ArticlePloS one2011
BAG3 directly interacts with mutated alphaB-crystallin to suppress its aggregation and toxicity.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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.
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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
- Autophagy activation via BAG3 gene therapy improves phenotype in a mouse model of LGMD1A.Molecular therapy. Advances · 2026Article
- O-GlcNAc modification of HSP27 alters its protein interactions and promotes refolding of proteins through the BAG3/HSP70 co-chaperone.Protein science : a publication of the Protein Society · 2024Article
- Genetic Insights into Primary Restrictive Cardiomyopathy.Journal of clinical medicine · 2022Review
- Understanding the molecular basis of cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2022Review
- Therapeutic targeting of BAG3: considering its complexity in cancer and heart disease.The Journal of clinical investigation · 2021Review
- Novel BAG3 Variants in African American Patients With Cardiomyopathy: Reduced β-Adrenergic Responsiveness in Excitation-Contraction.Journal of cardiac failure · 2020Article
- Proteinaceous Transformers: Structural and Functional Variability of Human sHsps.International journal of molecular sciences · 2020Review
- Small heat shock proteins in neurodegenerative diseases.Cell stress & chaperones · 2020Review
- Assembly and Maintenance of Sarcomere Thin Filaments and Associated Diseases.International journal of molecular sciences · 2020Review
- Expanding the Clinico-Genetic Spectrum of Myofibrillar Myopathy: Experience From a Chinese Neuromuscular Center.Frontiers in neurology · 2020Article
- Come Together: Protein Assemblies, Aggregates and the Sarcostat at the Heart of Cardiac Myocyte Homeostasis.Frontiers in physiology · 2020Review
- Review
- Inhibitors and chemical probes for molecular chaperone networks.The Journal of biological chemistry · 2019Review
- The Regulation of the Small Heat Shock Protein B8 in Misfolding Protein Diseases Causing Motoneuronal and Muscle Cell Death.Frontiers in neuroscience · 2019Review
- Small Heat Shock Proteins, Big Impact on Protein Aggregation in Neurodegenerative Disease.Frontiers in pharmacology · 2019Review
- Suppression of astrocytic autophagy by αB-crystallin contributes to α-synuclein inclusion formation.Translational neurodegeneration · 2019Article
- LGMD1D myopathy with cytoplasmic and nuclear inclusions in a Saudi family due to DNAJB6 mutation.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2018Article
- The Multifunctional Protein BAG3: A Novel Therapeutic Target in Cardiovascular Disease.JACC. Basic to translational science · 2018Article
- The role of heat shock proteins and co-chaperones in heart failure.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
A homozygous disruption or genetic mutation of the bag3 gene causes progressive myofibrillar myopathy in mouse and human skeletal and cardiac muscle disorder while mutations in the small heat shock protein αB-crystallin gene (CRYAB) are reported to be responsible for myofibrillar myopathy. Here, we demonstrate that BAG3 directly binds to wild-type αB-crystallin and the αB-crystallin mutant R120G, via the intermediate domain of BAG3. Peptides that inhibit this interaction in an in vitro binding assay indicate that two conserved Ile-Pro-Val regions of BAG3 are involved in the interaction with αB-crystallin, which is similar to results showing BAG3 binding to HspB8 and HspB6. BAG3 overexpression increased αB-crystallin R120G solubility and inhibited its intracellular aggregation in HEK293 cells. BAG3 suppressed cell death induced by αB-crystallin R120G overexpression in differentiating C2C12 mouse myoblast cells. Our findings indicate a novel function for BAG3 in inhibiting protein aggregation caused by the genetic mutation of CRYAB responsible for human myofibrillar myopathy.
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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.