Evidence map›Paper›PMID 31015486›Full record

ArticleNature communications2019

RUNX3 regulates cell cycle-dependent chromatin dynamics by functioning as a pioneer factor of the restriction-point.

Jung-Won Lee, Da-Mi Kim, Ju-Won Jang, Tae-Geun Park, Soo-Hyun Song, You-Soub Lee, Xin-Zi Chi, Il Yeong Park, Jin-Won Hyun, Yoshiaki Ito and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 56 citations in OpenAlex.

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  14. Cells · 2023
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  15. Epigenetic Abnormalities in Chondrosarcoma.International journal of molecular sciences · 2023
    Review
  16. Review
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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

11 authors at 3 institutions in 2 countries.

Jung-Won LeeDepartment of Biochemistry, School of Medicine, and Institute for Tumor Research, Chungbuk National University, Cheongju, 28644, South Korea.
Da-Mi KimDepartment of Biochemistry, School of Medicine, and Institute for Tumor Research, Chungbuk National University, Cheongju, 28644, South Korea.
Ju-Won JangDepartment of Biochemistry, School of Medicine, and Institute for Tumor Research, Chungbuk National University, Cheongju, 28644, South Korea.
Tae-Geun ParkDepartment of Biochemistry, School of Medicine, and Institute for Tumor Research, Chungbuk National University, Cheongju, 28644, South Korea.
Soo-Hyun SongDepartment of Biochemistry, School of Medicine, and Institute for Tumor Research, Chungbuk National University, Cheongju, 28644, South Korea.
You-Soub LeeDepartment of Biochemistry, School of Medicine, and Institute for Tumor Research, Chungbuk National University, Cheongju, 28644, South Korea.
Xin-Zi ChiDepartment of Biochemistry, School of Medicine, and Institute for Tumor Research, Chungbuk National University, Cheongju, 28644, South Korea.
Il Yeong ParkCollege of Pharmacy, Chungbuk National University, Cheongju, 361-763, South Korea.
Jin-Won HyunDepartment of Biochemistry, School of Medicine, Jeju National University, Jeju, 63243, South Korea.
Yoshiaki ItoCancer Science Institute of Singapore, National University of Singapore, 14 Medical Drive, Singapore, Singapore, 117599.
Suk-Chul BaeDepartment of Biochemistry, School of Medicine, and Institute for Tumor Research, Chungbuk National University, Cheongju, 28644, South Korea. scbae@chungbuk.ac.kr.ORCID http://orcid.org/0000-0002-4613-3517
Chungbuk National University · KRJeju National University · KRNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cellular decision regarding whether to undergo proliferation or death is made at the restriction (R)-point, which is disrupted in nearly all tumors. The identity of the molecular mechanisms that govern the R-point decision is one of the fundamental issues in cell biology. We found that early after mitogenic stimulation, RUNX3 binds to its target loci, where it opens chromatin structure by sequential recruitment of Trithorax group proteins and cell-cycle regulators to drive cells to the R-point. Soon after, RUNX3 closes these loci by recruiting Polycomb repressor complexes, causing the cell to pass through the R-point toward S phase. If the RAS signal is constitutively activated, RUNX3 inhibits cell cycle progression by maintaining R-point-associated genes in an open structure. Our results identify RUNX3 as a pioneer factor for the R-point and reveal the molecular mechanisms by which appropriate chromatin modifiers are selectively recruited to target loci for appropriate R-point decisions.

Indexed as

Gene Expression RegulationAnimalsButadienesCell Cycle CheckpointsCell Line, TumorCell ProliferationChromatinChromatin Assembly and DisassemblyCore Binding Factor Alpha 3 SubunitCyclin-Dependent Kinase 4Drosophila melanogasterEpithelial CellsHEK293 CellsHistone-Lysine N-MethyltransferaseHumansImidazolesButadienesCDK4 protein, humanChromatinCore Binding Factor Alpha 3 SubunitCyclin-Dependent Kinase 4Histone-Lysine N-MethyltransferaseImidazolesKMT2A protein, humanMAP2K1 protein, humanMAP Kinase Kinase 1MAP Kinase Kinase 4MTOR protein, humanMyeloid-Lymphoid Leukemia ProteinNitrilesp38 Mitogen-Activated Protein KinasespalbociclibPiperazinesPolycomb-Group ProteinsProtein Kinase InhibitorsPyridinesras ProteinsRNA, Small InterferingRunx3 protein, humanSB 203580SirolimusTOR Serine-Threonine KinasesU 0126

Identifiers

PMID31015486
PMCPMC6479060
OpenAlexW2950101086

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.