ArticlePloS one2013
Mapping of MN1 sequences necessary for myeloid transformation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Refinement of Risk-Stratification of Cytogenetically Normal Acute Myeloid Leukemia Adult Patients by MN1 Expression.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- Intrinsically disordered Meningioma-1 stabilizes the BAF complex to cause AML.Molecular cell · 2021Article
- NKL Homeobox Gene VENTX Is Part of a Regulatory Network in Human Conventional Dendritic Cells.International journal of molecular sciences · 2021Article
- Role of Meningioma 1 for maintaining the transformed state in MLL-rearranged acute myeloid leukemia: potential for therapeutic intervention?Haematologica · 2020Article
- MN1 C-terminal truncation syndrome is a novel neurodevelopmental and craniofacial disorder with partial rhombencephalosynapsis.Brain : a journal of neurology · 2020Article
- Article
- MN1 and PTEN gene expression in acute myeloid leukemia.Cancer biomarkers : section A of Disease markers · 2017Article
- MLL1 and DOT1L cooperate with meningioma-1 to induce acute myeloid leukemia.The Journal of clinical investigation · 2016Article
- Chromosome 22q12.1 microdeletions: confirmation of the MN1 gene as a candidate gene for cleft palate.European journal of human genetics : EJHG · 2016Article
- Cell fate decisions in malignant hematopoiesis: leukemia phenotype is determined by distinct functional domains of the MN1 oncogene.PloS one · 2014Article
- GFI1B, EVI5, MYB--additional genes that cooperate with the human BCL6 gene to promote the development of lymphomas.Blood cells, molecules & diseases · 2014Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The MN1 oncogene is deregulated in human acute myeloid leukemia and its overexpression induces proliferation and represses myeloid differentiation of primitive human and mouse hematopoietic cells, leading to myeloid leukemia in mouse models. To delineate the sequences within MN1 necessary for MN1-induced leukemia, we tested the transforming capacity of in-frame deletion mutants, using retroviral transduction of mouse bone marrow. We found that integrity of the regions between amino acids 12 to 458 and 1119 to 1273 are required for MN1's in vivo transforming activity, generating myeloid leukemia with some mutants also producing T-cell lympho-leukemia and megakaryocytic leukemia. Although both full length MN1 and a mutant that lacks the residues between 12-228 (Δ12-228 mutant) repressed myeloid differentiation and increased myeloproliferative activity in vitro, the mutant lost its transforming activity in vivo. Both MN1 and Δ12-228 increased the frequency of common myeloid progentiors (CMP) in vitro and microarray comparisons of purified MN1-CMP and Δ12-228-CMP cells showed many differentially expressed genes including Hoxa9, Meis1, Myb, Runx2, Cebpa, Cebpb and Cebpd. This collection of immediate MN1-responsive candidate genes distinguishes the leukemic activity from the in vitro myeloproliferative capacity of this oncoprotein.
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