Evidence map›Paper›PMID 24526115›Full record

ReviewCell cycle (Georgetown, Tex.)2014

The histone methyltransferase Dot1/DOT1L as a critical regulator of the cell cycle.

Wootae Kim, Minji Choi, Ja-Eun Kim

Open access · hybridAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

65 citing papers in PubMed, 112 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Neurod2 knockdown inmicroPublication biology · 2026
    Article
  8. Review
  9. Discovery of the first-in-class DOT1L PROTAC degrader.European journal of medicinal chemistry · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Connecting the DOTs on Cell Identity.Frontiers in cell and developmental biology · 2022
    Review
  20. Article

5 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Wootae KimDepartment of Pharmacology; School of Medicine; Kyung Hee University; Seoul, Republic of Korea; Department of Biomedical Science; Graduate School; Kyung Hee University; Seoul, Republic of Korea.
Minji ChoiDepartment of Pharmacology; School of Medicine; Kyung Hee University; Seoul, Republic of Korea; Department of Biomedical Science; Graduate School; Kyung Hee University; Seoul, Republic of Korea.
Ja-Eun KimDepartment of Pharmacology; School of Medicine; Kyung Hee University; Seoul, Republic of Korea; Department of Biomedical Science; Graduate School; Kyung Hee University; Seoul, Republic of Korea.
Indiana University School of MedicineKyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dot1/DOT1L catalyzes the methylation of histone H3 lysine 79 (H3K79), which regulates diverse cellular processes, such as development, reprogramming, differentiation, and proliferation. In regards to these processes, studies of Dot1/DOT1L-dependent H3K79 methylation have mainly focused on the transcriptional regulation of specific genes. Although the gene transcription mediated by Dot1/DOT1L during the cell cycle is not fully understood, H3K79 methylation plays a critical role in the progression of G 1 phase, S phase, mitosis, and meiosis. This modification may contribute to the chromatin structure that controls gene expression, replication initiation, DNA damage response, microtubule reorganization, chromosome segregation, and heterochromatin formation. Overall, Dot1/DOT1L is required to maintain genomic and chromosomal stability. This review summarizes the several functions of Dot1/DOT1L and highlights its role in cell cycle regulation.

Indexed as

Cell CycleAnimalsCellular ReprogrammingChromatinDNA DamageHistone-Lysine N-MethyltransferaseHistonesHumansLysineMethylationMethyltransferasesNeoplasmsChromatinDOT1L protein, humanHistone-Lysine N-MethyltransferaseHistonesLysineMethyltransferasescell cycledifferentiationDOT1LH3K79histone methyltransferasemeiosismitosisproliferationreplicationsenescence

Identifiers

PMID24526115
PMCPMC3979909
OpenAlexW2049703577

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.