promotes B-cell viability and gene expression in a B cell culture Zfp521 cyclin D1 system Salma Al Dallal, Kathryn Wolton, Kathryn E. Hentges* Faculty of Life Sciences, University of Manchester, Manchester UK M13 9PT *Author for correspondence: Kathryn E. Hentges Michael Smith Building Oxford Road Manchester M13 9PT UK Tel: +44 (0)161 275 1490 Email: Abstract Leukemia arises due to the dysregulated proliferation of hematopoietic progenitor cells. Errors in the multi-step commitment process result in excessive numbers of immature lymphocytes, causing malignant disease. Genes involved in the differentiation of lymphocytes are often associated with leukemia. One such gene, has been found to Zfp521, cause B-cell leukemia in mice when over-expressed. The role of in B-cell Zfp521 differentiation, and the mechanisms by which it leads to leukemic transformation, are unclear. In this study we report that knockdown causes apoptosis in a B-cell culture system Zfp521 and promotes down-regulation of genes acting at late stages of B-cell differentiation. We
Zfp521 promotes B-cell viability and cyclin D1 gene expression in a B cell culture system Salma Al Dallal, Kathryn Wolton, Kathryn E. Hentges* Faculty of Life Sciences, University of Manchester, Manchester UK M13 9PT *Author for correspondence: Kathryn E. Hentges Michael Smith Building Oxford Road Manchester M13 9PT UK Tel: +44 (0)161 275 1490 Email: Abstract Leukemia arises due to the dysregulated proliferation of hematopoietic progenitor cells. Errors in the multi-step commitment process result in excessive numbers of immature lymphocytes, causing malignant disease. Genes involved in the differentiation of lymphocytes are often associated with leukemia. One such gene, Zfp521, has been found to cause B-cell leukemia in mice when over-expressed. The role of Zfp521 in B-cell differentiation, and the mechanisms by which it leads to leukemic transformation, are unclear. In this study we report that Zfp521 knockdown causes apoptosis in a B-cell culture system and promotes down-regulation of genes acting at late stages of B-cell differentiation. We
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