Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A quantitative assay for human adrenal autoantibodies has been developed to aid in the detection and isolation of human adrenal antigens. To define the subcellular location(s) of the antigen(s) capable of binding with these antibodies, we have quantitated both antibody binding to various adrenal subcellular fractions and the adrenal autoantibody binding inhibition caused by each subcellular fraction. To further define the subcellular location of the autoantibody binding, each fraction was assayed for organelle-specific marker enzyme activities. Enzyme activities were correlated to adrenal autoantibody binding to each fraction by linear regression. Of the materials tested, both antibody binding and inhibition of binding were most highly correlated with adrenal subcellular fractions enriched with cytochrome-c reductase and 5'-nucleotidase (r = 0.98; P less than 0.05). Thus, our data support the localization of adrenal autoantigen(s) in the microsomes, plasma membrane, or both.
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PMID:Adrenal autoantibodies bind to adrenal subcellular fractions enriched in cytochrome-c reductase and 5'-nucleotidase. 229 42

Sporadic inclusion body myositis (sIBM) is a chronically progressing inflammatory myopathy most common in the aged population. Asymmetric muscle weakness and waste of the quadriceps and finger and wrist flexor muscles are characteristic features of sIBM. Histological findings suggest the involvement of a crosstalk of inflammatory and myodegenerative mechanisms in the pathogenesis of sIBM. As an etiological clue to sIBM, identification of autoantibodies against cytosolic 5'-nucleotidase 1A (NT5C1A) in plasma and serum samples from patients with sIBM has been attracting attention. So far, various methods with clinical utility have been established to detect anti-NT5C1A autoantibodies. The measurement of the autoantibodies is useful for the diagnosis of sIBM due to its high specificity. Moreover, the autoantibodies may have pathogenic roles in the development of the disease by stimulating catabolic conditions and/or causing dysfunction in protein degradation of skeletal muscles; however, the molecular mechanisms by which the sarcoplasmic autoantigen is recognized and involved in the degeneration of myofibers remain unclear.
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PMID:[Sporadic Inclusion Body Myositis and Autoantibodies]. 2963 92