Evidence map›Paper›PMID 27320916›Full record

ArticleCell reports2016

A Damage-Independent Role for 53BP1 that Impacts Break Order and Igh Architecture during Class Switch Recombination.

Pedro P Rocha, Ramya Raviram, Yi Fu, JungHyun Kim, Vincent M Luo, Arafat Aljoufi, Emily Swanzey, Alessandra Pasquarella, Alessia Balestrini, Emily R Miraldi and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Physiological role of the 3'IgH CBEs super-anchor in antibody class switching.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  6. A Tumor Suppressor Enhancer ofBlood cancer discovery · 2021
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
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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

14 authors at 4 institutions in 2 countries.

Pedro P RochaDepartment of Pathology, New York University School of Medicine, New York, NY 10016, USA. Electronic address: pereip02@nyumc.org.
Ramya RaviramDepartment of Pathology, New York University School of Medicine, New York, NY 10016, USA; Department of Biology, New York University, New York, NY 10003, USA.
Yi FuDepartment of Pathology, New York University School of Medicine, New York, NY 10016, USA.
JungHyun KimDepartment of Pathology, New York University School of Medicine, New York, NY 10016, USA.
Vincent M LuoDepartment of Pathology, New York University School of Medicine, New York, NY 10016, USA.
Arafat AljoufiDepartment of Pathology, New York University School of Medicine, New York, NY 10016, USA.
Emily SwanzeyDepartment of Developmental Genetics, New York University School of Medicine, New York, NY 10016, USA.
Alessandra PasquarellaLudwig Maximilians University and Munich Center for Integrated Protein Science (CiPSM), Biomedical Center, Planegg-Martinsried 80336, Germany.
Alessia BalestriniMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Emily R MiraldiSimons Center for Data Analysis, New York, NY 10010, USA.
Richard BonneauDepartment of Biology, New York University, New York, NY 10003, USA; Department of Computer Science, Courant Institute of Mathematical Sciences, New York, NY 10012, USA; Simons Center for Data Analysis, New York, NY 10010, USA.
John PetriniMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Gunnar SchottaLudwig Maximilians University and Munich Center for Integrated Protein Science (CiPSM), Biomedical Center, Planegg-Martinsried 80336, Germany.
Jane A SkokDepartment of Pathology, New York University School of Medicine, New York, NY 10016, USA. Electronic address: jane.skok@nyumc.org.
New York University · USLudwig-Maximilians-Universität München · DEMemorial Sloan Kettering Cancer Center · USSimons Foundation · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ANIRBAN MAITRA · 1985 to 2026
$83.1M
Regulation of the DNA damage response by the Mre11 complexR37GM059413 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI PETRINI, JOHN HJ · 2012 to 2020
$5.2M
The Mre11 complex: linking recombination to checkpointsR01GM059413 · NIGMS · UNIVERSITY OF WISCONSIN MADISON · PI PETRINI, JOHN HJ · 1999 to 2011
$5.2M
The Proneural Perivascular Niche and Therapeutic ResponseU54CA163167 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI HOLLAND, ERIC C. · 2011 to 2015
$4.6M
Role Of Nuclear Organization In Protecting Genome Stability During RecombinationR01GM086852 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI KLUGER, YUVAL, SKOK, JANE AMANDA · 2008 to 2016
$3.8M
Enhancer Driven Gene Regulation During Lymphocyte DevelopmentR01GM112192 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SKOK, JANE AMANDA · 2014 to 2016
$1.6M
The Role of RNA in Regulating recombination and allelic exclusionR21AI107069 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SKOK, JANE AMANDA · 2013 to 2014
$453k
A novel role for 53BP1 independent of damage that controls chromatin structureK99GM117302 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ROCHA, PEDRO P · 2016 to 2017
$180k
FASEB SRC on Genetic Recombination and Genome RearrangementsR13CA162528 · NCI · FEDERATION OF AMER SOC FOR EXPER BIOLOGY · PI PETRINI, JOHN HJ · 2011 to 2011
$5k
NCI NIH HHS P30 CA008748NCI NIH HHS P30 CA016087NCI NIH HHS R13 CA162528NCI NIH HHS U54 CA163167NIAID NIH HHS R21 AI107069NIGMS NIH HHS K99 GM117302NIGMS NIH HHS R01 GM059413NIGMS NIH HHS R01 GM086852NIGMS NIH HHS R01 GM112192NIGMS NIH HHS R37 GM059413
6 · The paper itself

Abstract

During class switch recombination (CSR), B cells replace the Igh Cμ or δ exons with another downstream constant region exon (CH), altering the antibody isotype. CSR occurs through the introduction of AID-mediated double-strand breaks (DSBs) in switch regions and subsequent ligation of broken ends. Here, we developed an assay to investigate the dynamics of DSB formation in individual cells. We demonstrate that the upstream switch region Sμ is first targeted during recombination and that the mechanism underlying this control relies on 53BP1. Surprisingly, regulation of break order occurs through residual binding of 53BP1 to chromatin before the introduction of damage and independent of its established role in DNA repair. Using chromosome conformation capture, we show that 53BP1 mediates changes in chromatin architecture that affect break order. Finally, our results explain how changes in Igh architecture in the absence of 53BP1 could promote inversional rearrangements that compromise CSR.

Indexed as

DNA Breaks, Double-StrandedRecombination, GeneticAnimalsBase SequenceChromatinImmunoglobulin Class SwitchingImmunoglobulin Heavy ChainsMiceProtein BindingSingle-Cell AnalysisTumor Suppressor p53-Binding Protein 1ChromatinImmunoglobulin Heavy ChainsTrp53bp1 protein, mouseTumor Suppressor p53-Binding Protein 1

Identifiers

PMID27320916
PMCPMC4927351
OpenAlexW2437539949

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.