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B lymphocytes are generated from hematopoietic stem cells, a process controlled by multiple transcription factors (i.e. PU.1, E2A etc.). In addition, concerted changes of chromatin structure at the target gene loci are required to achieve desired developmental outcomes. It is known that a compact chromatin state would prevent transcription factors from DNA-binding and gene expression initiation while a loose structure favors binding. However, the process by which chromatin remodeling affects B cell lymphopoiesis has not been fully understood. I am currently studying a novel B cell deficient mouse model in which B cell development is severely impaired due to a point mutation in a putative chromatin remodeling protein.
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