ArticleThe Journal of cell biology2020
Ecm29-mediated proteasomal distribution modulates excitatory GABA responses in the developing brain.
Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- More 26S and 30S proteasomes are beneficial in proteinopathy.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mechanisms of ubiquitin-independent proteasomal degradation and their roles in age-related neurodegenerative disease.Frontiers in cell and developmental biology · 2024Review
- Sodium channel endocytosis drives axon initial segment plasticity.Science advances · 2023Article
- A novel endoplasmic reticulum adaptation is critical for the long-lived Caenorhabditis elegans rpn-10 proteasomal mutant.Biochimica et biophysica acta. Gene regulatory mechanisms · 2023Article
- Endoplasmic Reticulum in Metaplasticity: From Information Processing to Synaptic Proteostasis.Molecular neurobiology · 2022Review
- Localized Proteasomal Degradation: From the Nucleus to Cell Periphery.Biomolecules · 2022Review
- Axonal Organelles as Molecular Platforms for Axon Growth and Regeneration after Injury.International journal of molecular sciences · 2021Review
- Ecm29-Dependent Proteasome Localization Regulates Cytoskeleton Remodeling at the Immune Synapse.Frontiers in cell and developmental biology · 2021Article
- The biogenesis of potassium transporters: implications of disease-associated mutations.Critical reviews in biochemistry and molecular biologyReview
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9 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Neuronal GABAergic responses switch from excitatory to inhibitory at an early postnatal period in rodents. The timing of this switch is controlled by intracellular Cl- concentrations, but factors determining local levels of cation-chloride cotransporters remain elusive. Here, we report that local abundance of the chloride importer NKCC1 and timely emergence of GABAergic inhibition are modulated by proteasome distribution, which is mediated through interactions of proteasomes with the adaptor Ecm29 and the axon initial segment (AIS) scaffold protein ankyrin G. Mechanistically, both the Ecm29 N-terminal domain and an intact AIS structure are required for transport and tethering of proteasomes in the AIS region. In mice, Ecm29 knockout (KO) in neurons increases the density of NKCC1 protein in the AIS region, a change that positively correlates with a delay in the GABAergic response switch. Phenotypically, Ecm29 KO mice showed increased firing frequency of action potentials at early postnatal ages and were hypersusceptible to chemically induced convulsive seizures. Finally, Ecm29 KO neurons exhibited accelerated AIS developmental positioning, reflecting a perturbed AIS morphological plastic response to hyperexcitability arising from proteasome inhibition, a phenotype rescued by ectopic Ecm29 expression or NKCC1 inhibition. Together, our findings support the idea that neuronal maturation requires regulation of proteasomal distribution controlled by Ecm29.
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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.