ReviewCell stress & chaperones2020
Consequences of mutations in the genes of the ER export machinery COPII in vertebrates.
Review in Cell stress & chaperones, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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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
9 citing papers in PubMed, 17 citations in OpenAlex.
- ER sensing of lipid metabolism drives PRA family-dependent regulation of COPII vesicle transport.Nature communications · 2026Article
- Defective anterograde protein-trafficking contributes to endoplasmic reticulum-stress in a CLN1 disease model.Neurobiology of disease · 2025Article
- A Report of a Child with SEC31A-Related Neurodevelopmental Disorder.International journal of molecular sciences · 2025Article
- SEC24C deficiency causes trafficking and glycosylation abnormalities in an epileptic encephalopathy with cataracts and dyserythropoeisis.JCI insight · 2025Article
- Compromised COPII vesicle trafficking leads to glycogenic hepatopathy.Disease models & mechanisms · 2024Article
- COPII cage assembly factor Sec13 integrates information flow regulating endomembrane function in response to human variation.Scientific reports · 2024Article
- COP I and II dependent trafficking controls ER-associated degradation in mammalian cells.iScience · 2023Article
- KLHL12 can form large COPII structures in the absence of CUL3 neddylation.Molecular biology of the cell · 2023Article
- Collagen has a unique SEC24 preference for efficient export from the endoplasmic reticulum.Traffic (Copenhagen, Denmark) · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Coat protein complex II (COPII) plays an essential role in the export of cargo molecules such as secretory proteins, membrane proteins, and lipids from the endoplasmic reticulum (ER). In yeast, the COPII machinery is critical for cell viability as most COPII knockout mutants fail to survive. In mice and fish, homozygous knockout mutants of most COPII genes are embryonic lethal, reflecting the essentiality of the COPII machinery in the early stages of vertebrate development. In humans, COPII mutations, which are often hypomorphic, cause diseases having distinct clinical features. This is interesting as the fundamental cellular defect of these diseases, that is, failure of ER export, is similar. Analyses of humans and animals carrying COPII mutations have revealed clues to why a similar ER export defect can cause such different diseases. Previous reviews have focused mainly on the deficit of secretory or membrane proteins in the final destinations because of an ER export block. In this review, we also underscore the other consequence of the ER export block, namely ER stress triggered by the accumulation of cargo proteins in the ER.
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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 Socratic graph.