ArticleThe Journal of biological chemistry2012
A novel approach to recovery of function of mutant proteins by slowing down translation.
Article in The Journal of biological chemistry, 2012. 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 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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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Barriers to the Pharmacologic Rescue of W1282X CFTR.Biochemistry · 2026Article
- Characterization of a Novel RNA Polymerase Mutant of Escherichia coli That Confers Thermotolerance and Chaperone Independence.Molecular microbiology · 2025Article
- A Proximity Complementation Assay to Identify Small Molecules That Enhance the Traffic of ABCA4 Misfolding Variants.International journal of molecular sciences · 2024Article
- Gain- and Loss-of-FunctionCells · 2022Article
- Translational suppression via IFG-1/eIF4G inhibits stress-induced RNA alternative splicing in Caenorhabditis elegans.Genetics · 2022Article
- Spatial covariance analysis reveals the residue-by-residue thermodynamic contribution of variation to the CFTR fold.Communications biology · 2022Article
- Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Slowing ribosome velocity restores folding and function of mutant CFTR.The Journal of clinical investigation · 2019Article
- HDAC inhibitors rescue multiple disease-causing CFTR variants.Human molecular genetics · 2019Article
- Correcting the F508del-CFTR variant by modulating eukaryotic translation initiation factor 3-mediated translation initiation.The Journal of biological chemistry · 2018Article
- Hsp70-Bag3 complex is a hub for proteotoxicity-induced signaling that controls protein aggregation.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Translation inhibition corrects aberrant localization of mutant alanine-glyoxylate aminotransferase: possible therapeutic approach for hyperoxaluria.Journal of molecular medicine (Berlin, Germany) · 2018Article
- Insights into the role and regulation of TCTP in skeletal muscle.Oncotarget · 2017Article
- Rescue of mutant rhodopsin traffic by metformin-induced AMPK activation accelerates photoreceptor degeneration.Human molecular genetics · 2017Article
- Reducing translation through eIF4G/IFG-1 improves survival under ER stress that depends on heat shock factor HSF-1 in Caenorhabditis elegans.Aging cell · 2016Article
- Ribosomal Stalk Protein Silencing Partially Corrects the ΔF508-CFTR Functional Expression Defect.PLoS biology · 2016Article
- Hijacked then lost in translation: the plight of the recombinant host cell in membrane protein structural biology projects.Current opinion in structural biology · 2015Review
- Dynamic changes in ribosome-associated proteome and phosphoproteome during deoxynivalenol-induced translation inhibition and ribotoxic stress.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
- Co-translational mechanisms of quality control of newly synthesized polypeptides.Translation (Austin, Tex.) · 2014Review
- Hsp33 controls elongation factor-Tu stability and allows Escherichia coli growth in the absence of the major DnaK and trigger factor chaperones.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Protein homeostasis depends on a balance of translation, folding, and degradation. Here, we demonstrate that mild inhibition of translation results in a dramatic and disproportional reduction in production of misfolded polypeptides in mammalian cells, suggesting an improved folding of newly synthesized proteins. Indeed, inhibition of translation elongation, which slightly attenuated levels of a copepod GFP mutant protein, significantly enhanced its function. In contrast, inhibition of translation initiation had minimal effects on copepod GFP folding. On the other hand, mild suppression of either translation elongation or initiation corrected folding defects of the disease-associated cystic fibrosis transmembrane conductance regulator mutant F508del. We propose that modulation of translation can be used as a novel approach to improve overall proteostasis in mammalian cells, as well as functions of disease-associated mutant proteins with folding deficiencies.
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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.