ArticleThe Journal of biological chemistry2014
Multiple sclerosis autoantigen myelin basic protein escapes control by ubiquitination during proteasomal degradation.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Review
- Myelin Basic Protein Fragmentation by Engineered Human Proteasomes with Different Catalytic Phenotypes Revealed Direct Peptide Ligands of MS-Associated and Protective HLA Class I Molecules.International journal of molecular sciences · 2023Article
- Role of Neddylation in Neurodegenerative Diseases.NeuroSci · 2022Review
- Modulating the Ubiquitin-Proteasome System: A Therapeutic Strategy for Autoimmune Diseases.Cells · 2022Review
- A short binding site in the KPC1 ubiquitin ligase mediates processing of NF-κB1 p105 to p50: A potential for a tumor-suppressive PROTAC.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Comprehensive Atlas of the Myelin Basic Protein Interaction Landscape.Biomolecules · 2021Article
- Review
- Cell type-specific transcriptomics identifies neddylation as a novel therapeutic target in multiple sclerosis.Brain : a journal of neurology · 2021Article
- Polyamines Counteract Carbonate-Driven Proteasome Stalling in Alkaline Conditions.Biomolecules · 2020Article
- Galectin-3 Exerts a Pro-differentiating and Pro-myelinating Effect Within a Temporal Window Spanning Precursors and Pre-oligodendrocytes: Insights into the Mechanisms of Action.Molecular neurobiology · 2020Article
- Article
- The Transcriptome of Type I Murine Astrocytes under Interferon-Gamma Exposure and Remyelination Stimulus.Molecules (Basel, Switzerland) · 2017Article
- mRNA expression profile of mouse oligodendrocytes in inflammatory conditions.Doklady. Biochemistry and biophysics · 2016Article
- Deimination of the myelin basic protein decelerates its proteasome-mediated metabolism.Doklady. Biochemistry and biophysics · 2016Article
- Ubiquitin-independent proteosomal degradation of myelin basic protein contributes to development of neurodegenerative autoimmunity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Antigen Presentation, Autoantigens, and Immune Regulation in Multiple Sclerosis and Other Autoimmune Diseases.Frontiers in immunology · 2015Review
- Clinical and experimental studies of multiple sclerosis in Russia: experience of the leading national research centers.Degenerative neurological and neuromuscular disease · 2015Article
- Glatiramer acetate and nanny proteins restrict access of the multiple sclerosis autoantigen myelin basic protein to the 26S proteasome.BioMed research international · 2014Article
- Article
- Multiple Sclerosis Is Associated with Immunoglobulin Germline Gene Variation of Transitional B Cells.Acta naturaeArticle
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The vast majority of cellular proteins are degraded by the 26S proteasome after their ubiquitination. Here, we report that the major component of the myelin multilayered membrane sheath, myelin basic protein (MBP), is hydrolyzed by the 26S proteasome in a ubiquitin-independent manner both in vitro and in mammalian cells. As a proteasomal substrate, MBP reveals a distinct and physiologically relevant concentration range for ubiquitin-independent proteolysis. Enzymatic deimination prevents hydrolysis of MBP by the proteasome, suggesting that an abnormally basic charge contributes to its susceptibility toward proteasome-mediated degradation. To our knowledge, our data reveal the first case of a pathophysiologically important autoantigen as a ubiquitin-independent substrate of the 26S proteasome.
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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.