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  • 1
    Electronic Resource
    Electronic Resource
    Peptide mapping and characterisation of glycation patterns of the glima 38 antigen recognised by autoantibodies in Type I diabetic patients (2000)
    Springer
    Diabetologia 43 (2000), S. 598-608 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Type I diabetes ; immunology ; autoantibodies ; target autoantigen ; 38 000 Mr autoantigen ; glima 38 ; proteolytic cleavage ; peptide mapping ; lectin binding ; deglycation.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Glima 38 is an N-glycated neuroendocrine membrane protein of Mr 38 000, which is recognised by autoantibodies in approximately 20 % of patients with Type I (insulin-dependent) diabetes mellitus. The aim of this study was to characterise the carbohydrate moiety and generate peptide maps of glima 38. Methods. Sera of high immunoreactivity to glima 38 were used to isolate 35-S methionine-labelled protein from βTC-3 cells and a neuronal cell line GT1.7. Tunicamycin was used to inhibit N-glycation of glima 38 and define the core protein. The carbohydrate moiety was characterised for tunicamycin sensitivity, lectin binding and susceptibility to different endoglycosidases. The protein moiety was subjected to digestion by proteases to define peptide maps. Results. The autoreactive epitopes in glima 38 recognised by Type I diabetic sera are conformational and independent of the carbohydrate moiety. Inhibition of N-glycation of glima 38 in vivo, shows a protein core of Mr 22 000 in both pancreatic β-(βTC3) and neuronal (GT1.7) cell lines. The carbohydrate moieties in the two cell types are distinct but contain a similar amount of terminal sialic acid residues and at least five oligosaccharide chains Glima 38 binds Triticum vulgare and Ricinus communis I lectins. Endoproteinase treatment of the Mr 22 000 core protein results in peptides of Mr 4500 and Mr 20 000 with Lys-C, and peptides of Mr 4 000 and Mr 11 000–12 000 with Glu-C/V8 and Asp-N proteases. Conclusion/interpretation. The biochemical properties of glima 38 define it as a new autoantigen in Type I diabetes and provide a basis for its purification. [Diabetologia (2000) 43: 598–608]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051349
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  • 2
    Electronic Resource
    Electronic Resource
    Zytogenetik und molekulare Untersuchungen sichern die histopathologischen Diagnosen von chronischen myelopro-liferativen Erkrankungen ab (1995)
    Springer
    Der Pathologe 16 (1995), S. 41-45 
    Details
    ISSN: 1432-1963
    Keywords: Schlüsselwörter Chronische myeloproliferative Erkrankungen ; Philadelphia-Translokation ; Zytogenetik ; Molekulargenetik ; Fluoreszenz-in-situ-Hybridisierung ; Histopathologie ; Key words Chronic myeloproliferative disorders ; Philadelphia-translocation ; Cytogenetics ; Molecular genetics ; Fluorescence in situ hybridization ; Histopathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The histopathological classification of chronic myeloproliferative disorders can be supported by applying cytogenetics and molecular genetics to the analysis of bone marrow or blood cells, as demonstrated in 253 cases evaluated. The Philadelphia translocation (9;22) is the most important genetic parameter, being specific for chronic myeloid leukemia. Conventional methods for the detection of the t(9;22) are karyotyping and Southern blot analysis of the bcr gene. The newly established technique of fluorescence in situ hybridization (FISH) allows visualization of bcr-abl fusion even in non dividing cells. Molecular cytogenetics for t(9;22) yield results that are rapid and reliable as well as easily quantifiable.
    Notes: Zusammenfassung Zytogenetische und molekulargenetische Untersuchungen von Knochenmark- oder Blutzellen sind für die histopathologische Klassifikation der chronischen myeloproliferativen Erkrankungen hilfreich, was durch die simultane Auswertung von 253 Fällen gezeigt wird. Insbesondere die Analyse der Philadelphia-Translokation (9;22) ist dabei für die Bestätigung oder den Ausschluß einer chronischen myeloischen Leukämie wichtig. Für den Nachweis der t(9;22) stehen die konventionelle Karyotypisierung mit Bestimmung des Philadelphia-Chromosoms und das Southernblotverfahren zur Analyse einer Umlagerung des bcr-Gens zur Verfügung. Durch die neuere Methode der Fluoreszenz-in-situ-Hybridisierung (FISH) kann auch eine bcr-abl-Fusion an Interphasekernen dargestellt werden. Diese molekulare Zytogenetik ist ein rasches und zuverlässiges Verfahren zum Nachweis der Philadelphia-Translokation, das zudem leicht quantifizierbare Ergebnisse liefert.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002920050074
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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