ArticlePloS one2010
Control of Alzheimer's amyloid beta toxicity by the high molecular weight immunophilin FKBP52 and copper homeostasis in Drosophila.
Article in PloS one, 2010. 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, 58 citations in OpenAlex.
- Balancing cellular copper levels via the post-translational regulation of copper transport.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Exploring the versatility ofFly · 2025Review
- Article
- FKBP52 in Neuronal Signaling and Neurodegenerative Diseases: A Microtubule Story.International journal of molecular sciences · 2022Review
- Hsc70-4 aggravates PolyQ-mediated neurodegeneration by modulating NF-κB mediated immune response inFrontiers in molecular neuroscience · 2022Article
- Review
- FKBP52 overexpression accelerates hippocampal-dependent memory impairments in a tau transgenic mouse model.NPJ aging and mechanisms of disease · 2021Article
- Modeling Neurodegenerative Disorders inInternational journal of molecular sciences · 2020Review
- Copper Redox Cycling Inhibits Aβ Fibre Formation and Promotes Fibre Fragmentation, while Generating a Dityrosine Aβ Dimer.Scientific reports · 2018Article
- Comparative analysis of FKBP family protein: evaluation, structure, and function in mammals and Drosophila melanogaster.BMC developmental biology · 2018Review
- Copper and Zinc Homeostasis: Lessons fromFrontiers in genetics · 2017Review
- Phenotypic differences betweenAnimal cells and systems · 2017Article
- The Role of Copper Chaperone Atox1 in Coupling Redox Homeostasis to Intracellular Copper Distribution.Antioxidants (Basel, Switzerland) · 2016Review
- The Ubiquitin-Proteasome System and Molecular Chaperone Deregulation in Alzheimer's Disease.Molecular neurobiology · 2016Review
- HSP90AB1: Helping the good and the bad.Gene · 2016Review
- Modeling the complex pathology of Alzheimer's disease in Drosophila.Experimental neurology · 2015Review
- Truncated Amyloid-β(11-40/42) from Alzheimer Disease Binds Cu2+ with a Femtomolar Affinity and Influences Fiber Assembly.The Journal of biological chemistry · 2015Article
- The emerging role of peptidyl-prolyl isomerase chaperones in tau oligomerization, amyloid processing, and Alzheimer's disease.Journal of neurochemistry · 2015Review
- Proteomics in Traditional Chinese Medicine with an Emphasis on Alzheimer's Disease.Evidence-based complementary and alternative medicine : eCAM · 2015Review
- Conserved metallomics in two insect families evolving separately for a hundred million years.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2014Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
FK506 binding proteins (FKBPs), also called immunophilins, are prolyl-isomerases (PPIases) that participate in a wide variety of cellular functions including hormone signaling and protein folding. Recent studies indicate that proteins that contain PPIase activity can also alter the processing of Alzheimer's Amyloid Precursor Protein (APP). Originally identified in hematopoietic cells, FKBP52 is much more abundantly expressed in neurons, including the hippocampus, frontal cortex, and basal ganglia. Given the fact that the high molecular weight immunophilin FKBP52 is highly expressed in CNS regions susceptible to Alzheimer's, we investigated its role in Abeta toxicity. Towards this goal, we generated Abeta transgenic Drosophila that harbor gain of function or loss of function mutations of FKBP52. FKBP52 overexpression reduced the toxicity of Abeta and increased lifespan in Abeta flies, whereas loss of function of FKBP52 exacerbated these Abeta phenotypes. Interestingly, the Abeta pathology was enhanced by mutations in the copper transporters Atox1, which interacts with FKBP52, and Ctr1A and was suppressed in FKBP52 mutant flies raised on a copper chelator diet. Using mammalian cultures, we show that FKBP52 (-/-) cells have increased intracellular copper and higher levels of Abeta. This effect is reversed by reconstitution of FKBP52. Finally, we also found that FKBP52 formed stable complexes with APP through its FK506 interacting domain. Taken together, these studies identify a novel role for FKBP52 in modulating toxicity of Abeta peptides.
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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.