PERK-mediated translational control is required for collagen secretion in chondrocytes
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M. Miyake | S. Oyadomari | J. Hirose | H. Mizuta | M. Morimoto | Miho Oyadomari | S. Taniuchi | Ryosuke Sato | S. Hisanaga
[1] C. Jorcyk,et al. Endoplasmic Reticulum Stress and Unfolded Protein Response in Cartilage Pathophysiology; Contributing Factors to Apoptosis and Osteoarthritis , 2017, International journal of molecular sciences.
[2] Hao Huang,et al. The Roles of Endoplasmic Reticulum Stress in the Pathophysiological Development of Cartilage and Chondrocytes. , 2017, Current pharmaceutical design.
[3] Masato Miyake,et al. Integrated stress response of vertebrates is regulated by four eIF2α kinases , 2016, Scientific Reports.
[4] J. Pelletier,et al. The unfolded protein response genes in human osteoarthritic chondrocytes: PERK emerges as a potential therapeutic target , 2016, Arthritis Research & Therapy.
[5] K. Horiuchi,et al. The unfolded protein response in skeletal development and homeostasis , 2016, Cellular and Molecular Life Sciences.
[6] D. Ron,et al. Skeletal muscle–specific eukaryotic translation initiation factor 2α phosphorylation controls amino acid metabolism and fibroblast growth factor 21–mediated non–cell-autonomous energy metabolism , 2015, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[7] Rosa Bartolomeo,et al. FGF signalling regulates bone growth through autophagy , 2015, Nature.
[8] L. Glimcher,et al. XBP1-Independent UPR Pathways Suppress C/EBP-β Mediated Chondrocyte Differentiation in ER-Stress Related Skeletal Disease , 2015, PLoS genetics.
[9] L. Glimcher,et al. Cartilage-specific ablation of XBP1 signaling in mouse results in a chondrodysplasia characterized by reduced chondrocyte proliferation and delayed cartilage maturation and mineralization. , 2015, Osteoarthritis and cartilage.
[10] W. Ladiges,et al. Deletion of P58IPK, the Cellular Inhibitor of the Protein Kinases PKR and PERK, Causes Bone Changes and Joint Degeneration in Mice , 2014, Front. Endocrinol..
[11] R. Kaufman,et al. Endoplasmic reticulum stress and oxidative stress in cell fate decision and human disease. , 2014, Antioxidants & redox signaling.
[12] S. Oyadomari,et al. Endoplasmic reticulum stress-induced apoptosis contributes to articular cartilage degeneration via C/EBP homologous protein. , 2014, Osteoarthritis and cartilage.
[13] Neville E. Sanjana,et al. Improved vectors and genome-wide libraries for CRISPR screening , 2014, Nature Methods.
[14] K. Chayama,et al. Multiplex genome engineering in human cells using all-in-one CRISPR/Cas9 vector system , 2014, Scientific Reports.
[15] Di Huang,et al. Endoplasmic Reticulum Stress-Unfolding Protein Response-Apoptosis Cascade Causes Chondrodysplasia in a col2a1 p.Gly1170Ser Mutated Mouse Model , 2014, PloS one.
[16] Fangzhou Song,et al. IRE1α dissociates with BiP and inhibits ER stress-mediated apoptosis in cartilage development. , 2013, Cellular signalling.
[17] P. Reynolds,et al. Osteoarthritis in temporomandibular joint of Col2a1 mutant mice. , 2013, Archives of oral biology.
[18] J. Hirose,et al. Intracellular accumulation of advanced glycation end products induces apoptosis via endoplasmic reticulum stress in chondrocytes , 2013, The FEBS journal.
[19] L. Shewchuk,et al. Discovery of 7-methyl-5-(1-{[3-(trifluoromethyl)phenyl]acetyl}-2,3-dihydro-1H-indol-5-yl)-7H-pyrrolo[2,3-d]pyrimidin-4-amine (GSK2606414), a potent and selective first-in-class inhibitor of protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK). , 2012, Journal of medicinal chemistry.
[20] P. Walter,et al. The Unfolded Protein Response: From Stress Pathway to Homeostatic Regulation , 2011, Science.
[21] Y. Oike,et al. Enhanced apoptotic and reduced protective response in chondrocytes following endoplasmic reticulum stress in osteoarthritic cartilage , 2011, International journal of experimental pathology.
[22] A. Saito,et al. Physiological unfolded protein response regulated by OASIS family members, transmembrane bZIP transcription factors , 2011, IUBMB life.
[23] A. Saito,et al. Endoplasmic Reticulum Stress Response Mediated by the PERK-eIF2α-ATF4 Pathway Is Involved in Osteoblast Differentiation Induced by BMP2* , 2010, The Journal of Biological Chemistry.
[24] H. Moss,et al. Atf4 regulates chondrocyte proliferation and differentiation during endochondral ossification by activating Ihh transcription , 2009, Development.
