ArticleNucleic acids research2004
Translational regulation of BACE-1 expression in neuronal and non-neuronal cells.
Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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
38 citing papers in PubMed, 81 citations in OpenAlex.
- Complex CDKL5 translational regulation and its potential role in CDKL5 deficiency disorder.Frontiers in cellular neuroscience · 2023Article
- Casein Kinase 2 dependent phosphorylation of eIF4B regulates BACE1 expression in Alzheimer's disease.Cell death & disease · 2021Article
- Integrated Stress Response Inhibitor Reverses Sex-Dependent Behavioral and Cell-Specific Deficits after Mild Repetitive Head Trauma.Journal of neurotrauma · 2020Article
- Amyloid Beta-Peptide Increases BACE1 Translation through the Phosphorylation of the Eukaryotic Initiation Factor-2Oxidative medicine and cellular longevity · 2020Article
- L-Type Amino Acid Transporter 1 (LAT1/Lat1)-Utilizing Prodrugs Can Improve the Delivery of Drugs into Neurons, Astrocytes and Microglia.Scientific reports · 2019Article
- BACE1 Translation: At the Crossroads Between Alzheimer's Disease Neurodegeneration and Memory Consolidation.Journal of Alzheimer's disease reports · 2019Review
- Astrocyte-Targeted Transporter-Utilizing Derivatives of Ferulic Acid Can Have Multifunctional Effects Ameliorating Inflammation and Oxidative Stress in the Brain.Oxidative medicine and cellular longevity · 2019Article
- Proteolytic ectodomain shedding of membrane proteins in mammals-hardware, concepts, and recent developments.The EMBO journal · 2018Review
- Inhibition of PKCδ reduces amyloid-β levels and reverses Alzheimer disease phenotypes.The Journal of experimental medicine · 2018Article
- PKR downregulation prevents neurodegeneration and β-amyloid production in a thiamine-deficient model.Cell death & disease · 2015Article
- Unfolded Protein Response and PERK Kinase as a New Therapeutic Target in the Pathogenesis of Alzheimer's Disease.Current medicinal chemistry · 2015Review
- PERK mediates eIF2α phosphorylation responsible for BACE1 elevation, CREB dysfunction and neurodegeneration in a mouse model of Alzheimer's disease.Neurobiology of aging · 2014Article
- MicroRNA-339-5p down-regulates protein expression of β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) in human primary brain cultures and is reduced in brain tissue specimens of Alzheimer disease subjects.The Journal of biological chemistry · 2014Article
- Article
- Roles of eIF2α kinases in the pathogenesis of Alzheimer's disease.Frontiers in molecular neuroscience · 2014Review
- Translational control by eIF2α kinases in long-lasting synaptic plasticity and long-term memory.Neurobiology of learning and memory · 2013Review
- Inhibition of GSK3β-mediated BACE1 expression reduces Alzheimer-associated phenotypes.The Journal of clinical investigation · 2013Article
- Physical evidence supporting a ribosomal shunting mechanism of translation initiation for BACE1 mRNA.Translation (Austin, Tex.) · 2013Article
- Depletion of GGA1 and GGA3 mediates postinjury elevation of BACE1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Accumulation of exogenous amyloid-beta peptide in hippocampal mitochondria causes their dysfunction: a protective role for melatonin.Oxidative medicine and cellular longevity · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
As the main beta-secretase of the central nervous system, BACE-1 is a key protein in the pathogenesis of Alzheimer's disease. Excessive expression of the protein might cause an overproduction of the neurotoxic beta-amyloid peptide. Therefore, a tight regulation of BACE-1 expression is expected in vivo. In addition to a possible transcriptional control, the BACE-1 transcript leader contains features that might constitute mechanisms of translational regulation of protein expression. Moreover, recent work has revealed an increase of BACE-1 protein and beta-secretase activity in some Alzheimer's disease patients, although a corresponding increase of transcript has not been reported. Here we show that BACE-1 translation could be modulated at multiple stages. The presence of several upstream ATGs strongly reduces the translation of the main open reading frame. This inhibition could be overcome with conditions that favour skipping of upstream ATGs. We also report an alternative splicing of the BACE-1 transcript leader that reduces the number of upstream ATGs. Finally, we show that translation driven by the BACE-1 transcript leader is increased in activated astrocytes independently of the splicing event, indicating yet another mechanism of translational control. Our findings might explain why increases in BACE-1 protein or activity are reported in the brain of Alzheimer's disease patients even in the absence of changes in transcript levels.
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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.