ArticleThe Biochemical journal2007
A reversible form of lysine acetylation in the ER and Golgi lumen controls the molecular stabilization of BACE1.
Article in The Biochemical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.
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
73 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.
- Insulin-like growth factor 1 associated research in Alzheimer's disease: an exploratory trends analysis.Frontiers in neurologyPooled it
- Metabolite import by SLC33A1 is required for ATF6 activation during endoplasmic reticulum stress.Life science alliance · 2026Article
- Review
- Lysine 473 Regulates the Progression of SLC7A11, the Cystine/Glutamate Exchanger, through the Secretory Pathway.International journal of molecular sciences · 2024Article
- The citrate transporters SLC13A5 and SLC25A1 elicit different metabolic responses and phenotypes in the mouse.Communications biology · 2023Article
- The Involvement of Post-Translational Modifications in Regulating the Development and Progression of Alzheimer's Disease.Molecular neurobiology · 2023Review
- Metabolic and Cellular Compartments of Acetyl-CoA in the Healthy and Diseased Brain.International journal of molecular sciences · 2022Review
- BACE1: More than just a β-secretase.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2022Review
- Finding New Ways How to Control BACE1.The Journal of membrane biology · 2022Article
- Increased expression of SLC25A1/CIC causes an autistic-like phenotype with altered neuron morphology.Brain : a journal of neurology · 2022Article
- SLC13A5/sodium-citrate co-transporter overexpression causes disrupted white matter integrity and an autistic-like phenotype.Brain communications · 2022Article
- Post-Translational Modifications of BACE1 in Alzheimer's Disease.Current neuropharmacology · 2022Article
- The aminosterol Claramine inhibits β-secretase 1-mediated insulin receptor cleavage.The Journal of biological chemistry · 2021Article
- The β-Secretase BACE1 in Alzheimer's Disease.Biological psychiatry · 2021Review
- Endoplasmic reticulum acetyltransferases Atase1 and Atase2 differentially regulate reticulophagy, macroautophagy and cellular acetyl-CoA metabolism.Communications biology · 2021Article
- Is It the Twilight of BACE1 Inhibitors?Current neuropharmacology · 2021Article
- The Pathophysiological Role of CoA.International journal of molecular sciences · 2020Review
- A Molecular Perspective on Sirtuin Activity.International journal of molecular sciences · 2020Review
- The endoplasmic reticulum acetyltransferases ATase1/NAT8B and ATase2/NAT8 are differentially regulated to adjust engagement of the secretory pathway.Journal of neurochemistry · 2020Article
- Regulation of coenzyme A levels by degradation: the 'Ins and Outs'.Progress in lipid research · 2020Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The lipid second messenger ceramide regulates the rate of beta cleavage of the Alzheimer's disease APP (amyloid precursor protein) by affecting the molecular stability of the beta secretase BACE1 (beta-site APP cleaving enzyme 1). Such an event is stimulated in the brain by the normal process of aging, and is under the control of the general aging programme mediated by the insulin-like growth factor 1 receptor. In the present study we report that BACE1 is acetylated on seven lysine residues of the N-terminal portion of the nascent protein. This process involves lysine acetylation in the lumen of the ER (endoplasmic reticulum) and is followed by deacetylation in the lumen of the Golgi apparatus, once the protein is fully mature. We also show that specific enzymatic activities acetylate (in the ER) and deacetylate (in the Golgi apparatus) the lysine residues. This process requires carrier-mediated translocation of acetyl-CoA into the ER lumen and is stimulated by ceramide. Site-directed mutagenesis indicates that lysine acetylation is necessary for nascent BACE1 to leave the ER and move ahead in the secretory pathway, and for the molecular stabilization of the protein.
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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.