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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 tion of PTH(1-34)-NH(2) and abaloparatide (a PTHrP derivative) with a single homologous beta-amino ac
13 cells up-regulated CCL2 and was blocked by a PTHrP antagonist, suggesting that prostate cancer-derive
16 (iii) blockage of ADAMTS-7 almost abolishes PTHrP-mediated inhibition of chondrocyte hypertrophy and
17 enesis, as blockage of ECM1 nearly abolishes PTHrP regulation of chondrocyte hypertrophy, and overexp
20 essed IHH and PTHrP expression in an allelic PTHrP-LacZ-knockin mouse and several versions of PTHrP-n
22 ytes, such as those derived by WNT, BMP, and PTHrP/IHH molecules, suggesting that the FAM20B-catalyze
24 his study is to determine 1) whether HGF and PTHrP have additive/synergistic effects on beta-cell gro
27 accompanied by marked reductions in Ihh and PTHrP as well as sFRP-1, an endogenous Wnt signaling ant
33 th recombinant FGF2/FGF9 decreased Ptch1 and PTHrP expression in superficial/polymorphic layers and p
35 ns and enabled the design of altered PTH and PTHrP peptides that adopt the ECD-binding mode of the op
36 n of osteoclast-promoting factors, RANKL and PTHrP, even after the osteoblast differentiation ceases
40 (TUBTS) - were used to immobilize whole anti-PTHrP antibodies and Fab' fragments to surfaces as biore
44 emonstrate a novel signaling linkage between PTHrP and Wnt signaling pathways that results in downreg
47 pression of ERK activation in these cells by PTHrP or a MEK inhibitor coincided with a delay in chond
48 ADAMTS-7 is an important target of canonical PTHrP signaling, since (i) PTHrP induces ADAMTS-7, (ii)
49 tracellular calcium, through studies of CaSR-PTHrP interactions in the MMTV-PymT transgenic mouse mod
50 ken together, our findings suggest that CaSR-PTHrP interactions might be a promising target for the d
51 lcium transients, while endoproteases cleave PTHrP, resulting in fragments with different cellular fu
54 vidence that Ihh signaling directly controls PTHrP expression and chondrocyte morphology in the growt
56 differentially regulate genes such as CXCR4, PTHrP, RUNX2, and TGFbeta1 that are associated with homi
57 bone metastatic breast cancer would decrease PTHrP expression and therefore osteolytic bone destructi
58 differentiation factor 5 were used to delete PTHrP from articular chondrocytes in the mid-region of m
59 results showed that prostate cancer-derived PTHrP acts in the bone marrow to potentiate CD11b(+)Gr1(
60 ist, suggesting that prostate cancer-derived PTHrP plays an important role in elevation of osteoblast
61 of prostate cancer, levels of tumor-derived PTHrP correlated with CD11b(+)Gr1(+) cell recruitment an
64 tial, suggesting that prostate tumor-derived PTHrP potentiates this activity of CD11b(+)Gr1(+) cells.
65 ive cascade is driven by tumor cell-derived, PTHrP-mediated induction of CCL2, which facilitates tumo
66 ensating in response to a partial Cre-driven PTHrP deletion, a finding that underscores the need to s
72 is new ultrasensitive, multiplexed assay for PTHrP and fragments is promising for clinical diagnosis,
73 Of importance, ECM1 seems to be critical for PTHrP action in chondrogenesis, as blockage of ECM1 near
74 ocytes, indicating that PP2A is critical for PTHrP-mediated regulation of chondrocyte hypertrophy.
77 mozygous for the deletion of the PTHrP gene (PTHrP-/- null; NL) compared to PTHrP+/+ (wild-type; WT)
81 peptide (PTHrP) and the parathyroid hormone-PTHrP receptor increase chondrocyte proliferation and de
85 rget of canonical PTHrP signaling, since (i) PTHrP induces ADAMTS-7, (ii) ADAMTS-7 is downregulated i
86 ing PCa, and targeting this newly identified PTHrP/p38/Hsp27/AR/p21 signaling pathway with either p38
87 plates of these mice exhibit a lack of Ihh, PTHrP-R, and Col10 expression indicating a loss of chond
89 ocumented in KO mice to suggest that the IHH-PTHrP axis is capable of compensating in response to a p
91 hanisms downstream or independent of the Ihh-PTHrP signaling pathway, a pivotal signaling system that
95 at PTH-2R is due to the presence of His-5 in PTHrP (Ile-5 in PTH), which interacts with the receptor'
96 nloading is associated with rapid changes in PTHrP expression and articular chondrocyte differentiati
97 ADAMTS-7, (ii) ADAMTS-7 is downregulated in PTHrP null mutant (PTHrP-/-) growth plate chondrocytes,
98 including multiple genes that participate in PTHrP-IHH, BMP and CNP signaling, and many genes that ha
99 es expression of Ihh target genes, including PTHrP and Col10a1, through its physical and functional i
100 nal target genes of Eda/NF-kappaB, including PTHrP, Wnt10a, and Wnt10b, as well as Egf family ligands
102 c stimulation of cAMP accumulation increased PTHrP production by normal and transformed breast cells.
