ArticleMolecular and cellular biology2008
Deletion of Mtg16, a target of t(16;21), alters hematopoietic progenitor cell proliferation and lineage allocation.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
60 citing papers in PubMed, 81 citations in OpenAlex.
- ASF1B promotes erythropoiesis by regulating the establishment and enrichment of H3.3 nucleosomes.Nucleic acids research · 2026Article
- Mtg16 NHR1 mutations cause defects in lymphopoiesis and the response to anemia.Experimental hematology · 2025Article
- Bone Marrow Niche in Cardiometabolic Disease: Mechanisms and Therapeutic Potential.Circulation research · 2025Review
- The ETO2 transcriptional cofactor maintains acute leukemia by driving a MYB/EP300-dependent stemness program.HemaSphere · 2024Article
- CBFA2T3 Is PPARA Sensitive and Attenuates Fasting-Induced Lipid Accumulation in Mouse Liver.Cells · 2024Article
- Advances in molecular characterization of pediatric acute megakaryoblastic leukemia not associated with Down syndrome; impact on therapy development.Frontiers in cell and developmental biology · 2023Review
- Article
- MTG8 interacts with LHX6 to specify cortical interneuron subtype identity.Nature communications · 2022Article
- Hemogen/BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis.Blood · 2022Article
- MTG16 regulates colonic epithelial differentiation, colitis, and tumorigenesis by repressing E protein transcription factors.JCI insight · 2022Article
- UBC9 inhibits myeloid differentiation in collaboration with AML1-MTG8.International journal of hematology · 2022Article
- Insufficiency of non-canonical PRC1 synergizes with JAK2V617F in the development of myelofibrosis.Leukemia · 2022Article
- The divergence between T cell and innate lymphoid cell fates controlled by E and Id proteins.Frontiers in immunology · 2022Review
- ILC Differentiation in the Thymus.Advances in experimental medicine and biology · 2022Article
- Reduction of RUNX1 transcription factor activity by a CBFA2T3-mimicking peptide: application to B cell precursor acute lymphoblastic leukemia.Journal of hematology & oncology · 2021Article
- Finding erythroid stress progenitors: cell surface markers revealed.Haematologica · 2020Article
- E proteins orchestrate dynamic transcriptional cascades implicated in the suppression of the differentiation of group 2 innate lymphoid cells.The Journal of biological chemistry · 2020Article
- Embryonic erythropoiesis and hemoglobin switching require transcriptional repressor ETO2 to modulate chromatin organization.Nucleic acids research · 2020Article
- The Transcription Co-Repressors MTG8 and MTG16 Regulate Exit of Intestinal Stem Cells From Their Niche and Differentiation Into Enterocyte vs Secretory Lineages.Gastroenterology · 2020Article
- The transcriptional corepressor CBFA2T3 inhibits all-The Journal of biological chemistry · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
While a number of DNA binding transcription factors have been identified that control hematopoietic cell fate decisions, only a limited number of transcriptional corepressors (e.g., the retinoblastoma protein [pRB] and the nuclear hormone corepressor [N-CoR]) have been linked to these functions. Here, we show that the transcriptional corepressor Mtg16 (myeloid translocation gene on chromosome 16), which is targeted by t(16;21) in acute myeloid leukemia, is required for hematopoietic progenitor cell fate decisions and for early progenitor cell proliferation. Inactivation of Mtg16 skewed early myeloid progenitor cells toward the granulocytic/macrophage lineage while reducing the numbers of megakaryocyte-erythroid progenitor cells. In addition, inactivation of Mtg16 impaired the rapid expansion of short-term stem cells, multipotent progenitor cells, and megakaryocyte-erythroid progenitor cells that is required under hematopoietic stress/emergency. This impairment appears to be a failure to proliferate rather than an induction of cell death, as expression of c-Myc, but not Bcl2, complemented the Mtg16(-/-) defect.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.