ArticleFrontiers in cellular neuroscience2017
PIN1 Modulates Huntingtin Levels and Aggregate Accumulation: An
Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Temperature-sensitive sodium beta-glycerophosphate/chitosan hydrogel loaded with all-trans retinoic acid regulates Pin1 to inhibit the formation of spinal cord injury-induced rat glial scar.Bioengineering & translational medicine · 2025Article
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- Pin1-catalyzed conformational regulation after phosphorylation: A distinct checkpoint in cell signaling and drug discovery.Science signaling · 2024Review
- Review
- The regulatory role of Pin1 in neuronal death.Neural regeneration research · 2023Review
- New PIN1 inhibitors identified through a pharmacophore-driven, hierarchical consensus docking strategy.Journal of enzyme inhibition and medicinal chemistry · 2022Article
- Roles of peptidyl-prolyl isomerase Pin1 in disease pathogenesis.Theranostics · 2021Review
- Nemo-like kinase reduces mutant huntingtin levels and mitigates Huntington's disease.Human molecular genetics · 2020Article
- Prolyl isomerase Pin1: a promoter of cancer and a target for therapy.Cell death & disease · 2018Review
- Pin1 Promotes Regulated Necrosis Induced by Glutamate in Rat Retinal Neurons via CAST/Calpain2 Pathway.Frontiers in cellular neuroscience · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is a dominantly inherited neurodegenerative disorder characterized by a polyglutamine expansion within the N-terminal region of huntingtin protein (HTT). Cellular mechanisms promoting mutant huntingtin (mHTT) clearance are of great interest in HD pathology as they can lower the level of the mutant protein and its toxic aggregated species, thus affecting disease onset and progression. We have previously shown that the prolyl-isomerase PIN1 represents a promising negative regulator of mHTT aggregate accumulation using a genetically precise HD mouse model, namely
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Registered trials
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