104 the effects of CaR activation on inhibiting PTHrP secretion by MMECs and blocked the effects of the
105 is study, we confirmed that the CaR inhibits PTHrP production by MMECs but stimulates PTHrP productio
106 multiplexed peptide assay to measure intact PTHrP 1-173 as well as circulating N-terminal and C-term
107 P) is produced by PCa cells and intermittent PTHrP exposure has bone anabolic effects, suggesting tha
108 at the transcript and protein levels in K14-PTHrP fibroblasts in vitro, while ovariectomy increases
111 ining cells from the ventral skin of the K14-PTHrP transgenic mice [which overexpress parathyroid hor
112 es of sorted Pdgfralpha-positive ventral K14-PTHrP and wild-type fibroblasts, identifying differentia
113 transgenic overexpression of the PPR ligand PTHrP have suggested that this ligand receptor combinati
114 wever, the molecular mechanisms that mediate PTHrP production by breast cancer cells are not entirely
117 MTS-7 is downregulated in PTHrP null mutant (PTHrP-/-) growth plate chondrocytes, and (iii) blockage
123 ppeared to be mediated by nuclear actions of PTHrP that decreased p27(kip1) levels and prevented nucl
124 o, or overexpressing Ihh in the cartilage of PTHrP(-/-) embryos or inactivating patched 1 (Ptch1), a
127 In confirmation, adenoviral delivery of PTHrP to murine primary vascular smooth muscle cells (VS
130 and for survival, and many of the effects of PTHrP on development are not mediated by its N terminus.
133 genesis of HHM in ATLL and the expression of PTHrP can be activated by nuclear factor kappaB (NF-kapp
135 ion by upregulating osteoblast expression of PTHrP, which promoted RANKL expression via PKA and its t
138 ing chondrocyte hypertrophy independently of PTHrP, which is particularly important in postnatal cart
142 xpression is completely abolished by loss of PTHrP signaling and ectopic reporter activity is induced
153 rix metalloproteinase-directed processing of PTHrP disables the osteolytic functions of the mature ho
155 ciency or, alternatively, the restoration of PTHrP or cyclo-oxygenase activity by the administration
157 issection revealed that through secretion of PTHrP, NEPCa cells could alter the p38/MAPK/Hsp27 signal
158 rowth zone appears to serve as the source of PTHrP-expressing proliferative chondrocytes that populat
159 The high resolution crystal structure of PTHrP bound to the extracellular domain (ECD) of PTH1R r
160 emonstrate that ADAMTS-7, a direct target of PTHrP signaling, negatively regulates endochondral bone
162 h that the midregion, NLS, and C terminus of PTHrP are crucial for the commitment of osteogenic and h
164 Thus, the opposing effects of the CaR on PTHrP production are because of alternate G-protein coup
166 ulation with ATP and either PTHrP (43-52) or PTHrP (70-77) increased proliferation, suggesting that t
167 nvironments in which elevated calcium and/or PTHrP levels contribute to breast cancer progression.
169 chondrocyte proliferation and maturation or PTHrP-induced chondrocyte proliferation and PTHrP-delaye
170 r of nuclear factor-kappaB ligand (RANKL) or PTHrP in vivo increased calvarial vessel density and ost
175 e serum parathyroid hormone-related peptide (PTHrP) and a mouse monoclonal antibody to PTHrP to immun
176 data implicates parathyroid-related peptide (PTHrP) and cyclo-oxygenase-2 (COX-2) as possible factors
177 between parathyroid hormone-related peptide (PTHrP) and Indian hedgehog (Ihh) signaling tightly regul
179 ressing parathyroid hormone-related peptide (PTHrP) are in the dental follicle and on the root surfac
180 TH) and parathyroid hormone-related peptide (PTHrP) bind and activate the PTH/PTHrP receptor (PTH-1R)
182 rathyroid hormone (PTH)/PTH-related peptide (PTHrP) receptor (PTHR1) in cells of the renal proximal t
184 r by binding to the PTH/PTH-related peptide (PTHrP) type 1 receptor (PPR), a G-protein-coupled recept
186 nist of parathyroid hormone-related peptide (PTHrP), are compared to the corresponding lactam analogu
187 ed bone Parathyroid Hormone related Peptide (PTHrP), prevented the decrease in serum Parathyroid Horm
191 ) increases secretion of extracellular PGE2, PTHrP, and ATP (by epiphyseal chondrocytes), which toget
192 ling by parathyroid hormone-related protein (PTHrP) and its parathyroid hormone/PTHrP receptor PPR.