[25] R. Boot-Handford,et al. The unfolded protein response and its relevance to connective tissue diseases , 2009, Cell and Tissue Research.
[26] Shinichi Kondo,et al. Regulation of endoplasmic reticulum stress response by a BBF2H7-mediated Sec23a pathway is essential for chondrogenesis , 2009, Nature Cell Biology.
[27] R. Boot-Handford,et al. Genetic diseases of connective tissues: cellular and extracellular effects of ECM mutations , 2009, Nature Reviews Genetics.
[28] Barbara C. McGrath,et al. PERK is essential for neonatal skeletal development to regulate osteoblast proliferation and differentiation , 2008, Journal of cellular physiology.
[29] Hiderou Yoshida,et al. Transcriptional induction of mammalian ER quality control proteins is mediated by single or combined action of ATF6alpha and XBP1. , 2007, Developmental cell.
[30] Barbara C. McGrath,et al. PERK EIF2AK3 control of pancreatic beta cell differentiation and proliferation is required for postnatal glucose homeostasis. , 2006, Cell metabolism.
[31] M. Paulsson,et al. Matrilin-3 mutations that cause chondrodysplasias interfere with protein trafficking while a mutation associated with hand osteoarthritis does not , 2005, Journal of Medical Genetics.
[32] W. Horton,et al. Multiple Signals Induce Endoplasmic Reticulum Stress in Both Primary and Immortalized Chondrocytes Resulting in Loss of Differentiation, Impaired Cell Growth, and Apoptosis* , 2005, Journal of Biological Chemistry.
[33] P. Beighton,et al. A mutation in the variable repeat region of the aggrecan gene (AGC1) causes a form of spondyloepiphyseal dysplasia associated with severe, premature osteoarthritis. , 2005, American journal of human genetics.
[34] D. Ron,et al. CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum. , 2004, Genes & development.
[35] R. Herken,et al. Expression of collagen type I and type II in consecutive stages of human osteoarthritis , 2004, Histochemistry and Cell Biology.
[36] T. Aigner,et al. Collagens--structure, function, and biosynthesis. , 2003, Advanced drug delivery reviews.
[37] D. Meredith,et al. Functional characterisation of glucose transport in bovine articular chondrocytes , 2003, Pflügers Archiv.
[38] R. Paules,et al. An integrated stress response regulates amino acid metabolism and resistance to oxidative stress. , 2003, Molecular cell.
[39] 橋本 祐介. Mutation (D472Y) in the type 3 repeat domain of cartilage oligomeric matrix protein affects its early vesicle trafficking in endoplasmic reticulum and induces apoptosis , 2003 .
[40] Peichuan Zhang,et al. The PERK Eukaryotic Initiation Factor 2α Kinase Is Required for the Development of the Skeletal System, Postnatal Growth, and the Function and Viability of the Pancreas , 2002, Molecular and Cellular Biology.
[41] A. Luini,et al. Small cargo proteins and large aggregates can traverse the Golgi by a common mechanism without leaving the lumen of cisternae , 2001, The Journal of cell biology.
[42] D. Ron,et al. Diabetes mellitus and exocrine pancreatic dysfunction in perk-/- mice reveals a role for translational control in secretory cell survival. , 2001, Molecular cell.
[43] A. Aszódi,et al. Distribution of the collagen-binding integrin alpha10beta1 during mouse development. , 2001, Cell and tissue research.
[44] M. Schapira,et al. Regulated translation initiation controls stress-induced gene expression in mammalian cells. , 2000, Molecular cell.
[45] K. Mori. Tripartite Management of Unfolded Proteins in the Endoplasmic Reticulum , 2000, Cell.
[46] D. Ron,et al. Perk is essential for translational regulation and cell survival during the unfolded protein response. , 2000, Molecular cell.
[47] A. Mikos,et al. Review: tissue engineering for regeneration of articular cartilage. , 2000, Biomaterials.
[48] Antonios G. Mikos,et al. TISSUE ENGINEERING FOR REGENERATION OF ARTICULAR CARTILAGE , 2000 .
[49] T. Atsumi,et al. Chondrogenic differentiation of clonal mouse embryonic cell line ATDC5 in vitro: differentiation-dependent gene expression of parathyroid hormone (PTH)/PTH-related peptide receptor , 1996, The Journal of cell biology.
[50] Y. Ikawa,et al. A chondrogenic cell line derived from a differentiating culture of AT805 teratocarcinoma cells. , 1990, Cell differentiation and development : the official journal of the International Society of Developmental Biologists.
[51] I. Silver. Measurement of pH and ionic composition of pericellular sites. , 1975, Philosophical transactions of the Royal Society of London. Series B, Biological sciences.
[52] C. Brighton,et al. Oxygen tension in zones of the epiphyseal plate, the metaphysis and diaphysis. An in vitro and in vivo study in rats and rabbits. , 1971, The Journal of bone and joint surgery. American volume.