Evidence map›Paper›PMID 25695197›Full record

ArticleCell cycle (Georgetown, Tex.)2015

DNA damage-induced nuclear translocation of Apaf-1 is mediated by nucleoporin Nup107.

Léonard Jagot-Lacoussiere, Audrey Faye, Heriberto Bruzzoni-Giovanelli, Bruno O Villoutreix, Jean-Christophe Rain, Jean-Luc Poyet

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024
    Review
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  9. Article
  10. Moonlighting Proteins: The Case of the Hexokinases.Frontiers in molecular biosciences · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
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

6 authors at 4 institutions in 1 country.

Léonard Jagot-Lacoussierea INSERM UMRS1160; Université Denis Diderot; Institut Universitaire d'Hématologie ; Hôpital Saint-Louis ; Paris , France.
Audrey Faye
Heriberto Bruzzoni-Giovanelli
Bruno O Villoutreix
Jean-Christophe Rain
Jean-Luc Poyet
Délégation Paris 7 · FRHybrigenics (France) · FRSorbonne Paris Cité · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Beside its central role in the mitochondria-dependent cell death pathway, the apoptotic protease activating factor 1 (Apaf-1) is involved in the DNA damage response through cell-cycle arrest induced by genotoxic stress. This non-apoptotic function requires a nuclear translocation of Apaf-1 during the G1-to-S transition. However, the mechanisms that trigger the nuclear accumulation of Apaf-1 upon DNA damage remain to be investigated. Here we show that the main 4 isoforms of Apaf-1 can undergo nuclear translocation and restore Apaf-1 deficient MEFs cell cycle arrest in the S phase following genotoxic stress through activation of Chk-1. Interestingly, DNA damage-dependent nuclear accumulation of Apaf-1 occurs independently of p53 and the retinoblastoma (pRb) pathway. We demonstrated that Apaf-1 associates with the nucleoporin Nup107 and this association is necessary for Apaf-1 nuclear import. The CED-4 domain of Apaf-1 directly binds to the central domain of Nup107 in an ATR-regulated, phosphorylation-dependent manner. Interestingly, expression of the Apaf-1-interacting domain of Nup107 interfered with Apaf-1 nuclear translocation upon genotoxic stress, resulting in a marked reduction of Chk-1 activation and cell cycle arrest. Thus, our results confirm the crucial role of Apaf-1 nuclear relocalization in mediating cell-cycle arrest induced by genotoxic stress and implicate Nup107 as a critical regulator of the DNA damage-induced intra-S phase checkpoint response.

Indexed as

DNA DamageAnimalsApoptotic Protease-Activating Factor 1Ataxia Telangiectasia Mutated ProteinsCell LineCell NucleusCheckpoint Kinase 1CisplatinHumansMiceNuclear Pore Complex ProteinsPhosphorylationProtein BindingProtein IsoformsProtein KinasesRetinoblastoma ProteinApoptotic Protease-Activating Factor 1Ataxia Telangiectasia Mutated ProteinsATR protein, humanCheckpoint Kinase 1CisplatinNuclear Pore Complex ProteinsNUP107 protein, humanProtein IsoformsProtein KinasesRetinoblastoma ProteinRNA, Small InterferingTumor Suppressor Protein p53Apaf-1Apaf-1, apoptotic protease activating factor 1ApoptosomeCARD, caspase activation recruitment domaincell cyclecisplatinDAPI, 4′-diamino-2-phenylindoleDNA damageGST, glutathione S-transferaseMEFs, Mouse Embryonic FibroblastsNSCLC, non-small cell lung cancernuclear pore complexnucleoporinNup107PI, propidium iodide

Identifiers

PMID25695197
PMCPMC4612455
OpenAlexW1596956160

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.