ArticleThe Journal of biological chemistry2010
Structure-function studies of the SLC17 transporter sialin identify crucial residues and substrate-induced conformational changes.
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 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Clinical and Genetic Characteristics of Free Sialic Acid Storage Disorder.Journal of inherited metabolic disease · 2026Article
- Profiling glycosphingolipid changes in mouse and human cellular models of lysosomal free sialic acid storage disorder.Molecular genetics and metabolism reports · 2025Article
- Lysosomal free sialic acid storage disorder iPSC-derived neural cells display altered glycosphingolipid metabolism.Scientific reports · 2025Article
- Investigating the Utility of Leukocyte Sialic Acid Measurements in Lysosomal Free Sialic Acid Storage Disorder.JIMD reports · 2025Article
- Lack of significant ganglioside changes inBiochemistry and biophysics reports · 2025Article
- Dissecting the impact of N-acetylmannosamine (ManNAc) on ganglioside levels in a sialin-deficient cell model.microPublication biology · 2025Article
- Changes in glycosphingolipid levels in plasma and cerebrospinal fluid of individuals with Lysosomal Free Sialic Acid Storage Disorder.Rare (Amsterdam, Netherlands) · 2025Article
- Altered sialin mRNA gene expression in type 2 diabetic male Wistar rats: implications for nitric oxide deficiency.Scientific reports · 2023Article
- Free sialic acid storage disorder: Progress and promise.Neuroscience letters · 2021Review
- Mutational Analysis of the GXXXG/A Motifs in the Human NaFrontiers in molecular biosciences · 2021Article
- Inherited disorders of lysosomal membrane transporters.Biochimica et biophysica acta. Biomembranes · 2020Review
- Structures suggest a mechanism for energy coupling by a family of organic anion transporters.PLoS biology · 2019Article
- Identification of a large intronic transposal insertion in SLC17A5 causing sialic acid storage disease.Orphanet journal of rare diseases · 2017Article
- The Structure and Function of OxlT, the Oxalate Transporter of Oxalobacter formigenes.The Journal of membrane biology · 2015Review
- Are vesicular neurotransmitter transporters potential treatment targets for temporal lobe epilepsy?Frontiers in cellular neuroscience · 2013Review
- Successful prediction of substrate-binding pocket in SLC17 transporter sialin.The Journal of biological chemistry · 2012Article
- SLC17: a functionally diverse family of organic anion transporters.Molecular aspects of medicineReview
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Salla disease and infantile sialic acid storage disorder are human diseases caused by loss of function of sialin, a lysosomal transporter that mediates H(+)-coupled symport of acidic sugars N-acetylneuraminic acid and glucuronic acid out of lysosomes. Along with the closely related vesicular glutamate transporters, sialin belongs to the SLC17 transporter family. Despite their critical role in health and disease, these proteins remain poorly understood both structurally and mechanistically. Here, we use substituted cysteine accessibility screening and radiotracer flux assays to evaluate experimentally a computationally generated three-dimensional structure model of sialin. According to this model, sialin consists of 12 transmembrane helices (TMs) with an overall architecture similar to that of the distantly related glycerol 3-phosphate transporter GlpT. We show that TM4 in sialin lines a large aqueous cavity that forms a part of the substrate permeation pathway and demonstrate substrate-induced alterations in accessibility of substituted cysteine residues in TM4. In addition, we demonstrate that one mutant, F179C, has a dramatically different effect on the apparent affinity and transport rate for N-acetylneuraminic acid and glucuronic acid, suggesting that it may be directly involved in substrate recognition and/or translocation. These findings offer a basis for further defining the transport mechanism of sialin and other SLC17 family members.
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Registered trials
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.