ArticleNeurochemical research2010
Defective GM3 synthesis in Cog2 null mutant CHO cells associates to mislocalization of lactosylceramide sialyltransferase in the Golgi complex.
Article in Neurochemical research, 2010. 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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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- COG Complex in Golgi Trafficking and Glycosylation.Sub-cellular biochemistry · 2026Review
- Identification of SYS1 as a Host Factor Required for Shiga Toxin-Mediated Cytotoxicity in Vero Cells.International journal of molecular sciences · 2021Article
- A large-scale genome-lipid association map guides lipid identification.Nature metabolism · 2020Article
- Maintaining order: COG complex controls Golgi trafficking, processing, and sorting.FEBS letters · 2019Review
- More than just sugars: Conserved oligomeric Golgi complex deficiency causes glycosylation-independent cellular defects.Traffic (Copenhagen, Denmark) · 2018Article
- COG Complex Complexities: Detailed Characterization of a Complete Set of HEK293T Cells Lacking Individual COG Subunits.Frontiers in cell and developmental biology · 2016Article
- Defects in the COG complex and COG-related trafficking regulators affect neuronal Golgi function.Frontiers in neuroscience · 2015Review
- Mislocalization of large ARF-GEFs as a potential mechanism for BFA resistance in COG-deficient cells.Experimental cell research · 2011Article
- Cog2 null mutant CHO cells show defective sphingomyelin synthesis.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The conserved oligomeric Golgi (COG) complex is a eight subunit (COG1 to 8) tethering complex involved in the retrograde trafficking of multiple Golgi processing proteins. Here we studied the glycolipid synthesis status in ldlC cells, a Cog2 null mutant CHO cell line. Biochemical studies revealed a block in the coupling between LacCer and GM3 synthesis, resulting in decreased levels of GM3 in these cells. Uncoupling was not attributable to decreased activity of the glycosyltransferase that uses LacCer as acceptor substrate (SialT1). Rather, immunocytochemical experiments evidenced a mislocalization of SialT1 as consequence of the lack of Cog2 in these cells. Co-immunoprecipitation experiments disclose a Cog2 mediated interaction of SialT1 with the COG complex member Cog1. Results indicate that cycling of some Golgi glycolipid glycosyltransferases depends on the participation of the COG complex and that deficiencies in COG complex subunits, by altering their traffic and localization, affect glycolipid composition.
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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.