ArticleMolecular biology of the cell2010
Folding-competent and folding-defective forms of ricin A chain have different fates after retrotranslocation from the endoplasmic reticulum.
Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 48 citations in OpenAlex.
- Dysregulation of ceramide metabolism causes phytoceramide-dependent induction of the unfolded protein response.Molecular biology of the cell · 2024Article
- Pathological implications of cellular stress in cardiovascular diseases.The international journal of biochemistry & cell biology · 2023Review
- Differences in Medium-Induced Conformational Plasticity Presumably Underlie Different Cytotoxic Activity of Ricin and Viscumin.Biomolecules · 2022Article
- Predicting gene phenotype by multi-label multi-class model based on essential functional features.Molecular genetics and genomics : MGG · 2021Article
- Article
- Sites of vulnerability on ricin B chain revealed through epitope mapping of toxin-neutralizing monoclonal antibodies.PloS one · 2020Article
- Review
- Toxins Utilize the Endoplasmic Reticulum-Associated Protein Degradation Pathway in Their Intoxication Process.International journal of molecular sciences · 2019Review
- Genome-wide CRISPR Analysis Identifies Substrate-Specific Conjugation Modules in ER-Associated Degradation.Molecular cell · 2019Article
- A Simple Fluorescence-based Reporter Assay to Identify Cellular Components Required for Ricin Toxin A Chain (RTA) Trafficking in Yeast.Journal of visualized experiments : JoVE · 2017Article
- Article
- Yeast Reporter Assay to Identify Cellular Components of Ricin Toxin A Chain Trafficking.Toxins · 2016Article
- Progress and challenges associated with the development of ricin toxin subunit vaccines.Expert review of vaccines · 2016Review
- Hydrophobicity of protein determinants influences the recognition of substrates by EDEM1 and EDEM2 in human cells.BMC cell biology · 2015Article
- Ricin trafficking in cells.Toxins · 2015Review
- Cytolethal distending toxins require components of the ER-associated degradation pathway for host cell entry.PLoS pathogens · 2014Article
- Protein folding as a driving force for dual protein targeting in eukaryotes.Frontiers in molecular biosciences · 2014Review
- Article
- Isoform-selective oligomer formation of Saccharomyces cerevisiae p24 family proteins.The Journal of biological chemistry · 2013Article
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
We report that a toxic polypeptide retaining the potential to refold upon dislocation from the endoplasmic reticulum (ER) to the cytosol (ricin A chain; RTA) and a misfolded version that cannot (termed RTA(Delta)), follow ER-associated degradation (ERAD) pathways in Saccharomyces cerevisiae that substantially diverge in the cytosol. Both polypeptides are dislocated in a step mediated by the transmembrane Hrd1p ubiquitin ligase complex and subsequently degraded. Canonical polyubiquitylation is not a prerequisite for this interaction because a catalytically inactive Hrd1p E3 ubiquitin ligase retains the ability to retrotranslocate RTA, and variants lacking one or both endogenous lysyl residues also require the Hrd1p complex. In the case of native RTA, we established that dislocation also depends on other components of the classical ERAD-L pathway as well as an ongoing ER-Golgi transport. However, the dislocation pathways deviate strikingly upon entry into the cytosol. Here, the CDC48 complex is required only for RTA(Delta), although the involvement of individual ATPases (Rpt proteins) in the 19S regulatory particle (RP) of the proteasome, and the 20S catalytic chamber itself, is very different for the two RTA variants. We conclude that cytosolic ERAD components, particularly the proteasome RP, can discriminate between structural features of the same substrate.
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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.