Evidence map›Paper›PMID 31731258›Full record

ArticleDNA repair2020

Absence of XRCC4 and its paralogs in human cells reveal differences in outcomes for DNA repair and V(D)J recombination.

Brian Ruis, Amy Molan, Taylor Takasugi, Eric A Hendrickson

Open access · greenAbstract read
In one paragraph

Article in DNA repair, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Phosphorylation of DNA-PKcs at the S2056 cluster ensures efficient and productive lymphocyte development in XLF-deficient mice.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  6. Article
  7. DNA damage and repair: underlying mechanisms leading to microcephaly.Frontiers in cell and developmental biology · 2023
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
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

4 authors at 1 institution in 1 country.

Brian RuisDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota Medical School, Minneapolis, MN, 55455, United States.
Amy MolanDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota Medical School, Minneapolis, MN, 55455, United States.
Taylor TakasugiDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota Medical School, Minneapolis, MN, 55455, United States.
Eric A HendricksonDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota Medical School, Minneapolis, MN, 55455, United States. Electronic address: hendr064@umn.edu.
University of Minnesota Medical Center · US

Funding

The mechanism of Cas9/CRISPR-initiated genome modification in human somatic cellsR01GM088351 · NIGMS · UNIVERSITY OF MINNESOTA · PI HENDRICKSON, ERIC A · 2010 to 2018
$2.3M
Ligase III regulates survival from crisis induced by gradual telomere shorteningR01CA190492 · NCI · UNIVERSITY OF MINNESOTA · PI HENDRICKSON, ERIC A · 2015 to 2019
$1.7M
Ku regulates non-homologous end joining pathways in human somatic cellsR01CA154461 · NCI · UNIVERSITY OF MINNESOTA · PI HENDRICKSON, ERIC A · 2011 to 2015
$1.6M
Ku86 Controls DNA Repair, Telomeres &Genomic StabilityR01GM069576 · NIGMS · UNIVERSITY OF MINNESOTA TWIN CITIES · PI HENDRICKSON, ERIC A · 2005 to 2008
$976k
NCI NIH HHS R01 CA154461NCI NIH HHS R01 CA190492NIGMS NIH HHS R01 GM069576NIGMS NIH HHS R01 GM088351
6 · The paper itself

Abstract

The repair of DNA double-stranded breaks (DSBs) is an essential function performed by the Classical Non-Homologous End-Joining (C-NHEJ) pathway in higher eukaryotes. C-NHEJ, in fact, does double duty as it is also required for the repair of the intermediates formed during lymphoid B- and T-cell recombination. Consequently, the failure to properly repair DSBs leads to both genomic instability and immunodeficiency. A critical DSB protein required for C-NHEJ is the DNA Ligase IV (LIGIV) accessory factor, X-Ray Cross Complementing 4 (XRCC4). XRCC4 is believed to stabilize LIGIV, participate in LIGIV activation, and to help tether the broken DSB ends together. XRCC4's role in these processes has been muddied by the identification of two additional XRCC4 paralogs, XRCC4-Like Factor (XLF), and Paralog of XRCC4 and XLF (PAXX). The roles that these paralogs play in C-NHEJ is partially understood, but, in turn, has itself been obscured by species-specific differences observed in the absence of one or the other paralogs. In order to investigate the role(s) that XRCC4 may play, with or without XLF and/or PAXX, in lymphoid variable(diversity)joining [V(D)J] recombination as well as in DNA DSB repair in human somatic cells, we utilized gene targeting to inactivate the XRCC4 gene in both parental and XLF

Indexed as

DNA-Binding ProteinsDNA Breaks, Double-StrandedDNA End-Joining RepairDNA Ligase ATPDNA Repair EnzymesEtoposideGene TargetingHCT116 CellsHumansV(D)J RecombinationDNA-Binding ProteinsDNA Ligase ATPDNA Repair EnzymesEtoposideLIG4 protein, humanNHEJ1 protein, humanPAXX protein, humanXRCC4 protein, humanAlternative-EJ (aEJ)Classic non-homologous end joining (C-NHEJ)Paralog of XRCC4 and XLF (PAXX)Variable(Diversity)Joining recombination [V(D)J recombination]X-ray cross complementing 4 (XRCC4)XRCC4-like factor (XLF)

Identifiers

PMID31731258
PMCPMC6952554
OpenAlexW2987060340

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.