ArticleMolecular and cellular biology2012
Prolyl isomerase Pin1 regulates neuronal differentiation via β-catenin.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 66 citations in OpenAlex.
- Article
- Overexpression of Pin1 regulated by TOP2A, which subsequently stabilizes Pyk2 to promote bortezomib resistance in multiple myeloma.Cancer gene therapy · 2025Article
- PIN1 is a novel interaction partner and a negative upstream regulator of the transcription factor NFIB.FEBS letters · 2024Article
- PIN1‑silencing mitigates keratinocyte proliferation and the inflammatory response in psoriasis by activating mitochondrial autophagy.Experimental and therapeutic medicine · 2024Article
- Pin1-catalyzed conformational regulation after phosphorylation: A distinct checkpoint in cell signaling and drug discovery.Science signaling · 2024Review
- Pin1 Downregulation Is Involved in Excess Retinoic Acid-Induced Failure of Neural Tube Closure.International journal of molecular sciences · 2024Article
- Review
- Skin-brain axis in Alzheimer's disease - Pathologic, diagnostic, and therapeutic implications: A Hypothetical Review.Aging and disease · 2024Review
- Prolyl Isomerase Pin1 Expression in the Spinal Motor Neurons of Patients With Sporadic Amyotrophic Lateral Sclerosis.Journal of clinical neurology (Seoul, Korea) · 2022Article
- The role of peptidyl-prolyl isomerase Pin1 in neuronal signaling in epilepsy.Frontiers in molecular neuroscience · 2022Review
- Inverse Correlation Between Alzheimer's Disease and Cancer: Short Overview.Molecular neurobiology · 2021Review
- The Peptidyl-prolyl Isomerase Pin1 in Neuronal Signaling: from Neurodevelopment to Neurodegeneration.Molecular neurobiology · 2021Review
- Cancer and Alzheimer's disease inverse relationship: an age-associated diverging derailment of shared pathways.Molecular psychiatry · 2021Review
- Recent advances in tau-directed immunotherapy against Alzheimer's disease: an overview of pre-clinical and clinical development.Metabolic brain disease · 2020Review
- Activity-dependent isomerization of Kv4.2 by Pin1 regulates cognitive flexibility.Nature communications · 2020Article
- Pinning Down the Transcription: A Role for Peptidyl-ProlylFrontiers in cell and developmental biology · 2020Review
- Post-translational Modifications of the Peptidyl-Prolyl Isomerase Pin1.Frontiers in cell and developmental biology · 2020Review
- Spontaneous functional full recovery from motor and sensory deficits in adult mice after mild spinal cord injury.Heliyon · 2019Article
- Tau Pathology in Chronic Traumatic Encephalopathy and Alzheimer's Disease: Similarities and Differences.Frontiers in neurology · 2019Review
- Oncogenic Hijacking of the PIN1 Signaling Network.Frontiers in oncology · 2019Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
The Wnt/β-catenin pathway promotes proliferation of neural progenitor cells (NPCs) at early stages and induces neuronal differentiation from NPCs at late stages, but the molecular mechanisms that control this stage-specific response are unclear. Pin1 is a prolyl isomerase that regulates cell signaling uniquely by controlling protein conformation after phosphorylation, but its role in neuronal differentiation is not known. Here we found that whereas Pin1 depletion suppresses neuronal differentiation, Pin1 overexpression enhances it, without any effects on gliogenesis from NPCs in vitro. Consequently, Pin1-null mice have significantly fewer upper layer neurons in the motor cortex and severely impaired motor activity during the neonatal stage. A proteomic approach identified β-catenin as a major substrate for Pin1 in NPCs, in which Pin1 stabilizes β-catenin. As a result, Pin1 knockout leads to reduced β-catenin during differentiation but not proliferation of NPCs in developing brains. Importantly, defective neuronal differentiation in Pin1 knockout NPCs is fully rescued in vitro by overexpression of β-catenin but not a β-catenin mutant that fails to act as a Pin1 substrate. These results show that Pin1 is a novel regulator of NPC differentiation by acting on β-catenin and provides a new postphosphorylation signaling mechanism to regulate developmental stage-specific functioning of β-catenin signaling in neuronal differentiation.
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What OpenQuestion holds
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.