ArticleNature communications2018
The mechanism of glycosphingolipid degradation revealed by a GALC-SapA complex structure.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 62 citations in OpenAlex.
- CircRNA Profiling Identifies Candidates Associated with Abdominal Fat Deposition in Ducks.Biology · 2026Article
- Validating a Human Cell Model of Null Galactosylceramidase (GALC) Enzyme Activity That Recapitulates Krabbe Disease.Journal of inherited metabolic disease · 2026Article
- Transport of sphingolipids by yeast Npc2 supports phase separation of the vacuole membrane.The Journal of biological chemistry · 2026Article
- Gut Microbiome-Sphingolipid Metabolism-Brain Axis Interactions: Neuroprotective Effects of Amitriptyline as Functional Inhibitor of Acid Sphingomyelinase in a Mouse Model of Tauopathy.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Molecular Dynamics Simulations of 4Computational and structural biotechnology journal · 2026Article
- Sphingolipid metabolic enzyme GLA expression in gliomas: prognostic implications and therapeutic potential.Frontiers in oncology · 2026Article
- Abnormal Splicing ofBiomedicines · 2025Article
- Brain accumulation of lactosylceramide characterizes GALC deficiency in a zebrafish model of Krabbe disease.Brain : a journal of neurology · 2025Article
- Transport of sphingolipids by yeast Npc2 supports phase separation of the vacuole membrane.bioRxiv : the preprint server for biology · 2025Article
- Molecular Characterization of the GALC Mutation Thr112Ala Causing Krabbe Disease.International journal of molecular sciences · 2025Article
- Conformational dynamics and membrane insertion mechanism of B4GALNT1 in ganglioside synthesis.Nature communications · 2025Article
- Sphingolipid Metabolism and Signalling Pathways in Heart Failure: From Molecular Mechanism to Therapeutic Potential.Journal of inflammation research · 2025Review
- Article
- Impact of an irreversible β-galactosylceramidase inhibitor on the lipid profile of zebrafish embryos.Computational and structural biotechnology journal · 2024Article
- A novel homozygousThe Journal of international medical research · 2024Article
- Glycosphingolipids in Cardiovascular Disease: Insights from Molecular Mechanisms and Heart Failure Models.Biomolecules · 2024Review
- Human Saposin B Ligand Binding and Presentation to α-Galactosidase A.bioRxiv : the preprint server for biology · 2024Article
- Structural dissection of two redox proteins from the shipworm symbiont Teredinibacter turnerae.IUCrJ · 2024Article
- Altered Sphingolipid Hydrolase Activities and Alpha-Synuclein Level in Late-Onset Schizophrenia.Metabolites · 2023Article
- Article
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
Abstract
Sphingolipids are essential components of cellular membranes and defects in their synthesis or degradation cause severe human diseases. The efficient degradation of sphingolipids in the lysosome requires lipid-binding saposin proteins and hydrolytic enzymes. The glycosphingolipid galactocerebroside is the primary lipid component of the myelin sheath and is degraded by the hydrolase β-galactocerebrosidase (GALC). This enzyme requires the saposin SapA for lipid processing and defects in either of these proteins causes a severe neurodegenerative disorder, Krabbe disease. Here we present the structure of a glycosphingolipid-processing complex, revealing how SapA and GALC form a heterotetramer with an open channel connecting the enzyme active site to the SapA hydrophobic cavity. This structure defines how a soluble hydrolase can cleave the polar glycosyl headgroups of these essential lipids from their hydrophobic ceramide tails. Furthermore, the molecular details of this interaction provide an illustration for how specificity of saposin binding to hydrolases is encoded.
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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.