Evidence map›Paper›PMID 29495487›Full record

ReviewBiomolecules2018

DOT1L and H3K79 Methylation in Transcription and Genomic Stability.

Katherine Wood, Michael Tellier, Shona Murphy

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
9.8field-weighted citation impact, top 1% 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

125 citing papers in PubMed, 213 citations in OpenAlex.

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65 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 1 country.

Katherine WoodDepartment of Biochemistry, University of Oxford, Oxford OX1 3RE, UK. katherine.wood-3@postgrad.manchester.ac.uk.ORCID 0000-0002-6459-2127
Michael TellierSir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK. michael.tellier@path.ox.ac.uk.
Shona MurphySir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK. shona.murphy@path.ox.ac.uk.ORCID 0000-0001-5276-9645
University of Oxford · GBUniversity of Manchester · GB

Funding

Medical Research Council G0400653Medical Research Council MR/M010716/1Wellcome TrustWellcome Trust WT106134AIA
6 · The paper itself

Abstract

The organization of eukaryotic genomes into chromatin provides challenges for the cell to accomplish basic cellular functions, such as transcription, DNA replication and repair of DNA damage. Accordingly, a range of proteins modify and/or read chromatin states to regulate access to chromosomal DNA. Yeast Dot1 and the mammalian homologue DOT1L are methyltransferases that can add up to three methyl groups to histone H3 lysine 79 (H3K79). H3K79 methylation is implicated in several processes, including transcription elongation by RNA polymerase II, the DNA damage response and cell cycle checkpoint activation. DOT1L is also an important drug target for treatment of mixed lineage leukemia (MLL)-rearranged leukemia where aberrant transcriptional activation is promoted by DOT1L mislocalisation. This review summarizes what is currently known about the role of Dot1/DOT1L and H3K79 methylation in transcription and genomic stability.

Indexed as

Genomic InstabilityTranscription Elongation, GeneticAnimalsHistone CodeHistone-Lysine N-MethyltransferaseHistonesHumansYeastsHistone-Lysine N-MethyltransferaseHistonesDot1DOT1Lgenome stabilityH3K79meRNA polymerase IItranscription

Identifiers

PMID29495487
PMCPMC5871980
OpenAlexW2791712220

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.