chondrocyte proliferation and de

80 tic bone metastases, but it is not known how PTHrP is upregulated in breast tumors.

81 rget of canonical PTHrP signaling, since (i) PTHrP induces ADAMTS-7, (ii) ADAMTS-7 is downregulated i

82 ing PCa, and targeting this newly identified PTHrP/p38/Hsp27/AR/p21 signaling pathway with either p38

83 plates of these mice exhibit a lack of Ihh, PTHrP-R, and Col10 expression indicating a loss of chond

84 portant role by dampening the effects of Ihh-PTHrP together with sFRP-1.

85 ocumented in KO mice to suggest that the IHH-PTHrP axis is capable of compensating in response to a p

86 We conclude that the IHH-PTHrP axis participates in the maintenance of articular

87 hanisms downstream or independent of the Ihh-PTHrP signaling pathway, a pivotal signaling system that

88 s in cross-talk between the BMP, FGF and Ihh/PTHrP pathways.

89 Thus, Zfp521 is an important PTHrP target gene that regulates growth plate chondrocyt

90 In PTHrP-knockout mice, mineralizing chondrocytes encroach

91 at PTH-2R is due to the presence of His-5 in PTHrP (Ile-5 in PTH), which interacts with the receptor'

92 nloading is associated with rapid changes in PTHrP expression and articular chondrocyte differentiati

93 ADAMTS-7, (ii) ADAMTS-7 is downregulated in PTHrP null mutant (PTHrP-/-) growth plate chondrocytes,

94 including multiple genes that participate in PTHrP-IHH, BMP and CNP signaling, and many genes that ha

95 rocytes when compared to the same regions in PTHrP(-/-) mice.

96 es expression of Ihh target genes, including PTHrP and Col10a1, through its physical and functional i

97 nal target genes of Eda/NF-kappaB, including PTHrP, Wnt10a, and Wnt10b, as well as Egf family ligands

98 enes that enhance bone metastases, including PTHrP, CTGF, CXCR4, and IL11.

99 c stimulation of cAMP accumulation increased PTHrP production by normal and transformed breast cells.

100 Runx2 directly regulates the TGFbeta-induced PTHrP levels.

101 the effects of CaR activation on inhibiting PTHrP secretion by MMECs and blocked the effects of the

102 is study, we confirmed that the CaR inhibits PTHrP production by MMECs but stimulates PTHrP productio

103 multiplexed peptide assay to measure intact PTHrP 1-173 as well as circulating N-terminal and C-term

104 P) is produced by PCa cells and intermittent PTHrP exposure has bone anabolic effects, suggesting tha

105 at the transcript and protein levels in K14-PTHrP fibroblasts in vitro, while ovariectomy increases

106 le ovariectomy increases Tgfb1 levels in K14-PTHrP ventral skin.

107 e overexpressing PTHrP in keratinocytes (K14-PTHrP).

108 ining cells from the ventral skin of the K14-PTHrP transgenic mice [which overexpress parathyroid hor

109 es of sorted Pdgfralpha-positive ventral K14-PTHrP and wild-type fibroblasts, identifying differentia

110 transgenic overexpression of the PPR ligand PTHrP have suggested that this ligand receptor combinati

111 wever, the molecular mechanisms that mediate PTHrP production by breast cancer cells are not entirely

112 In growing and adult mice, PTHrP expression in articular chondrocytes is load-induc

113 C-terminal and mid-molecule PTHrP peptides (1-100 pM) potentiated ATP-induced calciu

114 MTS-7 is downregulated in PTHrP null mutant (PTHrP-/-) growth plate chondrocytes, and (iii) blockage

115 Administration of neutralizing PTHrP monoclonal antibody reduced CD11b(+)Gr1(+) cells a

116 Notably, PTHrP(1-36) also enhances GSIS.

117 inactivated Ihh signaling in the absence of PTHrP during endochondral skeletal development.

118 ation arrest and apoptosis in the absence of PTHrP or CREB1.

119 af might mediate the proliferative action of PTHrP in chondrocytes.

120 ppeared to be mediated by nuclear actions of PTHrP that decreased p27(kip1) levels and prevented nucl

121 o, or overexpressing Ihh in the cartilage of PTHrP(-/-) embryos or inactivating patched 1 (Ptch1), a

122 In addition, the combination of PTHrP and BMP signaling is responsible for upregulating

123 Mice with conditional deletion of PTHrP (knockout [KO]) and littermate control mice were e

124 In confirmation, adenoviral delivery of PTHrP to murine primary vascular smooth muscle cells (VS

125 The achieved label-free detection of PTHrP at levels of 50 ng mL(-1) is with great interest t

126 were achieved for simultaneous detection of PTHrP isoforms and peptide fragments in 30 min.

