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anti-Human PTH Anticorps:
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Human Monoclonal PTH Primary Antibody pour IHC (fro), IHC (p) - ABIN2476062
Uzych: Hawaii and the AIDS epidemic. dans Hawaii medical journal 1990
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Human Monoclonal PTH Primary Antibody pour ELISA, WB - ABIN966922
French, Hamilton, Mattano, Sather, Devidas, Nachman, Relling: A PAI-1 (SERPINE1) polymorphism predicts osteonecrosis in children with acute lymphoblastic leukemia: a report from the Children's Oncology Group. dans Blood 2008
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Human Monoclonal PTH Primary Antibody pour ELISA, WB - ABIN1724741
Koshizuka, Ogata, Shiraki, Hosoi, Seichi, Takeshita, Nakamura, Kawaguchi: Distinct association of gene polymorphisms of estrogen receptor and vitamin D receptor with lumbar spondylosis in post-menopausal women. dans European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society 2006
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Human Monoclonal PTH Primary Antibody pour ELISA, ICC - ABIN260228
Koh, Hogue, Sosa: A Novel Ex Vivo Method for Visualizing Live-Cell Calcium Response Behavior in Intact Human Tumors. dans PLoS ONE 2016
The results support that Parathyroid hormone (PTH)(1-34) not only activates PTH1R but also uniquely senses Ca(2+).
This study revealed a dysequilibrium of the PTH-FGF23-vitamin D axis in RRMS, with lower plasma PTH, higher plasma iFGF23 and a lower serum 1,25(OH)2D to 25OHD ratio in RRMS compared with healthy control subjects.
Among subjects with preserved renal function, PTH levels were possibly associated with metabolic syndrome in females, whereas vitamin D levels exhibited a possible link to metabolic syndrome in males.
Data suggest that, in pregnant women with largely sufficient calcium intakes (via diet and dietary supplements), serum 25-hydroxyvitamin D (total of 25[OH]D2 and 25[OH]D3) is important for maintaining normal serum PTH levels; this study was conducted in group of white-skinned women at northern latitudes in Ireland.
In conclusion, Fetuin A, vitamin D, and intact PTH levels were all associated with sarcopenia in this geriatric population. Among them, intact PTH specifically indicates patients with sarcopenic left ventricular hypertrophy.
Dkk-1 and PTH levels in psoriatic arthritis are lower than healthy female controls, in contrast with rheumatoid arthritis, in which they are increased
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) and parathyroid hormone (PTH) in some, but not all studies. [REVIEW]
Parathyroid hormone controls bone and kidney homeostasis via GNAS and Gq-G11 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, either continuous or pulsatile, does not exhibit any positive effect, and indicates that exogenous PTH administration after fracture has no effect on HCs. 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.
Cys 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 and high glucose-induced Smad2/3 phosphorylation and consequent upregulation of fibronectin and type IV collagen within 4 h.
FGFR1c and PTHR signaling pathways converge on NHERF1 to inhibit PTH- and FGF23-sensitive phosphate transport and down-regulate NPT2A.
The present study supports the independent pathogenic effect of rs6254GA polymorphism on the development and severity of bone mineral density complications in patients with asymptomatic but not normocalcemic hyperparathyroidism.
These data demonstrate that lactate activates GPR81-PKC-Akt signaling to regulate osteoblast differentiation that mediated by parathyroid hormone treatment.
suppression of miR-185 targeting PTH could promote osteoblast growth and proliferation during fracture healing through activating Wnt/beta -catenin axis
lack of endogenous PTH may reduce VEGF expression in bone marrow mesenchymal stem cellsderived osteoblasts.
findings identify p38alpha MAPK as a key component of PTH signaling in osteoblast lineage cells and highlight its requirement in iPTH osteoanabolic activity
FGF23 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, and that the CaSR plays a collaborative role in the PTH anabolic effects on bone.
Mmp13 is selectively regulated of by 1,25-Dihydroxyvitamin D3, PTH, and Osterix through distal enhancers.
PTHrP and PTH mediate wasting through a common mechanism involving PTHR.
Usp2 is required for the PTH1-34-induced proliferation of osteoblasts
These results highlight the role of distal enhancers in the regulation of RANKL 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 signaling in bone are necessary to establish radial bone growth and optimize mineral acquisition during growth.
findings suggest that XLalphas 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 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.
Downregulation of PTH receptor expression mediated by intracellular oxidant stress as the mechanisms in hyperlipidemia-induced PTH resistance.
Chondrogenesis induced by PTH in mesenchymal progenitor cells is mediated by Runx1, which involves the activation of PKA.
PTH is not required to upregulate renal expression of Cyp27b1 during pregnancy or to stimulate recovery from loss of bone mineral content caused by lactation.
PTH deficiency itself impairs osteogenesis, osteoclastogenesis, and osteoclastic bone resorption, whereas subsequent upregulation of PTHrP in osteogenic cells compensates by increasing bone accrual.
Induced formation of aberrant crypt foci (ACF) caused by azoxymethane (AOM) injection in 'rescued' CaSR-/PTH- (C-/P-) double knockout colons compared with colons from control CaSR+/PTH+ (C+/P+) mice to study the role of CaSR.
These data highlight the ability of PTH to phosphorylate beta-catenin directly via PKA.
These data suggest that prostaglandin E2 acting via EP4R 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 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 DNA element in the hormone's promoter.
alternative cis-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 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