ReviewJournal of neuroscience research2009
Myelin under stress.
Review in Journal of neuroscience research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 48 citations in OpenAlex.
- Proteasome inhibitors rescue hypomyelination in iPSC based model of HIKESHI-associated leukodystrophy.Journal of translational medicine · 2026Article
- Review
- Peripheral Myelin Protein-22 and Its Prominence in Charcot-Marie-Tooth Disease.Chemical reviews · 2026Review
- Sleep loss induces cholesterol-associated myelin dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Activation of XBP1s attenuates disease severity in models of proteotoxic Charcot-Marie-Tooth type 1B.Brain : a journal of neurology · 2025Article
- GCN2-Mediated eIF2α Phosphorylation Is Required for Central Nervous System Remyelination.International journal of molecular sciences · 2025Article
- The Protective Effect of Nimodipine in Schwann Cells Is Related to the Upregulation of LMO4 and SERCA3 Accompanied by the Fine-Tuning of Intracellular Calcium Levels.International journal of molecular sciences · 2025Article
- Knockdown of Rab9 Recovers Defective Morphological Differentiation Induced by Chemical ER Stress Inducer or PMD-Associated PLP1 Mutant Protein in FBD-102b Cells.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024Article
- The Influence of Lysosomal Stress on Dental Pulp Stem Cell-Derived Schwann Cells.Biomolecules · 2024Article
- Activation of XBP1s attenuates disease severity in models of proteotoxic Charcot-Marie-Tooth type 1B.bioRxiv : the preprint server for biology · 2024Article
- A novel mouse model of CMT1B identifies hyperglycosylation as a new pathogenetic mechanism.Human molecular genetics · 2022Article
- Mechanisms and Treatments in Demyelinating CMT.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Calcineurin Activity Is Increased in Charcot-Marie-Tooth 1B Demyelinating Neuropathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Article
- Systemic hypoxia led to little retinal neuronal loss and dramatic optic nerve glial response.Experimental eye research · 2020Article
- Blocking Autophagy in Oligodendrocytes Limits Functional Recovery after Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Article
- Activating Transcription Factor-6α Deletion Modulates the Endoplasmic Reticulum Stress Response after Spinal Cord Injury but Does Not Affect Locomotor Recovery.Journal of neurotrauma · 2018Article
- Cellular Pathology of Pelizaeus-Merzbacher Disease Involving Chaperones Associated with Endoplasmic Reticulum Stress.Frontiers in molecular biosciences · 2017Review
- Endoplasmic reticulum stress and the unfolded protein response in disorders of myelinating glia.Brain research · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The capacity to fold proteins properly is fundamental for cell survival. Secreted and transmembrane proteins are synthesized in the endoplasmic reticulum (ER), an organelle that has the ability to discriminate between native and nonnative proteins, in a process called protein quality control. When folding is not properly achieved, misfolded proteins can accumulate. The terminally misfolded proteins are typically retrotranslocated into the cytoplasm for degradation by the proteasome, in a process known as endoplasmic reticulum-associated degradation. However, if the degradation is insufficient, accumulation of abnormal proteins in the ER activates the unfolded protein response (UPR), a complex set of new signals aimed to reduce further the load of abnormal protein in the ER. Massive synthesis of myelin lipids and proteins is necessary to support myelinogenesis. Not surprisingly, therefore, ER stress (including the UPR), the proteasome, and autophagy (lysosomes) have been implicated in myelin disorders, such as Pelizaeus-Merzbacher disease and vanishing white matter disease in the central nervous system and Charcot-Marie-Tooth neuropathies in the peripheral nervous system. Here we discuss recent evidence supporting an important role for ER stress in myelin disorders.
Indexed as
Identifiers
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.