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Scientific evidence of genetic association of serum PTH level among individuals with different pathologic conditions remains deficient and published results provide weak evidence (review and meta-analysis).
Clinical data on secondary hyperparathyroidism, mainly derived from patients with chronic kidney disease, indicate a potential inverse association between leptin (LEP (show LEP Proteins)) and parathyroid hormone (PTH) in some, but not all studies. [REVIEW]
Parathyroid hormone controls bone and kidney homeostasis via GNAS (show GNAS Proteins) and Gq-G11 (show STK19 Proteins) heterotrimeric G proteins. (Review)
Patients with chronic kidney disease undergoing parathyroidectomy for primary hyperparathyroidism have similar intraoperative parathyroid hormone degradation kinetics to those with normal kidney function.
PTH levels are significantly higher in untreated sustained hypertension patients than white-coat hypertension patients and normotensive subjects.
results revealed that PTH treatment on HCs (show HLCS Proteins), either continuous or pulsatile, does not exhibit any positive effect, and indicates that exogenous PTH administration after fracture has no effect on HCs (show HLCS Proteins). PTH may not have a positive effect at the fracture site during the early stage of fracture healing in which haematoma formation occurs.
Pre-incubation of muscle fibers or myotubes with physiological concentrations of PTH, concentration-dependently reduced uptake of labelled 25-hydroxyvitamin D3.
Baseline PTH level was not associated with changes in frailty status in men.
Elevated PTH induces the transition of endothelial cells to chondrogenic cells via endothelial-mesenchymal transition, possibly mediated by the nuclear translocation of beta-catenin (show CTNNB1 Proteins).
Cys (show DNAJC5 Proteins) mutation at the 25th residue of hPTH(1-34) may result in a high bone mass phenotype.
lack of endogenous PTH may reduce VEGF (show VEGFA Proteins) expression in bone marrow mesenchymal stem cellsderived osteoblasts.
findings identify p38alpha (show MAPK14 Proteins) MAPK (show MAPK1 Proteins) as a key component of PTH signaling in osteoblast lineage cells and highlight its requirement in iPTH osteoanabolic activity
FGF23 (show FGF23 Proteins) may be an important modulator of PTH signaling in bone and kidney.
These findings suggest that trabecular bone formation can occur independently of the CaSR (show CASR Proteins), and that the CaSR (show CASR Proteins) plays a collaborative role in the PTH anabolic effects on bone.
Mmp13 (show MMP13 Proteins) is selectively regulated of by 1,25-Dihydroxyvitamin D3, PTH, and Osterix (show SP7 Proteins) through distal enhancers.
PTHrP and PTH mediate wasting through a common mechanism involving PTHR (show PTH1R Proteins).
Usp2 (show USP2 Proteins) is required for the PTH1-34-induced proliferation of osteoblasts
These results highlight the role of distal enhancers in the regulation of RANKL (show TNFSF11 Proteins) expression by PTH and perhaps 1,25(OH)2D3 and suggest that the RL-D2 and RL-D5 enhancers contribute in either an additive or synergistic manner to regulate bone remodeling.
These results indicate that PTH-mediated inhibition of renal phosphate transport involves phosphorylation of S77 of the NHERF-1 PDZ I domain and the dissociation of NHERF-1/Npt2a complexes.
It was concluded that endogenously secreted PTH and GHR (show GHR Proteins) signaling in bone are necessary to establish radial bone growth and optimize mineral acquisition during growth.
These data highlight the ability of PTH to phosphorylate beta-catenin (show CTNNB1 Proteins) directly via PKA.
These data suggest that prostaglandin E2 acting via EP4R (show PTGER4 Proteins) on bone marrow macrophages committed to the osteoblast cell lineage, stimulated secretion of a factor or factors that acted to suppress PTH-stimulated osteoblast differentiation.
These results suggest that in vivo PTH treatment increased in vitro osteoclastogenesis and resorption without altering the number of osteoclast precursors.
Osteoblast 2-deoxyglucose uptake and glycogen (show GYS2 Proteins) synthesis were increased after exposure to low concentrations (0.1 nmol/l and above) of PTH.
Parathyroid hormone stimulated growth and decreased Col-X deposition via phosphotidylinositol-3,4,5 triphosphate kinase and mitogen activating protein kinase pathways in avian sterna.
likely involvement of the Sp family in regulating PTH gene expression through interactions with an Sp1 (show SP1 Proteins) DNA element in the hormone's promoter.
alternative cis (show CISH Proteins)-acting protein-binding elements may determine the regulation of PTH mRNA stability in response to changes in serum calcium and phosphate
a possible role for the Wnt (show WNT2 Proteins) signaling pathway in PTH actions in bone
Data suggest that calcium-mediated destabilization of parathyroid hormone mRNA requires gene transcription and involves increases in cytosolic Ca.
The protein encoded by this gene is a hormone secreted by parathyroid cells. This hormone elevates blood Ca2+ level by dissolving the salts in bone and preventing their renal excretion. Defects in this gene are a cause of familial isolated hypoparathyroidism (FIH).
, parathyroid hormone 1
, preproparathyroid hormone
, hypothalamic parathyroid hormone
, thyroid hormone
, parathyroid hormone