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Human PTH Protein expressed in Escherichia coli (E. coli) - ABIN666842
Hodsman, Hanley, Ettinger, Bolognese, Fox, Metcalfe, Lindsay: Efficacy and safety of human parathyroid hormone-(1-84) in increasing bone mineral density in postmenopausal osteoporosis. in The Journal of clinical endocrinology and metabolism 2003
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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.
Common genetic variants located near genes involved in vitamin D metabolism and calcium and renal phosphate transport associated with differences in circulating parathyroid hormone concentrations
PTH pretreatment prevented TGF-beta1 (show TGFB1 Proteins) and high glucose-induced Smad2 (show SMAD2 Proteins)/3 phosphorylation and consequent upregulation of fibronectin (show FN1 Proteins) and type IV collagen (show COL4 Proteins) within 4 h.
FGFR1c and PTHR signaling pathways converge on NHERF1 (show SLC9A3R1 Proteins) to inhibit PTH- and FGF23 (show FGF23 Proteins)-sensitive phosphate transport and down-regulate NPT2A (show SLC34A1 Proteins).
In patients receiving dual antiplatelet therapy for coronary artery disease, higher PTH levels are associated with an increased ADP-mediated platelet reactivity and suboptimal response to clopidogrel.
Parathyroid hormone gene rs6256 variants are not associated with susceptibility to colorectal cancer
PTH levels were significantly higher in patients with aldosterone producing adenomas.
Although there was a trend for a negative association in women, no statistically significant association was found between endogenous PTH and knee osteoarthritis.
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.
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 (show SLC9A3R1 Proteins) PDZ I domain and the dissociation of NHERF-1 (show SLC9A3R1 Proteins)/Npt2a (show SLC34A1 Proteins) 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.
findings suggest that XLalphas (show GNAS Proteins) enhances Gq/11 signaling to mediate the renal actions of PTH during early postnatal development.
bone adaptation during exercise is not only a function of dynamic loading, but also PTH release, and that PTH signaling contributes differently at the structural and tissue levels.
IGF1 (show IGF1 Proteins) signaling plays a greater role in the skeletal actions of cPTH in the female mouse than in the male mouse, which may underlie the sex differences in the response to cPTH.
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
, probable peptidyl-tRNA hydrolase