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The current work provides experimental support for a hypothesis that strain-specific patterns of PrPSc sialoglycoforms formed as a result of selective recruitment dictate strain-specific disease phenotypes. This work suggests a causative relationship between a strain-specific structure, posttranslational modifications and disease phenotype.Patients with common variable immunodeficiency associated with autoimmune cytopenias (CVID+AIC) generate few isotype-switched B cells with severely decreased frequencies of somatic hypermutations (SHM)