ArticleJournal of inherited metabolic disease2020
Fetal bovine serum impacts the observed N-glycosylation defects in TMEM165 KO HEK cells.
Article in Journal of inherited metabolic disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Prolonged duration induces divergent transcriptomic responses to manganese, distinct from concentration effects, in an SH-SY5Y neurotoxicity model.Neurotoxicology · 2026Article
- Article
- Putative role of TMEM165 in congenital cardiomyopathies.Frontiers in molecular neuroscience · 2025Review
- Insights into the regulation of cellular MnBiochimica et biophysica acta. Molecular basis of disease · 2023Article
- Chemical factors induce aggregative multicellularity in a close unicellular relative of animals.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Abnormal expression of lysosomal glycoproteins in patients with congenital disorders of glycosylation.BMC research notes · 2023Article
- Article
- Differential Effects of D-Galactose Supplementation on Golgi Glycosylation Defects in TMEM165 Deficiency.Frontiers in cell and developmental biology · 2022Article
- Manganese systemic distribution is modulated in vivo during tumor progression and affects tumor cell migration and invasion in vitro.Scientific reports · 2021Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
TMEM165 is involved in a rare genetic human disease named TMEM165-CDG (congenital disorders of glycosylation). It is Golgi localized, highly conserved through evolution and belongs to the uncharacterized protein family 0016 (UPF0016). The use of isogenic TMEM165 KO HEK cells was crucial in deciphering the function of TMEM165 in Golgi manganese homeostasis. Manganese is a major cofactor of many glycosylation enzymes. Severe Golgi glycosylation defects are observed in TMEM165 Knock Out Human Embryonic Kidney (KO HEK) cells and are rescued by exogenous manganese supplementation. Intriguingly, we demonstrate in this study that the observed Golgi glycosylation defect mainly depends on fetal bovine serum, particularly its manganese level. Our results also demonstrate that iron and/or galactose can modulate the observed glycosylation defects in TMEM165 KO HEK cells. While isogenic cultured cells are widely used to study the impact of gene defects on proteins' glycosylation patterns, these results emphasize the importance of the use of validated fetal bovine serum in glycomics studies.
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