ArticleThe EMBO journal2006
The mechanism of repression of the myeloid-specific c-fms gene by Pax5 during B lineage restriction.
Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 75 citations in OpenAlex.
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- Erythropoietin exposure disrupts B cell development and drives the emergence of myeloid-biased biphenotypic progenitors.Stem cell reports · 2026Article
- B-lineage commitment is dependent on a reversible epigenetic switch.Genes & development · 2026Article
- Review
- FOXO Dictates Initiation of B Cell Development and Myeloid Restriction in Common Lymphoid Progenitors.Frontiers in immunology · 2022Article
- Conserved DNA sequence features underlie pervasive RNA polymerase pausing.Nucleic acids research · 2021Article
- Different mutant RUNX1 oncoproteins program alternate haematopoietic differentiation trajectories.Life science alliance · 2021Article
- Dysregulation of NIPBL leads to impaired RUNX1 expression and haematopoietic defects.Journal of cellular and molecular medicine · 2020Article
- Molecular Regulation of Differentiation in Early B-Lymphocyte Development.International journal of molecular sciences · 2018Review
- Clonal conversion of B lymphoid leukemia reveals cross-lineage transfer of malignant states.Genes & development · 2016Article
- CSF-1 receptor signaling in myeloid cells.Cold Spring Harbor perspectives in biology · 2014Review
- Runx1 regulation of Pu.1 corepressor/coactivator exchange identifies specific molecular targets for leukemia differentiation therapy.The Journal of biological chemistry · 2014Article
- Hacking cell differentiation: transcriptional rerouting in reprogramming, lineage infidelity and metaplasia.EMBO molecular medicine · 2013Review
- The function of the conserved regulatory element within the second intron of the mammalian Csf1r locus.PloS one · 2013Article
- AML1/ETO and POU4F1 synergy drives B-lymphoid gene expression typical of t(8;21) acute myeloid leukemia.Leukemia · 2012Article
- Epigenetic regulation of B lymphocyte differentiation, transdifferentiation, and reprogramming.Comparative and functional genomics · 2012Article
- Article
- Repeat-element driven activation of proto-oncogenes in human malignancies.Cell cycle (Georgetown, Tex.) · 2010Article
- Common clonal origin of an acute B-lymphoblastic leukemia and a Langerhans' cell sarcoma: evidence for hematopoietic plasticity.Haematologica · 2010Article
- Aberrant expression of CD19 in AML with t(8;21) involves a poised chromatin structure and PAX5.Oncogene · 2010Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
The transcription factor Pax5 (BSAP) is required for the expression of a B-cell-specific genetic program and for B-cell differentiation, and also to suppress genes of alternative lineages. The molecular mechanism by which repression of myeloid genes occurs during early B-lineage restriction is unknown and in this study we addressed this question. One of the genes repressed by Pax5 in B cells is the colony-stimulating factor receptor 1 gene (csf1r or c-fms). We examined the changes in chromatin caused by Pax5 activity, and we show that Pax5 is directly recruited to c-fms resulting in the rapid loss of RNA polymerase II binding, followed by loss of transcription factor binding and DNaseI hypersensitivity at all cis-regulatory elements. We also show that Pax5 targets the basal transcription machinery of c-fms by interacting with a binding site within the major transcription start sites. Our results support a model by which Pax5 does not lead to major alterations in chromatin modification, but inhibits transcription by interfering with the action of myeloid transcription factors.
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Registered trials
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