Evidence map›Paper›PMID 24674624›Full record

ReviewDNA repair2014

Functional overlaps between XLF and the ATM-dependent DNA double strand break response.

Vipul Kumar, Frederick W Alt, Valentyn Oksenych

Abstract readReview
In one paragraph

Review in DNA repair, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
  2. Orientation Regulation of Class-switch Recombination in Human B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2024
    Article
  3. Review
  4. When DNA-damage responses meet innate and adaptive immunity.Cellular and molecular life sciences : CMLS · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. DNA Damage Response.Biomolecules · 2021
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. AnThe Journal of biological chemistry · 2020
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Vipul KumarHoward Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children's Hospital, Department of Genetics, Harvard Medical School, Boston, MA 02115, United States.
Frederick W AltHoward Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children's Hospital, Department of Genetics, Harvard Medical School, Boston, MA 02115, United States. Electronic address: alt@enders.tch.harvard.edu.
Valentyn OksenychHoward Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children's Hospital, Department of Genetics, Harvard Medical School, Boston, MA 02115, United States. Electronic address: oksenych@gmail.com.
Harvard University · US

Funding

Molecular, Cellular, & Developmental Dynamics PhD ProgramT32GM007226 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI VAN VACTOR, DAVID L. · 1985 to 2021
$14.4M
Role of TACI mutations in CVIDP01AI076210 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TERHORST, CORNELIS P · 2009 to 2013
$9.0M
Howard Hughes Medical InstituteNIAID NIH HHS AI076210NIAID NIH HHS P01 AI076210NIGMS NIH HHS GM007226-38NIGMS NIH HHS T32 GM007226
6 · The paper itself

Abstract

Developing B and T lymphocytes generate programmed DNA double strand breaks (DSBs) during the V(D)J recombination process that assembles exons that encode the antigen-binding variable regions of antibodies. In addition, mature B lymphocytes generate programmed DSBs during the immunoglobulin heavy chain (IgH) class switch recombination (CSR) process that allows expression of different antibody heavy chain constant regions that provide different effector functions. During both V(D)J recombination and CSR, DSB intermediates are sensed by the ATM-dependent DSB response (DSBR) pathway, which also contributes to their joining via classical non-homologous end-joining (C-NHEJ). The precise nature of the interplay between the DSBR and C-NHEJ pathways in the context of DSB repair via C-NHEJ remains under investigation. Recent studies have shown that the XLF C-NHEJ factor has functional redundancy with several members of the ATM-dependent DSBR pathway in C-NHEJ, highlighting unappreciated major roles for both XLF as well as the DSBR in V(D)J recombination, CSR and C-NHEJ in general. In this review, we discuss current knowledge of the mechanisms that contribute to the repair of DSBs generated during B lymphocyte development and activation with a focus on potential functionally redundant roles of XLF and ATM-dependent DSBR factors.

Indexed as

DNA Breaks, Double-StrandedDNA End-Joining RepairAnimalsAtaxia Telangiectasia Mutated ProteinsB-LymphocytesDNA-Binding ProteinsHistonesHumansImmunoglobulin Class SwitchingLymphocyte ActivationV(D)J RecombinationAtaxia Telangiectasia Mutated ProteinsDNA-Binding ProteinsHistones53BP1ATMCernunnosDNA-PKcsNHEJV(D)J recombination

Identifiers

PMID24674624
PMCPMC4017585
OpenAlexW2147539498

What OpenQuestion holds

Textmetadata
LicenceTDM
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.