Evidence map›Paper›PMID 33494786›Full record

ArticleMolecular brain2021

Mice with cleavage-resistant N-cadherin exhibit synapse anomaly in the hippocampus and outperformance in spatial learning tasks.

M Asada-Utsugi, K Uemura, M Kubota, Y Noda, Y Tashiro, T M Uemura, H Yamakado, M Urushitani, R Takahashi, S Hattori and 5 more

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 32% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. The intracellular domain of the epilepsy protein PCDH19 regulates spine density in cortical neurons in vivo viaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
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

15 authors at 5 institutions in 1 country.

M Asada-UtsugiSchool of Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
K UemuraDepartment of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
M KubotaSchool of Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Y NodaSchool of Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Y TashiroSchool of Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
T M UemuraDepartment of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
H YamakadoDepartment of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
M UrushitaniDepartment of Neurology, Shiga University of Medical Science, Seta-Tsukinowa-Cho Otsu, Shiga, 520-2192, Japan.
R TakahashiDepartment of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
S HattoriDivision of Systems Medical Science, Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, 470-1192, Japan.
T MiyakawaDivision of Systems Medical Science, Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, 470-1192, Japan.
N Ageta-IshiharaDivision of Biological Sciences, Department of Molecular Biology, Nagoya University Graduate School of Science, Nagoya, 464-8602, Japan.
K KobayashiDepartment of Pharmacology, Graduate School of Medicine, Nippon Medical School, Tokyo, 113-8602, Japan.
M KinoshitaDivision of Biological Sciences, Department of Molecular Biology, Nagoya University Graduate School of Science, Nagoya, 464-8602, Japan.
A KinoshitaSchool of Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan. kinoshita.ayae.6v@kyoto-u.ac.jp.
Kyoto University · JPNagoya University · JPFujita Health University · JPNippon Medical School · JPShiga University of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

N-cadherin is a homophilic cell adhesion molecule that stabilizes excitatory synapses, by connecting pre- and post-synaptic termini. Upon NMDA receptor (NMDAR) activation by glutamate, membrane-proximal domains of N-cadherin are cleaved serially by a-disintegrin-and-metalloprotease 10 (ADAM10) and then presenilin 1(PS1, catalytic subunit of the γ-secretase complex). To assess the physiological significance of the initial N-cadherin cleavage, we engineer the mouse genome to create a knock-in allele with tandem missense mutations in the mouse N-cadherin/Cadherin-2 gene (Cdh2

Indexed as

Spatial LearningTask Performance and AnalysisADAM10 ProteinAllelesAnimalsBehavior, AnimalCadherinsCell MembraneCHO CellsCricetulusFearGene Knock-In TechniquesHippocampusMemoryMiceMice, Inbred C57BLADAM10 ProteinCadherinsMutant ProteinsADAM10HippocampusN-cadherinSynapseWorking memory

Identifiers

PMID33494786
PMCPMC7831172
OpenAlexW3112842599

What OpenQuestion holds

Textmetadata
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.