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1 en play a crucial role in the development of pseudoachondroplasia.
2 ts and COOH-terminal globular region lead to pseudoachondroplasia.
3 e critical cellular and clinical features of pseudoachondroplasia.
5 indings suggest that the secretory defect in pseudoachondroplasia and multiple epiphyseal dysplasia i
6 sociated with two human skeletal dysplasias, pseudoachondroplasia and multiple epiphyseal dysplasia,
7 xtracellular matrix, have been identified in pseudoachondroplasia and multiple epiphyseal dysplasia,
8 eoarthritis (OA) are phenotypes of inherited pseudoachondroplasia and multiple epiphyseal dysplasia.
9 gene have been linked to the development of pseudoachondroplasia and multiple epiphyseal dysplasia.
10 gene to the 4, 6 or 7mers in the etiology of pseudoachondroplasia and multiple epiphyseal dysplasia.
11 tein (COMP) lead to two skeletal dysplasias, pseudoachondroplasia and multiple epiphyseal dysplasia.
13 SP5 mutations cause two skeletal dysplasias, pseudoachondroplasia and multiple epiphyseal dysplasia;
14 COMP) have been linked to the development of pseudoachondroplasia and multiple epiphyseal dysplasia;
15 hanisms underlying D469del-COMP pathology in pseudoachondroplasia and suggest that oxidative stress a
16 signated MUT3 that accounts for 30% of human pseudoachondroplasia cases, to determine if the mutation
19 OMP and the most common mutant form found in pseudoachondroplasia, MUT3, using a mammalian expression
21 rotein (COMP) cause two skeletal dysplasias, pseudoachondroplasia (PSACH) and multiple epiphyseal dys
25 tions in COMP cause two skeletal dysplasias, pseudoachondroplasia (PSACH) and multiple epiphyseal dys
27 ve identified a novel missense mutation in a pseudoachondroplasia (PSACH) patient in one of the type
32 COMP previously identified in a patient with pseudoachondroplasia resulted in abnormal sequestration
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