Evidence map›Paper›PMID 17635954›Full record

ArticleThe Journal of experimental medicine2007

Cyclophilin A participates in the nuclear translocation of apoptosis-inducing factor in neurons after cerebral hypoxia-ischemia.

Changlian Zhu, Xiaoyang Wang, Johanna Deinum, Zhiheng Huang, Jianfeng Gao, Nazanine Modjtahedi, Martha R Neagu, Michael Nilsson, Peter S Eriksson, Henrik Hagberg and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed
6.4field-weighted citation impact, top 2% 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

100 citing papers in PubMed, 223 citations in OpenAlex.

  1. Review
  2. Neuroprotective Effects of Furanoditerpenes fromACS chemical neuroscience · 2026
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  6. Review
  7. Review
  8. AssessingPharmaceutics · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Non-Immunosuppressive Cyclophilin Inhibitors.Angewandte Chemie (International ed. in English) · 2022
    Review
  13. Article
  14. Article
  15. Revisiting Regulated Cell Death Responses in Viral Infections.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

40 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

13 authors at 6 institutions in 4 countries.

Changlian ZhuCenter for Brain Repair and Rehabilitation, Institute of Neuroscience and Physiology, Göteborg University, 405 30 Göteborg, Sweden. changlian.zhu@neuro.gu.se
Xiaoyang Wang
Johanna Deinum
Zhiheng Huang
Jianfeng Gao
Nazanine Modjtahedi
Martha R Neagu
Michael Nilsson
Peter S Eriksson
Henrik Hagberg
Jeremy Luban
Guido Kroemer
Klas Blomgren
Third Affiliated Hospital of Zhengzhou University · CNColumbia University · USInstitut Gustave Roussy · FRAstraZeneca (Sweden) · SEDrottning Silvias barn- och ungdomssjukhus · SEUniversity of Gothenburg · SE

Funding

Cyclophilin A Function in the Immune SystemR01AI059159 · NIAID · UNIVERSITY OF GENEVA · PI LUBAN, JEREMY · 2006 to 2011
$1.4M
NIAID NIH HHS R01 AI059159NIAID NIH HHS R01 AI59159
6 · The paper itself

Abstract

Upon cerebral hypoxia-ischemia (HI), apoptosis-inducing factor (AIF) can move from mitochondria to nuclei, participate in chromatinolysis, and contribute to the execution of cell death. Previous work (Cande, C., N. Vahsen, I. Kouranti, E. Schmitt, E. Daugas, C. Spahr, J. Luban, R.T. Kroemer, F. Giordanetto, C. Garrido, et al. 2004. Oncogene. 23:1514-1521) performed in vitro suggests that AIF must interact with cyclophilin A (CypA) to form a proapoptotic DNA degradation complex. We addressed the question as to whether elimination of CypA may afford neuroprotection in vivo. 9-d-old wild-type (WT), CypA(+/-), or CypA(-/-) mice were subjected to unilateral cerebral HI. The infarct volume after HI was reduced by 47% (P = 0.0089) in CypA(-/-) mice compared with their WT littermates. Importantly, CypA(-/-) neurons failed to manifest the HI-induced nuclear translocation of AIF that was observed in WT neurons. Conversely, CypA accumulated within the nuclei of damaged neurons after HI, and this nuclear translocation of CypA was suppressed in AIF-deficient harlequin mice. Immunoprecipitation of AIF revealed coprecipitation of CypA, but only in injured, ischemic tissue. Surface plasmon resonance revealed direct molecular interactions between recombinant AIF and CypA. These data indicate that the lethal translocation of AIF to the nucleus requires interaction with CypA, suggesting a model in which two proteins that normally reside in separate cytoplasmic compartments acquire novel properties when moving together to the nucleus.

Indexed as

Active Transport, Cell NucleusAnimalsApoptosisApoptosis Inducing FactorBrainCell NucleusCyclophilin ACytoplasmHypoxia-Ischemia, BrainMiceMice, TransgenicModels, BiologicalNeuronsOxidative StressProtein BindingApoptosis Inducing FactorCyclophilin A

Identifiers

PMID17635954
PMCPMC2118669
OpenAlexW2158213789

What OpenQuestion holds

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LicenceCC BY-NC-SA
Read underepoch 390

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.