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anti-Human PTH1R Antibodies:
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Human Polyclonal PTH1R Primary Antibody for ICC, IHC (p) - ABIN3043983
Li, He, Yao, Song, Zeng, Peng, Rosol, Deng: TGF-? Induces Degradation of PTHrP Through Ubiquitin-Proteasome System in Hepatocellular Carcinoma. in Journal of Cancer 2015
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Cow (Bovine) Monoclonal PTH1R Primary Antibody for IHC (p), WB - ABIN444936
Madiraju, Gawri, Wang, Antoniou, Mwale: Mechanism of parathyroid hormone-mediated suppression of calcification markers in human intervertebral disc cells. in European cells & materials 2013
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Human Monoclonal PTH1R Primary Antibody for ICC, IHC - ABIN969372
Dean, Vilardaga, Potts, Gardella: Altered selectivity of parathyroid hormone (PTH) and PTH-related protein (PTHrP) for distinct conformations of the PTH/PTHrP receptor. in Molecular endocrinology (Baltimore, Md.) 2007
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PTHR1 expression in U2OS cells was reduced by 0.18-, and 0.41-fold at 80, and 100 muM, respectively.
High PTH1R expression is associated with crohn's disease.
this study reports the cryo-electron microscopy structure of human PTH1R bound to a long-acting PTH analog and the stimulatory G protein.
We further find that Ca(2+) allostery in the PTHR is strongly affected by the point mutation recently identified in the PTH (PTH(R25C)) as a new cause of hypocalcemia in humans.
The results of this research confirm that mutations of the PTH1R gene are responsible for eruption failure with a varied clinical presentation consistent with previous descriptions of primary failure of eruption (PFE). These phenotypes can be found early at the level of the deciduous and then in the permanent dentition.
The results support that Parathyroid hormone (PTH)(1-34) not only activates PTH1R but also uniquely senses Ca(2+).
These results pinpoint the ubiquitinated Lys residues in PTHR controlling MAPK signaling and cell proliferation and survival.
findings confirm the expression of CaSR in human BM-derived MSCs and unravel a prominent role for the interplay between CaSR and PTH1R in regulating MSC fate and the choice of pathway for bone formation.
the decreased expression of PTH1R may be the main cause of hypercalcemia in HCC. Decreased expression of PTH1R was associated with tumor size, Edmondson Grade, serum AFP level and poor overall survival, and was a poor prognosis in HCC.
the results indicated that the beta-alanine induced expression of PTHR1 has a positive relationship with invasion and metastasis of osteosarcoma cells.
Functional studies (IFA) showed a variation in expression between the WT and mutant PTH1R. In silico analysis showed structural differences between WT and mutant PTH1R proteins, particularly in the regions of the 3rd intracellular loop and the 6th transmembrane domain required for efficient PTH1R function.
Heterozygous mutations in the ATP4A and PTH1R genes were identified in a family with type I gastric neuroendocrine tumors plus hypothyroidism and rheumatoid arthritis
It seems likely that Mut-PTH1R may be, at least in part, co-localized with Wt-PTH1R by forming a heterodimer, leading to affect the function to each other in Jansen type metaphyseal chondrodysplasia.
PTH1R mutation is associated with Primary Failure of Tooth Eruption.
Data suggest that GCGR (glucagon receptor) activation proceeds via a mechanism in which transmembrane helix 6 (TM6) is held in an inactive conformation by a conserved polar core and a hydrophobic lock (involving intracellular loop 3, IC3); mutations in the corresponding polar core of GCGR or PTH1R disrupt these inhibitory elements, allow TM6 to swing outward, and induce constitutive G protein signaling.
data highlight sequences in PTHR that contribute to NHERF1 interaction and can be altered to prevent phosphorylation-mediated inhibition
Overt hypercalcemia is not always encountered in Jansen Metaphyseal Chondrodysplasia due to Heterozygous H223R-PTH1R Mutation.
data are consistent with the hypothesis that the pattern of C-terminal tail phosphorylation on PTH1R may determine the signaling outcome following receptor activation.
the data presented in this manuscript demonstrate a critical function of VPS35 in regulating PTH1R trafficking. This event and VPS35-interaction with PPP1R14C appear to be essential for turning off PTH1R's endosomal signaling, and promoting PTH1R-mediated catabolic response and bone remodeling.
