Proteasomal degradation of Runx2 shortens parathyroid hormone-induced anti-apoptotic signaling in osteoblasts. A putative explanation for why intermittent administration is needed for bone anabolism.
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Down-regulation of ubiquitin ligase Cbl induced by twist haploinsufficiency in Saethre-Chotzen syndrome results in increased PI3K/Akt signaling and osteoblast proliferationT lymphocytes amplify the anabolic activity of parathyroid hormone through Wnt10b signalingEffects of PTH on osteocyte functionCatabolic and anabolic actions of parathyroid hormone on the skeletonApoptotic osteocytes and the control of targeted bone resorptionControl of bone mass and remodeling by PTH receptor signaling in osteocytesCritical role of activating transcription factor 4 in the anabolic actions of parathyroid hormone in boneRegulation of gene expression in osteoblasts.Parathyroid hormone-responsive Smad3-related factor, Tmem119, promotes osteoblast differentiation and interacts with the bone morphogenetic protein-Runx2 pathwayMutational analysis of sclerostin shows importance of the flexible loop and the cystine-knot for Wnt-signaling inhibitionDysapoptosis of osteoblasts and osteocytes increases cancellous bone formation but exaggerates cortical porosity with age.Nmp4/CIZ suppresses parathyroid hormone-induced increases in trabecular bone.ClC-3 chloride channel mediates the role of parathyroid hormone [1-34] on osteogenic differentiation of osteoblastsParathyroid hormone: anabolic and catabolic actions on the skeletonSelective small molecule compounds increase BMP-2 responsiveness by inhibiting Smurf1-mediated Smad1/5 degradationNmp4/CIZ: road block at the intersection of PTH and load.Osteoblastogenesis and tumor growth in myeloma.Advances in the understanding of myeloma bone disease and tumour growth.Amelioration of type I diabetes-induced osteoporosis by parathyroid hormone is associated with improved osteoblast survivalRunx2 trans-activation mediated by the MSX2-interacting nuclear target requires homeodomain interacting protein kinase-3.Genetic and transcriptional control of bone formationT cells: critical bone regulators in health and disease.Phospholipase C signaling via the parathyroid hormone (PTH)/PTH-related peptide receptor is essential for normal bone responses to PTH.PTH1-34 alleviates radiotherapy-induced local bone loss by improving osteoblast and osteocyte survival.The immune system and bone.Decreased oxidative stress and greater bone anabolism in the aged, when compared to the young, murine skeleton with parathyroid hormone administration.A review of osteocyte function and the emerging importance of sclerostinIntermittent PTHrP(1-34) exposure augments chondrogenesis and reduces hypertrophy of mesenchymal stromal cells.Novel actions of bisphosphonates in bone: preservation of osteoblast and osteocyte viability.Consequences of daily administered parathyroid hormone on myeloma growth, bone disease, and molecular profiling of whole myelomatous bone.The Role of RUNX2 in Osteosarcoma Oncogenesis.A bisphosphonate that does not affect osteoclasts prevents osteoblast and osteocyte apoptosis and the loss of bone strength induced by glucocorticoids in mice.PTH1-34 blocks radiation-induced osteoblast apoptosis by enhancing DNA repair through canonical Wnt pathwaySix months of disuse during hibernation does not increase intracortical porosity or decrease cortical bone geometry, strength, or mineralization in black bear (Ursus americanus) femurs.Modifications in bone matrix of estrogen-deficient rats treated with intermittent PTHThe sclerostin-independent bone anabolic activity of intermittent PTH treatment is mediated by T-cell-produced Wnt10bPrevention of glucocorticoid induced-apoptosis of osteoblasts and osteocytes by protecting against endoplasmic reticulum (ER) stress in vitro and in vivo in female mice.Anabolic and catabolic regimens of human parathyroid hormone 1-34 elicit bone- and envelope-specific attenuation of skeletal effects in Sost-deficient mice.Parathyroid hormone (PTH)-induced bone gain is blunted in SOST overexpressing and deficient miceOsteoprotegerin prevents glucocorticoid-induced osteocyte apoptosis in mice
P2860
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P2860
Proteasomal degradation of Runx2 shortens parathyroid hormone-induced anti-apoptotic signaling in osteoblasts. A putative explanation for why intermittent administration is needed for bone anabolism.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh-hant
name
Proteasomal degradation of Run ...... is needed for bone anabolism.
@en
Proteasomal degradation of Run ...... is needed for bone anabolism.
@nl
type
label
Proteasomal degradation of Run ...... is needed for bone anabolism.
@en
Proteasomal degradation of Run ...... is needed for bone anabolism.
@nl
prefLabel
Proteasomal degradation of Run ...... is needed for bone anabolism.
@en
Proteasomal degradation of Run ...... is needed for bone anabolism.
@nl
P2093
P2860
P356
P1476
Proteasomal degradation of Run ...... is needed for bone anabolism.
@en
P2093
A Afshan Ali
Charles A O'Brien
Igor Gubrij
Lilian I Plotkin
Paula K Roberson
Robert L Jilka
Robert S Weinstein
Stavros C Manolagas
P2860
P304
50259-50272
P356
10.1074/JBC.M307444200
P407
P577
2003-10-01T00:00:00Z