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anti-Human PTH Antikörper:
anti-Mouse (Murine) PTH Antikörper:
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Human Monoclonal PTH Primary Antibody für IHC (fro), IHC (p) - ABIN2476062
Uzych: Hawaii and the AIDS epidemic. in Hawaii medical journal 1990
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Human Monoclonal PTH Primary Antibody für 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. in Blood 2008
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Human Monoclonal PTH Primary Antibody für 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. in 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 für ELISA, ICC - ABIN260228
Koh, Hogue, Sosa: A Novel Ex Vivo Method for Visualizing Live-Cell Calcium Response Behavior in Intact Human Tumors. in PLoS ONE 2016
Parathyroid hormone controls bone and kidney homeostasis via GNAS (zeige GNAS Antikörper) and Gq-G11 (zeige STK19 Antikörper) 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 (zeige HLCS Antikörper), either continuous or pulsatile, does not exhibit any positive effect, and indicates that exogenous PTH administration after fracture has no effect on HCs (zeige HLCS Antikörper). 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 (zeige CTNNB1 Antikörper).
Cys (zeige DNAJC5 Antikörper) 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 (zeige TGFB1 Antikörper) and high glucose-induced Smad2 (zeige SMAD2 Antikörper)/3 phosphorylation and consequent upregulation of fibronectin (zeige FN1 Antikörper) and type IV collagen (zeige COL4 Antikörper) within 4 h.
findings identify p38alpha (zeige MAPK14 Antikörper) MAPK (zeige MAPK1 Antikörper) as a key component of PTH signaling in osteoblast lineage cells and highlight its requirement in iPTH osteoanabolic activity
FGF23 (zeige FGF23 Antikörper) 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 (zeige CASR Antikörper), and that the CaSR (zeige CASR Antikörper) plays a collaborative role in the PTH anabolic effects on bone.
Mmp13 (zeige MMP13 Antikörper) is selectively regulated of by 1,25-Dihydroxyvitamin D3, PTH, and Osterix (zeige SP7 Antikörper) through distal enhancers.
PTHrP and PTH mediate wasting through a common mechanism involving PTHR (zeige PTH1R Antikörper).
Usp2 (zeige USP2 Antikörper) is required for the PTH1-34-induced proliferation of osteoblasts
These results highlight the role of distal enhancers in the regulation of RANKL (zeige TNFSF11 Antikörper) 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 (zeige GHR Antikörper) signaling in bone are necessary to establish radial bone growth and optimize mineral acquisition during growth.
findings suggest that XLalphas (zeige GNAS Antikörper) enhances Gq/11 signaling to mediate the renal actions of PTH during early postnatal development.
These data highlight the ability of PTH to phosphorylate beta-catenin (zeige CTNNB1 Antikörper) directly via PKA.
These data suggest that prostaglandin E2 acting via EP4R (zeige PTGER4 Antikörper) 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 (zeige GYS2 Antikörper) 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 (zeige SP1 Antikörper) DNA element in the hormone's promoter.
alternative cis (zeige CISH Antikörper)-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 (zeige WNT2 Antikörper) 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