The α1,6-fucosyltransferase, FUT8, is the sole enzyme catalyzing the core-fucosylation of N-glycoproteins in mammalian systems. Previous studies using free N-glycans as acceptor substrates indicated that a terminal β1,2-GlcNAc moiety on the Man-α1,3-Man arm of N-glycan substrates is required for efficient FUT8-catalyzed core-fucosylation. In contrast, we recently demonstrated that, in a proper protein context, FUT8 could also fucosylate Man5GlcNAc2 without a GlcNAc at the non-reducing end. We describe here a further study of the substrate specificity of FUT8 using a range of N-glycans containing different aglycones. We found that FUT8 could fucosylate most of high-mannose and complex-type N-glycans, including highly branched N-glycans from chicken ovalbumin, when the aglycone moiety is modified with a 9-fluorenylmethyloxycarbonyl (Fmoc) moiety or in a suitable peptide/protein context, even if they lack the terminal GlcNAc moiety on the Man-α1,3-Man arm. FUT8 could also fucosylate paucimannose structures when they are on glycoprotein substrates. Such core-fucosylated paucimannosylation is a prominent feature of lysosomal proteins of human neutrophils and several types of cancers. We also found that sialylation of N-glycans significantly reduced their activity as a substrate of FUT8. Kinetic analysis demonstrated that Fmoc aglycone modification could either improve the turnover rate or decrease the KM value depending on the nature of the substrates, thus significantly enhancing the overall efficiency of FUT8 catalyzed fucosylation. Our results indicate that an appropriate aglycone context of N-glycans could significantly broaden the acceptor substrate specificity of FUT8 beyond what has previously been thought.
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http://dx.doi.org/10.1042/BCJ20210138 | DOI Listing |
Cell Insight
February 2025
Hubei Province Key Laboratory of Allergy and Immunology, Department of Allergy Zhongnan Hospital of Wuhan University, Department of Immunology Wuhan University Taikang Medical School (School of Basic Medical Sciences), Wuhan, 430071, China.
Adv Sci (Weinh)
November 2024
Institute of Clinical Science, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Intrahepatic cholangiocarcinoma (ICC) is a highly lethal malignancy that currently lacks effective clinical treatments. Eliminating stem cell-like cancer cells is an extremely promising but challenging strategy for treating ICC. A recently developed synthetic retinoid, sulfarotene, abrogates proliferation, and induces apoptosis of tumor-repopulating cells (TRCs) that exhibit stem cell-like properties, yet its effect and underlying mechanisms remain elusive in ICC.
View Article and Find Full Text PDFMol Neurobiol
November 2024
The Children's Hospital, School of Medicine, National Clinical Research Center for Child Health, Zhejiang University, Hangzhou, 310052, China.
Core fucosylation at N-glycans, which is uniquely catalyzed by fucosyltransferase FUT8, plays essential roles in post-translational regulation of protein function. Aberrant core fucosylation leads to neurological disorders in individuals with congenital glycosylation disorders (CDG). However, the underlying mechanisms for these neurological defects remain largely unknown.
View Article and Find Full Text PDFMol Med
November 2024
Department of Nephrology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, 116011, PR China.
Background: Activation of pericytes leads to renal interstitial fibrosis, but the regulatory mechanism of pericytes in the progression from AKI to CKD remains poorly understood. CD36 activation plays a role in the progression of CKD. However, the significance of CD36 during AKI-CKD, especially in pericyte, remains to be fully defined.
View Article and Find Full Text PDFJ Biol Chem
December 2024
Institut für Parasitologie, Veterinärmedizinische Universität, Wien, Austria. Electronic address:
N-glycans with complex core chitobiose modifications are observed in various free-living and parasitic nematodes but are absent in mammals. Using Caenorhabditis elegans as a model, we demonstrated that the core N-acetylglucosamine (GlcNAc) residues are modified by three fucosyltransferases (FUTs), namely FUT-1, FUT-6, and FUT-8. Interestingly, FUT-6 can only fucosylate N-glycans lacking the α1,6-mannose upper arm, indicating that a specific α-mannosidase is required to generate substrates for subsequent FUT-6 activity.
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