Evidence map›Paper›PMID 24837676›Full record

ArticleMolecular cell2014

Catalytic and noncatalytic roles of the CtIP endonuclease in double-strand break end resection.

Nodar Makharashvili, Anthony T Tubbs, Soo-Hyun Yang, Hailong Wang, Olivia Barton, Yi Zhou, Rajashree A Deshpande, Ji-Hoon Lee, Markus Lobrich, Barry P Sleckman and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
10.7field-weighted citation impact, top 1% 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

116 citing papers in PubMed, 176 citations in OpenAlex.

  1. Article
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  9. Syk-dependent homologous recombination activation promotes cancer resistance to DNA targeted therapy.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2024
    Article
  10. Review
  11. Review
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  16. Article
  17. Critical DNA damaging pathways in tumorigenesis.Seminars in cancer biology · 2022
    Review
  18. Article
  19. Review
  20. Article

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

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

12 authors at 4 institutions in 2 countries.

Nodar MakharashviliThe Howard Hughes Medical Institute and Department of Molecular Biosciences, Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA.
Anthony T TubbsDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Soo-Hyun YangThe Howard Hughes Medical Institute and Department of Molecular Biosciences, Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA.
Hailong WangDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.
Olivia BartonRadiation Biology and DNA Repair, Darmstadt University of Technology, 64287 Darmstadt, Germany.
Yi ZhouThe Howard Hughes Medical Institute and Department of Molecular Biosciences, Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA.
Rajashree A DeshpandeThe Howard Hughes Medical Institute and Department of Molecular Biosciences, Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA.
Ji-Hoon LeeThe Howard Hughes Medical Institute and Department of Molecular Biosciences, Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA.
Markus LobrichRadiation Biology and DNA Repair, Darmstadt University of Technology, 64287 Darmstadt, Germany.
Barry P SleckmanDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Xiaohua WuDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.
Tanya T PaullThe Howard Hughes Medical Institute and Department of Molecular Biosciences, Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA. Electronic address: tpaull@utexas.edu.
Howard Hughes Medical Institute · USScripps Research Institute · USTechnische Universität Darmstadt · DEWashington University in St. Louis · US

Funding

ATM FUNCTION DURING V(D)J RECOMBINATIONR01AI074953 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI SLECKMAN, BARRY P · 2009 to 2023
$5.9M
Role of the Mre11/Rad50/Nbs1 complex in DNA damage response pathwaysR01CA102361 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI WU, XIAOHUA · 2003 to 2012
$4.1M
S-phase checkpoint and rereplication in mammalian cellsR01GM080677 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI WU, XIAOHUA · 2010 to 2018
$2.9M
Mrell/Rad50/Nbs1 and DNA double strand break repairR01CA094008 · NCI · UNIVERSITY OF TEXAS AUSTIN · PI PAULL, TANYA T · 2002 to 2011
$2.8M
Role of BRCA1 and its association protein CtlP in DNA double-strand break repairR01CA140972 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI WU, XIAOHUA · 2010 to 2014
$2.2M
NCI NIH HHS CA094008NCI NIH HHS CA102361NCI NIH HHS CA140972NCI NIH HHS R01 CA094008NCI NIH HHS R01 CA102361NCI NIH HHS R01 CA140972NIAID NIH HHS AI074953NIAID NIH HHS R01 AI074953NIGMS NIH HHS R01 GM080677
6 · The paper itself

Abstract

The carboxy-terminal binding protein (CtBP)-interacting protein (CtIP) is known to function in 5' strand resection during homologous recombination, similar to the budding yeast Sae2 protein, but its role in this process is unclear. Here, we characterize recombinant human CtIP and find that it exhibits 5' flap endonuclease activity on branched DNA structures, independent of the MRN complex. Phosphorylation of CtIP at known damage-dependent sites and other sites is essential for its catalytic activity, although the S327 and T847 phosphorylation sites are dispensable. A catalytic mutant of CtIP that is deficient in endonuclease activity exhibits wild-type levels of homologous recombination at restriction enzyme-generated breaks but is deficient in processing topoisomerase adducts and radiation-induced breaks in human cells, suggesting that the nuclease activity of CtIP is specifically required for the removal of DNA adducts at sites of DNA breaks.

Indexed as

DNA Breaks, Double-StrandedBinding SitesCarrier ProteinsCatalysisCell LineCell SurvivalDNADNA-Binding ProteinsDNA End-Joining RepairEndodeoxyribonucleasesEndonucleasesHumansNuclear ProteinsPhosphorylationProtein Processing, Post-TranslationalRadiation, IonizingCarrier ProteinsDNADNA-Binding ProteinsEndodeoxyribonucleasesEndonucleasesNuclear ProteinsRBBP8 protein, human

Identifiers

PMID24837676
PMCPMC4079050
OpenAlexW2075477236

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.