ArticleThe Journal of cell biology1999
Apoptotic activities of wild-type and Alzheimer's disease-related mutant presenilins in Drosophila melanogaster.
Article in The Journal of cell biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- Analysis of hidradenitis suppurativa-linked mutations in four genes and the effects of PSEN1-P242LfsX11 on cytokine and chemokine expression in macrophages.Human molecular genetics · 2019Pooled it
- Article
- Lipophorin receptors genetically modulate neurodegeneration caused by reduction of Psn expression in the aging Drosophila brain.Genetics · 2024Article
- Gamma secretase activity modulates BMP-7-induced dendritic growth in primary rat sympathetic neurons.Autonomic neuroscience : basic & clinical · 2023Article
- Presenilin-1 (PSEN1) Mutations: Clinical Phenotypes beyond Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Cell competition from development to neurodegeneration.Disease models & mechanisms · 2021Review
- Synaptic homeostats: latent plasticity revealed at the Drosophila neuromuscular junction.Cellular and molecular life sciences : CMLS · 2021Review
- Pharmacological Treatment of Alzheimer's Disease: Insights fromInternational journal of molecular sciences · 2020Review
- Genetic Dissection of Alzheimer's Disease UsingInternational journal of molecular sciences · 2020Review
- Heparan Sulfate Structure Affects Autophagy, Lifespan, Responses to Oxidative Stress, and Cell Degeneration inG3 (Bethesda, Md.) · 2020Article
- Beyond Host Defense: Deregulation ofFrontiers in immunology · 2020Review
- Drosophila Full-Length Amyloid Precursor Protein Is Required for Visual Working Memory and Prevents Age-Related Memory Impairment.Current biology : CB · 2018Article
- AKAP200 promotes Notch stability by protecting it from Cbl/lysosome-mediated degradation in Drosophila melanogaster.PLoS genetics · 2018Article
- Article
- APC/CDevelopmental cell · 2017Article
- Swing Boat: Inducing and Recording Locomotor Activity in aFrontiers in behavioral neuroscience · 2017Article
- Review
- A neuroprotective function of NSF1 sustains autophagy and lysosomal trafficking in Drosophila.Genetics · 2015Article
- Drosophila domino Exhibits Genetic Interactions with a Wide Spectrum of Chromatin Protein-Encoding Loci.PloS one · 2015Article
- β-Amyloid: the key peptide in the pathogenesis of Alzheimer's disease.Frontiers in pharmacology · 2015Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mutant human presenilins cause early-onset familial Alzheimer's disease and render cells susceptible to apoptosis in cultured cell models. We show that loss of presenilin function in Drosophila melanogaster increases levels of apoptosis in developing tissues. Moreover, overexpression of presenilin causes apoptotic and neurogenic phenotypes resembling those of Presenilin loss-of-function mutants, suggesting that presenilin exerts a dominant negative effect when expressed at high levels. In Drosophila S2 cells, Psn overexpression leads to reduced Notch receptor synthesis affecting levels of the intact approximately 300-kD precursor and its approximately 120-kD processed COOH-terminal derivatives. Presenilin-induced apoptosis is cell autonomous and can be blocked by constitutive Notch activation, suggesting that the increased cell death is due to a developmental mechanism that eliminates improperly specified cell types. We describe a genetic model in which the apoptotic activities of wild-type and mutant presenilins can be assessed, and we find that Alzheimer's disease-linked mutant presenilins are less effective at inducing apoptosis than wild-type presenilin.
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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.