ArticleMolecular psychiatry2021
Behavioral, circuitry, and molecular aberrations by region-specific deficiency of the high-risk autism gene Cul3.
Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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.
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.
Who cites it
48 citing papers in PubMed, 72 citations in OpenAlex.
- Review
- USP15 mutation associated with autism spectrum disorder alters progenitor fate and neuronal maturation in human brain organoids.Molecules and cells · 2026Article
- β-catenin deficiency in forebrain excitatory neurons induces fear memory deficits and physiological alterations.Brain communications · 2026Article
- Distinct neural dynamics in the ventral hippocampus and medial prefrontal cortex during social information processing.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Comprehensive behavioral characterization and impaired hippocampal synaptic transmission in R1117X Shank3 mutant mice.Translational psychiatry · 2025Article
- Discovery of a NovelMolecular syndromology · 2025Article
- CSN-CRL Complexes: New Regulators of Adipogenesis.Biomolecules · 2025Review
- The Cul3 ubiquitin ligase engages Insomniac as an adaptor to impact sleep and synaptic homeostasis.PLoS genetics · 2025Article
- Ras, RhoA, and vascular pharmacology in neurodevelopment and aging.Neurochemistry international · 2024Review
- Article
- Ubiquitin system mutations in neurological diseases.Trends in biochemical sciences · 2024Review
- Increased gene dosage of RFWD2 causes autistic-like behaviors and aberrant synaptic formation and function in mice.Molecular psychiatry · 2024Article
- A prefrontal-thalamic circuit encodes social information for social recognition.Nature communications · 2024Article
- Severity of Autism Spectrum Disorder Symptoms Associated with de novo Variants and Pregnancy-Induced Hypertension.Journal of autism and developmental disorders · 2024Article
- Neuronal knockdown of Cullin3 as a Drosophila model of autism spectrum disorder.Scientific reports · 2024Article
- Autism risk geneFrontiers in cellular neuroscience · 2024Article
- Distinct and Convergent Alterations of Entorhinal Cortical Circuits in Two Mouse Models for Alzheimer's Disease and Related Disorders.Journal of Alzheimer's disease : JAD · 2024Article
- The SMYD3-MAP3K2 signaling axis promotes tumor aggressiveness and metastasis in prostate cancer.Science advances · 2023Article
- Dissecting the Relationship Between Neuropsychiatric and Neurodegenerative Disorders.Molecular neurobiology · 2023Review
- Deficiency of Cullin 3, a Protein Encoded by a Schizophrenia and Autism Risk Gene, Impairs Behaviors by Enhancing the Excitability of Ventral Tegmental Area (VTA) DA Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Cullin 3 (Cul3) gene, which encodes a core component of the E3 ubiquitin ligase complex that mediates proteasomal degradation, has been identified as a true high-risk factor for autism. Here, by combining behavioral, electrophysiological, and proteomic approaches, we have examined how Cul3 deficiency contributes to the etiology of different aspects of autism. Heterozygous mice with forebrain Cul3 deletion displayed autism-like social interaction impairment and sensory-gating deficiency. Region-specific deletion of Cul3 leads to distinct phenotypes, with social deficits linked to the loss of Cul3 in prefrontal cortex (PFC), and stereotypic behaviors linked to the loss of Cul3 in striatum. Correlated with these behavioral alterations, Cul3 deficiency in forebrain or PFC induces NMDA receptor hypofunction, while Cul3 loss in striatum causes a cell type-specific alteration of neuronal excitability in striatal circuits. Large-scale profiling has identified sets of misregulated proteins resulting from Cul3 deficiency in different regions, including Smyd3, a histone methyltransferase involved in gene transcription. Inhibition or knockdown of Smyd3 in forebrain Cul3-deficient mice ameliorates social deficits and restores NMDAR function in PFC. These results have revealed for the first time a potential molecular mechanism underlying the manifestation of different autism-like behavioral deficits by Cul3 deletion in cortico-striatal circuits.
Indexed as
Identifiers
What OpenQuestion holds
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.