Evidence map›Paper›PMID 21209208›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Fas/CD95 regulatory protein Faim2 is neuroprotective after transient brain ischemia.

Arno Reich, Christopher Spering, Karen Gertz, Christoph Harms, Ellen Gerhardt, Golo Kronenberg, Klaus A Nave, Markus Schwab, Simone C Tauber, Anja Drinkut and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed, 58 citations in OpenAlex.

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  15. Ion and pH Sensitivity of a TMBIM CaStructure (London, England : 1993) · 2019
    Article
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  17. TMBIM-mediated CaBiochimica et biophysica acta. Molecular cell research · 2017
    Review
  18. MiR-3202 - Promoted H5V Cell Apoptosis by Directly Targeting Fas Apoptotic Inhibitory Molecule 2 (FAIM2) in High Glucose Condition.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  19. Interaction of ARC and Daxx: A Novel Endogenous Target to Preserve Motor Function and Cell Loss after Focal Brain Ischemia in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
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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

16 authors at 5 institutions in 1 country.

Arno ReichDepartment of Neurology, University Hospital and Medical School, RWTH Aachen University, D-52074 Aachen, Germany.
Christopher Spering
Karen Gertz
Christoph Harms
Ellen Gerhardt
Golo Kronenberg
Klaus A Nave
Markus Schwab
Simone C Tauber
Anja Drinkut
Kristian Harms
Chrstioph P Beier
Aaron Voigt
Sandra Göbbels
Matthias Endres
Jörg B Schulz
Charité - Universitätsmedizin Berlin · DERWTH Aachen University · DEUniversity of Göttingen · DEMax Planck Institute of Experimental Medicine · DEMax Planck Society · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Death receptor (DR) signaling has a major impact on the outcome of numerous neurological diseases, including ischemic stroke. DRs mediate not only cell death signals, but also proinflammatory responses and cell proliferation. Identification of regulatory proteins that control the switch between apoptotic and alternative DR signaling opens new therapeutic opportunities. Fas apoptotic inhibitory molecule 2 (Faim2) is an evolutionary conserved, neuron-specific inhibitor of Fas/CD95-mediated apoptosis. To investigate its role during development and in disease models, we generated Faim2-deficient mice. The ubiquitous null mutation displayed a viable and fertile phenotype without overt deficiencies. However, lack of Faim2 caused an increase in susceptibility to combined oxygen-glucose deprivation in primary neurons in vitro as well as in caspase-associated cell death, stroke volume, and neurological impairment after cerebral ischemia in vivo. These processes were rescued by lentiviral Faim2 gene transfer. In summary, we provide evidence that Faim2 is a novel neuroprotective molecule in the context of cerebral ischemia.

Indexed as

Analysis of VarianceAnimalsBrain InfarctionCaspase 3Caspase 8Cell DeathCells, CulturedCerebral CortexDisease Models, Animalfas ReceptorGene Expression RegulationGlucoseGreen Fluorescent ProteinsHypoxiaIn Situ Nick-End LabelingIschemic Attack, TransientCaspase 3Caspase 8fas ReceptorGlucoseGreen Fluorescent Proteinslifeguard protein, mouseMembrane ProteinsNerve Tissue ProteinsPhosphopyruvate Hydratase

Identifiers

PMID21209208
PMCPMC6622730
OpenAlexW2080857698

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.