ArticleThe Journal of biological chemistry2014
Biochemical characterization of mutants in chaperonin proteins CCT4 and CCT5 associated with hereditary sensory neuropathy.
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 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- The Human Lens Fiber Cytoskeletome Reveals Neuronal Signatures and the Presence of Chaperonins, Proteasome, Signaling, and Redox Regulators.Investigative ophthalmology & visual science · 2026Article
- Chaperonin in health and disease.Molecular biomedicine · 2026Review
- Proteome Microarray-Guided Global View: Multiple Pharmacological Targets of Icariin.Drug design, development and therapy · 2026Article
- Identification of metabolic reprogramming-associated biomarkers in endometriosis through integrated bioinformatics analysis.Hereditas · 2025Article
- Pan-cancer analysis reveals immunological and prognostic significance of CCT5 in human tumors.Scientific reports · 2025Article
- Retinal Pigment Epithelium Under Oxidative Stress: Chaperoning Autophagy and Beyond.International journal of molecular sciences · 2025Review
- CCT and Cullin1 Regulate the TORC1 Pathway to Promote Dendritic Arborization in Health and Disease.Cells · 2024Article
- Review
- Structural and Dynamic Disturbances Revealed by Molecular Dynamics Simulations Predict the Impact on Function of CCT5 Chaperonin Mutations Associated with Rare Severe Distal Neuropathies.International journal of molecular sciences · 2023Article
- Chaperonin-Containing TCP1 Subunit 5 Protects Against the Effect of Mer Receptor Tyrosine Kinase Knockdown in Retinal Pigment Epithelial Cells by Interacting With Filamentous Actin and Activating the LIM-Kinase 1/Cofilin Pathway.Frontiers in medicine · 2022Article
- The TRiCky Business of Protein Folding in Health and Disease.Frontiers in cell and developmental biology · 2022Review
- Roles of the miR-139-5p/CCT5 axis in hepatocellular carcinoma: a bioinformatic analysis.International journal of medical sciences · 2021Article
- Homeostatic Roles of the Proteostasis Network in Dendrites.Frontiers in cellular neuroscience · 2020Review
- Co-expression of CCT subunits hints at TRiC assembly.Cell stress & chaperones · 2019Article
- Myelin Pathology: Involvement of Molecular Chaperones and the Promise of Chaperonotherapy.Brain sciences · 2019Article
- Bridging human chaperonopathies and microbial chaperonins.Communications biology · 2019Review
- Quantitative analysis of the impact of a human pathogenic mutation on the CCT5 chaperonin subunit using a proxy archaeal ortholog.Biochemistry and biophysics reports · 2017Article
- Structure of the human TRiC/CCT Subunit 5 associated with hereditary sensory neuropathy.Scientific reports · 2017Article
- CCT2 Mutations Evoke Leber Congenital Amaurosis due to Chaperone Complex Instability.Scientific reports · 2016Article
- Internal (His)₆-tagging delivers a fully functional hetero-oligomeric class II chaperonin in high yield.Scientific reports · 2016Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Hereditary sensory neuropathies are a class of disorders marked by degeneration of the nerve fibers in the sensory periphery neurons. Recently, two mutations were identified in the subunits of the eukaryotic cytosolic chaperonin TRiC, a protein machine responsible for folding actin and tubulin in the cell. C450Y CCT4 was identified in a stock of Sprague-Dawley rats, whereas H147R CCT5 was found in a human Moroccan family. As with many genetically identified mutations associated with neuropathies, the underlying molecular basis of the mutants was not defined. We investigated the biochemical properties of these mutants using an expression system in Escherichia coli that produces homo-oligomeric rings of CCT4 and CCT5. Full-length versions of both mutant protein chains were expressed in E. coli at levels approaching that of the WT chains. Sucrose gradient centrifugation revealed chaperonin-sized complexes of both WT and mutant chaperonins, but with reduced recovery of C450Y CCT4 soluble subunits. Electron microscopy of negatively stained samples of C450Y CCT4 revealed few ring-shaped species, whereas WT CCT4, H147R CCT5, and WT CCT5 revealed similar ring structures. CCT5 complexes were assayed for their ability to suppress aggregation of and refold the model substrate γd-crystallin, suppress aggregation of mutant huntingtin, and refold the physiological substrate β-actin in vitro. H147R CCT5 was not as efficient in chaperoning these substrates as WT CCT5. The subtle effects of these mutations are consistent with the homozygous disease phenotype, in which most functions are carried out during development and adulthood, but some selective function is lost or reduced.
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