Multiple signals induce endoplasmic reticulum stress in both primary and immortalized chondrocytes resulting in loss of differentiation, impaired cell growth, and apoptosis.
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SEPS1 protects RAW264.7 cells from pharmacological ER stress agent-induced apoptosisTemperature regulates limb length in homeotherms by directly modulating cartilage growthChondrocyte Apoptosis in the Pathogenesis of OsteoarthritisEndoplasmic reticulum stress in chondrodysplasias caused by mutations in collagen types II and XWFS1-deficiency increases endoplasmic reticulum stress, impairs cell cycle progression and triggers the apoptotic pathway specifically in pancreatic beta-cellsInduction of unfolded protein response during neuronal induction of rat bone marrow stromal cells and mouse embryonic stem cellsGene expression profile of the cartilage tissue spontaneously regenerated in vivo by using a novel double-network gel: comparisons with the normal articular cartilage.Both endoplasmic reticulum and mitochondria are involved in disc cell apoptosis and intervertebral disc degeneration in rats.Periovulatory expression of hyaluronan and proteoglycan link protein 1 (Hapln1) in the rat ovary: hormonal regulation and potential function.Unfolded protein response is required for the definitive endodermal specification of mouse embryonic stem cells via Smad2 and β-catenin signaling.Deletion of P58(IPK), the Cellular Inhibitor of the Protein Kinases PKR and PERK, Causes Bone Changes and Joint Degeneration in MiceSCCA1/SERPINB3 promotes oncogenesis and epithelial-mesenchymal transition via the unfolded protein response and IL6 signalingCOL10A1 nonsense and frame-shift mutations have a gain-of-function effect on the growth plate in human and mouse metaphyseal chondrodysplasia type Schmid.Oxidative stress in secondary osteoarthritis: from cartilage destruction to clinical presentation?Epithelial Xbp1 is required for cellular proliferation and differentiation during mammary gland developmentCCAAT/Enhancer-binding protein homologous protein (CHOP) decreases bone formation and causes osteopenia.Endoplasmic reticulum stress induces the expression of COX-2 through activation of eIF2α, p38-MAPK and NF-κB in advanced glycation end products stimulated human chondrocytes.Differential regulation of CHOP-10/GADD153 gene expression by MAPK signaling in pancreatic beta-cells.Monosodium Urate Crystal-Induced Chondrocyte Death via Autophagic Process.Thyroglobulin From Molecular and Cellular Biology to Clinical Endocrinology.Interleukin-1β induced Stress Granules Sequester COX-2 mRNA and Regulates its Stability and Translation in Human OA ChondrocytesCCN2/CTGF is required for matrix organization and to protect growth plate chondrocytes from cellular stress.Increased expression of the Akt/PKB inhibitor TRB3 in osteoarthritic chondrocytes inhibits insulin-like growth factor 1-mediated cell survival and proteoglycan synthesisAging and osteoarthritis: the role of chondrocyte senescence and aging changes in the cartilage matrix.Cartilage homeostasis in health and rheumatic diseases.Advanced osteoarthritis in humans is associated with altered collagen VI expression and upregulation of ER-stress markers Grp78 and bag-1.Epithelial-mesenchymal transition induces endoplasmic-reticulum-stress response in human colorectal tumor cells.The role of X-box binding protein-1 in tumorigenicity.Physiology and pathophysiology of nitrosative and oxidative stress in osteoarthritic joint destruction.Melatonin-mediated Bim up-regulation and cyclooxygenase-2 (COX-2) down-regulation enhances tunicamycin-induced apoptosis in MDA-MB-231 cells.Apoptosis signaling pathways in osteoarthritis and possible protective role of melatonin.Increased hexosamine biosynthetic pathway flux dedifferentiates INS-1E cells and murine islets by an extracellular signal-regulated kinase (ERK)1/2-mediated signal transmission pathway.The presence of extracellular matrix alters the chondrocyte response to endoplasmic reticulum stress.Involvement of p38 MAPK in regulation of MMP13 mRNA in chondrocytes in response to surviving stress to endoplasmic reticulumEndoplasmic reticulum stress mediates nitric oxide-induced chondrocyte apoptosis.Mouse pancreatic islets are resistant to indoleamine 2,3 dioxygenase-induced general control nonderepressible-2 kinase stress pathway and maintain normal viability and function.Inhibitory effect ofquercetinon titaniumparticle-inducedendoplasmic reticulum stress (ERS)-related apoptosisandin vivoosteolysis.The unfolded protein response genes in human osteoarthritic chondrocytes: PERK emerges as a potential therapeutic target.Calcium channel blocker verapamil enhances endoplasmic reticulum stress and cell death induced by proteasome inhibition in myeloma cells.Endoplasmic reticulum stress inhibits collagen synthesis independent of collagen-modifying enzymes in different chondrocyte populations and dermal fibroblasts.
P2860
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P2860
Multiple signals induce endoplasmic reticulum stress in both primary and immortalized chondrocytes resulting in loss of differentiation, impaired cell growth, and apoptosis.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
2005年论文
@zh
2005年论文
@zh-cn
name
Multiple signals induce endopl ...... ed cell growth, and apoptosis.
@en
type
label
Multiple signals induce endopl ...... ed cell growth, and apoptosis.
@en
prefLabel
Multiple signals induce endopl ...... ed cell growth, and apoptosis.
@en
P2093
P2860
P356
P1476
Multiple signals induce endopl ...... ed cell growth, and apoptosis.
@en
P2093
Denise McBurney
Sara G Carlson
Walter E Horton
P2860
P304
31156-31165
P356
10.1074/JBC.M501069200
P407
P577
2005-07-05T00:00:00Z