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Blood, Vol. 113, Issue 16, 3706-3715, April 16, 2009
Analysis of somatic hypermutation in X-linked hyper-IgM syndrome shows specific deficiencies in mutational targeting
Blood Longo et al.
113: 3706
Supplemental materials for: Longo et al
Files in this Data Supplement:
- Table S1. Mutation pattern of nonproductive light chain rearrangements in X-HIgM (%) (PDF, 14.7 KB)
- Table S2. Mutation frequency of VH rearrangements of X-HIgM patients (PDF, 20.5 KB)
- Table S3. Mutation frequency of VH rearrangements of X-HIgM patients (PDF, 15 KB)
- Table S4. Initial gene list for microarray analysis (PDF, 72.2 KB)
- Figure S1. The expression of genes involved in SHM and/or DNA repair are increased in GC B cells (JPG, 757 KB)
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The dendogram displays the relative gene expression in tonsil naïve (CD38−IgD+), activated naïve (CD38++IgD+), GC dark zone (CD38++IgD−) and PB naïve (CD19+IgD+) and memory (CD19+IgD−) cells. Hierarchical clustering identifies the genes by gene expression profiling that are differentially upregulated (red) or downregulated (green) in the various normal B cell subpopulations. Gene expression is displayed over a 4-fold range is analyzed by using MAS5 normalization.
- Figure S2. A single node from the Fig. S1 dendogram reveals a tight cluster of genes upregulated in GC B cells (JPG, 391 KB)
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- Figure S3. The expression of genes involved in SHM and/or DNA repair are increased in GC B cells (JPG, 361 KB)
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The dendogram displays a reanalysis using RMA normalization of the same microarray data presented in Fig. S1. Gene expression is displayed over a 4-fold range.
- Figure S4. The expression of genes involved in SHM and/or DNA repair is increased in GC B cells (JPG, 252 KB)
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A second set of tonsillar populations from three additional donors was analyzed using RMA normalization to determine the expression of genes involved in SHM.
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