127 and for survival, and many of the effects of PTHrP on development are not mediated by its N terminus.

128 The pro-angiogenic effects of PTHrP or RANKL were absent in metatarsal explants or cal

129 Runx2-dependent and -independent effects of PTHrP, we examined embryonic tibiae and femurs from litt

130 en the complementary therapeutic efficacy of PTHrP(1-36) in postmenopausal osteoporosis.

131 genesis of HHM in ATLL and the expression of PTHrP can be activated by nuclear factor kappaB (NF-kapp

132 The expression of PTHrP is a property of infectious granulomas regardless

133 ion by upregulating osteoblast expression of PTHrP, which promoted RANKL expression via PKA and its t

134 nts are the predominant circulating forms of PTHrP.

135 521 (Zfp521) as a downstream target gene of PTHrP signaling.

136 ing chondrocyte hypertrophy independently of PTHrP, which is particularly important in postnatal cart

137 aded surgically to examine load-induction of PTHrP and IHH.

138 We found elevated serum levels of PTHrP while the patient was hypercalcemic that became un

139 Loss of PTHrP or its receptor (Pthr1) abolishes the expression o

140 xpression is completely abolished by loss of PTHrP signaling and ectopic reporter activity is induced

141 ents and to examine underlying mechanisms of PTHrP overproduction.

142 Neutralization of PTHrP in tumour-bearing mice blocked adipose tissue brow

143 Thus, neutralization of PTHrP might hold promise for ameliorating cancer cachexi

144 y buds and that BMP4 can rescue outgrowth of PTHrP(-/-) mammary buds.

145 More importantly, overexpression of PTHrP causes a significant approximately threefold incre

146 By contrast, overexpression of PTHrP in basal keratinocytes induces inappropriate diffe

147 senchyme markers caused by overexpression of PTHrP in basal keratinocytes.

148 ter activity is induced by overexpression of PTHrP.

149 f ECM1 rescues disorganized growth plates of PTHrP-null mice.

150 The future therapeutic potential of PTHrP(1-36) for the treatment of diabetes is especially

151 rix metalloproteinase-directed processing of PTHrP disables the osteolytic functions of the mature ho

152 We propose that excess production of PTHrP is the cause of hypercalcemia in granulomatous inf

153 ciency or, alternatively, the restoration of PTHrP or cyclo-oxygenase activity by the administration

154 As a result of PTHrP signaling, the mammary mesenchyme supports mammary

155 issection revealed that through secretion of PTHrP, NEPCa cells could alter the p38/MAPK/Hsp27 signal

156 rowth zone appears to serve as the source of PTHrP-expressing proliferative chondrocytes that populat

157 The high resolution crystal structure of PTHrP bound to the extracellular domain (ECD) of PTH1R r

158 emonstrate that ADAMTS-7, a direct target of PTHrP signaling, negatively regulates endochondral bone

159 acking the midregion, NLS, and C terminus of PTHrP (Pthrp(Delta/Delta)) was developed.

160 h that the midregion, NLS, and C terminus of PTHrP are crucial for the commitment of osteogenic and h

161 P-LacZ-knockin mouse and several versions of PTHrP-null mice.

162 Thus, the opposing effects of the CaR on PTHrP production are because of alternate G-protein coup

163 ated with the opposing effects of the CaR on PTHrP production.

164 ulation with ATP and either PTHrP (43-52) or PTHrP (70-77) increased proliferation, suggesting that t

165 nvironments in which elevated calcium and/or PTHrP levels contribute to breast cancer progression.

166 c signaling pathways activated by HGF and/or PTHrP.

167 chondrocyte proliferation and maturation or PTHrP-induced chondrocyte proliferation and PTHrP-delaye

168 r of nuclear factor-kappaB ligand (RANKL) or PTHrP in vivo increased calvarial vessel density and ost

169 ration in primary islet cells overexpressing PTHrP and/or HGF.

170 alyzed doubly transgenic mice overexpressing PTHrP and HGF in the beta-cell.

171 n the ventral surface of mice overexpressing PTHrP in keratinocytes (K14-PTHrP).