194 tion of parathyroid hormone-related protein (PTHrP) and participate in the regulation of calcium and
196 yroid hormone (PTH) and PTH-related protein (PTHrP) are two related peptides that control calcium/pho
201 derived parathyroid-hormone-related protein (PTHrP) has an important role in wasting, through driving
202 role of parathyroid hormone-related protein (PTHrP) in fetal calcium homeostasis and placental calciu
203 express parathyroid hormone-related protein (PTHrP) in their developing epidermis and mammary glands]
204 nt with parathyroid hormone related protein (PTHrP) increased explant angiogenesis, which was complet
207 ions of parathyroid hormone-related protein (PTHrP) on morphogenesis, cell proliferation, apoptosis,
208 hat the parathyroid hormone-related protein (PTHrP) potentiates CD11b(+)Gr1(+) cells in the bone marr
209 or signaling at the PTH/PTH-related protein (PTHrP) receptor (PPR) in intramembranous bone formation
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
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 ator of parathyroid hormone-related protein (PTHrP), which is produced by bone metastatic tumor cells
218 both a parathyroid hormone-related protein (PTHrP)-dependent and -independent manner by activating t
219 derived parathyroid hormone-related protein (PTHrP)-mediated signaling through the epidermal growth f
224 (PTH, 84 residues) and PTH-related protein (PTHrP, 141 residues) are natural agonists of PTHR1, and
225 HH) and parathyroid hormone-related protein (PTHrP, PTHLH) negatively regulate the transition from pr
226 wn that parathyroid hormone-related protein (PTHrP; also known as parathyroid hormone-like peptide, P
227 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
228 marker (parathyroid hormone-related protein, PTHrP) in a real clinical scenario such as cell culture
230 modeling, but also to the regulation of PTH, PTHrP, 1,25-Dyhydroxyvitamin D (1,25(OH)2D), osteoclasto
231 s a rotamer toggle switch to accommodate PTH/PTHrP sequence divergence, and the latter adapting to th
232 rast, signaling by constitutively active PTH/PTHrP receptor (caPPR), whose expression was regulated b
234 enes, such as type II collagen (Col2a1), PTH/PTHrP receptor (Pth1r) and type X collagen (Col10a1), is
235 otomers forms an alpha-helix that mimics PTH/PTHrP by occupying the peptide binding groove of the opp
236 ndicated that constitutive activation of PTH/PTHrP receptor signaling in osteoblastic cells suppresse
237 d roles of parathyroid hormone receptor (PTH/PTHrP receptor) signaling in osteoblasts in unloading-in
238 y Indian hedgehog and acting through the PTH/PTHrP receptor (PPR), is crucial for normal cartilage de
240 respectively, through activation of the PTH/PTHrP receptor (PTH1R), a class B G protein-coupled rece
242 velopment ex vivo and found that recombinant PTHrP, Wnt3A, and Egf family ligands stimulate embryonic
245 rocyte-targeted deletion of Zfp521 resembled PTHrP(-/-) and chondrocyte-specific PTHR1(-/-) mice, wit
247 iral restoration of p27(kip1) fully reverses PTHrP-induced cell cycle progression, indicating that PT
251 t Gli2 is required for TGF-beta to stimulate PTHrP expression and that blocking Hh-independent Gli2 a
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
257 ATP) alone and in combination with synthetic PTHrP peptides on calcium transients in HaCaT cells.
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
270 s PCa progresses, led to the hypothesis that PTHrP could be a negative regulator of DKK1 expression i
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
279 e has bone anabolic effects, suggesting that PTHrP could contribute to the excess bone mineralization
280 logy or the tissue involved, suggesting that PTHrP expression is part of the normal granulomatous imm
281 component of the Wnt pathway, attenuates the PTHrP-induced abnormal differentiation of the ventral sk
282 ast to a straight, continuous PTH helix, the PTHrP helix is gently curved and C-terminally "unwound."
286 enchymal, canonical Wnt pathway mediates the PTHrP-dependent specification of the mammary mesenchyme.
288 d in mice homozygous for the deletion of the PTHrP gene (PTHrP-/- null; NL) compared to PTHrP+/+ (wil
289 ot formation, underscoring importance of the PTHrP-PPR system during root morphogenesis and tooth eru
293 e PTHrP gene (PTHrP-/- null; NL) compared to PTHrP+/+ (wild-type; WT) and PTHrP+/- (heterozygous; HZ)
294 rs and abrogated angiogenesis in response to PTHrP or RANKL in explants and in vivo but did not decre
295 ling in the developing cartilage by treating PTHrP(-/-) limb explants with sonic hedgehog (Shh) prote
296 helial cells in MMTV-PymT mice reduced tumor PTHrP expression and inhibited tumor cell proliferation
299 CD11b(+)Gr1(+) cells isolated from mice with PTHrP-overexpressing tumors exhibited relatively increas