Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Increased expression of SLC25A1/CIC causes an autistic-like phenotype with altered neuron morphology.

Brain : a journal of neurology - 18 Apr 2022

Rigby Michael J, Orefice Nicola Salvatore, Lawton Alexis J, Ma Min, Shapiro Samantha L, Yi Sue Y, Dieterich Inca A, Frelka Alyssa, Miles Hannah N, Pearce Robert A, Yu John Paul J, Li Lingjun, Denu John M, Puglielli Luigi

Abstract excerpt

N ε-lysine acetylation within the lumen of the endoplasmic reticulum is a recently characterized protein quality control system that positively selects properly folded glycoproteins in the early secretory pathway. Overexpression of the endoplasmic reticulum acetyl-CoA transporter AT-1 in mouse forebrain neurons results in increased dendritic branching, spine formation and an autistic-like phenotype that is...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Acetyl Coenzyme A
Share to Autism Spectrum Disorder

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Autistic Disorder

Share to Citric Acid

Share to Mitochondrial Proteins

Share to Neurons

Share to Organic Anion Transporters

Share to Proteomics

Source

Open in PubMed Open full text

Identifiers

PMID: 35203088
DOI: 10.1093/brain/awab295
PMCID: PMC9014753

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Increased expression of SLC25A1/CIC causes an autistic-like phenotype with altered neuron morphology.PMID 35203088Read ↗

Increased expression of ATase1/NAT8B or ATase2/NAT8 in the mouse results in an autistic-like phenotype with altered dendritic branching and spine formation.Semantic proximity Read ↗

Increased expression of AT-1/SLC33A1 causes an autistic-like phenotype in mice by affecting dendritic branching and spine formation.Semantic proximity Read ↗

Deficient Import of Acetyl-CoA into the ER Lumen Causes Neurodegeneration and Propensity to Infections, Inflammation, and CancerSemantic proximity Read ↗

Acetyl-CoA flux from the cytosol to the ER regulates engagement and quality of the secretory pathway.Semantic proximity Read ↗

Increased transport of acetyl-CoA into the endoplasmic reticulum causes a progeria-like phenotype.Semantic proximity Read ↗

The citrate transporters SLC13A5 and SLC25A1 elicit different metabolic responses and phenotypes in the mouse.Semantic proximity Read ↗

Dysregulation of Multiple Solute Carrier genes and Metabolic Deficits in <i>SLC1A4</i> -Mutant Human iPSC-Derived Hippocampal NeuronsSemantic proximity Read ↗

ATP-Citrate lyase fuels axonal transport across speciesSemantic proximity Read ↗

Overexpression of ATase1 and ATase2 disrupts the secretome and causes a progeria phenotype.Semantic proximity Read ↗

AGC1 Deficiency: Pathology and Molecular and Cellular Mechanisms of the Disease.Semantic proximity Read ↗

Nacc1 Mutation in Mice Models Rare Neurodevelopmental Disorder with Underlying Synaptic Dysfunction.Semantic proximity Read ↗

RNA editing-mediated regulation of calcium-dependent activator protein for secretion (CAPS1) localization and its impact on synaptic transmission.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.