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.
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Authors | Shanique K E Edwards, Anand Desai, Yan Liu, Carissa R Moore, Ping Xie |
Journal | Leukemia research
(Leuk Res)
Vol. 38
Issue 3
Pg. 393-401
(Mar 2014)
ISSN: 1873-5835 [Electronic] England |
PMID | 24418753
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2013 Elsevier Ltd. All rights reserved. |
Chemical References |
- Antibodies
- CTNNB1 protein, human
- Lipopolysaccharides
- Proliferating Cell Nuclear Antigen
- Protein Isoforms
- SOXD Transcription Factors
- Sox5 protein, mouse
- TNF Receptor-Associated Factor 3
- beta Catenin
- p27 antigen
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Topics |
- Animals
- Antibodies
(pharmacology)
- B-Lymphocytes
(drug effects, metabolism, pathology)
- Cell Cycle
(genetics)
- Cell Nucleus
(genetics, metabolism, ultrastructure)
- Cell Proliferation
- Gene Expression Regulation, Neoplastic
- Humans
- Lipopolysaccharides
(pharmacology)
- Lymphocyte Activation
(drug effects)
- Mice
- Proliferating Cell Nuclear Antigen
(genetics, metabolism)
- Protein Isoforms
(genetics, metabolism)
- SOXD Transcription Factors
(genetics, metabolism)
- Signal Transduction
- TNF Receptor-Associated Factor 3
(deficiency, genetics)
- beta Catenin
(genetics, metabolism)
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