ArticleTraffic (Copenhagen, Denmark)2018
More than just sugars: Conserved oligomeric Golgi complex deficiency causes glycosylation-independent cellular defects.
Article in Traffic (Copenhagen, Denmark), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- COG Complex in Golgi Trafficking and Glycosylation.Sub-cellular biochemistry · 2026Review
- Siamese Twins: The Multimodular Mechanisms of Golgi Maturation and Glycan Synthesis Are Coupled at Their Core.Sub-cellular biochemistry · 2026Review
- Diagnostic and Therapeutic Approaches in Congenital Disorders of Glycosylation.Handbook of experimental pharmacology · 2025Review
- Validation of Candidate Host Cell Entry Factors for Bovine Herpes Virus Type-1 Based on a Genome-Wide CRISPR Knockout Screen.Viruses · 2024Article
- Split but merge: Golgi fragmentation in physiological and pathological conditions.Molecular biology reports · 2024Review
- COG-imposed Golgi functional integrity determines the onset of dark-induced senescence.Nature plants · 2023Article
- Syntaxin-5's flexibility in SNARE pairing supports Golgi functions.Traffic (Copenhagen, Denmark) · 2023Article
- Review
- Acute COG complex inactivation unveiled its immediate impact on Golgi and illuminated the nature of intra-Golgi recycling vesicles.Traffic (Copenhagen, Denmark) · 2023Article
- Article
- Towards understanding the extensive diversity of protein N-glycan structures in eukaryotes.Biological reviews of the Cambridge Philosophical Society · 2022Review
- GARP dysfunction results in COPI displacement, depletion of Golgi v-SNAREs and calcium homeostasis proteins.Frontiers in cell and developmental biology · 2022Article
- Getting Sugar Coating Right! The Role of the Golgi Trafficking Machinery in Glycosylation.Cells · 2021Review
- Congenital disorder of glycosylation caused by starting site-specific variant in syntaxin-5.Nature communications · 2021Article
- The Golgi-associated retrograde protein (GARP) complex plays an essential role in the maintenance of the Golgi glycosylation machinery.Molecular biology of the cell · 2021Article
- Proteoglycan synthesis in conserved oligomeric Golgi subunit deficient HEK293T cells is affected differently, depending on the lacking subunit.Traffic (Copenhagen, Denmark) · 2021Article
- Golgi-Dependent Copper Homeostasis Sustains Synaptic Development and Mitochondrial Content.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Development and Initial Characterization of Cellular Models for COG Complex-Related CDG-II Diseases.Frontiers in genetics · 2021Article
- Article
- Golgi inCOGnito: From vesicle tethering to human disease.Biochimica et biophysica acta. General subjects · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The conserved oligomeric Golgi (COG) complex controls membrane trafficking and ensures Golgi homeostasis by orchestrating retrograde vesicle trafficking within the Golgi. Human COG defects lead to severe multisystemic diseases known as COG-congenital disorders of glycosylation (COG-CDG). To gain better understanding of COG-CDGs, we compared COG knockout cells with cells deficient to 2 key enzymes, Alpha-1,3-mannosyl-glycoprotein 2-beta-N-acetylglucosaminyltransferase and uridine diphosphate-glucose 4-epimerase (GALE), which contribute to proper N- and O-glycosylation. While all knockout cells share similar defects in glycosylation, these defects only account for a small fraction of observed COG knockout phenotypes. Glycosylation deficiencies were not associated with the fragmented Golgi, abnormal endolysosomes, defective sorting and secretion or delayed retrograde trafficking, indicating that these phenotypes are probably not due to hypoglycosylation, but to other specific interactions or roles of the COG complex. Importantly, these COG deficiency specific phenotypes were also apparent in COG7-CDG patient fibroblasts, proving the human disease relevance of our CRISPR knockout findings. The knowledge gained from this study has important implications, both for understanding the physiological role of COG complex in Golgi homeostasis in eukaryotic cells, and for better understanding human diseases associated with COG/Golgi impairment.
Indexed as
Identifiers
What OpenQuestion holds
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.