ArticleScientific reports2016
Lost region in amyloid precursor protein (APP) through TALEN-mediated genome editing alters mitochondrial morphology.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Amyloid precursor protein interacts with the mitochondrial phosphatase PGAM5 and regulates mitochondrial respiration.bioRxiv : the preprint server for biology · 2026Article
- The reciprocal relationship between amyloid precursor protein and mitochondrial function.Journal of neurochemistry · 2024Review
- Gene therapy for CNS disorders: modalities, delivery and translational challenges.Nature reviews. Neuroscience · 2024Review
- Interactions between amyloid, amyloid precursor protein, and mitochondria.Biochemical Society transactions · 2023Article
- Amyloid precursor protein and mitochondria.Current opinion in neurobiology · 2023Review
- Mitochondrial supercomplex assembly regulates metabolic features and glutamine dependency in mammalian cells.Theranostics · 2023Article
- New Insights into the Gut Microbiota in Neurodegenerative Diseases from the Perspective of Redox Homeostasis.Antioxidants (Basel, Switzerland) · 2022Review
- A CHCHD6-APP axis connects amyloid and mitochondrial pathology in Alzheimer's disease.Acta neuropathologica · 2022Article
- Current landscape of gene-editing technology in biomedicine: Applications, advantages, challenges, and perspectives.MedComm · 2022Review
- Exploring the Involvement of the Amyloid Precursor Protein A673T Mutation against Amyloid Pathology and Alzheimer's Disease in Relation to Therapeutic Editing Tools.Pharmaceutics · 2022Review
- Potential for Ketotherapies as Amyloid-Regulating Treatment in Individuals at Risk for Alzheimer's Disease.Frontiers in neuroscience · 2022Review
- Oxidative-Signaling in Neural Stem Cell-Mediated Plasticity: Implications for Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Accumulation of amyloid precursor protein C-terminal fragments triggers mitochondrial structure, function, and mitophagy defects in Alzheimer's disease models and human brains.Acta neuropathologica · 2021Article
- Relationships between Mitochondrial Dysfunction and Neurotransmission Failure in Alzheimer's Disease.Aging and disease · 2020Review
- Systematic analysis of a mitochondrial disease-causing ND6 mutation in mitochondrial deficiency.Molecular genetics & genomic medicine · 2020Article
- Applications of genome editing technology in the targeted therapy of human diseases: mechanisms, advances and prospects.Signal transduction and targeted therapy · 2020Review
- A key role for MAM in mediating mitochondrial dysfunction in Alzheimer disease.Cell death & disease · 2018Review
- Mitochondria and Mitochondrial Cascades in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2018Review
- Amyloid precursor protein processing and bioenergetics.Brain research bulletin · 2017Review
- Metabolic dysfunction and mitochondrial failure in Alzheimer's disease: integrating pathophysiology, clinical evidence and emerging interventions.Frontiers in neurologyReview
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) deposition in the brain. Aβ plaques are produced through sequential β/γ cleavage of amyloid precursor protein (APP), of which there are three main APP isoforms: APP695, APP751 and APP770. KPI-APPs (APP751 and APP770) are known to be elevated in AD, but the reason remains unclear. Transcription activator-like (TAL) effector nucleases (TALENs) induce mutations with high efficiency at specific genomic loci, and it is thus possible to knock out specific regions using TALENs. In this study, we designed and expressed TALENs specific for the C-terminus of APP in HeLa cells, in which KPI-APPs are predominantly expressed. The KPI-APP mutants lack a 12-aa region that encompasses a 5-aa trans-membrane (TM) region and 7-aa juxta-membrane (JM) region. The mutated KPI-APPs exhibited decreased mitochondrial localization. In addition, mitochondrial morphology was altered, resulting in an increase in spherical mitochondria in the mutant cells through the disruption of the balance between fission and fusion. Mitochondrial dysfunction, including decreased ATP levels, disrupted mitochondrial membrane potential, increased ROS generation and impaired mitochondrial dehydrogenase activity, was also found. These results suggest that specific regions of KPI-APPs are important for mitochondrial localization and function.
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