ArticleCarcinogenesis2008
MN1 affects expression of genes involved in hematopoiesis and can enhance as well as inhibit RAR/RXR-induced gene expression.
Article in Carcinogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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
16 citing papers in PubMed, 29 citations in OpenAlex.
- Sustained Transcriptional Response to Lipopolysaccharide and Interleukin-4 in an Immortalized Mouse Microglial Cell Line.Molecular neurobiology · 2026Article
- BRD9-containing non-canonical BAF complex maintains somatic cell transcriptome and acts as a barrier to human reprogramming.Stem cell reports · 2022Article
- MN1 overexpression with varying tumor grade is a promising predictor of survival of glioma patients.Human molecular genetics · 2021Article
- Review
- Post-natal all-trans-retinoic acid biosynthesis.Methods in enzymology · 2020Article
- Gene expression profile in patients with Gaucher disease indicates activation of inflammatory processes.Scientific reports · 2019Article
- The ten-year evolutionary trajectory of a highly recurrent paediatric high grade neuroepithelial tumour with MN1:BEND2 fusion.Scientific reports · 2018Article
- Article
- The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid.Cell cycle (Georgetown, Tex.) · 2014Article
- The enhancer landscape during early neocortical development reveals patterns of dense regulation and co-option.PLoS genetics · 2013Article
- The leukemia-associated fusion protein MN1-TEL blocks TEL-specific recognition sequences.PloS one · 2012Article
- Review
- The ETS family member TEL binds to nuclear receptors RAR and RXR and represses gene activation.PloS one · 2011Article
- Tetracycline regulator expression alters the transcriptional program of mammalian cells.PloS one · 2010Article
- CITED2 and NCOR2 in anti-oestrogen resistance and progression of breast cancer.British journal of cancer · 2009Article
- Meningioma 1 is required for appropriate osteoblast proliferation, motility, differentiation, and function.The Journal of biological chemistry · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The oncoprotein meningioma 1 (MN1) is overexpressed in several subtypes of acute myeloid leukemia (AML) and overexpression was associated with a poor response to chemotherapy. MN1 is a cofactor of retinoic acid receptor/retinoic x receptor (RAR/RXR)-mediated transcription and this study identified genes in the promonocytic cell line U937 that were regulated by MN1. We found that MN1 can both stimulate and inhibit transcription. Combining MN1 expression with all-trans retinoic acid (ATRA), the ligand of the RAR/RXR dimer, showed that MN1 could both enhance and repress ATRA effects. Many of the identified genes are key players in hematopoiesis and leukemogenesis (e.g. MEIS1 and BMI1). Another interesting target is DHRS9. DHRS9 is involved in the synthesis of ATRA from vitamin A. MN1 inhibited DHRS9 expression and completely abolished its induction by ATRA. MN1 is also the target of a rare AML-causing translocation encoding the MN1-TEL protein. MN1-TEL induces expression of only a few genes and its most pronounced effect is inhibition of a large group of ATRA-induced genes including DHRS9. In conclusion, both MN1 and MN1-TEL interfere with the ATRA pathway and this might explain the differentiation block in leukemias in which these genes are involved.
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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.