An inducible cartilage oligomeric matrix protein mouse model recapitulates human pseudoachondroplasia phenotype
about
Mechanisms and models of endoplasmic reticulum stress in chondrodysplasiaD469del-COMP retention in chondrocytes stimulates caspase-independent necroptosisAntioxidant and anti-inflammatory agents mitigate pathology in a mouse model of pseudoachondroplasiaA novel COMP mutation in a pseudoachondroplasia family of Chinese origin.The ECM-cell interaction of cartilage extracellular matrix on chondrocytes.Chondrocyte-specific pathology during skeletal growth and therapeutics in a murine model of pseudoachondroplasiaPseudoachondroplasia/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 pseudoachondroplasiaIncreased classical endoplasmic reticulum stress is sufficient to reduce chondrocyte proliferation rate in the growth plate and decrease bone growth.Revisiting the matricellular concept.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).A novel form of chondrocyte stress is triggered by a COMP mutation causing pseudoachondroplasia.A novel transgenic mouse model of growth plate dysplasia reveals that decreased chondrocyte proliferation due to chronic ER stress is a key factor in reduced bone growth.Extracellular matrix and developing growth plate.Novel therapeutic interventions for pseudoachondroplasia.Chop (Ddit3) is essential for D469del-COMP retention and cell death in chondrocytes in an inducible transgenic mouse model of pseudoachondroplasia.Lubricin binds cartilage proteins, cartilage oligomeric matrix protein, fibronectin and collagen II at the cartilage surfaceMutant cartilage oligomeric matrix cartilage (COMP) compromises bone integrity, joint function and the balance between adipogenesis and osteogenesis.Antisense Reduction of Mutant COMP Reduces Growth Plate Chondrocyte Pathology.Cartilage oligomeric matrix protein: COMPopathies and beyond.Cell-nonautonomous local and systemic responses to cell arrest enable long-bone catch-up growth in developing mice.
P2860
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P2860
An inducible cartilage oligomeric matrix protein mouse model recapitulates human pseudoachondroplasia phenotype
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
2009年论文
@zh
2009年论文
@zh-cn
name
An inducible cartilage oligome ...... pseudoachondroplasia phenotype
@en
type
label
An inducible cartilage oligome ...... pseudoachondroplasia phenotype
@en
prefLabel
An inducible cartilage oligome ...... pseudoachondroplasia phenotype
@en
P2093
P2860
P1476
An inducible cartilage oligome ...... pseudoachondroplasia phenotype
@en
P2093
Alka C Veerisetty
Brian J Poindexter
Huiqiu R Wang
Jacqueline T Hecht
Joseph L Alcorn
Karen L Posey
Pieman Liu
Roger Bick
P2860
P304
P356
10.2353/AJPATH.2009.090184
P407
P577
2009-09-17T00:00:00Z