ArticleDisease models & mechanisms2014
Absence of strong strain effects in behavioral analyses of Shank3-deficient mice.
Article in Disease models & mechanisms, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 53 citations in OpenAlex.
- Aberrant Fear: Biological Underpinnings Relevant to Psychosis, Antipsychotic Drugs, and Psychotherapeutic Treatments, a Translational Approach.International journal of molecular sciences · 2026Review
- SHANK3 Deficiency in AgRP Neurons Inhibits Diet-Induced Obesity by Activating p38α.Neuroscience bulletin · 2026Article
- A Frank Assessment of SHANK: Impacts of Pathogenic Variations in SHANK3 on Preclinical Models of Phelan McDermid Syndrome.Autism research : official journal of the International Society for Autism Research · 2025Review
- Risk factors for barbering in laboratory mice.Scientific reports · 2025Article
- Behavioral decline in Shank3Molecular autism · 2024Article
- Behavioral regression in shank3Research square · 2024Article
- Transcriptional determinism and stochasticity contribute to the complexity of autism-associated SHANK family genes.Cell reports · 2024Article
- Transcriptional Determinism and Stochasticity Contribute to the Complexity of Autism AssociatedbioRxiv : the preprint server for biology · 2024Article
- Haploinsufficiency ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Article
- Postsynaptic Protein Shank3a Deficiency Synergizes with Alzheimer's Disease Neuropathology to Impair Cognitive Performance in the 3xTg-AD Murine Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Immune activation during pregnancy exacerbates ASD-related alterations in Shank3-deficient mice.Molecular autism · 2023Article
- The Effects of Prenatal and Postnatal Exposure to 50-Hz and 3 mT Electromagnetic Field on Rat Testicular Development.Medicina (Kaunas, Lithuania) · 2022Article
- Review
- Restoring glutamate receptosome dynamics at synapses rescues autism-like deficits in Shank3-deficient mice.Molecular psychiatry · 2021Article
- Developmental and Behavioral Phenotypes in a Mouse Model of DDX3X Syndrome.Biological psychiatry · 2021Article
- LMT USV Toolbox, a Novel Methodological Approach to Place Mouse Ultrasonic Vocalizations in Their Behavioral Contexts-A Study in Female and Male C57BL/6J Mice and inFrontiers in behavioral neuroscience · 2021Article
- Tandospirone, a Partial 5-HT1A Receptor Agonist, Administered Systemically or Into Anterior Cingulate Attenuates Repetitive Behaviors in Shank3B Mice.The international journal of neuropsychopharmacology · 2020Article
- A standardized social preference protocol for measuring social deficits in mouse models of autism.Nature protocols · 2020Article
- Neural Mechanisms Underlying Repetitive Behaviors in Rodent Models of Autism Spectrum Disorders.Frontiers in cellular neuroscience · 2020Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Haploinsufficiency of SHANK3, caused by chromosomal abnormalities or mutations that disrupt one copy of the gene, leads to a neurodevelopmental syndrome called Phelan-McDermid syndrome, symptoms of which can include absent or delayed speech, intellectual disability, neurological changes and autism spectrum disorders. The SHANK3 protein forms a key structural part of the post-synaptic density. We previously generated and characterized mice with a targeted disruption of Shank3 in which exons coding for the ankyrin-repeat domain were deleted and expression of full-length Shank3 was disrupted. We documented specific deficits in synaptic function and plasticity, along with reduced reciprocal social interactions, in Shank3 heterozygous mice. Changes in phenotype owing to a mutation at a single locus are quite frequently modulated by other loci, most dramatically when the entire genetic background is changed. In mice, each strain of laboratory mouse represents a distinct genetic background and alterations in phenotype owing to gene knockout or transgenesis are frequently different across strains, which can lead to the identification of important modifier loci. We have investigated the effect of genetic background on phenotypes of Shank3 heterozygous, knockout and wild-type mice, using C57BL/6, 129SVE and FVB/Ntac strain backgrounds. We focused on observable behaviors with the goal of carrying out subsequent analyses to identify modifier loci. Surprisingly, there were very modest strain effects over a large battery of analyses. These results indicate that behavioral phenotypes associated with Shank3 haploinsufficiency are largely strain-independent.
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Registered trials
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.