ArticleFrontiers in cellular neuroscience2016
Effects of Pin1 Loss in Hdh(Q111) Knock-in Mice.
Article in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- 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
- Modelling the Human Blood-Brain Barrier in Huntington Disease.International journal of molecular sciences · 2022Article
- Neuroinflammation in Huntington's Disease: A Starring Role for Astrocyte and Microglia.Current neuropharmacology · 2022Review
- The kingdom of the prolyl-isomerase Pin1: The structural and functional convergence and divergence of Pin1.Frontiers in cell and developmental biology · 2022Review
- Juvenile Huntington's Disease and Other PolyQ Diseases, Update on Neurodevelopmental Character and Comparative Bioinformatic Review of Transcriptomic and Proteomic Data.Frontiers in cell and developmental biology · 2021Review
- Roles of peptidyl-prolyl isomerase Pin1 in disease pathogenesis.Theranostics · 2021Review
- Analysis of LINE1 Retrotransposons in Huntington's Disease.Frontiers in cellular neuroscience · 2021Article
- Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form.Nature communications · 2020Article
- Pin1 Is Regulated by CaMKII Activation in Glutamate-Induced Retinal Neuronal Regulated Necrosis.Frontiers in cellular neuroscience · 2019Article
- Pin1 Promotes Regulated Necrosis Induced by Glutamate in Rat Retinal Neurons via CAST/Calpain2 Pathway.Frontiers in cellular neuroscience · 2017Article
- PIN1 Modulates Huntingtin Levels and Aggregate Accumulation: AnFrontiers in cellular neuroscience · 2017Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is a fatal, dominantly inherited, neurodegenerative disorder due to a pathological expansion of the CAG repeat in the coding region of the HTT gene. In the quest for understanding the molecular basis of neurodegeneration, we have previously demonstrated that the prolyl isomerase Pin1 plays a crucial role in mediating p53-dependent apoptosis triggered by mutant huntingtin (mHtt) in vitro. To assess the effects of the lack of Pin1 in vivo, we have bred Pin1 knock-out mice with Hdh(Q111) knock-in mice, a genetically precise model of HD. We show that Pin1 genetic ablation modifies a portion of Hdh(Q111) phenotypes in a time-dependent fashion. As an early event, Pin1 activity reduces the DNA damage response (DDR). In midlife mice, by taking advantage of next-generation sequencing technology, we show that Pin1 activity modulates a portion of the alterations triggered by mHtt, extending the role of Pin1 to two additional Hdh(Q111) phenotypes: the unbalance in the "synthesis/concentration of hormones", as well as the alteration of "Wnt/β-catenin signaling". In aging animals, Pin1 significantly increases the number of mHtt-positive nuclear inclusions while it reduces gliosis. In summary, this work provides further support for a role of Pin1 in HD pathogenesis.
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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.