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

Deficient Import of Acetyl-CoA into the ER Lumen Causes Neurodegeneration and Propensity to Infections, Inflammation, and Cancer

14 May 2014

Abstract excerpt

The import of acetyl-CoA into the ER lumen by AT-1/SLC33A1 is essential for the N(ε)-lysine acetylation of ER-resident and ER-transiting proteins. A point-mutation (S113R) in AT-1 has been associated with a familial form of spastic paraplegia. Here, we report that AT-1S113R is unable to form homodimers in the ER membrane and is devoid of acetyl-CoA transport activity. The reduced influx of acetyl-CoA into the ER...

Read the complete abstract on PubMed

Topics

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

Share to Autophagy in Disease and Therapy
Share to Endoplasmic Reticulum Stress and Disease
Share to Hereditary Neurological Disorders

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 24828632
DOI: 10.1523/jneurosci.0077-14.2014

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Deficient Import of Acetyl-CoA into the ER Lumen Causes Neurodegeneration and Propensity to Infections, Inflammation, and CancerPMID 24828632Read ↗

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 ↗

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

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

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 ↗

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

Deficient ER Acetyl-CoA Import in Acinar Cells Leads to Chronic PancreatitisSemantic proximity Read ↗

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

NATs at a glanceSemantic proximity Read ↗

Mutations in ACY1, the gene encoding aminoacylase 1, cause a novel inborn error of metabolism.Semantic proximity Read ↗

N-acetylaspartate catabolism determines cytosolic acetyl-CoA levels and histone acetylation in brown adipocytes.Semantic proximity Read ↗

[Alpha-1-antitrypsin deficiency].Semantic proximity Read ↗

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