In one paragraphArticle in Acta neuropathologica communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
13 authors.
Yulia Kostritskaia *Institute of Biological Information Processing, Molekular- und Zellphysiologie (IBI-1), Forschungszentrum Jülich, 52428, Jülich, Germany.ORCID 0000-0001-9933-2918 Daniela Bulla-Miely *Department of Neurology and Epileptology, Hertie Institute for Clinical Brain Research, University of Tübingen, 72076, Tübingen, Germany.ORCID 0009-0006-1241-1853 Miriam EngelsInstitute of Biological Information Processing, Molekular- und Zellphysiologie (IBI-1), Forschungszentrum Jülich, 52428, Jülich, Germany.ORCID 0000-0001-7801-4929 Jan MeyerInstitute of Neurobiology, Heinrich-Heine-Universität Düsseldorf, 40225, Düsseldorf, Germany.ORCID 0000-0002-3351-8653 Juliane L BernsInstitute for Cellular Neurosciences II, Universitätsklinikum Bonn, 53127, Bonn, Germany.ORCID 0009-0002-5003-4922 Sabrina BehuetInstitute of Neuroscience and Medicine, Strukturelle und funktionelle Organisation des Gehirns (INM-1), Forschungszentrum Jülich GmbH, 52428, Jülich, Germany.ORCID 0000-0002-4975-786X Sebastian BludauInstitute of Neuroscience and Medicine, Strukturelle und funktionelle Organisation des Gehirns (INM-1), Forschungszentrum Jülich GmbH, 52428, Jülich, Germany.ORCID 0000-0001-6173-9050 Christine R RoseInstitute of Neurobiology, Heinrich-Heine-Universität Düsseldorf, 40225, Düsseldorf, Germany.ORCID 0000-0002-9684-3592 Albert BeckerInstitute for Cellular Neurosciences II, Universitätsklinikum Bonn, 53127, Bonn, Germany.ORCID 0000-0003-2661-3705 Thomas GenschInstitute of Biological Information Processing, Molekular- und Zellphysiologie (IBI-1), Forschungszentrum Jülich, 52428, Jülich, Germany.ORCID 0000-0002-3903-4705 Ulrike B S Hedrich *Department of Neurology and Epileptology, Hertie Institute for Clinical Brain Research, University of Tübingen, 72076, Tübingen, Germany.ORCID 0000-0003-3801-1306 Christoph Fahlke *Institute of Biological Information Processing, Molekular- und Zellphysiologie (IBI-1), Forschungszentrum Jülich, 52428, Jülich, Germany.ORCID 0000-0001-8602-9952 Peter Kovermann *Institute of Biological Information Processing, Molekular- und Zellphysiologie (IBI-1), Forschungszentrum Jülich, 52428, Jülich, Germany. p.kovermann@fz-juelich.de.ORCID 0000-0001-5296-4918 Funding
No grant is acknowledged in the PubMed record.
6 · The paper itselfAbstract
A missense variant in SLC1A3, which results in a proline to arginine substitution in the glial excitatory amino acid transporter 1 (EAAT1), causes a severe form of episodic ataxia type 6, characterized by recurrent attacks of ataxia and epilepsy. EAATs are dual function transport proteins, and the P290R variant reduces secondary active glutamate transport rates, while enhancing the anion channel activity. Here, we used complementary electrophysiological, imaging, biochemical and neuropathological techniques to characterize the cellular mechanisms underlying epileptic seizures in a mouse model of episodic ataxia type 6, the heterozygous Slc1a3
Indexed as
AtaxiaExcitatory Amino Acid Transporter 1gamma-Aminobutyric AcidNeural InhibitionAnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLMice, TransgenicExcitatory Amino Acid Transporter 1gamma-Aminobutyric AcidSlc1a3 protein, mouseChloride homeostasisDentate gyrusEpilepsyGlutamate transportersRadial glia-like cellsTonic inhibition
Identifiers
PMID42563189
PMCPMC13449690
What OpenQuestion holds
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