ReviewStem cells international2017
Emerging Roles of MTG16 in Cell-Fate Control of Hematopoietic Stem Cells and Cancer.
Review in Stem cells international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Mtg16 NHR1 mutations cause defects in lymphopoiesis and the response to anemia.Experimental hematology · 2025Article
- CBFA2T3-GLIS2 mediates transcriptional regulation of developmental pathways through a gene regulatory network.Nature communications · 2024Article
- Article
- 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
- The NCOR-HDAC3 co-repressive complex modulates the leukemogenic potential of the transcription factor ERG.Nature communications · 2023Article
- Identification of cancer stemness and M2 macrophage-associated biomarkers in lung adenocarcinoma.Heliyon · 2023Article
- Article
- HDAC I/IIb selective inhibitor Purinostat Mesylate combined with GLS1 inhibition effectively eliminates CML stem cells.Bioactive materials · 2023Article
- 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
- Physioxia-induced downregulation of Tet2 in hematopoietic stem cells contributes to enhanced self-renewal.Blood · 2022Article
- RUNX1T1 function in cell fate.Stem cell research & therapy · 2022Review
- MTG16 regulates colonic epithelial differentiation, colitis, and tumorigenesis by repressing E protein transcription factors.JCI insight · 2022Article
- Molecular Landscapes and Models of Acute Erythroleukemia.HemaSphere · 2021Review
- Reduction of RUNX1 transcription factor activity by a CBFA2T3-mimicking peptide: application to B cell precursor acute lymphoblastic leukemia.Journal of hematology & oncology · 2021Article
- AKAP Signaling Islands: Venues for Precision Pharmacology.Trends in pharmacological sciences · 2020Review
- The transcriptional corepressor CBFA2T3 inhibits all-The Journal of biological chemistry · 2020Article
- Circ_0008532 promotes bladder cancer progression by regulation of the miR-155-5p/miR-330-5p/MTGR1 axis.Journal of experimental & clinical cancer research : CR · 2020Article
- Off to a Bad Start: Cancer Initiation by Pluripotency Regulator PRDM14.Trends in genetics : TIG · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
MTG16 (myeloid translocation gene on chromosome 16) and its related proteins, MTG8 and MTGR1, define a small family of transcriptional corepressors. These corepressors share highly conserved domain structures yet have distinct biological functions and tissue specificity. In vivo studies have shown that, of the three MTG corepressors, MTG16 is uniquely important for the regulation of hematopoietic stem/progenitor cell (HSPC) proliferation and differentiation. Apart from this physiological function, MTG16 is also involved in carcinomas and leukemias, acting as the genetic target of loss of heterozygosity (LOH) aberrations in breast cancer and recurrent translocations in leukemia. The frequent involvement of MTG16 in these disease etiologies implies an important developmental role for this transcriptional corepressor. Furthermore, mounting evidence suggests that MTG16 indirectly alters the disease course of several leukemias via its regulatory interactions with a variety of pathologic fusion proteins. For example, a recent study has shown that MTG16 can repress not only wild-type E2A-mediated transcription, but also leukemia fusion protein E2A-Pbx1-mediated transcription, suggesting that MTG16 may serve as a potential therapeutic target in acute lymphoblastic leukemia expressing the E2A-Pbx1 fusion protein. Given that leukemia stem cells share similar regulatory pathways with normal HSPCs, studies to further understand how MTG16 regulates cell proliferation and differentiation could lead to novel therapeutic approaches for leukemia treatment.
Identifiers
What OpenQuestion holds
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.