Regulation of B lymphocyte and macrophage development by graded expression of PU.1.

By R. DeKoter, Harinder Singh. Science, 2000

793 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/6112dbca9eb7e54acee700e73328ccda34b5d755

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Citations in the corpus

Transcriptional regulation of macrophage polarization: enabling diversity with identity (2011, background): “1, which must be constantly expressed at high levels to induce and then maintain macrophage differentiatio”
Stepwise reprogramming of B cells into macrophages. (2004, positive): “1 / fetal liver cursor cells reprograms them into megakaryocytic/ery- precursors promote B cell differentiation, while high levthroid (MEP) cells, eosinophils, or mast cells, lineages els promote macrophage differentiation (DeKoter and Singh, 2000).”
GM-CSF regulates alveolar macrophage differentiation and innate immunity in the lung through PU.1. (2001, background): “However, the global and transduction of mAM cells with a retroviral vector expressing murine PU.1 and, as a selectable marker, also green fluorescent proteinparallel regulation of phagocytosis of gram-negative and (GFP) (DeKoter and Singh, 2000).”
Pulmonary alveolar proteinosis: progress in the first 44 years. (2002, background): “1 levels on lineage commitment, with low levels leading to B-lineage differentiation and high levels leading to macrophage lineage differentiation [119].”
Hematopoiesis: an evolving paradigm for stem cell biology. (2008, background): “1 expression directs macrophage differentiation, whereas low-level expression promotes B cell formation (DeKoter and Singh, 2000).”
Master Transcription Factors Determine Cell-Type-Specific Responses to TGF-β Signaling (2011, positive): “We performed ChIP-seq analysis for Myod1 in myotubes (Davis et al., 1987; Tapscott, 2005) and PU.1 in pro-B cells (DeKoter and Singh, 2000; Nutt and Kee, 2007) and found that sites bound by Oct4, Myod1, and PU.1 were largely unique (Figure 4A; Table S1).”
Mutations of the transcription factor PU.1 are not associated with acute lymphoblastic leukaemia (2006, positive): “…was recently hypothesised that differing concentrations of the PU.1 protein regulate the development of B-lymphocytes as compared with macrophages (DeKoter and Singh, 2000): A low concentration of PU.1 protein (one-fifth to one-seventh as much) was proposed to induce a B-cell fate, whereas a high…”
microRNA-155 Regulates the Generation of Immunoglobulin Class-Switched Plasma Cells (2007, methodology): “1 expressing vectors were kindly provided by Rodney DeKoter (DeKoter and Singh, 2000).”
Suppression of IL-12 Transcription in Macrophages Following Fcγ Receptor Ligation1 (2001, background): “1 protein induces the B cell fate, whereas a high concentration promotes macrophage differentiation and blocks B cell development) (31).”
ChIP-seq guidelines and practices of the ENCODE and modENCODE consortia (2012, methodology): “Higher expression is known to result in occupancy of sites not necessarily occupied at physiological levels (DeKoter and Singh 2000; Fernandez et al. 2003).”
The ETS-domain transcription factor family (2001, background): “1, with high levels promoting macrophage differentiation and low levels inducing the B-cell fat”
Eosinophils: Biological Properties and Role in Health and Disease (2008, background): “The expression level of PU.1 specifies distinct cell lineage fates, with low levels specifying lymphocytic and high levels myeloid differentiation (De Koter & Singh 2000; Du et al. 2002).”