Evidence map›Paper›PMID 20133803›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Alternative end-joining catalyzes robust IgH locus deletions and translocations in the combined absence of ligase 4 and Ku70.

Cristian Boboila, Mila Jankovic, Catherine T Yan, Jing H Wang, Duane R Wesemann, Tingting Zhang, Alex Fazeli, Lauren Feldman, Andre Nussenzweig, Michel Nussenzweig and 1 more

Erratum issuedAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
–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

106 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Polλ promotes microhomology-mediated end-joining.Nature structural & molecular biology · 2023
    Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Tools for Efficient Genome Editing; ZFN, TALEN, and CRISPR.Methods in molecular biology (Clifton, N.J.) · 2022
    Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. DNA damage-induced phosphorylation of CtIP at a conserved ATM/ATR site T855 promotes lymphomagenesis in mice.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article

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

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

11 authors.

Cristian BoboilaDepartment of Genetics, Harvard Medical School, Boston, MA 02115, USA.
Mila Jankovic
Catherine T Yan
Jing H Wang
Duane R Wesemann
Tingting Zhang
Alex Fazeli
Lauren Feldman
Andre Nussenzweig
Michel Nussenzweig
Frederick W Alt

Funding

The Role of BCL-6 in Berminal Center FormationP01CA092625 · NCI · DANA-FARBER CANCER INSTITUTE · PI SHIPP, MARGARET A · 2001 to 2011
$32.9M
DNA RepairZIABC010283 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI NUSSENZWEIG, ANDRE A. · 2009 to 2025
$27.0M
Relationship between DNA damage detection and signalingZIABC010959 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI NUSSENZWEIG, ANDRE A. · 2009 to 2025
$27.0M
Transcriptional Regulation of the Allergic ResponseP01AI031541 · NIAID · CHILDREN'S HOSPITAL BOSTON · PI GEHA, RAIF SALIM · 1999 to 2007
$8.0M
Class Switch Recombination in B LymphocytesR37AI037526 · NIAID · ROCKEFELLER UNIVERSITY · PI NUSSENZWEIG, MICHEL C · 2014 to 2023
$5.4M
SIGNALLING PATHWAYS IN AUTOIMMUNITYR01AI037526 · NIAID · ROCKEFELLER UNIVERSITY · PI NUSSENZWEIG, MICHEL C · 1994 to 2012
$5.0M
Mechanisms that Regulate Antibody Class Switch Recombination and Somatic HypermutationR37AI077595 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI Frederick W. Alt · 2019 to 2026
$4.6M
Molecular Mechanisms of Class Switch RecombinationR01AI077595 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI ALT, FREDERICK W. · 2009 to 2018
$4.3M
Pathobiology of Cancer at the Host and Population LevelT32CA009382 · NCI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI YUAN, ZHI-MIN · 1985 to 2012
$2.9M
MOLECULAR BASIS OF IMMUNE FUNCTION IN HEALTH AND DISEASEU19AI031541 · NIAID · CHILDREN'S HOSPITAL BOSTON · PI GEHA, RAIF SALIM · 1995 to 1998
–
Howard Hughes Medical InstituteNCI NIH HHS CA092625NCI NIH HHS P01 CA092625NCI NIH HHS T32 CA009382NCI NIH HHS T32CA09382-26NIAID NIH HHS AI037526NIAID NIH HHS AI077595NIAID NIH HHS P01 AI031541NIAID NIH HHS R01 AI037526NIAID NIH HHS R01 AI077595NIAID NIH HHS R37 AI037526NIAID NIH HHS R37 AI077595NIAID NIH HHS U19 AI031541
6 · The paper itself

Abstract

Class switch recombination (CSR) in B lymphocytes is initiated by introduction of multiple DNA double-strand breaks (DSBs) into switch (S) regions that flank immunoglobulin heavy chain (IgH) constant region exons. CSR is completed by joining a DSB in the donor S mu to a DSB in a downstream acceptor S region (e.g., S gamma1) by end-joining. In normal cells, many CSR junctions are mediated by classical nonhomologous end-joining (C-NHEJ), which employs the Ku70/80 complex for DSB recognition and XRCC4/DNA ligase 4 for ligation. Alternative end-joining (A-EJ) mediates CSR, at reduced levels, in the absence of C-NHEJ, even in combined absence of Ku70 and ligase 4, demonstrating an A-EJ pathway totally distinct from C-NHEJ. Multiple DSBs are introduced into S mu during CSR, with some being rejoined or joined to each other to generate internal switch deletions (ISDs). In addition, S-region DSBs can be joined to other chromosomes to generate translocations, the level of which is increased by absence of a single C-NHEJ component (e.g., XRCC4). We asked whether ISD and S-region translocations occur in the complete absence of C-NHEJ (e.g., in Ku70/ligase 4 double-deficient B cells). We found, unexpectedly, that B-cell activation for CSR generates substantial ISD in both S mu and S gamma1 and that ISD in both is greatly increased by the absence of C-NHEJ. IgH chromosomal translocations to the c-myc oncogene also are augmented in the combined absence of Ku70 and ligase 4. We discuss the implications of these findings for A-EJ in normal and abnormal DSB repair.

Indexed as

DNA Breaks, Double-StrandedAnimalsAntigens, NuclearBase SequenceBlotting, SouthernB-LymphocytesDNA-Binding ProteinsDNA Ligase ATPDNA LigasesDNA PrimersDNA RepairGenes, mycImmunoglobulin Class SwitchingImmunoglobulin Heavy ChainsImmunoglobulin Switch RegionIn Situ Hybridization, FluorescenceAntigens, NuclearDNA-Binding ProteinsDNA Ligase ATPDNA LigasesDNA PrimersImmunoglobulin Heavy ChainsKu AutoantigenXrcc6 protein, mouse

Identifiers

PMID20133803
PMCPMC2840344

What OpenQuestion holds

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Registered trials

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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.