Evidence map›Paper›PMID 23241889›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

The histone methyltransferase MMSET regulates class switch recombination.

Huadong Pei, Xiaosheng Wu, Tongzheng Liu, Kefei Yu, Diane F Jelinek, Zhenkun Lou

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

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  15. Histone methyltransferase MMSET promotes AID-mediated DNA breaks at the donor switch region during class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2017
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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 4 institutions in 2 countries.

Huadong PeiDivision of Oncology Research, Mayo Clinic, Rochester, MN 55905, USA.
Xiaosheng Wu
Tongzheng Liu
Kefei Yu
Diane F Jelinek
Zhenkun Lou
Mayo Clinic · USMayo Clinic in Arizona · USMayo Clinic in Florida · USMichigan State University · US

Funding

Targeted MV-CEA as a Potent Antitumor Agent against GBMP50CA108961 · NCI · MAYO CLINIC ROCHESTER · PI O'NEILL, BRIAN PATRICK · 2004 to 2015
$22.5M
Ubiquitination and the DNA Damage Response PathwayR01CA130996 · NCI · MAYO CLINIC ROCHESTER · PI LOU, ZHENKUN · 2008 to 2018
$3.3M
Regultion of p53 DeubiquitinationR01CA148940 · NCI · MAYO CLINIC ROCHESTER · PI LOU, ZHENKUN · 2011 to 2015
$1.6M
Role of the BCR in B Cell Chronic Lymphocytic LeukemiaR01CA136591 · NCI · MAYO CLINIC ROCHESTER · PI JELINEK, DIANE F · 2009 to 2013
$1.5M
Targeted DNA cleavage at switch regions in immunoglobulin class switch recombinatR01AI081817 · NIAID · MICHIGAN STATE UNIVERSITY · PI YU, KEFEI · 2009 to 2013
$1.5M
The Role of MMSET in DNA damage response and ChemoradioresistanceR01CA151329 · NCI · MAYO CLINIC ROCHESTER · PI LOU, ZHENKUN · 2010 to 2011
$645k
NCI NIH HHS CA108961NCI NIH HHS CA130996NCI NIH HHS P50 CA108961NCI NIH HHS R01 CA130996NCI NIH HHS R01 CA136591NCI NIH HHS R01 CA148940NCI NIH HHS R01 CA151329NIAID NIH HHS R01 AI081817
6 · The paper itself

Abstract

Wolf-Hirschhorn syndrome (WHS) is a genetic disease with characteristic facial features and developmental disorders. Of interest, loss of the MMSET gene (also known as WHSC1) is considered to be responsible for the core phenotypes of this disease. Patients with WHS also display Ab deficiency, although the underlying cause of this deficiency is unclear. Recent studies suggest that the histone methyltransferase activity of MMSET plays an important role in the DNA damage response by facilitating the recruitment of 53BP1 to sites of DNA damage. We hypothesize that MMSET also regulates class switch recombination (CSR) through its effect on 53BP1. In this study, we show that MMSET indeed plays an important role in CSR through its histone methyltransferase activity. Knocking down MMSET expression impaired 53BP1 recruitment as well as the germline transcription of the Igh switch regions, resulting in defective CSR but no effect on cell growth and viability. These results suggest that defective CSR caused by MMSET deficiency could be a cause of Ab deficiency in WHS patients.

Indexed as

Cell LineGene Expression RegulationGenetic LociHistone-Lysine N-MethyltransferaseHistonesHumansImmunoglobulin Class SwitchingImmunoglobulin Heavy ChainsIntracellular Signaling Peptides and ProteinsMethylationProtein BindingRepressor ProteinsTranscription, GeneticTumor Suppressor p53-Binding Protein 1V(D)J RecombinationWolf-Hirschhorn SyndromeHistone-Lysine N-MethyltransferaseHistonesImmunoglobulin Heavy ChainsIntracellular Signaling Peptides and ProteinsNSD2 protein, humanRepressor ProteinsTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1

Identifiers

PMID23241889
PMCPMC3775478
OpenAlexW1824521228

What OpenQuestion holds

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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.