ArticleThe Journal of clinical investigation2008
Pin1 has opposite effects on wild-type and P301L tau stability and tauopathy.
Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
73 citing papers in PubMed, 114 citations in OpenAlex.
- Targeting the crosstalk between Alzheimer's disease and gastrointestinal cancers.Molecular medicine (Cambridge, Mass.) · 2026Review
- Association between Benzodiazepine and Dementia Risk in Treating Depression after Breast Cancer Diagnosis: A Nationwide Population-Based Cohort Study.Yonsei medical journal · 2025Article
- Common Signaling Pathways in Cancer and Alzheimer's Disease May Point to New Treatments.Current topics in medicinal chemistry · 2025Review
- Advancing Alzheimer's research by improving disease modeling of secondary tauopathy.NPJ dementia · 2025Review
- Pin1-catalyzed conformational regulation after phosphorylation: A distinct checkpoint in cell signaling and drug discovery.Science signaling · 2024Review
- TauCell death & disease · 2024Article
- Review
- Causal relationship between Alzheimer's disease and prostate cancer: a bidirectional Mendelian randomization analysis.Frontiers in endocrinology · 2024Article
- "Cyclophilin A" Enzymatic Effect on the Aggregation Behavior of 1N4R Tau Protein: An Overlooked Crucial Determinant that should be Re-considered in Alzheimer's Disease Pathogenesis.Current Alzheimer research · 2024Article
- The role of the Pin1-Frontiers in cell and developmental biology · 2024Review
- Traumatic brain injury and the pathways to cerebral tau accumulation.Frontiers in neurology · 2023Review
- Spinal Cord Injury Causes Prominent Tau Pathology Associated with Brain Post-Injury Sequela.Molecular neurobiology · 2022Article
- Neuropathological and behavioral features of an APP/PS1/MAPT (6xTg) transgenic model of Alzheimer's disease.Molecular brain · 2022Article
- Actin-binding protein filamin-A drives tau aggregation and contributes to progressive supranuclear palsy pathology.Science advances · 2022Article
- The kingdom of the prolyl-isomerase Pin1: The structural and functional convergence and divergence of Pin1.Frontiers in cell and developmental biology · 2022Review
- Cis P-tau underlies vascular contribution to cognitive impairment and dementia and can be effectively targeted by immunotherapy in mice.Science translational medicine · 2021Article
- The Pin1-CaMKII-AMPA Receptor Axis Regulates Epileptic Susceptibility.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- Emerging Evidences for an Implication of the Neurodegeneration-Associated Protein TAU in Cancer.Brain sciences · 2020Review
- Melatonin directly binds and inhibits death-associated protein kinase 1 function in Alzheimer's disease.Journal of pineal research · 2020Article
- Optical induction of autophagy via Transcription factor EB (TFEB) reduces pathological tau in neurons.PloS one · 2020Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Tau pathology is a hallmark of many neurodegenerative diseases including Alzheimer disease (AD) and frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17). Genetic tau mutations can cause FTDP-17, and mice overexpressing tau mutants such as P301L tau are used as AD models. However, since no tau mutations are found in AD, it remains unclear how appropriate tau mutant mice are as an AD model. The prolyl isomerase Pin1 binds and isomerizes tau and has been implicated in protecting against neurodegeneration, but whether such Pin1 regulation is affected by tau mutations is unknown. Consistent with earlier findings that Pin1 KO induces tauopathy, here we demonstrate that Pin1 knockdown or KO increased WT tau protein stability in vitro and in mice and that Pin1 overexpression suppressed the tauopathy phenotype in WT tau transgenic mice. Unexpectedly, Pin1 knockdown or KO decreased P301L tau protein stability and abolished its robust tauopathy phenotype in mice. In contrast, Pin1 overexpression exacerbated the tauopathy phenotype in P301L tau mice. Thus, Pin1 has opposite effects on the tauopathy phenotype depending on whether the tau is WT or a P301L mutant, indicating the need for disease-specific therapies for tauopathies.
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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.