Evidence map›Paper›PMID 24746816›Full record

ArticleCell reports2014

Impaired p32 regulation caused by the lymphoma-prone RECQ4 mutation drives mitochondrial dysfunction.

Jiin-Tarng Wang, Xiaohua Xu, Aileen Y Alontaga, Yuan Chen, Yilun Liu

Abstract read
In one paragraph

Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Molecular Mechanisms of the RECQ4 Pathogenic Mutations.Frontiers in molecular biosciences · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Borrowing nuclear DNA helicases to protect mitochondrial DNA.International journal of molecular sciences · 2015
    Review
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

5 authors.

Jiin-Tarng WangDepartment of Radiation Biology, Beckman Research Institute, City of Hope, Duarte, CA 91010-3000, USA.
Xiaohua XuDepartment of Radiation Biology, Beckman Research Institute, City of Hope, Duarte, CA 91010-3000, USA.
Aileen Y AlontagaDepartment of Molecular Medicine, Beckman Research Institute, City of Hope, Duarte, CA 91010-3000, USA.
Yuan ChenDepartment of Molecular Medicine, Beckman Research Institute, City of Hope, Duarte, CA 91010-3000, USA.
Yilun LiuDepartment of Radiation Biology, Beckman Research Institute, City of Hope, Duarte, CA 91010-3000, USA. Electronic address: yiliu@coh.org.

Funding

SUMO modification and DNA damage response in cancer therapyR01GM086171 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHEN, YUAN · 2008 to 2020
$5.2M
The molecular basis of RECQ4-associated genetic disorders and cancer predispositiR01CA151245 · NCI · YALE UNIVERSITY · PI LIU, YILUN · 2011 to 2015
$1.7M
SENP:Conformational Dynamics and Inhibition by Small MoleculesR01GM102538 · NIGMS · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI CHEN, YUAN · 2012 to 2015
$1.7M
NCI NIH HHS R01 CA151245NIGMS NIH HHS R01 GM 086171NIGMS NIH HHS R01 GM086171NIGMS NIH HHS R01 GM102538
6 · The paper itself

Abstract

Mitochondrial DNA (mtDNA) encodes proteins that are important for ATP biogenesis. Therefore, changes in mtDNA copy number will have profound consequences on cell survival and proliferation. RECQ4 DNA helicase participates in both nuclear DNA and mtDNA synthesis. However, the mechanism that balances the distribution of RECQ4 in the nucleus and mitochondria is unknown. Here, we show that RECQ4 forms protein complexes with Protein Phosphatase 2A (PP2A), nucleophosmin (NPM), and mitochondrial p32 in different cellular compartments. Critically, the interaction with p32 negatively controls the transport of both RECQ4 and its chromatin-associated replication factor, MCM10, from the nucleus to mitochondria. Amino acids that are deleted in the most common cancer-associated RECQ4 mutation are required for the interaction with p32. Hence, this RECQ4 mutant, which is no longer regulated by p32 and is enriched in the mitochondria, interacts with the mitochondrial replication helicase PEO1 and induces abnormally high levels of mtDNA synthesis.

Indexed as

Carrier ProteinsCell NucleusCell ProliferationDNA, MitochondrialHEK293 CellsHumansLymphomaMetabolomeMinichromosome Maintenance ProteinsMitochondriaMitochondrial ProteinsNuclear ProteinsNucleophosminProtein BindingProtein Interaction MapsProtein Phosphatase 2C1QBP protein, humanCarrier ProteinsDNA, MitochondrialMCM10 protein, humanMinichromosome Maintenance ProteinsMitochondrial ProteinsNPM1 protein, humanNuclear ProteinsNucleophosminProtein Phosphatase 2RecQ HelicasesRECQL4 protein, humanRNA, Small Interfering

Identifiers

PMID24746816
PMCPMC4029353

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Registered trials

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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.