172 The paraneoplastic PTHrP has also been implicated in tumor progression and

173 e serum parathyroid hormone-related peptide (PTHrP) and a mouse monoclonal antibody to PTHrP to immun

174 data implicates parathyroid-related peptide (PTHrP) and cyclo-oxygenase-2 (COX-2) as possible factors

175 between parathyroid hormone-related peptide (PTHrP) and Indian hedgehog (Ihh) signaling tightly regul

176 Parathyroid hormone-related peptide (PTHrP) and the parathyroid hormone-PTHrP receptor increa

177 ressing parathyroid hormone-related peptide (PTHrP) are in the dental follicle and on the root surfac

178 TH) and parathyroid hormone-related peptide (PTHrP) bind and activate the PTH/PTHrP receptor (PTH-1R)

179 Parathyroid hormone-related peptide (PTHrP) is recognized as the major causative agent of hum

180 rathyroid hormone (PTH)/PTH-related peptide (PTHrP) receptor (PTHR1) in cells of the renal proximal t

181 ends on parathyroid hormone-related peptide (PTHrP) signaling pathway.

182 r by binding to the PTH/PTH-related peptide (PTHrP) type 1 receptor (PPR), a G-protein-coupled recept

183 tion of parathyroid hormone-related peptide (PTHrP), a key regulator of bone development.

184 nist of parathyroid hormone-related peptide (PTHrP), are compared to the corresponding lactam analogu

185 ated by parathyroid hormone-related peptide (PTHrP).

186 marker, parathyroid hormone-related peptide (PTHrP).

187 ) increases secretion of extracellular PGE2, PTHrP, and ATP (by epiphyseal chondrocytes), which toget

188 because the Hh pathway regulates physiologic PTHrP expression in the developing growth plate.

189 cause osteolytic lesions in vivo and produce PTHrP (MDA-MB-231, RWGT2, and PC-3) but is not expressed

190 Parathyroid hormone-related protein (PTHrP) and macrophage inflammatory protein-1 alpha (MIP-

191 tion of parathyroid hormone-related protein (PTHrP) and participate in the regulation of calcium and

192 sion of parathyroid hormone-related protein (PTHrP) and the morphology of chondrocytes.

193 yroid hormone (PTH) and PTH-related protein (PTHrP) are two related peptides that control calcium/pho

194 GF) and parathyroid hormone-related protein (PTHrP) as two potent beta-cell mitogens.

195 g (IHH)-parathyroid hormone-related protein (PTHrP) axis.

196 Parathyroid hormone-related protein (PTHrP) contributes to the development and metastatic pro

197 whereas parathyroid hormone-related protein (PTHrP) delays this process.

198 Parathyroid hormone-related protein (PTHrP) enhances rodent beta-cell growth and function thr

199 derived parathyroid-hormone-related protein (PTHrP) has an important role in wasting, through driving

200 role of parathyroid hormone-related protein (PTHrP) in fetal calcium homeostasis and placental calciu

201 express parathyroid hormone-related protein (PTHrP) in their developing epidermis and mammary glands]

202 nt with parathyroid hormone related protein (PTHrP) increased explant angiogenesis, which was complet

203 Parathyroid hormone-related protein (PTHrP) is a critical regulator of bone resorption and au

204 Parathyroid hormone-related protein (PTHrP) is essential to maintain a pool of dividing, imma

205 Parathyroid hormone-related protein (PTHrP) is produced by PCa cells and intermittent PTHrP e

206 ions of parathyroid hormone-related protein (PTHrP) on morphogenesis, cell proliferation, apoptosis,

207 hat the parathyroid hormone-related protein (PTHrP) potentiates CD11b(+)Gr1(+) cells in the bone marr

208 or signaling at the PTH/PTH-related protein (PTHrP) receptor (PPR) in intramembranous bone formation

209 e (PTH)/parathyroid hormone-related protein (PTHrP) receptor (PPR) signaling inhibits proliferation a

210 rathyroid hormone (PTH)/PTH-related protein (PTHrP) receptor (PTHR1) and is characterized by widening

211 des and parathyroid hormone-related protein (PTHrP) regulate keratinocyte proliferation and different

212 Parathyroid hormone-related protein (PTHrP) regulates cell fate and specifies the mammary mes

213 Parathyroid hormone-related protein (PTHrP) regulates the rate of differentiation of growth c

214 Parathyroid hormone-related protein (PTHrP) treatment of osteoblastic cells up-regulated CCL2

215 vels of parathyroid hormone-related protein (PTHrP), known to induce osteoclastogenesis, were also ob

216 Parathyroid hormone (PTH)-related protein (PTHrP), regulated by Indian hedgehog and acting through

217 both a parathyroid hormone-related protein (PTHrP)-dependent and -independent manner by activating t

218 derived parathyroid hormone-related protein (PTHrP)-mediated signaling through the epidermal growth f

219 yroid hormone (PTH) and PTH-related protein (PTHrP).

