ArticleCell death & disease2021
Small heat-shock protein HSPB3 promotes myogenesis by regulating the lamin B receptor.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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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
18 citing papers in PubMed, 24 citations in OpenAlex.
- HSP60 and HSP10 depletion provoke distinct biological responses.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Article
- Caenorhabditis elegans small heat-shock protein HSP-12.6 has a highly specialized protective function towards muscle thick filaments in vivo.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Article
- Small heat shock proteins and biomolecular condensates.Cellular and molecular life sciences : CMLS · 2026Review
- Therapeutic potency and the related mechanism of deinoxanthin in experimental animal and cell models of periodontitis.Scientific reports · 2026Article
- Genome-wide association study identifies candidate genes affecting body conformation traits of Zhongwei goat.BMC genomics · 2025Article
- A new insight on alleviating the inhibitory effect of aflatoxin B1 on muscle development in grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2024Article
- HuD impairs neuromuscular junctions and induces apoptosis in human iPSC and Drosophila ALS models.Nature communications · 2024Article
- Article
- The major inducible small heat shock protein HSP20-3 in the tardigrade Ramazzottius varieornatus forms filament-like structures and is an active chaperone.Cell stress & chaperones · 2024Article
- Transcriptomic Response of Differentiating Porcine Myotubes to Thermal Stress and Donor Piglet Age.International journal of molecular sciences · 2023Article
- Review
- Heat Shock Proteins: Important Helpers for the Development, Maintenance and Regeneration of Skeletal Muscles.Muscles (Basel, Switzerland) · 2023Review
- Tardigrade small heat shock proteins can limit desiccation-induced protein aggregation.Communications biology · 2023Article
- Article
- The Role of Small Heat Shock Proteins in Protein Misfolding Associated Motoneuron Diseases.International journal of molecular sciences · 2022Review
- Insights on Human Small Heat Shock Proteins and Their Alterations in Diseases.Frontiers in molecular biosciences · 2022Review
- Identification of Potential Biomarkers and Immune Infiltration Characteristics in Ulcerative Colitis by Combining Results from Two Machine Learning Algorithms.Computational and mathematical methods in medicine · 2022Article
- HLH-1 Modulates Muscle Proteostasis DuringFrontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
24 authors at 11 institutions in 5 countries.
Funding
Abstract
One of the critical events that regulates muscle cell differentiation is the replacement of the lamin B receptor (LBR)-tether with the lamin A/C (LMNA)-tether to remodel transcription and induce differentiation-specific genes. Here, we report that localization and activity of the LBR-tether are crucially dependent on the muscle-specific chaperone HSPB3 and that depletion of HSPB3 prevents muscle cell differentiation. We further show that HSPB3 binds to LBR in the nucleoplasm and maintains it in a dynamic state, thus promoting the transcription of myogenic genes, including the genes to remodel the extracellular matrix. Remarkably, HSPB3 overexpression alone is sufficient to induce the differentiation of two human muscle cell lines, LHCNM2 cells, and rhabdomyosarcoma cells. We also show that mutant R116P-HSPB3 from a myopathy patient with chromatin alterations and muscle fiber disorganization, forms nuclear aggregates that immobilize LBR. We find that R116P-HSPB3 is unable to induce myoblast differentiation and instead activates the unfolded protein response. We propose that HSPB3 is a specialized chaperone engaged in muscle cell differentiation and that dysfunctional HSPB3 causes neuromuscular disease by deregulating LBR.
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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.