Evidence map›Paper›PMID 21724828›Full record

ReviewGenes & development2011

The diverse functions of Dot1 and H3K79 methylation.

Anh Tram Nguyen, Yi Zhang

Open access · diamondAbstract readReview
In one paragraph

Review in Genes & development, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 348 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
348citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

348 citing papers in PubMed, 2 syntheses or guidelines pooled it, 580 citations in OpenAlex.

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288 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

2 authors at 1 institution in 2 countries.

Anh Tram NguyenHoward Hughes Medical Institute, Chevy Chase, Maryland 20815, USA.
Yi Zhang
Howard Hughes Medical Institute · US

Funding

Role of histone methyltransferases hDOTIL in leukemogenesisR01CA119133 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZHANG, YI · 2006 to 2009
$1.0M
Howard Hughes Medical InstituteNCI NIH HHS CA119133NCI NIH HHS R01 CA119133
6 · The paper itself

Abstract

DOT1 (disruptor of telomeric silencing; also called Kmt4) was initially discovered in budding yeast in a genetic screen for genes whose deletion confers defects in telomeric silencing. Since the discovery ∼10 years ago that Dot1 and its mammalian homolog, DOT1L (DOT1-Like), possess histone methyltransferase activity toward histone H3 Lys 79, great progress has been made in characterizing their enzymatic activities and the role of Dot1/DOT1L-mediated H3K79 methylation in transcriptional regulation, cell cycle regulation, and the DNA damage response. In addition, gene disruption in mice has revealed that mouse DOT1L plays an essential role in embryonic development, hematopoiesis, cardiac function, and the development of leukemia. The involvement of DOT1L enzymatic activity in leukemogenesis driven by a subset of MLL (mixed-lineage leukemia) fusion proteins raises the possibility of targeting DOT1L for therapeutic intervention.

Indexed as

AnimalsCell CycleDNA RepairGene Expression Regulation, EnzymologicHistone-Lysine N-MethyltransferaseHistonesHumansMethylationMethyltransferasesDot1l protein, mouseHistone-Lysine N-MethyltransferaseHistonesMethyltransferases

Identifiers

PMID21724828
PMCPMC3134078
OpenAlexW2094498537

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.