ArticlePloS one2013
N-glycosylation is required for secretion and mitosis in C. elegans.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Glycan remodelling of live adult Schistosoma mansoni worms by chemical inhibition of α-mannosidases.International journal for parasitology · 2026Article
- Distinct responses to non-autonomous UPRCommunications biology · 2025Article
- Targeting EDEM protects against ER stress and improves development and survival in C. elegans.PLoS genetics · 2022Article
- Inhibition of the oligosaccharyl transferase in Caenorhabditis elegans that compromises ER proteostasis suppresses p38-dependent protection against pathogenic bacteria.PLoS genetics · 2020Article
- UPRScience advances · 2020Article
- Article
- RNAi screening of human glycogene orthologs in the nematode Caenorhabditis elegans and the construction of the C. elegans glycogene database.Glycobiology · 2015Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-glycosylation of proteins is an essential process, and N-glucans serve as important beacons in protein folding and ER associated degradation. More importantly, N-glycosylation increases the structural repertoire of proteins because the addition of the N-glucan on proteins will serve as a base for further sugar additions in the Golgi apparatus, and hence complex three-dimensional structures can be build. N-glycosylation is mediated by the ER-resident OST complex, which is essential throughout eukaryotes. Partial knockdown of conserved OST complex members, such as C. elegans RIBO-1, led to an embryonic lethal phenotype. Although the ER morphology was not grossly altered in ribo-1(RNAi) oocytes and embryos, secretion of yolk and of the yolk receptor RME-2 was perturbed in those worms. Perhaps as a consequence of reduced arrival of N-glycosylated proteins at the plasma membrane, cytokinesis occurred less efficiently leading to multinuclear cells. Unexpectedly, we detected a chromosome segregation defect in ribo-1(RNAi) embryos suggesting an essential role of at least one N-glycosylated protein in metaphase-anaphase transition.
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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.