ArticleOncogene2007
The MN1-TEL myeloid leukemia-associated fusion protein has a dominant-negative effect on RAR-RXR-mediated transcription.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 27 citations in OpenAlex.
- MN1 altered astroblastoma with APC and LRP1B gene mutations: a unique variant in the cervical spine of a pediatric patient.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2023Article
- Review
- Meningioma 1 is indispensable for mixed lineage leukemia-rearranged acute myeloid leukemia.Haematologica · 2020Article
- ETV6 in hematopoiesis and leukemia predisposition.Seminars in hematology · 2017Review
- MLL1 and DOT1L cooperate with meningioma-1 to induce acute myeloid leukemia.The Journal of clinical investigation · 2016Article
- Article
- The leukemia-associated fusion protein MN1-TEL blocks TEL-specific recognition sequences.PloS one · 2012Article
- Retinoids regulate stem cell differentiation.Journal of cellular physiology · 2011Review
- The ETS family member TEL binds to nuclear receptors RAR and RXR and represses gene activation.PloS one · 2011Article
- MN1 affects expression of genes involved in hematopoiesis and can enhance as well as inhibit RAR/RXR-induced gene expression.Carcinogenesis · 2008Article
- Molecular mechanisms of ETS transcription factor-mediated tumorigenesis.Critical reviews in biochemistry and molecular biologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The translocation t(12;22)(p13;q11) creates an MN1-TEL fusion gene leading to acute myeloid leukemia. MN1 is a transcription coactivator of the retinoic acid and vitamin D receptors, and TEL (ETV6) is a member of the E26-transformation-specific family of transcription factors. In MN1-TEL, the transactivating domains of MN1 are combined with the DNA-binding domain of TEL. We show that MN1-TEL inhibits retinoic acid receptor (RAR)-mediated transcription, counteracts coactivators such as p160 and p300, and acts as a dominant-negative mutant of MN1. Compared to MN1, the same transactivation domains in MN1-TEL are poorly stimulated by p160, p300 or histone deacetylase inhibitors, indicating that the block of RAR-mediated transcription by MN1-TEL is caused by dysfunctional transactivation domains rather than by recruitment of corepressors. The mechanism leading to myeloid leukemia in t(12;22) thus differs from the translocations that involve RAR itself.
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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.