Evidence map›Paper›PMID 39386666›Full record

ArticlebioRxiv : the preprint server for biology2024

Senataxin and DNA-PKcs Redundantly Promote Non-Homologous End Joining Repair of DNA Double Strand Breaks During V(D)J Recombination.

Bo-Ruei Chen, Thu Pham, Lance D Reynolds, Nghi Dang, Yanfeng Zhang, Kimberly Manalang, Gabriel Matos-Rodrigues, Jason Romero Neidigk, Andre Nussenzweig, Jessica K Tyler and 1 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Bo-Ruei ChenDivision of Hematology and Oncology, University of Alabama at Birmingham, Birmingham, AL 35233.ORCID 0000-0001-6404-2099
Thu PhamDivision of Hematology and Oncology, University of Alabama at Birmingham, Birmingham, AL 35233.
Lance D ReynoldsDivision of Hematology and Oncology, University of Alabama at Birmingham, Birmingham, AL 35233.
Nghi DangDivision of Hematology and Oncology, University of Alabama at Birmingham, Birmingham, AL 35233.
Yanfeng ZhangO'Neal Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL 35233.
Kimberly ManalangDivision of Hematology and Oncology, University of Alabama at Birmingham, Birmingham, AL 35233.
Gabriel Matos-RodriguesLaboratory of Genome Integrity, National Cancer Institute, Bethesda, MD 20892.
Jason Romero NeidigkDivision of Hematology and Oncology, University of Alabama at Birmingham, Birmingham, AL 35233.
Andre NussenzweigLaboratory of Genome Integrity, National Cancer Institute, Bethesda, MD 20892.
Jessica K TylerDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY 10065.
Barry P SleckmanDivision of Hematology and Oncology, University of Alabama at Birmingham, Birmingham, AL 35233.

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MICHAEL JAMES BERTRAM · 1985 to 2026
$165.9M
THE V(D)J RECOMBINATION REACTION AND ITS IMPACT ON LYMPHOCYTE DEVELOPMENTR01AI047829 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI SLECKMAN, BARRY P · 2000 to 2021
$7.0M
Chromatin's Role in Repair of Radiation-induced Damage.R01CA095641 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI TYLER, JESSICA K · 2002 to 2023
$5.2M
Novel pathways that regulate DNA double-strand break repair events in mammalian cellsR35GM139816 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI TYLER, JESSICA K · 2021 to 2025
$2.1M
NCI NIH HHS P30 CA013148NCI NIH HHS R01 CA095641NIAID NIH HHS R01 AI047829NIGMS NIH HHS R35 GM139816
6 · The paper itself

Abstract

Non-homologous end joining (NHEJ) is required for repairing DNA double strand breaks (DSBs) generated by the RAG endonuclease during lymphocyte antigen receptor gene assembly by V(D)J recombination. The Ataxia telangiectasia mutated (ATM) and DNA-dependent protein kinase catalytic subunit (DNA-PKcs) kinases regulate functionally redundant pathways required for NHEJ. Here we report that loss of the senataxin helicase leads to a significant defect in RAG DSB repair upon inactivation of DNA-PKcs. The NHEJ function of senataxin is redundant with the RECQL5 helicase and the HLTF translocase and is epistatic with ATM. Co-inactivation of ATM, RECQL5 and HLTF results in an NHEJ defect similar to that from the combined deficiency of DNA-PKcs and senataxin or losing senataxin, RECQL5 and HLTF. These data suggest that ATM and DNA-PKcs regulate the functions of senataxin and RECQL5/HLTF, respectively to provide redundant support for NHEJ.

Identifiers

PMID39386666
PMCPMC11463457

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.