220 such as parathyroid hormone-related protein (PTHrP).

221 ctivate parathyroid hormone-related protein (PTHrP).

222 (PTH, 84 residues) and PTH-related protein (PTHrP, 141 residues) are natural agonists of PTHR1, and

223 HH) and parathyroid hormone-related protein (PTHrP, PTHLH) negatively regulate the transition from pr

224 wn that parathyroid hormone-related protein (PTHrP; also known as parathyroid hormone-like peptide, P

225 that PTH(1-34), but not PTH-related protein, PTHrP(1-36), or M-PTH(1-14) (M = Ala/Aib(1),Aib(3),Gln(1

226 marker (parathyroid hormone-related protein, PTHrP) in a real clinical scenario such as cell culture

227 ulated through the parathyroid hormone (PTH)/PTHrP receptor (PTH1R) signaling pathway.

228 s a rotamer toggle switch to accommodate PTH/PTHrP sequence divergence, and the latter adapting to th

229 rast, signaling by constitutively active PTH/PTHrP receptor (caPPR), whose expression was regulated b

230 provide a template for designing better PTH/PTHrP therapeutics.

231 enes, such as type II collagen (Col2a1), PTH/PTHrP receptor (Pth1r) and type X collagen (Col10a1), is

232 otomers forms an alpha-helix that mimics PTH/PTHrP by occupying the peptide binding groove of the opp

233 ndicated that constitutive activation of PTH/PTHrP receptor signaling in osteoblastic cells suppresse

234 d roles of parathyroid hormone receptor (PTH/PTHrP receptor) signaling in osteoblasts in unloading-in

235 y Indian hedgehog and acting through the PTH/PTHrP receptor (PPR), is crucial for normal cartilage de

236 ed peptide (PTHrP) bind and activate the PTH/PTHrP receptor (PTH-1R).

237 respectively, through activation of the PTH/PTHrP receptor (PTH1R), a class B G protein-coupled rece

238 Binding studies performed with PTH/PTHrP hybrid ligands having reciprocal exchanges of resi

239 velopment ex vivo and found that recombinant PTHrP, Wnt3A, and Egf family ligands stimulate embryonic

240 PS-341 reduced PTHrP and MIP-1 alpha expression in tumor cells in vivo.

241 ity, increased apoptosis, and down-regulated PTHrP expression in ATLL cells in vitro.

242 e Hedgehog (Hh) signaling pathway, regulates PTHrP expression in metastatic breast cancer because the

243 rocyte-targeted deletion of Zfp521 resembled PTHrP(-/-) and chondrocyte-specific PTHR1(-/-) mice, wit

244 eas enforced overexpression of Gli2 restored PTHrP activity.

245 iral restoration of p27(kip1) fully reverses PTHrP-induced cell cycle progression, indicating that PT

246 In contrast, Runx2(-/-)/PTHrP(-/-) mice exhibited limited vascular invasion and

247 In both tibia and femur, Runx2(-/-)/PTHrP(-/-) mice exhibited expanded regions of proliferat

248 Second, PTHrP has lower affinity than PTH for PTH-2R because of

249 olytic cancer cell lines that do not secrete PTHrP (MCF-7, ZR-75, and T47D).

250 Since PTHrP is found in many normal and malignant cells, poten

251 t Gli2 is required for TGF-beta to stimulate PTHrP expression and that blocking Hh-independent Gli2 a

252 ells, the CaR has been reported to stimulate PTHrP production by breast cancer cells.

253 CaSR activation stimulated PTHrP production by breast cancer cells in vitro and in

254 ) reduced endogenous and TGF-beta-stimulated PTHrP mRNA expression, but did not alter tumor cell prol

255 its PTHrP production by MMECs but stimulates PTHrP production by Comma-D cells (immortalized murine m

256 locked the effects of the CaR on stimulating PTHrP production in Comma-D and MCF-7 cells.

