ArticleThe Journal of biological chemistry2010
Requirement of the mTOR kinase for the regulation of Maf1 phosphorylation and control of RNA polymerase III-dependent transcription in cancer cells.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 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
107 citing papers in PubMed, 183 citations in OpenAlex.
- Signaling to make human ribosomes: Connections between the cytoplasm and the nucleolus.Molecular cell · 2026Review
- Nucleolus as a cornerstone linking proliferation and metabolism to cellular responses to stress: involvement of transcription factors MYC and p53.Frontiers in molecular biosciences · 2026Review
- mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics.Signal transduction and targeted therapy · 2025Review
- Aurora-A-mediated cytosolic localization of Maf1 promotes cell proliferation via regulating mitochondrial function in HCC.Cell death discovery · 2025Article
- CDK9 is a dependency in GATA-3 driven and MCL-1 independent T-cell Lymphomas.Blood cancer journal · 2025Article
- Maf1 cooperates with progesterone receptor to repress RNA polymerase III transcription of select tRNAs.Nucleic acids research · 2025Article
- The Central FacilitaTOR: Coordinating Transcription and Translation in Eukaryotes.International journal of molecular sciences · 2025Review
- Circadian Control of Protein Synthesis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- MAF1 inhibits hepatocarcinogenesis by fostering an immunostimulatory tumor microenvironment.Journal for immunotherapy of cancer · 2025Article
- mTORC1, the maestro of cell metabolism and growth.Genes & development · 2025Review
- The dynamics and functional impact of tRNA repertoires during early embryogenesis in zebrafish.The EMBO journal · 2024Article
- Uncoupling of mTORC1 from E2F activity maintains DNA damage and senescence.Nature communications · 2024Article
- Nuclear mTOR Signaling Orchestrates Transcriptional Programs Underlying Cellular Growth and Metabolism.Cells · 2024Review
- Oxidative Stress, Transfer RNA Metabolism, and Protein Synthesis.Antioxidants & redox signaling · 2024Review
- Selective gene expression maintains human tRNA anticodon pools during differentiation.Nature cell biology · 2024Article
- Maf1 is an intrinsic suppressor against spontaneous neural repair and functional recovery after ischemic stroke.Journal of advanced research · 2023Article
- Regulation of ribosomal RNA gene copy number, transcription and nucleolus organization in eukaryotes.Nature reviews. Molecular cell biology · 2023Review
- A multi-organ analysis of the role of mTOR in fetal alcohol spectrum disorders.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Review
- Transcription by the Three RNA Polymerases under the Control of the TOR Signaling Pathway inBiomolecules · 2023Review
- The coordinated management of ribosome and translation during injury and regeneration.Frontiers in cell and developmental biology · 2023Review
47 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
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mammalian target of rapamycin (mTOR) regulates growth via promoting translation and transcription. Here, employing an mTOR active-site inhibitor WYE-125132 (WYE-132), we have performed quantitative phospho-proteomics and identified a Ser-75-containing phosphopeptide from Maf1, a known repressor of RNA polymerase III (Pol III) transcription. Treatment of cancer cells with WYE-132 or the rapamycin analog CCI-779 led to a rapid loss of the phosphorylation at Ser-75, whereas this effect was not seen in cells treated with cytotoxic agents or unrelated inhibitors. WYE-132-induced Maf1 dephosphorylation correlated with its accumulation in the nucleus and a marked decline in the cellular levels of pre-tRNAs. Depletion of cellular Maf1 via small interfering RNA increased basal pre-tRNA and rendered tRNA synthesis refractory to mTOR inhibitors. Maf1 mutant proteins carrying S75A alone or with S60A, T64A, and S68A (Maf1-S75A, Maf1-4A) progressively enhanced basal repression of tRNA in actively proliferating cells and attenuated amino acid-induced tRNA transcription. Gene alignment revealed conservation of all four Ser/Thr sites in high eukaryotes, further supporting a critical role of these residues in Maf1 function. Interestingly, mTOR inhibition led to an increase in the occupancy of Maf1 on a set of Pol III-dependent genes, with concomitant reduction in the binding of Pol III and Brf1. Unexpectedly, mTORC1 itself was also enriched at the same set of Pol III templates, but this association was not influenced by mTOR inhibitor treatment. Our results highlight a new and unique mode of regulation of Pol III transcription by mTOR and suggest that normalization of Pol III activity may contribute to the therapeutic efficacy of mTOR inhibitors.
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.