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• W2061372381 abstract "In this paper, we describe the unexpected outgrowth of B lineage cells from PU.1−/− fetal liver cultures. The cells express all early B cell genes tested, including the putative PU.1 target genes IL-7R and EBF but not B220, and can produce immunoglobulin M. However, we observed a delay in the PU.1−/− B cell outgrowth and reduced precursor frequencies, indicating that although PU.1 is not strictly required for B cell commitment, it facilitates B cell development. We also ablated PU.1 in CD19-expressing B lineage cells in vivo, using a Cre-lox approach that allows them to be tracked. PU.1 excision resulted in a shift from B-2 cells to B-1–like cells, which dramatically increased with the age of the mice. Our data indicate that this shift is predominantly caused by a B-2 to B-1 cell reprogramming. Furthermore, we found that B-2 cells express substantially more PU.1 than B-1 cells, which is consistent with the idea that maintenance of the B-2 cell phenotype requires relatively high levels of PU.1, but B-1 cells require little." @default.
• W2061372381 created "2016-06-24" @default.
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• W2061372381 creator A5061537073 @default.
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• W2061372381 date "2005-11-21" @default.
• W2061372381 modified "2023-10-14" @default.
• W2061372381 title "PU.1 is not strictly required for B cell development and its absence induces a B-2 to B-1 cell switch" @default.
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• W2061372381 doi "https://doi.org/10.1084/jem.20051089" @default.
• W2061372381 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2212978" @default.
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