257 ATP) alone and in combination with synthetic PTHrP peptides on calcium transients in HaCaT cells.

258 To target PTHrP, we employed a microfluidic immunoarray featuring

259 Furthermore, the amino terminus PTHrP(1-36) peptide is sufficient to increase replicatio

260 1R is expressed in human beta-cells and that PTHrP has the potential to enhance human beta-cell proli

261 h multiple mutated DKK1 promoter assays that PTHrP, through c-Jun activation, downregulated the DKK1

262 We conclude that PTHrP is an important regulator of fetal calcium homeost

263 In this report, we demonstrate that PTHrP acts, in part, by sensitizing mesenchymal cells to

264 Our results demonstrate that PTHrP mediates energy wasting in fat tissues and contrib

265 We demonstrate that PTHrP or forskolin administration can block induction of

266 To test this, we first demonstrated that PTHrP downregulated DKK1 mRNA and protein expression.

267 In this study, we document that PTHrP modulates Wnt/beta-catenin signaling in the mammar

268 We found that PTHrP increases the expression of Zfp521, a zinc finger

269 We have found that PTHrP/forskolin administration represses the transcripti

270 s PCa progresses, led to the hypothesis that PTHrP could be a negative regulator of DKK1 expression i

271 This study tested the hypothesis that PTHrP might have a regulatory role in articular chondroc

272 ion of Runx1, Runx2, and Sox9 indicates that PTHrP is a modulator of transcriptional activation durin

273 uced cell cycle progression, indicating that PTHrP mediates its cell cycle acceleration in VSM via p2

274 gs, in conjunction with the observation that PTHrP expression increases and DKK1 expression decreases

275 anistic investigations in vivo revealed that PTHrP elevated Y418 phosphorylation levels in Src family

276 tion (ChIP) and re-ChIP assays revealed that PTHrP mediated this effect through inducing c-Jun to bin

277 acellular domain (ECD) of PTH1R reveals that PTHrP binds as an amphipathic alpha-helix to the same hy

278 Together, these data suggest that PTHrP expression and osteolysis in vivo in human breast

279 Our data suggest that PTHrP signaling sensitizes the mammary mesenchyme to the

280 Taken together, these results suggest that PTHrP signals block chondrocyte hypertrophy by, in part,

281 e has bone anabolic effects, suggesting that PTHrP could contribute to the excess bone mineralization

282 logy or the tissue involved, suggesting that PTHrP expression is part of the normal granulomatous imm

283 component of the Wnt pathway, attenuates the PTHrP-induced abnormal differentiation of the ventral sk

284 ast to a straight, continuous PTH helix, the PTHrP helix is gently curved and C-terminally "unwound."

285 Our results identify the PTHrP-cAMP-CREB1 axis as an attractive pathway for thera

286 , chondrocyte hypertrophy was delayed in the PTHrP(-/-) embryo.

287 , accelerated chondrocyte hypertrophy in the PTHrP(-/-) embryos.

288 enchymal, canonical Wnt pathway mediates the PTHrP-dependent specification of the mammary mesenchyme.

289 Moreover, the fetal skins of the PTHrP and PPR knockouts (KOs) had reciprocal increases i

290 d in mice homozygous for the deletion of the PTHrP gene (PTHrP-/- null; NL) compared to PTHrP+/+ (wil

291 ot formation, underscoring importance of the PTHrP-PPR system during root morphogenesis and tooth eru

292 e divergence, and the latter adapting to the PTHrP curvature.

293 e (PTHrP) and a mouse monoclonal antibody to PTHrP to immunostain biopsies.

294 e PTHrP gene (PTHrP-/- null; NL) compared to PTHrP+/+ (wild-type; WT) and PTHrP+/- (heterozygous; HZ)

295 rs and abrogated angiogenesis in response to PTHrP or RANKL in explants and in vivo but did not decre

296 ling in the developing cartilage by treating PTHrP(-/-) limb explants with sonic hedgehog (Shh) prote

297 helial cells in MMTV-PymT mice reduced tumor PTHrP expression and inhibited tumor cell proliferation

298 To examine whether PTHrP suppresses chondrocyte hypertrophy via Runx2-depen

299 ATP induced calcium transients, while PTHrP peptides did not.

300 CD11b(+)Gr1(+) cells isolated from mice with PTHrP-overexpressing tumors exhibited relatively increas

301 adenoviral PTHrP constructs or treated with PTHrP peptides.