Evidence map›Paper›PMID 25724647›Full record

ArticleThe Journal of biological chemistry2015

δ-Catenin Regulates Spine Architecture via Cadherin and PDZ-dependent Interactions.

Li Yuan, Eunju Seong, James L Beuscher, Jyothi Arikkath

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.8field-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

27 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Roles and regulation of δ-catenin in tumorigenesis and neuronal diseases.Frontiers in cell and developmental biology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. The autism-associated loss of δ-catenin functions disrupts social behavior.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. Loss ofFrontiers in neuroscience · 2023
    Article
  13. Article
  14. Article
  15. Delta-Catenin as a Modulator of Rho GTPases in Neurons.Frontiers in cellular neuroscience · 2022
    Review
  16. Review
  17. Article
  18. Disruption ofHGG advances · 2020
    Article
  19. Article
  20. 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

4 authors at 2 institutions in 1 country.

Li YuanFrom the Department of Pharmacology and Experimental Neuroscience.
Eunju SeongDevelopmental Neuroscience, Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, Nebraska 68198.
James L BeuscherDevelopmental Neuroscience, Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, Nebraska 68198.
Jyothi ArikkathFrom the Department of Pharmacology and Experimental Neuroscience, Developmental Neuroscience, Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, Nebraska 68198 Jyothi.arikkath@unmc.edu.
University of Nebraska Medical Center · USNebraska Medical Center · US

Funding

UNMC Histology/Imaging and Creighton University Imaging Core FacilityP30GM110768 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SMITH, SHELLEY D · 2014 to 2018
$5.1M
The Molecular Biology of Neurosurgery SystemsP20GM103471 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SMITH, SHELLEY D · 2012 to 2013
$4.1M
NIGMS NIH HHS 5P20GM103471-10NIGMS NIH HHS P20 GM103471NIGMS NIH HHS P30 GM110768
6 · The paper itself

Abstract

The ability of neurons to maintain spine architecture and modulate it in response to synaptic activity is a crucial component of the cellular machinery that underlies information storage in pyramidal neurons of the hippocampus. Here we show a critical role for δ-catenin, a component of the cadherin-catenin cell adhesion complex, in regulating spine head width and length in pyramidal neurons of the hippocampus. The loss of Ctnnd2, the gene encoding δ-catenin, has been associated with the intellectual disability observed in the cri du chat syndrome, suggesting that the functional roles of δ-catenin are vital for neuronal integrity and higher order functions. We demonstrate that loss of δ-catenin in a mouse model or knockdown of δ-catenin in pyramidal neurons compromises spine head width and length, without altering spine dynamics. This is accompanied by a reduction in the levels of synaptic N-cadherin. The ability of δ-catenin to modulate spine architecture is critically dependent on its ability to interact with cadherin and PDZ domain-containing proteins. We propose that loss of δ-catenin during development perturbs synaptic architecture leading to developmental aberrations in neural circuit formation that contribute to the learning disabilities in a mouse model and humans with cri du chat syndrome.

Indexed as

AnimalsArmadillo Domain ProteinsCadherinsCateninsCri-du-Chat SyndromeDelta CateninDisease Models, AnimalHumansMiceNerve Tissue ProteinsPyramidal CellsRatsSpineSynapsesArmadillo Domain ProteinsCadherinsCateninsCdh2 protein, mouseCtnnd2 protein, ratDelta CateninN-cadherin, ratNerve Tissue ProteinsCadherinCateninDendritic SpineHippocampusNeuronPDZSpine ArchitectureSpine Dynamic

Identifiers

PMID25724647
PMCPMC4409256
OpenAlexW1981859983

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.