ArticleThe Journal of biological chemistry
The promiscuous binding pocket of SLC35A1 ensures redundant transport of CDP-ribitol to the Golgi.
Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 21 citations in OpenAlex.
- STREMI: a dual-function upstream ORF-encoded regulator of mitochondrial cristae architecture.EMBO reports · 2026Article
- Biosynthetic and genetic pathways related to sialic acid metabolism.The Journal of biological chemistry · 2026Review
- Molecular Modeling and Gene Ontology Implicate SLC35F4 and SLC35F5 as Golgi-Associated Importers of Flavin-Adenine-Dinucleotide.International journal of molecular sciences · 2026Article
- Biosynthesis and Regulation of Laminin-Binding O-Mannosyl Glycans Related to Muscular Dystrophy.Advances in experimental medicine and biology · 2026Review
- The dual-coding gene SLC35A4 protects against oxidative stress.Protein science : a publication of the Protein Society · 2025Article
- Small open reading frame-encoded microproteins in cancer: identification, biological functions and clinical significance.Molecular cancer · 2025Review
- Non-canonical ORFs-derived protein products in mitochondria: A multifaceted exploration of their functions in health and disease.Protein science : a publication of the Protein Society · 2025Review
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- Analysis of cancer-associated glycosyltransferases reveals novel targets of non-small cell lung cancer pathogenesis.Frontiers in oncology · 2025Article
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- Identification of SLC35A1 as an essential host factor for the transduction of multi-serotype recombinant adeno-associated virus (AAV) vectors.bioRxiv : the preprint server for biology · 2024Article
- Novel GNE missense variants impair de novo sialylation and cause defective angiogenesis in the developing brain in mice.Blood advances · 2024Article
- Identification of a short, single site matriglycan that maintains neuromuscular function in the mouse.bioRxiv : the preprint server for biology · 2023Article
- Parkinson's disease protein PARK7 prevents metabolite and protein damage caused by a glycolytic metabolite.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Novel Insights into the Prognosis and Immunological Value of the SLC35A (Solute Carrier 35A) Family Genes in Human Breast Cancer.Biomedicines · 2021Article
- Biosynthetic Mechanisms and Biological Significance of Glycerol Phosphate-Containing Glycan in Mammals.Molecules (Basel, Switzerland) · 2021Review
- NAA80 bi-allelic missense variants result in high-frequency hearing loss, muscle weakness and developmental delay.Brain communications · 2021Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The glycoprotein α-dystroglycan helps to link the intracellular cytoskeleton to the extracellular matrix. A unique glycan structure attached to this protein is required for its interaction with extracellular matrix proteins such as laminin. Up to now, this is the only mammalian glycan known to contain ribitol phosphate groups. Enzymes in the Golgi apparatus use CDP-ribitol to incorporate ribitol phosphate into the glycan chain of α-dystroglycan. Since CDP-ribitol is synthesized in the cytoplasm, we hypothesized that an unknown transporter must be required for its import into the Golgi apparatus. We discovered that CDP-ribitol transport relies on the CMP-sialic acid transporter SLC35A1 and the transporter SLC35A4 in a redundant manner. These two transporters are closely related, but bulky residues in the predicted binding pocket of SLC35A4 limit its size. We hypothesized that the large binding pocket SLC35A1 might accommodate the bulky CMP-sialic acid and the smaller CDP-ribitol, whereas SLC35A4 might only accept CDP-ribitol. To test this, we expressed SLC35A1 with mutations in its binding pocket in SLC35A1 KO cell lines. When we restricted the binding site of SLC35A1 by introducing the bulky residues present in SLC35A4, the mutant transporter was unable to support sialylation of proteins in cells but still supported ribitol phosphorylation. This demonstrates that the size of the binding pocket determines the substrate specificity of SLC35A1, allowing a variety of cytosine nucleotide conjugates to be transported. The redundancy with SLC35A4 also explains why patients with SLC35A1 mutations do not show symptoms of α-dystroglycan deficiency.
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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.