PTH1R mutation causing primary failure of tooth eruption in a consanguineous Saudi family.
acute calcemic response to PTH in vivo in mice lacking PTH receptors in osteocytes vs littermate controls, is resported.
Knock-down of PTHR1 reveals its pro-malignant effects in osteosarcoma cells.
ZFPM2, LEF1, NR4A2, HAS2, and RHOC might be potential targets of PTHR1 in osteosarcoma.
Pth1r in DMP1-8kb-expressing cells is required to maintain basal levels of bone resorption but is dispensable for the catabolic action of chronic PTH elevation.
Results provide in vivo evidence of a role for RAMP2 in placental development distinct from the RAMP2-calcitonin receptor-like receptor/adrenomedullin signaling paradigm; decreases Pthr1 expression and causes a blunted response to systemic parathyroid hormone; and identify additional pathways underlying the endocrine and fertility defects of the previously characterized Ramp2 heterozygous adult females.
Activation of PTHrP-cyclic AMP-CREB1 signaling following p53 loss is essential for osteosarcoma initiation and maintenance.
A critical role for SNX27-retromer mediated transport of PTHR in normal bone development.
PTHrP and PTH mediate wasting through a common mechanism involving PTHR.
we propose that PTH has a direct effect on osteoblasts and osteoclasts, and that this effect is mediated through PTH1R, thus contributing to bone remodeling
Ihh and PTH1R signaling in limb mesenchyme are both essential to regulate proper development of digit structures, although they appear to use different mechanisms.
cells expressing osterix are mesenchymal progenitors contributing to all relevant cell types during morphogenesis.
PTH1R regulates systemic mineral ion homeostasis and induction of FGF23.
PTH1R is an important component of mechanical signal transduction in osteocytic MLO-Y4 cells.
These studies reveal that PTH1R signaling in osteoblasts regulates cartilaginous growth plate for postnatal growth of bone.
Cbfbeta functions in upregulating Ihh expression to promoter chondrocyte proliferation and osteoblast differentiation, and inhibiting PPR expression to enhance chondrocyte differentiation.
Osteocytic gp130 is required to maintain PTH1R expression in the osteoblast lineage, and for the stimulation of osteoblast differentiation that occurs in response to PTH.
PTH receptor signaling enhances bone resorption by directly regulating Rankl gene expression in osteocytes.
Data suggest that parathyroid hormone (PTH) receptor signaling could enhance the therapeutic potential of the pathway.
Data indicate that PTH/PTH-related peptide (PTHrP) type 1 receptor (PPR) signaling in osteocytes is required for bone remodeling.
PTH-induced phosphorylation of the PTHR1 in is important in regulating acute ligand responses
Loss of function of either PTHR1 or PTHrP in zebrafish leads to a localized aortic defect that is Notch dependent.
The expression of the PTH/PTHrP receptor in dairy cows before and after parturition is reported.
This study reveals clear genetic-statistical evidence for a link of KRT8, FAF1 and PTH1R with some of leg weakness related traits in pigs.
These findings reveal that direct ezrin interactions promote PTH1R apical localization and signaling in LLC-PK1 cells.
PTHLH and PTHR1 were evaluated as functional candidate genes for their effects on number and shape of teats in pigs
The protein encoded by this gene is a member of the G-protein coupled receptor family 2. This protein is a receptor for parathyroid hormone (PTH) and for parathyroid hormone-like hormone (PTHLH). The activity of this receptor is mediated by G proteins which activate adenylyl cyclase and also a phosphatidylinositol-calcium second messenger system. Defects in this receptor are known to be the cause of Jansen's metaphyseal chondrodysplasia (JMC), chondrodysplasia Blomstrand type (BOCD), as well as enchodromatosis. Two transcript variants encoding the same protein have been found for this gene.
, PTH/PTHrP type I receptor
, PTH1 receptor
, parathyroid hormone receptor 1
, parathyroid hormone/parathyroid hormone-related peptide receptor
, parathyroid hormone/parathyroid hormone-related protein receptor
, seven transmembrane helix receptor
, PTH-related peptide receptor
, PTH/PTHrP receptor
, parathyroid hormone 1 receptor
, parathyroid hormone/parathyroid hormone-related peptide receptor-like
, parathyroid hormone receptor-1
, parathyroid receptor
, LOW QUALITY PROTEIN: parathyroid hormone/parathyroid hormone-related peptide receptor
, Parathyroid hormone/parathyroid hormone-related peptide receptor