Evidence map›Paper›PMID 23401855›Full record

ArticleMolecular and cellular biology2013

The MCM8-MCM9 complex promotes RAD51 recruitment at DNA damage sites to facilitate homologous recombination.

Jonghoon Park, David T Long, Kyung Yong Lee, Tarek Abbas, Etsuko Shibata, Masamitsu Negishi, Yunhai Luo, John C Schimenti, Agnieszka Gambus, Johannes C Walter and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.

  1. Pooled it
  2. Structural Activation of DNA Unwinding by MCM8/9/HROB.bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. MCM8-9 helicase activity protects primordial germ cell development to prevent premature ovarian insufficiency.Proceedings of the National Academy of Sciences of the United States of America · 2026
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24 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

11 authors at 4 institutions in 2 countries.

Jonghoon ParkDepartment of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia, USA.
David T Long
Kyung Yong Lee
Tarek Abbas
Etsuko Shibata
Masamitsu Negishi
Yunhai Luo
John C Schimenti
Agnieszka Gambus
Johannes C Walter
Anindya Dutta
University of Virginia · USCornell University · USHarvard University · USUniversity of Birmingham · GB

Funding

Women's Oncology Program - WONP30CA044579 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Thomas P. Loughran · 1987 to 2026
$72.1M
The role of MCM8-9 in genomic instability of cancersR01CA060499 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Anindya Dutta · 1994 to 2026
$8.6M
The Fanconi anemia pathway: role in DNA interstrand cross-link repairR01HL098316 · NHLBI · HARVARD MEDICAL SCHOOL · PI Johannes Walter · 2010 to 2026
$6.3M
Regulation of TIP60 by the ubiquitin-proteasome pathwayR01GM084465 · NIGMS · UNIVERSITY OF VIRGINIA · PI DUTTA, ANINDYA · 2008 to 2017
$2.4M
The Role of CRL4-Cdt2 E3 Ubiquitin Ligase in Genomic Stability and CancerR00CA140774 · NCI · UNIVERSITY OF VIRGINIA · PI ABBAS, TAREK A. · 2012 to 2014
$725k
NCI NIH HHS P30 CA044579NCI NIH HHS R00 CA140774NCI NIH HHS R01 CA060499NHLBI NIH HHS R01 HL098316NIGMS NIH HHS R01 GM084465
6 · The paper itself

Abstract

The minichromosome maintenance protein homologs MCM8 and MCM9 have previously been implicated in DNA replication elongation and prereplication complex (pre-RC) formation, respectively. We found that MCM8 and MCM9 physically associate with each other and that MCM8 is required for the stability of MCM9 protein in mammalian cells. Depletion of MCM8 or MCM9 in human cancer cells or the loss of function MCM9 mutation in mouse embryo fibroblasts sensitizes cells to the DNA interstrand cross-linking (ICL) agent cisplatin. Consistent with a role in the repair of ICLs by homologous recombination (HR), knockdown of MCM8 or MCM9 significantly reduces HR repair efficiency. Chromatin immunoprecipitation analysis using human DR-GFP cells or Xenopus egg extract demonstrated that MCM8 and MCM9 proteins are rapidly recruited to DNA damage sites and promote RAD51 recruitment. Thus, these two metazoan-specific MCM homologs are new components of HR and may represent novel targets for treating cancer in combination with DNA cross-linking agents.

Indexed as

Homologous RecombinationRecombinational DNA RepairAnimalsCell Cycle ProteinsCell Line, TumorCell SurvivalChromatin ImmunoprecipitationCisplatinDNA-Binding ProteinsDNA DamageGreen Fluorescent ProteinsHEK293 CellsHeLa CellsHumansMiceMinichromosome Maintenance ProteinsCell Cycle ProteinsCisplatinDNA-Binding ProteinsGreen Fluorescent ProteinsMCM8 protein, humanMCM9 protein, humanMinichromosome Maintenance ProteinsRAD51 protein, humanRad51 RecombinaseRNA, Small Interfering

Identifiers

PMID23401855
PMCPMC3624244
OpenAlexW2025862317

What OpenQuestion holds

Textmetadata
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.