Chop (Ddit3) is essential for D469del-COMP retention and cell death in chondrocytes in an inducible transgenic mouse model of pseudoachondroplasia. - Wikidata - awgldk - TriplyDB

Chop (Ddit3) is essential for D469del-COMP retention and cell death in chondrocytes in an inducible transgenic mouse model of pseudoachondroplasia.

Chop (Ddit3) is essential for D469del-COMP retention and cell death in chondrocytes in an inducible transgenic mouse model of pseudoachondroplasia.

http://www.wikidata.org/entity/Q41905281

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Mechanisms and models of endoplasmic reticulum stress in chondrodysplasia Antioxidant and anti-inflammatory agents mitigate pathology in a mouse model of pseudoachondroplasia Chondrocyte-specific pathology during skeletal growth and therapeutics in a murine model of pseudoachondroplasia Utilization of the cellular stress response to sensitize cancer cells to TRAIL-mediated apoptosis.Pseudoachondroplasia/COMP - translating from the bench to the bedside.Abnormal chondrocyte apoptosis in the cartilage growth plate is influenced by genetic background and deletion of CHOP in a targeted mouse model of pseudoachondroplasia The utility of mouse models to provide information regarding the pathomolecular mechanisms in human genetic skeletal diseases: The emerging role of endoplasmic reticulum stress (Review).New therapeutic targets in rare genetic skeletal diseases.Extracellular matrix and developing growth plate.Novel therapeutic interventions for pseudoachondroplasia.Mutant cartilage oligomeric matrix cartilage (COMP) compromises bone integrity, joint function and the balance between adipogenesis and osteogenesis.Skeletal Characterization of the Fgfr3 Mouse Model of Achondroplasia Using Micro-CT and MRI Volumetric Imaging.Antisense Reduction of Mutant COMP Reduces Growth Plate Chondrocyte Pathology.Inhibiting the integrated stress response pathway prevents aberrant chondrocyte differentiation thereby alleviating chondrodysplasia

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P2860

Chop (Ddit3) is essential for D469del-COMP retention and cell death in chondrocytes in an inducible transgenic mouse model of pseudoachondroplasia.

http://www.wikidata.org/entity/Q41905281

description

2011 nî lūn-bûn

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J.AJPATH.2011.10.035

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The American Journal of Pathology

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Chop (Ddit3) is essential for ...... model of pseudoachondroplasia.

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Alka C Veerisetty

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Francoise Coustry

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Jacqueline T Hecht

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Joseph L Alcorn

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Karen L Posey

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Peiman Liu

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P2860

Cartilage oligomeric matrix protein is a calcium-binding protein, and a mutation in its type 3 repeats causes conformational changes

Mutations in cartilage oligomeric matrix protein causing pseudoachondroplasia and multiple epiphyseal dysplasia affect binding of calcium and collagen I, II, and IX

AIF promotes chromatinolysis and caspase-independent programmed necrosis by interacting with histone H2AX

Cartilage oligomeric matrix protein/thrombospondin 5 supports chondrocyte attachment through interaction with integrins

Interaction of cartilage oligomeric matrix protein/thrombospondin 5 with aggrecan

Interactions between the cartilage oligomeric matrix protein and matrilins. Implications for matrix assembly and the pathogenesis of chondrodysplasias

Pseudoachondroplasia and multiple epiphyseal dysplasia due to mutations in the cartilage oligomeric matrix protein gene

Cartilage oligomeric matrix protein-deficient mice have normal skeletal development.

Diverse mutations in the gene for cartilage oligomeric matrix protein in the pseudoachondroplasia-multiple epiphyseal dysplasia disease spectrum

Reduced cell proliferation and increased apoptosis are significant pathological mechanisms in a murine model of mild pseudoachondroplasia resulting from a mutation in the C-terminal domain of COMP

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