ArticleThe Journal of biological chemistry2010
Slc35c2 promotes Notch1 fucosylation and is required for optimal Notch signaling in mammalian cells.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 58 citations in OpenAlex.
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- Directed evolution of novel AAV variants using the MCMS library for enhanced CNS tropism and reduced liver targeting in mice.Molecular therapy. Methods & clinical development · 2025Article
- GDP-fucose transporter SLC35C1: a potential regulatory role in cytosolic GDP-fucose and fucosylated glycan synthesis.FEBS open bio · 2025Article
- Review
- ProteinMolecules (Basel, Switzerland) · 2025Review
- Proximal partners of the organellar N-terminal acetyltransferase NAA60: insights into Golgi structure and transmembrane protein topology.Open biology · 2025Article
- Genetics of glycosylation in mammalian development and disease.Nature reviews. Genetics · 2024Review
- Article
- In vivo evidence for GDP-fucose transport in the absence of transporter SLC35C1 and putative transporter SLC35C2.The Journal of biological chemistry · 2023Article
- Origin of cytoplasmic GDP-fucose determines its contribution to glycosylation reactions.The Journal of cell biology · 2022Article
- Delivery of Nucleotide Sugars to the Mammalian Golgi: A Very Well (un)Explained Story.International journal of molecular sciences · 2022Review
- L-fucose, a sugary regulator of antitumor immunity and immunotherapies.Molecular carcinogenesis · 2022Review
- A spoonful of L-fucose-an efficient therapy for GFUS-CDG, a new glycosylation disorder.EMBO molecular medicine · 2021Article
- A long non-coding RNA (Lrap) modulates brain gene expression and levels of alcohol consumption in rats.Genes, brain, and behavior · 2021Review
- Therapeutic Monosaccharides: Looking Back, Moving Forward.Biochemistry · 2020Review
- Differential Labeling of Glycoproteins with Alkynyl Fucose Analogs.International journal of molecular sciences · 2020Article
- Expanding the molecular and clinical phenotypes of FUT8-CDG.Journal of inherited metabolic disease · 2020Article
- Article
- SLC35A5 Protein-A Golgi Complex Member with Putative Nucleotide Sugar Transport Activity.International journal of molecular sciences · 2019Article
- CDG Therapies: From Bench to Bedside.International journal of molecular sciences · 2018Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mammalian Notch receptors require modification by fucose on epidermal growth factor-like (EGF) repeats of their extracellular domain to respond optimally to signal induction by canonical Notch ligands. Inactivation of the Golgi GDP-fucose transporter Slc35c1 in mouse or human does not cause marked defects in Notch signaling during development, and shows milder fucosylation defects than those observed in mice unable to synthesize GDP-fucose, indicating the existence of another mechanism for GDP-fucose transport into the secretory pathway. We show here that fibroblasts from mice or humans lacking Slc35c1 exhibit robust Notch signaling in co-culture signaling assays. A potential candidate for a second GDP-fucose transporter is the related gene Slc35c2. Overexpression of Slc35c2 reduces expression of the fucosylated epitopes Lewis X and sialylated Lewis X in CHO cells, indicating competition with Slc35c1. The fucosylation of a Notch1 EGF repeat fragment that occurs in the endoplasmic reticulum was increased in CHO transfectants overexpressing Slc35c2. In CHO cells with low levels of Slc35c2, both Delta1- and Jagged1-induced Notch signaling were reduced, and the fucosylation of a Notch1 fragment was also decreased. Immunofluorescence microscopy of rat intestinal epithelial cells and HeLa cells, and analysis of rat liver membrane fractions showed that Slc35c2 is primarily colocalized with markers of the cis-Golgi network and endoplasmic reticulum-Golgi intermediate compartment (ERGIC). The combined results suggest that Slc35c2 is either a GDP-fucose transporter that competes with Slc35c1 for GDP-fucose, or a factor that otherwise enhances the fucosylation of Notch and is required for optimal Notch signaling in mammalian cells.
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