ArticleNature communications2022
SLITRK2 variants associated with neurodevelopmental disorders impair excitatory synaptic function and cognition in mice.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Molecular continuity between axon guidance and synaptic function.Molecules and cells · 2026Review
- GluA1 C80 Peptide Impairs Short-Term Spatial Memory in Mice by Interfering with the 4.1N Binding Site.Neuroscience bulletin · 2026Article
- Bazedoxifene reverses sexually dimorphic autistic-like abnormalities in biallelic MDGA1-mutant mice.EMBO molecular medicine · 2026Article
- Autism-associated ARHGEF9 variants impair GABAergic synapses and ultrasonic communication by reducing gephyrin phosphorylation.Molecular psychiatry · 2026Article
- A decade of progress in understanding LRRTM and Slitrk synaptic cell-adhesion molecules.Molecules and cells · 2026Review
- PRPF8-associated retinitis pigmentosa variant induces human neural retina-autonomous photoreceptor defects.Scientific reports · 2026Article
- Single-nucleus multiomics reveals the disrupted regulatory programs in three brain regions of sporadic early-onset Alzheimer's disease.Science advances · 2025Article
- Paralogs of Slitrk cell adhesion molecules configure excitatory synapse specificity via distinct cellular mechanisms.PLoS biology · 2025Article
- Enhanced Protein Synthesis and Hippocampus-Dependent Memory via Inhibition of YTHDF2-Mediated mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- EphB2 receptor tyrosine kinase-mediated excitatory synaptic functions are negatively modulated by MDGA2.Progress in neurobiology · 2025Article
- Article
- Analysis of short tandem repeats linked to polyglutamine diseases from whole-genome sequencing reveals intermediate alleles ofBrain communications · 2025Article
- SLITRK2 as a prognostic and immunological biomarker in gastric cancer.Discover oncology · 2024Article
- Insight into the Association between Slitrk Protein and Neurodevelopmental and Neuropsychiatric Conditions.Biomolecules · 2024Review
- Rare variation in non-coding regions with evolutionary signatures contributes to autism spectrum disorder risk.Cell genomics · 2024Article
- Identification of brain-enriched proteins in CSF as biomarkers of relapsing remitting multiple sclerosis.Clinical proteomics · 2024Article
- Plasma proteomics show altered inflammatory and mitochondrial proteins in patients with neurologic symptoms of post-acute sequelae of SARS-CoV-2 infection.Brain, behavior, and immunity · 2023Article
- Loss-of-function variant in the LRR domain of SLITRK2 implicated in a neurodevelopmental disorder.Frontiers in genetics · 2023Article
- Developmental control of noradrenergic system by SLITRK1 and its implications in the pathophysiology of neuropsychiatric disorders.Frontiers in molecular neuroscience · 2022Review
Corrections and comments
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Authors and funding
40 authors at 20 institutions in 9 countries.
Funding
Abstract
SLITRK2 is a single-pass transmembrane protein expressed at postsynaptic neurons that regulates neurite outgrowth and excitatory synapse maintenance. In the present study, we report on rare variants (one nonsense and six missense variants) in SLITRK2 on the X chromosome identified by exome sequencing in individuals with neurodevelopmental disorders. Functional studies showed that some variants displayed impaired membrane transport and impaired excitatory synapse-promoting effects. Strikingly, these variations abolished the ability of SLITRK2 wild-type to reduce the levels of the receptor tyrosine kinase TrkB in neurons. Moreover, Slitrk2 conditional knockout mice exhibited impaired long-term memory and abnormal gait, recapitulating a subset of clinical features of patients with SLITRK2 variants. Furthermore, impaired excitatory synapse maintenance induced by hippocampal CA1-specific cKO of Slitrk2 caused abnormalities in spatial reference memory. Collectively, these data suggest that SLITRK2 is involved in X-linked neurodevelopmental disorders that are caused by perturbation of diverse facets of SLITRK2 function.
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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 Socratic graph.