ArticleHuman molecular genetics2009
AIP-1 ameliorates beta-amyloid peptide toxicity in a Caenorhabditis elegans Alzheimer's disease model.
Article in Human molecular genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 59 citations in OpenAlex.
- Modulation of host proteostasis by Prevotella corporis via induction of the heat shock response.Cell stress & chaperones · 2026Article
- DAB2IP: unifying cardiovascular pathogenesis and cardiovascular brain crosstalk.Frontiers in cardiovascular medicine · 2026Review
- Simple model systems reveal conserved mechanisms of Alzheimer's disease and related tauopathies.Molecular neurodegeneration · 2023Review
- Modeling Alzheimer's Disease inBiomedicines · 2022Review
- UsingFrontiers in pharmacology · 2022Review
- A modular degron library for synthetic circuits in mammalian cells.Nature communications · 2019Article
- Multiomic Profiling Identifies cis-Regulatory Networks Underlying Human Pancreatic β Cell Identity and Function.Cell reports · 2019Article
- Putative autoantibodies in the cerebrospinal fluid of Alzheimer's disease patients.F1000Research · 2019Article
- Neuronal Cell Death.Physiological reviews · 2018Review
- What Can We Learn About Human Disease from the Nematode C. elegans?Methods in molecular biology (Clifton, N.J.) · 2018Review
- The Proteasome and Oxidative Stress in Alzheimer's Disease.Antioxidants & redox signaling · 2016Review
- Royal jelly promotes DAF-16-mediated proteostasis to tolerate β-amyloid toxicity in C. elegans model of Alzheimer's disease.Oncotarget · 2016Article
- Selective Binding of AIRAPL Tandem UIMs to Lys48-Linked Tri-Ubiquitin Chains.Structure (London, England : 1993) · 2016Article
- Loss of the proteostasis factor AIRAPL causes myeloid transformation by deregulating IGF-1 signaling.Nature medicine · 2016Article
- Current advances in the functional studies of fatty acids and fatty acid-derived lipids inWorm · 2016Review
- Identifying Aβ-specific pathogenic mechanisms using a nematode model of Alzheimer's disease.Neurobiology of aging · 2015Article
- 20S proteasome activation promotes life span extension and resistance to proteotoxicity in Caenorhabditis elegans.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- The Mechanistic Links Between Proteasome Activity, Aging and Age-related Diseases.Current genomics · 2014Article
- The ubiquitin proteasome system in Caenorhabditis elegans and its regulation.Redox biology · 2014Review
- A cocoa peptide protects Caenorhabditis elegans from oxidative stress and β-amyloid peptide toxicity.PloS one · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Multiple neurodegenerative diseases are causally linked to aggregation-prone proteins. Cellular mechanisms involving protein turnover may be key defense mechanisms against aggregating protein disorders. We have used a transgenic Caenorhabditis elegans Alzheimer's disease model to identify cellular responses to proteotoxicity resulting from expression of the human beta amyloid peptide (Abeta). We show up-regulation of aip-1 in Abeta-expressing animals. Mammalian homologues of AIP-1 have been shown to associate with, and regulate the function of, the 26S proteasome, leading us to hypothesize that induction of AIP-1 may be a protective cellular response directed toward modulating proteasomal function in response to toxic protein aggregation. Using our transgenic model, we show that overexpression of AIP-1 protected against, while RNAi knockdown of AIP-1 exacerbated, Abeta toxicity. AIP-1 overexpression also reduced accumulation of Abeta in this model, which is consistent with AIP-1 enhancing protein degradation. Transgenic expression of one of the two human aip-1 homologues (AIRAPL), but not the other (AIRAP), suppressed Abeta toxicity in C. elegans, which advocates the biological relevance of the data to human biology. Interestingly, AIRAPL and AIP-1 contain a predicted farnesylation site, which is absent from AIRAP. This farnesylation site was shown by others to be essential for an AIP-1 prolongevity function. Consistent with this, we show that an AIP-1 mutant lacking the predicted farnesylation site failed to protect against Abeta toxicity. Our results implicate AIP-1 in the regulation of protein turnover and protection against Abeta toxicity and point at AIRAPL as the functional mammalian homologue of AIP-1.
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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.