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      Expression and function of a novel isoform of Sox5 in malignant B cells.

      Leukemia Research
      Animals, Antibodies, pharmacology, B-Lymphocytes, drug effects, metabolism, pathology, Cell Cycle, genetics, Cell Nucleus, ultrastructure, Cell Proliferation, Gene Expression Regulation, Neoplastic, Humans, Lipopolysaccharides, Lymphocyte Activation, Mice, Proliferating Cell Nuclear Antigen, Protein Isoforms, SOXD Transcription Factors, Signal Transduction, TNF Receptor-Associated Factor 3, deficiency, beta Catenin

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          Abstract

          Using a mouse model with the tumor suppressor TRAF3 deleted from B cells, we identified Sox5 as a gene strikingly up-regulated in B lymphomas. Sox5 proteins were not detected in normal or premalignant TRAF3(-/-) B cells even after treatment with B cell stimuli. The Sox5 expressed in TRAF3(-/-) B lymphomas represents a novel isoform of Sox5, and was localized in the nucleus of malignant B cells. Overexpression of Sox5 inhibited cell cycle progression, and up-regulated the protein levels of p27 and β-catenin in human multiple myeloma cells. Together, our findings indicate that Sox5 regulates the proliferation of malignant B cells. Copyright © 2013 Elsevier Ltd. All rights reserved.

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