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Article

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

The Journal of experimental medicine - 27 Jun 2016

Hullinger Rikki, Li Mi, Wang Jingxin, Peng Yajing, Dowell James A, Bomba-Warczak Ewa, Mitchell Heather A, Burger Corinna, Chapman Edwin R, Denu John M, Li Lingjun, Puglielli Luigi

Abstract excerpt

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...

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Share to Acetyl Coenzyme A
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 27242167
DOI: 10.1084/jem.20151776
PMCID: PMC4925020

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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.

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