ArticleThe Journal of experimental medicine2016
Increased expression of AT-1/SLC33A1 causes an autistic-like phenotype in mice by affecting dendritic branching and spine formation.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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.
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Who cites it
33 citing papers in PubMed, 39 citations in OpenAlex.
- Overexpression of endoplasmic reticulum acetyl-CoA transporter AT-1 alters neuronal metabolism, growth, and synaptic activity.iScience · 2026Article
- Stearoyl-CoA Desaturase (SCD) Gene Based Molecular Breeding Enhances Nutritional Quality and Growth Performance in the Oyster (Crassostrea angulata).Marine biotechnology (New York, N.Y.) · 2026Article
- Pharmacological Inhibition of SLC33A1 Promotes Endoplasmic Reticulum Hyperoxidation and Induces Adaptive IRE1/XBP1s Signaling.bioRxiv : the preprint server for biology · 2026Article
- Acetyl-CoA availability regulates neuronal metabolism, growth, and synaptic activity.bioRxiv : the preprint server for biology · 2026Article
- Increased expression of ATase1/NAT8B or ATase2/NAT8 in the mouse results in an autistic-like phenotype with altered dendritic branching and spine formation.Molecular psychiatry · 2026Article
- Overexpression of ATase1 and ATase2 disrupts the secretome and causes a progeria phenotype.Life science alliance · 2025Article
- Genomic structural equation modeling decodes skeletal aging: novel loci discovery and multisystem genetic crosstalk.Journal of translational medicine · 2025Article
- Direct connexin-26 interactions with membrane proteins functionally relevant to the cochlea.Human genetics · 2025Article
- Mechanistic insights into the acetyl-CoA recognition by SLC33A1.Cell discovery · 2025Article
- Article
- The Fourth Annual Symposium of the Midwest Aging Consortium.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
- CaScientific reports · 2024Article
- Spatial selectivity of ATase inhibition in mouse models of Charcot-Marie-Tooth disease.Brain communications · 2024Article
- The citrate transporters SLC13A5 and SLC25A1 elicit different metabolic responses and phenotypes in the mouse.Communications biology · 2023Article
- Metabolic and Cellular Compartments of Acetyl-CoA in the Healthy and Diseased Brain.International journal of molecular sciences · 2022Review
- Increased expression of SLC25A1/CIC causes an autistic-like phenotype with altered neuron morphology.Brain : a journal of neurology · 2022Article
- ATase inhibition rescues age-associated proteotoxicity of the secretory pathway.Communications biology · 2022Article
- SLC13A5/sodium-citrate co-transporter overexpression causes disrupted white matter integrity and an autistic-like phenotype.Brain communications · 2022Article
- Coenzyme a Biochemistry: From Neurodevelopment to Neurodegeneration.Brain sciences · 2021Review
- ATG9A regulates proteostasis through reticulophagy receptors FAM134B and SEC62 and folding chaperones CALR and HSPB1.iScience · 2021Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
The import of acetyl-CoA into the lumen of the endoplasmic reticulum (ER) by AT-1/SLC33A1 regulates Nε-lysine acetylation of ER-resident and -transiting proteins. Specifically, lysine acetylation within the ER appears to influence the efficiency of the secretory pathway by affecting ER-mediated quality control. Mutations or duplications in AT-1/SLC33A1 have been linked to diseases such as familial spastic paraplegia, developmental delay with premature death, and autism spectrum disorder with intellectual disability. In this study, we generated an AT-1 Tg mouse model that selectively overexpresses human AT-1 in neurons. These animals demonstrate cognitive deficits, autistic-like social behavior, aberrations in synaptic plasticity, an increased number of dendritic spines and branches, and widespread proteomic changes. We also found that AT-1 activity regulates acetyl-CoA flux, causing epigenetic modulation of the histone epitope H3K27 and mitochondrial adaptation. In conclusion, our results indicate that increased expression of AT-1 can cause an autistic-like phenotype by affecting key neuronal metabolic pathways.
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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.