ArticleProceedings of the National Academy of Sciences of the United States of America2018
BACE1 SUMOylation increases its stability and escalates the protease activity in Alzheimer's disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.
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
29 citing papers in PubMed, 45 citations in OpenAlex.
- Disturbed Spatial Learning and Hippocampal Molecular and Histological Alterations in Middle-Aged Rats with a History of Polycystic Ovary Syndrome.International journal of endocrinology and metabolism · 2027Article
- The role of SUMOylation in regulating proteins that drive neuronal disease progression.Biochemistry and biophysics reports · 2026Review
- Epigenetic Changes in Alzheimer's Disease and Interventions for Therapy.Neuropsychiatric disease and treatment · 2026Review
- Gnb5 is a negative regulator of the BACE1-mediated Aβ generation and ameliorates cognitive deficits in a mouse model of Alzheimer's disease.PLoS biology · 2025Article
- Age-related p53 SUMOylation accelerates senescence and tau pathology in Alzheimer's disease.Cell death and differentiation · 2025Article
- SUMOylation balance: a key determinant in synapse physiology.Frontiers in physiology · 2025Review
- Unveiling the multifaceted pathogenesis and therapeutic drugs of Alzheimer's disease: A comprehensive review.Heliyon · 2024Review
- Protein modification in neurodegenerative diseases.MedComm · 2024Review
- A positive feedback inhibition of isocitrate dehydrogenase 3β on paired-box gene 6 promotes Alzheimer-like pathology.Signal transduction and targeted therapy · 2024Article
- ADME profiling, molecular docking, DFT, and MEP analysis reveal cissamaline, cissamanine, and cissamdine fromRSC advances · 2024Article
- Paralogue-Specific Roles of SUMO1 and SUMO2/3 in Protein Quality Control and Associated Diseases.Cells · 2023Review
- SUMOylation of AnxA6 facilitates EGFR-PKCα complex formation to suppress epithelial cancer growth.Cell communication and signaling : CCS · 2023Article
- The Involvement of Post-Translational Modifications in Regulating the Development and Progression of Alzheimer's Disease.Molecular neurobiology · 2023Review
- Fangchinoline alleviates cognitive impairments through enhancing autophagy and mitigating oxidative stress in Alzheimer's disease models.Frontiers in cell and developmental biology · 2023Article
- Review
- BACE1: More than just a β-secretase.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2022Review
- In Silico Molecular Docking Analysis of Karanjin against Alzheimer's and Parkinson's Diseases as a Potential Natural Lead Molecule for New Drug Design, Development and Therapy.Molecules (Basel, Switzerland) · 2022Article
- Post-Translational Modifications of BACE1 in Alzheimer's Disease.Current neuropharmacology · 2022Article
- Delta- and beta- secretases crosstalk amplifies the amyloidogenic pathway in Alzheimer's disease.Progress in neurobiology · 2021Article
- The aminosterol Claramine inhibits β-secretase 1-mediated insulin receptor cleavage.The Journal of biological chemistry · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Amyloid beta (Aβ) is a major pathological marker in Alzheimer's disease (AD), which is principally regulated by the rate-limiting β-secretase (i.e., BACE1) cleavage of amyloid precursor protein (APP). However, how BACE1 activity is posttranslationally regulated remains incompletely understood. Here, we show that BACE1 is predominantly SUMOylated at K501 residue, which escalates its protease activity and stability and subsequently increases Aβ production, leading to cognitive defect seen in the AD mouse model. Compared with a non-SUMOylated K501R mutant, injection of wild-type BACE1 significantly increases Aβ production and triggers cognitive dysfunction. Furthermore, overexpression of wild-type BACE1, but not non-SUMOylated K501R mutant, facilitates senile plaque formation and aggravates the cognitive deficit seen in the APP/PS1 AD mouse model. Together, our data strongly suggest that K501 SUMOylation on BACE1 plays a critical role in mediating its stability and enzymatic activity.
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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.