Evidence map›Paper›PMID 30232008›Full record

ArticleCell reports2018

Loss of PICH Results in Chromosomal Instability, p53 Activation, and Embryonic Lethality.

Eliene Albers, Mauro Sbroggiò, David Pladevall-Morera, Anna H Bizard, Alexandra Avram, Patricia Gonzalez, Javier Martin-Gonzalez, Ian D Hickson, Andres J Lopez-Contreras

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
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  4. Research advances in the molecular classification of gastric cancer.Cellular oncology (Dordrecht, Netherlands) · 2024
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  5. DNA strand breaks at centromeres: Friend or foe?Seminars in cell & developmental biology · 2024
    Review
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  16. Observational
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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

9 authors at 2 institutions in 2 countries.

Eliene AlbersDepartment of Cellular and Molecular Medicine, Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Copenhagen 2200, Denmark.
Mauro SbroggiòDepartment of Cellular and Molecular Medicine, Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Copenhagen 2200, Denmark.
David Pladevall-MoreraDepartment of Cellular and Molecular Medicine, Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Copenhagen 2200, Denmark.
Anna H BizardDepartment of Cellular and Molecular Medicine, Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Copenhagen 2200, Denmark.
Alexandra AvramDepartment of Cellular and Molecular Medicine, Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Copenhagen 2200, Denmark.
Patricia GonzalezHistopathology Core Unit, Spanish National Cancer Research Centre, Madrid 28029, Spain.
Javier Martin-GonzalezTransgenic Core Facility, Department of Experimental Medicine, University of Copenhagen, Copenhagen 2200, Denmark.
Ian D HicksonDepartment of Cellular and Molecular Medicine, Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Copenhagen 2200, Denmark.
Andres J Lopez-ContrerasDepartment of Cellular and Molecular Medicine, Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Copenhagen 2200, Denmark. Electronic address: ajlopez@sund.ku.dk.
University of Copenhagen · DKSpanish National Cancer Research Centre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PICH is a DNA translocase necessary for the resolution of ultrafine anaphase DNA bridges and to ensure the fidelity of chromosomal segregation. Here, we report the generation of an animal model deficient for PICH that allowed us to investigate its physiological relevance. Pich KO mice lose viability during embryonic development due to a global accumulation of DNA damage. However, despite the presence of chromosomal instability, extensive p53 activation, and increased apoptosis throughout the embryo, Pich KO embryos survive until day 12.5 of embryonic development. The absence of p53 failed to improve the viability of the Pich KO embryos, suggesting that the observed developmental defects are not solely due to p53-induced apoptosis. Moreover, Pich-deficient mouse embryonic fibroblasts exhibit chromosomal instability and are resistant to RAS

Indexed as

Chromosomal InstabilityAnimalsApoptosisCells, CulturedDNA DamageDNA HelicasesEmbryonic DevelopmentMiceTumor Suppressor Protein p53DNA HelicasesErcc6L protein, mouseTumor Suppressor Protein p53DNA damageErcc6lgenomic instabilityPichUFBsultrafine anaphase DNA bridgesX chromosome inactivation

Identifiers

PMID30232008
PMCPMC6167640
OpenAlexW2892150717

What OpenQuestion holds

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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.