Cartilage Oligomeric Matrix Protein-Deficient Mice Have Normal Skeletal Development
نویسندگان
چکیده
منابع مشابه
Cartilage oligomeric matrix protein-deficient mice have normal skeletal development.
Cartilage oligomeric matrix protein (COMP) belongs to the thrombospondin family and is a homopentamer primarily expressed in cartilage. Mutations in the COMP gene result in the autosomal dominant chondrodysplasias pseudoachondroplasia (PSACH) and some types of multiple epiphyseal dysplasia (MED), which are characterized by mild to severe short-limb dwarfism and early-onset osteoarthritis. We ha...
متن کاملCartilage Oligomeric Matrix Protein (COMP): A Biomarker of Arthritis
Arthritis is a chronic disease with a significant impact on the population. It damages the cartilage, synovium, and bone of the joints causing pain, impairment, and disability in patients. Current methods for diagnosis of and monitoring the disease are only able to detect clinical manifestations of arthritis late in the process. However, with the recent onset of successful treatments for rheuma...
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INTRODUCTION Complexes between cartilage oligomeric matrix protein (COMP) and the complement activation product C3b have been found in the circulation of patients with rheumatoid arthritis and systemic lupus erythematosus. In systemic sclerosis (SSc) COMP expression in the skin is upregulated both in lesional and non-lesional skin, which is also reflected in an increased amount of circulating C...
متن کاملADAMTS-12 associates with and degrades cartilage oligomeric matrix protein.
Loss of articular cartilage because of extracellular matrix breakdown is the hallmark of arthritis. Degradative fragments of cartilage oligomeric matrix protein (COMP), a prominent noncollagenous matrix component in articular cartilage, have been observed in the cartilage, synovial fluid, and serum of arthritis patients. The molecular mechanism of COMP degradation and the enzyme(s) responsible ...
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ژورنال
عنوان ژورنال: Molecular and Cellular Biology
سال: 2002
ISSN: 0270-7306,1098-5549
DOI: 10.1128/mcb.22.12.4366-4371.2002