期刊
CELL
卷 119, 期 1, 页码 75-86出版社
CELL PRESS
DOI: 10.1016/j.cell.2004.09.014
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资金
- NIAID NIH HHS [AI34000] Funding Source: Medline
- NIDDK NIH HHS [DK60647, DK065961] Funding Source: Medline
- NIGMS NIH HHS [GM20675, GM47310] Funding Source: Medline
The transcriptional repressor BCL-6 regulates B lymphocyte cell fate during the germinal center reaction by preventing terminal differentiation of B lymphocytes into plasma cells until appropriate signals are received. Here, we report a cofactor, MTA3, a cell type-specific subunit of the corepressor complex Mi-2/ NuRD, for BCL-6-dependent cell fate determination. MTA3 is expressed in the same pattern in germinal centers as BCL-6. BCL-6 physically interacts with Mi-2/NuRD and this interaction is sensitive to BCL-6 acetylation status. Depletion of MTA3 by RNAi impairs BCL-6-dependent repression and alters the cell-specific transcriptional pattern characteristic of the B lymphocyte. Remarkably, exogenous expression of BCL-6 in a plasma cell line leads, in an MTA3-dependent manner, to repression of plasma cell-specific transcripts, reactivation of the B cell transcriptional program, expression of B lymphocyte cell surface markers, and reprogramming of cell fate.
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