ArticleNature communications2023
Structures of liganded glycosylphosphatidylinositol transamidase illuminate GPI-AP biogenesis.
Article in Nature communications, 2023. 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, 27 citations in OpenAlex.
- Molecular insights into Candida auris glycosylphosphatidylinositol transamidase.Protein & cell · 2026Article
- Mechanisms of Quality Control in GPI-Anchored Proteins: The Central Role of the Lipid Anchor.International journal of molecular sciences · 2026Review
- Conformational epitope engagement by anti-MSLN ADC RC88 confers resistance to soluble mesothelin.Antibody therapeutics · 2026Article
- Clonal expansion mechanisms in paroxysmal nocturnal hemoglobinuria.International journal of hematology · 2026Review
- Metabolites beyond metabolism: Exploring their atypical roles in protein modification and signaling transduction.Chinese medical journal · 2026Review
- An atypical venus fly trap domain receptor regulates motility and phagocytosis in the protozoan parasite Entamoeba histolytica.PLoS pathogens · 2026Article
- O-mannosylation of misfolded ER proteins promotes ERAD.The EMBO journal · 2026Article
- Integrative analysis identifies PIGK as an oncogenic glycosylphosphatidylinositol transamidase subunit with prognostic, immunological, and therapeutic relevance in head and neck cancer.International journal of medical sciences · 2026Article
- Molecular Insights into Fungal Glycosylphosphatidylinositol Transamidase Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Structural Insights into the Glycosylphosphatidylinositol Mannosyltransferase I Complex fromJournal of fungi (Basel, Switzerland) · 2025Article
- Biosynthesis of GPI anchored proteins, its deficiencies and treatment.Journal of human genetics · 2025Review
- Modeling glycans with AlphaFold 3: capabilities, caveats, and limitations.Glycobiology · 2025Article
- Structure-based design of covalent nanobody binders for a thermostable green fluorescence protein.Acta biochimica et biophysica Sinica · 2024Article
- PIGK defects induce apoptosis in Purkinje cells and acceleration of neuroectodermal differentiation.Cell death & disease · 2024Article
- A novel homozygous variant of the PIGK gene caused by paternal disomy in a patient with neurodevelopmental disorder, cerebellar atrophy, and seizures.Journal of human genetics · 2024Article
- A nanobody interaction with SARS-COV-2 Spike allows the versatile targeting of lentivirus vectors.Journal of virology · 2024Article
- Precise control of transmembrane current via regulating bionic lipid membrane composition.Science advances · 2024Article
- Inherited glycosylphosphatidylinositol deficiency: a review from molecular and clinical perspectives.Acta biochimica et biophysica Sinica · 2024Review
- Protein lipidation in health and disease: molecular basis, physiological function and pathological implication.Signal transduction and targeted therapy · 2024Review
- Proteomic screens of SEL1L-HRD1 ER-associated degradation substrates reveal its role in glycosylphosphatidylinositol-anchored protein biogenesis.Nature communications · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many eukaryotic receptors and enzymes rely on glycosylphosphatidylinositol (GPI) anchors for membrane localization and function. The transmembrane complex GPI-T recognizes diverse proproteins at a signal peptide region that lacks consensus sequence and replaces it with GPI via a transamidation reaction. How GPI-T maintains broad specificity while preventing unintentional cleavage is unclear. Here, substrates- and products-bound human GPI-T structures identify subsite features that enable broad proprotein specificity, inform catalytic mechanism, and reveal a multilevel safeguard mechanism against its promiscuity. In the absence of proproteins, the catalytic site is invaded by a locally stabilized loop. Activation requires energetically unfavorable rearrangements that transform the autoinhibitory loop into crucial catalytic cleft elements. Enzyme-proprotein binding in the transmembrane and luminal domains respectively powers the conformational rearrangement and induces a competent cleft. GPI-T thus integrates various weak specificity regions to form strong selectivity and prevent accidental activation. These findings provide important mechanistic insights into GPI-anchored protein biogenesis.
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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.