morinlab.bib
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+@article{gyoryTranscriptionFactorEbf12012,
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+ title = {Transcription factor {Ebf1} regulates differentiation stage-specific signaling, proliferation, and survival of {B} cells},
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+ volume = {26},
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+ issn = {1549-5477},
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+ doi = {10.1101/gad.187328.112},
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+ abstract = {The transcription factor Ebf1 is an important determinant of early B lymphopoiesis. To gain insight into the functions of Ebf1 at distinct stages of differentiation, we conditionally inactivated Ebf1. We found that Ebf1 is required for the proliferation, survival, and signaling of pro-B cells and peripheral B-cell subsets, including B1 cells and marginal zone B cells. The proliferation defect of Ebf1-deficient pro-B cells and the impaired expression of multiple cell cycle regulators are overcome by transformation with v-Abl. The survival defect of transformed Ebf1(fl/fl) pro-B cells can be rescued by the forced expression of the Ebf1 targets c-Myb or Bcl-x(L). In mature B cells, Ebf1 deficiency interferes with signaling via the B-cell-activating factor receptor (BAFF-R)- and B-cell receptor (BCR)-dependent Akt pathways. Moreover, Ebf1 is required for germinal center formation and class switch recombination. Genome-wide analyses of Ebf1-mediated gene expression and chromatin binding indicate that Ebf1 regulates both common and distinct sets of genes in early and late stage B cells. By regulating important components of transcription factor and signaling networks, Ebf1 appears to be involved in the coordination of cell proliferation, survival, and differentiation at multiple stages of B lymphopoiesis.},
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+ language = {eng},
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+ number = {7},
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+ journal = {Genes \& Development},
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+ author = {Györy, Ildiko and Boller, Sören and Nechanitzky, Robert and Mandel, Elizabeth and Pott, Sebastian and Liu, Edison and Grosschedl, Rudolf},
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+ month = apr,
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+ year = {2012},
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+ pmid = {22431510},
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+ pmcid = {PMC3323878},
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+ keywords = {Animals, B-Lymphocytes, Cell Differentiation, Cell Proliferation, Cell Survival, Gene Expression Regulation, Genome-Wide Association Study, Immunoglobulin Heavy Chains, Mice, Mice, Inbred C57BL, Mice, Transgenic, Signal Transduction, Trans-Activators, Transcription, Genetic},
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+ pages = {668--682},
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+}
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+
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@article{schejbelInactivatingBTKMutations2022,
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title = {Inactivating {BTK} mutations in large {B}-cell lymphoma in a real-world cohort: {Strong} correlation with {BCL2} translocation},
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volume = {3},