ArticleMolecular and cellular biology1998
The AML1-MTG8 leukemic fusion protein forms a complex with a novel member of the MTG8(ETO/CDR) family, MTGR1.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed, 155 citations in OpenAlex.
- Mtg16 NHR1 mutations cause defects in lymphopoiesis and the response to anemia.Experimental hematology · 2025Article
- MTGR1 is required to maintain small intestinal stem cell populations.Cell death and differentiation · 2024Article
- [Establishment of leukemia cell model with inducible AML1-ETO expression and its effect on fatty acid metabolism in leukemia cells].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2023Article
- Zinc finger myeloid Nervy DEAF-1 type (ZMYND) domain containing proteins exert molecular interactions to implicate in carcinogenesis.Discover oncology · 2022Review
- RUNX1T1 function in cell fate.Stem cell research & therapy · 2022Review
- UBC9 inhibits myeloid differentiation in collaboration with AML1-MTG8.International journal of hematology · 2022Article
- RUNX1-ETO Depletion in t(8;21) AML Leads to C/EBPα- and AP-1-Mediated Alterations in Enhancer-Promoter Interaction.Cell reports · 2019Article
- Myeloid translocation gene CBFA2T3 directs a relapse gene program and determines patient-specific outcomes in AML.Blood advances · 2019Article
- RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia.International journal of molecular sciences · 2019Review
- 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
- Loss of RUNX1/AML1 arginine-methylation impairs peripheral T cell homeostasis.British journal of haematology · 2015Article
- AML1/ETO cooperates with HIF1α to promote leukemogenesis through DNMT3a transactivation.Leukemia · 2015Article
- Myeloid translocation gene-16 co-repressor promotes degradation of hypoxia-inducible factor 1.PloS one · 2015Article
- Article
- RUNX1: A microRNA hub in normal and malignant hematopoiesis.International journal of molecular sciences · 2013Review
- The transcriptional co-repressor myeloid translocation gene 16 inhibits glycolysis and stimulates mitochondrial respiration.PloS one · 2013Article
- Childhood acute myeloid leukemia with bone marrow eosinophilia caused by t(16;21)(q24;q22).International journal of hematology · 2012Article
- Myeloid translocation gene 16 is required for maintenance of haematopoietic stem cell quiescence.The EMBO journal · 2012Article
- RUNX1 and RUNX1-ETO: roles in hematopoiesis and leukemogenesis.Frontiers in bioscience (Landmark edition) · 2012Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The AML1-CBFbeta transcription factor complex is essential for the definitive hematopoiesis of all lineages and is the most frequent target of chromosomal rearrangements in human leukemia. In the t(8;21) translocation associated with acute myeloid leukemia (AML), the AML1(CBFA2/PEBP2alphaB) gene is juxtaposed to the MTG8(ETO/CDR) gene. We show here that the resultant AML1-MTG8 gene product specifically and strongly interacts with an 85-kDa phosphoprotein. Molecular cloning of cDNA indicated that the AML1-MTG8-binding protein (MTGR1) is highly related to MTG8 and similar to Drosophila Nervy. Comparison of amino acid sequences among MTGR1, MTG8, and Nervy revealed four evolutionarily conserved regions (NHR1 to NHR4). Ectopic expression of AML1-MTG8 in L-G murine myeloid progenitor cells inhibits differentiation to mature neutrophils and induces cell proliferation in response to granulocyte colony-stimulating factor (G-CSF). Analysis with C-terminal deletion mutants of AML1-MTG8 indicated that the region of 51 residues (488 to 538), which contains NHR2, is essential for the induction of G-CSF-dependent cell proliferation. Immunoprecipitation analysis indicates that this region is required for AML1-MTG8 to form a stable complex with MTGR1. Overexpression of MTGR1 stimulates AML1-MTG8 to induce G-CSF-dependent proliferation of L-G cells and to interfere with AML1-dependent transcription. These results suggest that AML1-MTG8 could function as a complex with MTGR1 and that the complex might be important in promoting leukemogenesis.
Indexed as
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.