ArticleOncogene2005
Mnt transcriptional repressor is functionally regulated during cell cycle progression.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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
18 citing papers in PubMed, 34 citations in OpenAlex.
- The Development and Clinical Applications of Oral Arsenic Trioxide for Acute Promyelocytic Leukaemia and Other Diseases.Pharmaceutics · 2022Review
- Review
- Review
- The regulatory function of tandem repeat VNTR2-1 in hTERT gene involves basic Helix-loop-helix family transcription factors.Environmental and molecular mutagenesis · 2021Article
- miR-139-5p Regulates the Proliferation of Acute Promyelocytic Leukemia Cells by Targeting MNT.Journal of oncology · 2021Article
- The MNT transcription factor autoregulates its expression and supports proliferation in MYC-associated factor X (MAX)-deficient cells.The Journal of biological chemistry · 2020Article
- Therapeutic Inhibition of Myc in Cancer. Structural Bases and Computer-Aided Drug Discovery Approaches.International journal of molecular sciences · 2018Review
- A machine learning approach to integrate big data for precision medicine in acute myeloid leukemia.Nature communications · 2018Article
- MNT and Emerging Concepts of MNT-MYC Antagonism.Genes · 2017Article
- Proteomic discovery of MNT as a novel interacting partner of E3 ubiquitin ligase E6AP and a key mediator of myeloid differentiation.Oncotarget · 2016Article
- Functional interactions among members of the MAX and MLX transcriptional network during oncogenesis.Biochimica et biophysica acta · 2015Review
- MYC cofactors: molecular switches controlling diverse biological outcomes.Cold Spring Harbor perspectives in medicine · 2014Review
- An overview of MYC and its interactome.Cold Spring Harbor perspectives in medicine · 2014Review
- The E-box binding factors Max/Mnt, MITF, and USF1 act coordinately with FoxO to regulate expression of proapoptotic and cell cycle control genes by phosphatidylinositol 3-kinase/Akt/glycogen synthase kinase 3 signaling.The Journal of biological chemistry · 2011Article
- Mitotic cell-cycle progression is regulated by CPEB1 and CPEB4-dependent translational control.Nature cell biology · 2010Article
- MYCN-regulated microRNAs repress estrogen receptor-alpha (ESR1) expression and neuronal differentiation in human neuroblastoma.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Myc's broad reach.Genes & development · 2008Review
- Identification of small molecules that induce apoptosis in a Myc-dependent manner and inhibit Myc-driven transformation.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Myc/Max/Mad network of transcription factors regulates cell proliferation, differentiation, and transformation. Similar to other proteins of the network, Mnt forms heterodimers with Max and binds CACGTG E-Box elements. Transcriptional repression by Mnt is mediated through association with mSin3, and deletion of the mSin3-interacting domain (SID) converts Mnt to a transcriptional activator. Mnt is coexpressed with Myc in proliferating cells and has been suggested to be a modulator of Myc function. We report that Mnt is expressed both in growth-arrested and proliferating mouse fibroblasts and is phosphorylated when resting cells are induced to re-enter the cell cycle. Importantly, the interaction between Mnt and mSin3 is disrupted upon serum stimulation resulting in decreased Mnt-associated HDAC activity. Furthermore, we demonstrate that Mnt binds and recruits mSin3 to the Myc target gene cyclin D2 in quiescent mouse fibroblasts. Interference with Mnt expression by RNAi resulted in upregulation of cyclin D2 expression in growth-arrested fibroblasts, supporting the view that Mnt represses cyclin D2 transcription in quiescent cells. Our data suggest a model in which phosphorylation of Mnt at cell cycle entry results in disruption of Mnt-mSin3-HDAC1 interaction, which allows induction of Myc target genes by release of Mnt-mediated transcriptional repression.
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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.