ArticleThe Journal of biological chemistry2016
Early Growth Response 1 (Egr-1) Is a Transcriptional Activator of β-Secretase 1 (BACE-1) in the Brain.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Overcoming the blood‒brain barrier: nanomedicine strategies for targeted delivery and multimodal therapy in Alzheimer's disease.Drug delivery · 2026Review
- Effects of Wheat Malt Extract on Molecular and Behavioral Markers in Aged APP/PS1 and Wild-Type Mice.International journal of molecular sciences · 2026Article
- Memory-Associated Immediate Early Genes: Roles in Synaptic Function, Memory Processes, and Neurological Diseases.Molecular neurobiology · 2025Review
- Sex-Dependent Phenotypic and Histomorphometric Biomarkers in the APPswe/PS1dE9/Blg Mouse Model of Alzheimer's Disease.Brain sciences · 2025Article
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- Deep fusion of incomplete multi-omic data for molecular mechanism of Alzheimer's disease.Scientific reports · 2025Article
- Single-Cell Transcriptional Profiling and Gene Regulatory Network Modeling in Tg2576 Mice Reveal Gender-Dependent Molecular Features Preceding Alzheimer-Like Pathologies.Molecular neurobiology · 2024Article
- Sex differences in hippocampal β-amyloid accumulation in the triple-transgenic mouse model of Alzheimer's disease and the potential role of local estrogens.Frontiers in neuroscience · 2023Article
- Large-scale genetic screens identify BET-1 as a cytoskeleton regulator promoting actin function and life span.Aging cell · 2023Article
- Fasting-mimicking diet cycles reduce neuroinflammation to attenuate cognitive decline in Alzheimer's models.Cell reports · 2022Article
- Manganese-Induced Toxicity inInternational journal of molecular sciences · 2022Article
- Krüppel-like factor 5 accelerates the pathogenesis of Alzheimer's disease via BACE1-mediated APP processing.Alzheimer's research & therapy · 2022Article
- EGR1 Enhances Lymphangiogenesis via SOX18-Mediated Activation of JAK2/STAT3 Pathway.Computational and mathematical methods in medicine · 2022Article
- Article
- NREM delta power and AD-relevant tauopathy are associated with shared cortical gene networks.Scientific reports · 2021Article
- Article
- Early Growth Response 1 Suppresses Macrophage Phagocytosis by Inhibiting NRF2 Activation Through Upregulation of Autophagy DuringFrontiers in cellular and infection microbiology · 2021Article
- Dimeric Transmembrane Orientations of APP/C99 Regulate γ-Secretase Processing Line Impacting Signaling and Oligomerization.iScience · 2020Article
- The association between CD69 and EGR1 levels, and CHD patients without reflow after PCI.Experimental and therapeutic medicine · 2019Article
- Vulnerability and resilience to Alzheimer's disease: early life conditions modulate neuropathology and determine cognitive reserve.Alzheimer's research & therapy · 2018Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulation of amyloid-β peptide (Aβ) in the brain is regarded as central to Alzheimer's disease (AD) pathogenesis. Aβ is generated by a sequential cleavage of amyloid precursor protein (APP) by β-secretase 1 (BACE-1) followed by γ-secretase. BACE-1 cleavage of APP is the committed step in Aβ synthesis. Understanding the mechanism by which BACE-1 is activated leading to Aβ synthesis in the brain can provide better understanding of AD pathology and help to develop novel therapies. In this study, we found that the levels of Aβ and BACE-1 are significantly reduced in the brains of mice lacking transcription factor early growth response 1 (Egr-1) when compared with the WT. We demonstrate that in COS-7 cells, Egr-1 binds to the BACE-1 promoter and activates BACE-1 transcription. In rat hippocampal primary neurons, overexpression of Egr-1 induces BACE-1 expression, activates BACE-1, promotes amyloidogenic APP processing, and enhances Aβ synthesis. In mouse hippocampal primary neurons, knockdown of BACE-1 almost completely blocks Egr-1-induced amyloidogenic APP processing and Aβ synthesis. Our data indicate that Egr-1 promotes Aβ synthesis via transcriptional activation of BACE-1 and suggest that Egr-1 plays role in activation of BACE-1 and acceleration of Aβ synthesis in AD brain. Egr-1 is a potential therapeutic target for AD.
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