ArticleMolecular neurobiology2018
HERC1 Ubiquitin Ligase Is Required for Normal Axonal Myelination in the Peripheral Nervous System.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Glia of the heart's nervous system.Nature reviews. Neuroscience · 2025Review
- HERC1 E3 Ubiquitin Ligase Is Necessary for Autophagy Processes and for the Maintenance and Homeostasis of Vesicles in Motor Nerve Terminals, but Not for Proteasomal Activity.International journal of molecular sciences · 2025Article
- First Case of Macrocephaly, Dysmorphic Facies, and Psychomotor Retardation Harboring Co-inherited Variants in HERC1 and PMP22 Genes from Iran: Two Novel Variants.Archives of Iranian medicine · 2024Article
- Regulation of MAPK Signaling Pathways by the Large HERC Ubiquitin Ligases.International journal of molecular sciences · 2023Review
- Article
- Decreased MEF2A Expression Regulated by Its Enhancer Methylation Inhibits Autophagy and May Play an Important Role in the Progression of Alzheimer's Disease.Frontiers in neuroscience · 2021Article
- Maternal separation leads to regional hippocampal microglial activation and alters the behavior in the adolescence in a sex-specific manner.Brain, behavior, & immunity - health · 2020Article
- The Ubiquitin Proteasome System in Neuromuscular Disorders: Moving Beyond Movement.International journal of molecular sciences · 2020Review
- The HERC1 ubiquitin ligase regulates presynaptic membrane dynamics of central synapses.Scientific reports · 2020Article
- HERC1 Ubiquitin Ligase Is Required for Hippocampal Learning and Memory.Frontiers in neuroanatomy · 2020Article
- HERCing: Structural and Functional Relevance of the Large HERC Ubiquitin Ligases.Frontiers in physiology · 2019Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
A missense mutation in HERC1 provokes loss of cerebellar Purkinje cells, tremor, and unstable gait in tambaleante (tbl) mice. Recently, we have shown that before cerebellar degeneration takes place, the tbl mouse suffers from a reduction in the number of vesicles available for release at the neuromuscular junction (NMJ). The aim of the present work was to study to which extent the alteration in HERC1 may affect other cells in the nervous system and how this may influence the motor dysfunction observed in these mice. The functional analysis showed a consistent delay in the propagation of the action potential in mutant mice in comparison with control littermates. Morphological analyses of glial cells in motor axons revealed signs of compact myelin damage as tomacula and local hypermyelination foci. Moreover, we observed an alteration in non-myelinated terminal Schwann cells at the level of the NMJ. Additionally, we found a significant increment of phosphorylated Akt-2 in the sciatic nerve. Based on these findings, we propose a molecular model that could explain how mutated HERC1 in tbl mice affects the myelination process in the peripheral nervous system. Finally, since the myelin abnormalities found in tbl mice are histological hallmarks of neuropathic periphery diseases, tbl mutant mice could be considered as a new mouse model for this type of diseases.
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Registered trials
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