ArticleGlycoconjugate journal2011
Comparative analysis of involvement of UGT1 and UGT2 splice variants of UDP-galactose transporter in glycosylation of macromolecules in MDCK and CHO cell lines.
Article in Glycoconjugate journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Cytosolic UDP-Gal biosynthetic machinery is required for dimerization of SLC35A2 in the Golgi membrane and its interaction with B4GalT1.Frontiers in molecular biosciences · 2025Article
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- Delivery of Nucleotide Sugars to the Mammalian Golgi: A Very Well (un)Explained Story.International journal of molecular sciences · 2022Review
- Article
- Review
- Four New Cases of SLC35A2-CDG With Novel Mutations and Clinical Features.Frontiers in genetics · 2021Article
- Novel Insights into Selected Disease-Causing Mutations within theInternational journal of molecular sciences · 2020Article
- Biosynthesis of GlcNAc-richThe Journal of biological chemistry · 2020Article
- SLC35A2-CDG: Functional characterization, expanded molecular, clinical, and biochemical phenotypes of 30 unreported Individuals.Human mutation · 2019Article
- Article
- A new case of UDP-galactose transporter deficiency (SLC35A2-CDG): molecular basis, clinical phenotype, and therapeutic approach.Journal of inherited metabolic disease · 2015Article
- UDP-galactose (SLC35A2) and UDP-N-acetylglucosamine (SLC35A3) Transporters Form Glycosylation-related Complexes with Mannoside Acetylglucosaminyltransferases (Mgats).The Journal of biological chemistry · 2015Article
- Structure and function of nucleotide sugar transporters: Current progress.Computational and structural biotechnology journal · 2014Review
- UDP-N-acetylglucosamine transporter (SLC35A3) regulates biosynthesis of highly branched N-glycans and keratan sulfate.The Journal of biological chemistry · 2013Article
- Mosaicism of the UDP-galactose transporter SLC35A2 causes a congenital disorder of glycosylation.American journal of human genetics · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleotide sugar transporters deliver nucleotide sugars into the Golgi apparatus and endoplasmic reticulum. This study aimed to further characterize mammalian UDP-galactose transporter (UGT) in MDCK and CHO cell lines. MDCK-RCA(r) and CHO-Lec8 mutant cell lines are defective in UGT transporter, although they exhibit some level of galactosylation. Previously, only single forms of UGT were identified in both cell lines, UGT1 in MDCK cells and UGT2 in CHO cells. We have identified the second UGT splice variants in CHO (UGT1) and MDCK (UGT2) cells. Compared to UGT1, UGT2 is more abundant in nearly all examined mammalian tissues and cell lines, but MDCK cells exhibit different relative distribution of both splice variants. Complementation analysis demonstrated that both UGT splice variants are necessary for N- and O-glycosylation of proteins. Both mutant cell lines produce chondroitin-4-sulfate at only a slightly lower level compared to wild-type cells. This defect is corrected by overexpression of both UGT splice variants. MDCK-RCA(r) mutant cells do not produce keratan sulfate and this effect is not corrected by either UGT splice variant, overexpressed either singly or in combination. Here we demonstrate that both UGT splice variants are important for glycosylation of proteins. In contrast to MDCK cells, MDCK-RCA(r) mutant cells may possess an additional defect within the keratan sulfate biosynthesis pathway.
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