1999
DOI: 10.2169/internalmedicine.38.523
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Autoantibodies in Connective Tissue Diseases. Clinical Significance and Analysis of Target Autoantigens.

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Cited by 25 publications
(15 citation statements)
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References 86 publications
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“…It is a member of group D SOX-proteins [6] and is ubiquitously expressed in human tissues with highest expressions in pancreas, placenta and kidney [5]. Because autoantibodies against proteins associated with DNA replication and transcription are well known to be present in patients with rheumatic diseases [7], we decided that sera from those patients could serve as optimal controls to determine the specificity of SOX-13Ab. We observed SOX-13Ab in 4.0±11.4 % of those patients which clearly shows their non-diabetes specific nature.…”
Section: Discussionmentioning
confidence: 99%
“…It is a member of group D SOX-proteins [6] and is ubiquitously expressed in human tissues with highest expressions in pancreas, placenta and kidney [5]. Because autoantibodies against proteins associated with DNA replication and transcription are well known to be present in patients with rheumatic diseases [7], we decided that sera from those patients could serve as optimal controls to determine the specificity of SOX-13Ab. We observed SOX-13Ab in 4.0±11.4 % of those patients which clearly shows their non-diabetes specific nature.…”
Section: Discussionmentioning
confidence: 99%
“…These include antibodies reactive with nuclear antigens, membrane proteins, cytoplasmic proteins, and secreted products. Many autoantigens are intracellular enzymes and regulatory factors required for cellular function, especially gene replication, transcription, RNA processing, and protein synthesis 121. Interestingly, these molecules have little in common in terms of structure, subcellular localization, or biological function.…”
Section: Etiology Of Sjogren Syndrome and Sjogren Syndrome-like DImentioning
confidence: 99%
“…Other associated autoantibodies include anti-DNA protein kinase complex antibodies and anti-U2 RNP antibodies, rare antibodies that usually coexist with anti-U1 RNP. 8 The aetiology and pathogenic mechanisms of PM-Scl overlap remain unknown. A strong association of anti-PM-Scl antibody with HLA DR3 and an increased frequency of HLA DQA*0501 suggest a genetic influence.…”
Section: Scleroderma-polymyositis Overlap Syndrome (Pm-scl)mentioning
confidence: 99%