ArticleCurrent biology : CB2020
Pre-emptive Quality Control of a Misfolded Membrane Protein by Ribosome-Driven Effects.
Article in Current biology : CB, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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
31 citing papers in PubMed, 51 citations in OpenAlex.
- Principles of ribosome-associated protein quality control during the synthesis of CFTR.The EMBO journal · 2026Article
- The coordinated action of UFMylation and the RQC pathways clears arrested polypeptides at the ER.The EMBO journal · 2026Article
- Sec61β maintains cytoplasmic proteostasis via ARIH1-mediated translational repression upon ER stress.EMBO reports · 2026Article
- The EMC acts as a chaperone for membrane proteins.Nature communications · 2025Article
- SARS-CoV-2 Nsp2 recruits GIGYF2 near viral replication sites and supports viral protein production.Nucleic acids research · 2025Article
- Cytoplasmic mRNA decay and quality control machineries in eukaryotes.Nature reviews. Genetics · 2025Review
- EMC3 is critical for CFTR function and calcium mobilization in the mouse intestinal epithelium.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Ribosomal frameshifting selectively modulates the assembly, function, and pharmacological rescue of a misfolded CFTR variant.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Ribosomal Frameshifting Selectively Modulates the Assembly, Function, and Pharmacological Rescue of a Misfolded CFTR Variant.bioRxiv : the preprint server for biology · 2024Article
- Control of mRNA fate by its encoded nascent polypeptide.Molecular cell · 2023Review
- A selectivity filter in the ER membrane protein complex limits protein misinsertion at the ER.The Journal of cell biology · 2023Article
- A TAle of Two Pathways: Tail-Anchored Protein Insertion at the Endoplasmic Reticulum.Cold Spring Harbor perspectives in biology · 2023Review
- Elexacaftor/VX-445-mediated CFTR interactome remodeling reveals differential correction driven by mutation-specific translational dynamics.bioRxiv : the preprint server for biology · 2023Article
- Monosomes buffer translational stress to allow for active ribosome elongation.Frontiers in molecular biosciences · 2023Article
- HDLBP binds ER-targeted mRNAs by multivalent interactions to promote protein synthesis of transmembrane and secreted proteins.Nature communications · 2022Article
- Article
- EMC is required for biogenesis of Xport-A, an essential chaperone of Rhodopsin-1 and the TRP channel.EMBO reports · 2022Article
- Ending a bad start: Triggers and mechanisms of co-translational protein degradation.Frontiers in molecular biosciences · 2022Review
- The trinity of ribosome-associated quality control and stress signaling for proteostasis and neuronal physiology.BMB reports · 2021Review
- Detecting and Rescuing Stalled Ribosomes.Trends in biochemical sciences · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Cells possess multiple mechanisms that protect against the accumulation of toxic aggregation-prone proteins. Here, we identify a pre-emptive pathway that reduces synthesis of membrane proteins that have failed to properly assemble in the endoplasmic reticulum (ER). We show that loss of the ER membrane complex (EMC) or mutation of the Sec61 translocon causes reduced synthesis of misfolded forms of the yeast ABC transporter Yor1. Synthesis defects are rescued by various ribosomal mutations, as well as by reducing cellular ribosome abundance. Genetic and biochemical evidence point to a ribosome-associated quality-control pathway triggered by ribosome collisions when membrane domain insertion and/or folding fails. In support of this model, translation initiation also contributes to synthesis defects, likely by modulating ribosome abundance on the message. Examination of translation efficiency across the yeast membrane proteome revealed that polytopic membrane proteins have relatively low ribosome abundance, providing evidence for translational tuning to balance protein synthesis and folding. We propose that by modulating translation rates of poorly folded proteins, cells can pre-emptively protect themselves from potentially toxic aberrant transmembrane proteins.
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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.