Evidence map›Paper›PMID 30622182›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

The methyltransferase SETD6 regulates Mitotic progression through PLK1 methylation.

Michal Feldman, Zlata Vershinin, Inna Goliand, Natalie Elia, Dan Levy

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 48 citations in OpenAlex.

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  6. KDM5D histone demethylase mediates p38α inactivation via its enzymatic activity to inhibit cancer progression.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  16. Deletion of Mouse Setd4 Promotes the Recovery of Hematopoietic Failure.International journal of radiation oncology, biology, physics · 2020
    Article
  17. Article
  18. The Journal of biological chemistry · 2020
    Article
  19. 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

5 authors at 1 institution in 1 country.

Michal FeldmanThe Shraga Segal Department of Microbiology, Immunology and Genetics, Ben-Gurion University of the Negev, 84105 Be'er-Sheva, Israel; femichal@post.bgu.ac.il ledan@post.bgu.ac.il.
Zlata VershininThe Shraga Segal Department of Microbiology, Immunology and Genetics, Ben-Gurion University of the Negev, 84105 Be'er-Sheva, Israel.
Inna GoliandThe National Institute for Biotechnology in the Negev, Ben-Gurion University of the Negev, 84105 Be'er-Sheva, Israel.
Natalie EliaThe National Institute for Biotechnology in the Negev, Ben-Gurion University of the Negev, 84105 Be'er-Sheva, Israel.
Dan LevyThe Shraga Segal Department of Microbiology, Immunology and Genetics, Ben-Gurion University of the Negev, 84105 Be'er-Sheva, Israel; femichal@post.bgu.ac.il ledan@post.bgu.ac.il.ORCID 0000-0003-0719-0305
Ben-Gurion University of the Negev · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lysine methylation, catalyzed by protein lysine methyltransferases (PKMTs), is a key player in regulating intracellular signaling pathways. However, the role of PKMTs and the methylation of nonhistone proteins during the cell cycle are largely unexplored. In a recent proteomic screen, we identified that the PKMT SETD6 methylates PLK1-a key regulator of mitosis and highly expressed in tumor cells. In this study, we provide evidence that SETD6 is involved in cell cycle regulation. SETD6-deficient cells were observed to progress faster through the different mitotic steps toward the cytokinesis stage. Mechanistically, we found that during mitosis SETD6 binds and methylates PLK1 on two lysine residues: K209 and K413. Lack of methylation of these two residues results in increased kinase activity of PLK1, leading to accelerated mitosis and faster cellular proliferation, similarly to SETD6-deficient cells. Taken together, our findings reveal a role for SETD6 in regulating mitotic progression, suggesting a pathway through which SETD6 methylation activity contributes to normal mitotic pace.

Indexed as

Cell CycleCell Cycle ProteinsCell Line, TumorCell ProliferationCytokinesisHeLa CellsHumansLysineMethylationMitosisPolo-Like Kinase 1Protein MethyltransferasesProtein Serine-Threonine KinasesProteomicsProto-Oncogene ProteinsSignal TransductionCell Cycle ProteinsLysinePolo-Like Kinase 1Protein MethyltransferasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsSETD6 protein, humancell cyclelysine methylationmitosisPLK1SETD6

Identifiers

PMID30622182
PMCPMC6347700
OpenAlexW2910840103

What OpenQuestion holds

Textmetadata
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.