Evidence map›Paper›PMID 31776402›Full record

ArticleScientific reports2019

Phosphorylation of the histone demethylase KDM5B and regulation of the phenotype of triple negative breast cancer.

I-Ju Yeh, Emily Esakov, Justin D Lathia, Masaru Miyagi, Ofer Reizes, Monica M Montano

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. cGAS/STING-Independent Induction of Type I Interferon by Inhibitors of the Histone Methylase KDM5B.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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  5. Review
  6. Review
  7. Article
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  9. Article
  10. Hypoxia Stimulates SUMOylation-Dependent Stabilization of KDM5B.Frontiers in cell and developmental biology · 2021
    Article
  11. Article
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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

6 authors at 2 institutions in 1 country.

I-Ju YehDepartment of Pharmacology, Case Western Reserve University Cleveland, Cleveland, OH, 44106, USA.
Emily EsakovDepartment of Cellular and Molecular Medicine, Cleveland Clinic Lerner Research Institute, 9500 Euclid Ave., Cleveland, OH, 44195, USA.
Justin D LathiaDepartment of Cellular and Molecular Medicine, Cleveland Clinic Lerner Research Institute, 9500 Euclid Ave., Cleveland, OH, 44195, USA.
Masaru MiyagiDepartment of Pharmacology, Case Western Reserve University Cleveland, Cleveland, OH, 44106, USA.
Ofer ReizesDepartment of Cellular and Molecular Medicine, Cleveland Clinic Lerner Research Institute, 9500 Euclid Ave., Cleveland, OH, 44195, USA.
Monica M MontanoDepartment of Pharmacology, Case Western Reserve University Cleveland, Cleveland, OH, 44106, USA. mxm126@case.edu.
Case Western Reserve University · USCleveland Clinic Lerner College of Medicine · US

Funding

HEXIM1 regulation of transcriptional networks critical for tumor suppressionR01CA195558 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MONTANO, MONICA · 2016 to 2020
$1.8M
NCI NIH HHS R01 CA195558
6 · The paper itself

Abstract

Epigenetic modifications are known to play critical roles in the expression of genes related to differentiation and dedifferentiation. Histone lysine demethylase KDM5B (PLU-1) catalyzes the demethylation of histone H3 on Lys 4 (H3K4), which results in the repression of gene expression. KDM5B is involved in regulation of luminal and basal cell specific gene expression in breast cancers. However, the mechanisms by which KDM5B is regulated in breast cancer, in particular in response to post-translational signals is not well-defined. Here, we demonstrate that KDM5B is phosphorylated at Ser1456 by the cyclin-dependent kinase 1 (CDK1). Phosphorylation of KDM5B at Ser1456 attenuated the occupancy of KDM5B on the promoters of pluripotency genes. Moreover, KDM5B inhibited the expression of pluripotency genes, SOX2 and NANOG, and decreased the stem cell population in triple-negative breast cancer cell lines (TNBC). We previously reported that the tumor suppressor HEXIM1 is a mediator of KDM5B recruitment to its target genes, and HEXIM1 is required for the inhibition of nuclear hormone receptor activity by KDM5B. Similarly, HEXIM1 is required for regulation of pluripotency genes by KDM5B.

Indexed as

Cell Line, TumorEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticHumansJumonji Domain-Containing Histone DemethylasesNuclear ProteinsPhenotypePhosphorylationRepressor ProteinsRNA-Binding ProteinsTranscription FactorsTriple Negative Breast NeoplasmsHEXIM1 protein, humanJumonji Domain-Containing Histone DemethylasesKDM5B protein, humanNuclear ProteinsRepressor ProteinsRNA-Binding ProteinsTranscription Factors

Identifiers

PMID31776402
PMCPMC6881367
OpenAlexW2990388687

What OpenQuestion holds

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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.