ArticleMolecular and cellular biology2011
Mtg16/Eto2 contributes to murine T-cell development.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 32 citations in OpenAlex.
- Mtg16 NHR1 mutations cause defects in lymphopoiesis and the response to anemia.Experimental hematology · 2025Article
- CBFA2T3 Is PPARA Sensitive and Attenuates Fasting-Induced Lipid Accumulation in Mouse Liver.Cells · 2024Article
- MTG16 regulates colonic epithelial differentiation, colitis, and tumorigenesis by repressing E protein transcription factors.JCI insight · 2022Article
- 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
- Definition of a small core transcriptional circuit regulated by AML1-ETO.Molecular cell · 2021Article
- 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
- The Pluripotency Regulator PRDM14 Requires Hematopoietic Regulator CBFA2T3 to Initiate Leukemia in Mice.Molecular cancer research : MCR · 2019Article
- Off to a Bad Start: Cancer Initiation by Pluripotency Regulator PRDM14.Trends in genetics : TIG · 2019Review
- Myeloid translocation gene CBFA2T3 directs a relapse gene program and determines patient-specific outcomes in AML.Blood advances · 2019Article
- Emerging Roles of MTG16 in Cell-Fate Control of Hematopoietic Stem Cells and Cancer.Stem cells international · 2017Review
- New insights into transcriptional and leukemogenic mechanisms of AML1-ETO and E2A fusion proteins.Frontiers in biology · 2016Article
- Control of developmentally primed erythroid genes by combinatorial co-repressor actions.Nature communications · 2015Article
- The transcriptional corepressor MTGR1 regulates intestinal secretory lineage allocation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- ANTI-MTG16 ANTIBODIES REVEAL MTG16 SUBCELLULAR DISTRIBUTION AND NUCLEOCYTOPLASMIC TRANSPORT IN ERYTHROLEUKEMIA CELLS.Antibody technology journal · 2015Article
- Enforced expression of E47 has differential effects on Lmo2-induced T-cell leukemias.Leukemia research · 2015Article
- Myeloid translocation gene-16 co-repressor promotes degradation of hypoxia-inducible factor 1.PloS one · 2015Article
- ETO family protein Mtg16 regulates the balance of dendritic cell subsets by repressing Id2.The Journal of experimental medicine · 2014Article
- Differential involvement of E2A-corepressor interactions in distinct leukemogenic pathways.Nucleic acids research · 2014Article
- The transcriptional co-repressor myeloid translocation gene 16 inhibits glycolysis and stimulates mitochondrial respiration.PloS one · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mtg16/Eto2 is a transcriptional corepressor that is disrupted by t(16;21) in acute myeloid leukemia. Using mice lacking Mtg16, we found that Mtg16 is a critical regulator of T-cell development. Deletion of Mtg16 led to reduced thymocyte development in vivo, and after competitive bone marrow transplantation, there was a nearly complete failure of Mtg16(-/-) cells to contribute to thymocyte development. This defect was recapitulated in vitro as Mtg16(-/-) Lineage(-)/Sca1(+)/c-Kit(+) (LSK) cells of the bone marrow or DN1 cells of the thymus failed to produce CD4(+)/CD8(+) cells in response to a Notch signal. Complementation of these defects by reexpressing Mtg16 showed that 3 highly conserved domains were somewhat dispensable for T-cell development but required the capacity of Mtg16 to suppress E2A-dependent transcriptional activation and to bind to the Notch intracellular domain. Thus, Mtg16 integrates the activities of signaling pathways and nuclear factors in the establishment of T-cell fate specification.
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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.