Evidence map›Paper›PMID 41615455›Full record

ArticleCellular and molecular life sciences : CMLS2026

Mice carrying a GluN2B protein-truncating variant have altered NMDA receptor subunit composition and their behavior recapitulates patient phenotypes.

Klevinda Fili, Viktor Kuchtiak, Eni Tomovic, Miriam Candelas Serra, Agnieszka Kubik-Zahorodna, Karel Harant, Paulina Bozikova, Jiri Cerny, Miloslav Korinek, Barbora Hrcka Krausova and 7 more

Abstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

17 authors.

Klevinda FiliInstitute of Physiology, Czech Academy of Sciences(CAS), Videnska 1083, Prague 4, 142 00, Czech Republic.ORCID http://orcid.org/0000-0003-2039-7802
Viktor KuchtiakInstitute of Physiology, Czech Academy of Sciences(CAS), Videnska 1083, Prague 4, 142 00, Czech Republic.ORCID http://orcid.org/0000-0002-1833-3386
Eni TomovicInstitute of Physiology, Czech Academy of Sciences(CAS), Videnska 1083, Prague 4, 142 00, Czech Republic.ORCID http://orcid.org/0000-0001-9991-5259
Miriam Candelas SerraInstitute of Physiology, Czech Academy of Sciences(CAS), Videnska 1083, Prague 4, 142 00, Czech Republic.ORCID http://orcid.org/0000-0001-9663-1621
Agnieszka Kubik-ZahorodnaCzech Centre for Phenogenomics, Institute of Molecular Genetics, Czech Academy of Sciences, Vestec, 25050, Czech Republic.ORCID http://orcid.org/0000-0002-2331-3814
Karel HarantProteomics Core Facility, Faculty of Science, Charles University, Biocev, Vestec, 25050, Czech Republic.ORCID http://orcid.org/0000-0002-9654-5392
Paulina BozikovaInstitute of Physiology, Czech Academy of Sciences(CAS), Videnska 1083, Prague 4, 142 00, Czech Republic.ORCID http://orcid.org/0000-0002-6553-8421
Jiri CernyInstitute of Physiology, Czech Academy of Sciences(CAS), Videnska 1083, Prague 4, 142 00, Czech Republic.ORCID http://orcid.org/0000-0002-1969-9304
Miloslav KorinekInstitute of Physiology, Czech Academy of Sciences(CAS), Videnska 1083, Prague 4, 142 00, Czech Republic.ORCID http://orcid.org/0000-0001-5115-4489
Barbora Hrcka KrausovaInstitute of Physiology, Czech Academy of Sciences(CAS), Videnska 1083, Prague 4, 142 00, Czech Republic.ORCID http://orcid.org/0000-0001-5395-982X
Vera AbramovaInstitute of Physiology, Czech Academy of Sciences(CAS), Videnska 1083, Prague 4, 142 00, Czech Republic.ORCID https://orcid.org/0009-0004-7135-7039
Mark DobrovolskiInstitute of Physiology, Czech Academy of Sciences(CAS), Videnska 1083, Prague 4, 142 00, Czech Republic.ORCID https://orcid.org/0000-0003-2834-9872
Fatma Elzahraa S Abdel RahmanInstitute of Physiology, Czech Academy of Sciences(CAS), Videnska 1083, Prague 4, 142 00, Czech Republic.ORCID http://orcid.org/0000-0002-6312-7514
Jan ProchazkaCzech Centre for Phenogenomics, Institute of Molecular Genetics, Czech Academy of Sciences, Vestec, 25050, Czech Republic.ORCID https://orcid.org/0000-0003-4675-8995
Ales BalikInstitute of Physiology, Czech Academy of Sciences(CAS), Videnska 1083, Prague 4, 142 00, Czech Republic.ORCID https://orcid.org/0000-0002-7059-6095
Tereza SmejkalovaInstitute of Physiology, Czech Academy of Sciences(CAS), Videnska 1083, Prague 4, 142 00, Czech Republic. tereza.smejkalova@fgu.cas.cz.ORCID https://orcid.org/0000-0003-1297-7786
Ladislav VyklickyInstitute of Physiology, Czech Academy of Sciences(CAS), Videnska 1083, Prague 4, 142 00, Czech Republic. ladislav.vyklicky@fgu.cas.cz.ORCID http://orcid.org/0000-0002-0015-0098

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathogenic variants in GRIN2B, encoding the NMDA receptor (NMDAR) GluN2B subunit, are linked to intellectual disability (ID) and related neurodevelopmental disorders. While most disease-associated variants are missense, protein-truncating variants (PTVs) may cause haploinsufficiency with less severe phenotypes. Here, we characterize a knock-in mouse model carrying the GluN2B-L825Ffs*15 PTV (Grin2b

Indexed as

Behavior, AnimalIntellectual DisabilityReceptors, N-Methyl-D-AspartateAnimalsDisease Models, AnimalExcitatory Postsynaptic PotentialsFemaleGene Knock-In TechniquesHippocampusHumansMaleMiceMice, Inbred C57BLNeuronsPhenotypeProtein SubunitsNR2B NMDA receptorProtein SubunitsReceptors, N-Methyl-D-AspartateChannelopathyGluN2BGlutamate receptorsGrin genesTransgenic mice models

Identifiers

PMID41615455
PMCPMC12876548

What OpenQuestion holds

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LicenceCC BY
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.