ArticleProceedings of the National Academy of Sciences of the United States of America2019
The proteasome regulator PI31 is required for protein homeostasis, synapse maintenance, and neuronal survival in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Structural basis for regulation of the proteasome 20S core particle by the Parkinsonism-associated proteins FBXO7 and PI31.bioRxiv : the preprint server for biology · 2026Article
- Variants in the proteasome regulator PSMF1 cause a phenotypic spectrum from parkinsonism to perinatal lethality.Nature communications · 2026Article
- Magical moments in protease biology: proteasome autocatalytic activation and PI31-mediated inhibition.Trends in biochemical sciences · 2026Review
- White matter injury after brain ischemia.Experimental neurology · 2026Review
- Regulation via compartmentation: adaptive localization of the proteasome under stress.Biochemical Society transactions · 2025Review
- Early proteasome downregulation and dysfunction drive proteostasis failure in Alzheimer's disease.Brain : a journal of neurology · 2025Article
- PI31 expression is neuroprotective in a mouse model of early-onset parkinsonism.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- PI31 is a positive regulator of 20S immunoproteasome assembly.Journal of cell science · 2025Article
- Understanding neurodevelopmental proteasomopathies as new rare disease entities: A review of current concepts, molecular biomarkers, and perspectives.Genes & diseases · 2024Review
- Mechanisms of ubiquitin-independent proteasomal degradation and their roles in age-related neurodegenerative disease.Frontiers in cell and developmental biology · 2024Review
- Rational design of proteasome inhibitors based on the structure of the endogenous inhibitor PI31/Fub1.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Structure, Function, and Allosteric Regulation of the 20S Proteasome by the 11S/PA28 Family of Proteasome Activators.Biomolecules · 2023Review
- NMJ-related diseases beyond the congenital myasthenic syndromes.Frontiers in cell and developmental biology · 2023Review
- How neurons maintain their axons long-term: an integrated view of axon biology and pathology.Frontiers in neuroscience · 2023Review
- An Altered Neurovascular System in Aging-Related Eye Diseases.International journal of molecular sciences · 2022Review
- Comprehensive Analysis of Proteasomal Complexes in Mouse Brain Regions Detects ENO2 as a Potential Partner of the Proteasome in the Striatum.Cellular and molecular neurobiology · 2022Article
- Yeast PI31 inhibits the proteasome by a direct multisite mechanism.Nature structural & molecular biology · 2022Article
- Keeping synapses in shape: degradation pathways in the healthy and aging brain.Neuronal signaling · 2022Review
- Proteasome complexes experience profound structural and functional rearrangements throughout mammalian spermatogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Protein clearance strategies for disease intervention.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Proteasome-mediated degradation of intracellular proteins is essential for cell function and survival. The proteasome-binding protein PI31 (Proteasomal Inhibitor of 31kD) promotes 26S assembly and functions as an adapter for proteasome transport in axons. As localized protein synthesis and degradation is especially critical in neurons, we generated a conditional loss of PI31 in spinal motor neurons (MNs) and cerebellar Purkinje cells (PCs). A cKO of PI31 in these neurons caused axon degeneration, neuronal loss, and progressive spinal and cerebellar neurological dysfunction. For both MNs and PCs, markers of proteotoxic stress preceded axonal degeneration and motor dysfunction, indicating a critical role for PI31 in neuronal homeostasis. The time course of the loss of MN and PC function in developing mouse central nervous system suggests a key role for PI31 in human neurodegenerative diseases.
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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.