ArticleHaematologica2021
Slc35a1 deficiency causes thrombocytopenia due to impaired megakaryocytopoiesis and excessive platelet clearance in the liver.
Article in Haematologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Biosynthetic and genetic pathways related to sialic acid metabolism.The Journal of biological chemistry · 2026Review
- FUT1- and GAL3ST2-mediated cellular glycan remodeling broadly restricts sialic acid-dependent viral infections.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A Novel Missense Variant in Ultrarare SLC35A1-CDG Alters Cellular Glycosylation, Lipid, and Energy Metabolism Without Affecting CDG Serum Markers.Human mutation · 2025Review
- Novel GNE missense variants impair de novo sialylation and cause defective angiogenesis in the developing brain in mice.Blood advances · 2024Article
- Endothelial Slc35a1 Deficiency Causes Loss of LSEC Identity and Exacerbates Neonatal Lipid Deposition in the Liver in Mice.Cellular and molecular gastroenterology and hepatology · 2024Article
- Neurodevelopmental defects in human cortical organoids withScience advances · 2023Article
- Toward Automatic Inference of Glycan Linkages Using MSJournal of the American Society for Mass Spectrometry · 2023Article
- Platelet ITGA2B inhibits caspase-8 and Rip3/Mlkl-dependent platelet death though PTPN6 during sepsis.iScience · 2023Article
- Inherited Thrombocytopenia Caused by Variants in Crucial Genes for Glycosylation.International journal of molecular sciences · 2023Review
- Novel variants in GALE cause syndromic macrothrombocytopenia by disrupting glycosylation and thrombopoiesis.Blood · 2023Article
- Clinical and molecular findings in three Japanese patients with N-acetylneuraminic acid synthetase-congenital disorder of glycosylation (NANS-CDG).Scientific reports · 2022Article
- Overlapping and unique substrate specificities of ST3GAL1 and 2 during hematopoietic and megakaryocytic differentiation.Blood advances · 2022Article
- Sialic acid and platelet count regulation: Implications in immune thrombocytopenia.Research and practice in thrombosis and haemostasis · 2022Article
- Current therapeutic strategies and perspectives in refractory ITP: What have we learned recently?Frontiers in immunology · 2022Review
- Kupffer cell receptor CLEC4F is important for the destruction of desialylated platelets in mice.Cell death and differentiation · 2021Article
- Platelet desialylation and TFH cells-the novel pathway of immune thrombocytopenia.Experimental hematology & oncology · 2021Review
- NANS-CDG: Delineation of the Genetic, Biochemical, and Clinical Spectrum.Frontiers in neurology · 2021Article
- Novel Insights into Selected Disease-Causing Mutations within theInternational journal of molecular sciences · 2020Article
- Platelets and Defective N-Glycosylation.International journal of molecular sciences · 2020Review
- The promiscuous binding pocket of SLC35A1 ensures redundant transport of CDP-ribitol to the Golgi.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Sialic acid is a common terminal residue of glycans on proteins and acidic sphingolipids such as gangliosides and has important biological functions. The sialylation process is controlled by more than 20 different sialyltransferases, many of which exhibit overlapping functions. Thus, it is difficult to determine the overall biological function of sialylation by targeted deletion of individual sialyltransferases. To address this issue, we established a mouse line with the Slc35a1 gene flanked by loxP sites. Slc35a1 encodes the cytidine-5’-monophosphate (CMP)-sialic acid transporter that transports CMP-sialic acid from the cytoplasm into the Golgi apparatus for sialylation. Here we report our study regarding the role of sialylation on megakaryocytes and platelets using a mouse line with significantly reduced sialylation in megakaryocytes and platelets (Plt Slc35a1– /–). The major phenotype of Plt Slc35a1–/– mice was thrombocytopenia. The number of bone marrow megakaryocytes in Plt Slc35a1–/– mice was reduced, and megakaryocyte maturation was also impaired. In addition, an increased number of desialylated platelets was cleared by Küpffer cells in the liver of Plt Slc35a1–/– mice. This study provides new insights into the role of sialylation in platelet homeostasis and the mechanisms of thrombocytopenia in diseases associated with platelet desialylation, such as immune thrombocytopenia and a rare congenital disorder of glycosylation (CDG), SLC35A1-CDG, which is caused by SLC35A1 mutations.
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