Evidence map›Paper›PMID 26067234›Full record

ArticleeLife2015

MAF1 represses CDKN1A through a Pol III-dependent mechanism.

Yu-Ling Lee, Yuan-Ching Li, Chia-Hsin Su, Chun-Hui Chiao, I-Hsuan Lin, Ming-Ta Hsu

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. IL-15 Priming Alters IFN-γ Regulation in Murine NK Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023
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  9. Planar cell polarity geneEMBO reports · 2018
    Article
  10. Article
  11. Maf1 phenotypes and cell physiology.Biochimica et biophysica acta. Gene regulatory mechanisms · 2018
    Review
  12. Article
  13. Article
  14. Maf1, A New PTEN Target Linking RNA and Lipid Metabolism.Trends in endocrinology and metabolism: TEM · 2016
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Yu-Ling LeeInstitute of Biochemistry and Molecular Biology, School of Life Science, National Yang-Ming University, Taipei, Taiwan.ORCID http://orcid.org/0000-0003-1897-9918
Yuan-Ching LiInstitute of Biochemistry and Molecular Biology, School of Life Science, National Yang-Ming University, Taipei, Taiwan.
Chia-Hsin SuInstitute of Biochemistry and Molecular Biology, School of Life Science, National Yang-Ming University, Taipei, Taiwan.
Chun-Hui ChiaoInstitute of Biochemistry and Molecular Biology, School of Life Science, National Yang-Ming University, Taipei, Taiwan.
I-Hsuan LinInstitute of Biochemistry and Molecular Biology, School of Life Science, National Yang-Ming University, Taipei, Taiwan.ORCID http://orcid.org/0000-0002-6207-1299
Ming-Ta HsuInstitute of Biochemistry and Molecular Biology, School of Life Science, National Yang-Ming University, Taipei, Taiwan.
National Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MAF1 represses Pol III-mediated transcription by interfering with TFIIIB and Pol III. Herein, we found that MAF1 knockdown induced CDKN1A transcription and chromatin looping concurrently with Pol III recruitment. Simultaneous knockdown of MAF1 with Pol III or BRF1 (subunit of TFIIIB) diminished the activation and looping effect, which indicates that recruiting Pol III was required for activation of Pol II-mediated transcription and chromatin looping. Chromatin-immunoprecipitation analysis after MAF1 knockdown indicated enhanced binding of Pol III and BRF1, as well as of CFP1, p300, and PCAF, which are factors that mediate active histone marks, along with the binding of TATA binding protein (TBP) and POLR2E to the CDKN1A promoter. Simultaneous knockdown with Pol III abolished these regulatory events. Similar results were obtained for GDF15. Our results reveal a novel mechanism by which MAF1 and Pol III regulate the activity of a protein-coding gene transcribed by Pol II.

Indexed as

Gene Expression RegulationCell LineChromatin ImmunoprecipitationCyclin-Dependent Kinase Inhibitor p21DNAGene Knockdown TechniquesHumansPromoter Regions, GeneticProtein BindingRepressor ProteinsRNA Polymerase IIICDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DNAMAF1 protein, humanRepressor ProteinsRNA Polymerase IIIbiochemistryCDKN1Acell biologyhumanMAF1Pol III

Identifiers

PMID26067234
PMCPMC4480132
OpenAlexW1932665887

What OpenQuestion holds

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Registered trials

None linked

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.