Ask about this productRelated genes to: FUT6 antibody
- Gene:
- FUT6 NIH gene
- Name:
- fucosyltransferase 6
- Previous symbol:
- -
- Synonyms:
- FT1A, FCT3A, FucT-VI, FLJ40754
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-04-15
- Date modifiied:
- 2015-11-23
Related products to: FUT6 antibody
Related articles to: FUT6 antibody
- Pertussis (whooping cough) is caused by the bacterium Bordetella pertussis. Among the virulence factors produced by B. pertussis, pertussis toxin (PT) is responsible for key disease symptoms, including impacts on the immune system. PT is an AB5 toxin, consisting of a single catalytic A subunit and five B subunits. The B pentamer recognizes cell surface glycans and facilitates intracellular delivery of the catalytic A subunit. PT also impacts host cell signaling via mechanisms that do not depend on the catalytic activity of the A subunit. In particular, PT promotes signaling through the T-cell receptor (TCR), leading to activation of extracellular signal-regulated kinase (ERK) cascades. PT prefers to bind sialylated and N-linked glycans, but other aspects of PT's glycan binding specificity remain underexplored. Here we report that the absence of fucose on mammalian cell surfaces leads to increased binding by PT. Using pharmacological inhibitors in a human bronchial epithelial cell line, we observe that sialylation and N-linked glycosylation promote PT binding while fucosylation interferes with PT binding. Similarly, CHO and Colo205 cells deficient in fucosylation exhibited enhanced PT binding as compared to the corresponding wild-type cell lines. Genetic knockout of FUT3/FUT5/FUT6 or of FUT8 led to increased PT binding, suggesting that specific fucosylated epitopes mediate protection from PT. The functional impact of altered PT binding was examined in Jurkat T cells, where removal of cell surface non-core fucose led to increased PT-dependent ERK phosphorylation. In sum, our study identifies a role for fucosylation in protecting mammalian cells from PT. - Source: PubMed
Konada Rohit Sai ReddyNischan NicoleSilva AuroraKohler Jennifer J - Despite the importance of the gut microbiome to health, the role of human genetic variation in shaping its composition remains poorly understood. Here we report genome-wide association analyses of harmonized metagenomic data from 16,017 adults in four Swedish population-based studies, with replication in 12,652 people from the Norwegian HUNT study. We identified variants in the OR51E1-OR51E2 locus, encoding sensors for microbiome-derived fatty acids, associated with microbial richness. We further identified 15 study-wide significant genetic associations (P < 5.4 × 10) involving eight loci and 14 common bacterial species, of which 11 associations at six loci were replicated. The results confirm previously reported associations at LCT, ABO and FUT2, and provide evidence for new loci MUC12, CORO7-HMOX2, SLC5A11, FOXP1 and FUT3-FUT6, with supporting data from metabolomics and gene expression analyses. Our findings link gut microbial variation genetically to gastrointestinal functions, including enteroendocrine fatty acid sensing, bile composition and mucosal layer composition. - Source: PubMed
Publication date: 2026/02/13
Dekkers Koen FPertiwi KamalitaBaldanzi GabrielLundmark PerHammar UlfMoksnes Marta RiiseCoward EivindNethander MariaSalih Ghassan AliMiari MariamNguyen DiemSayols-Baixeras SergiEklund Aron CHolm Jacob BakNielsen H BjørnVolpiano Camila GazollaMéric GuillaumeThangam ManonanthiniHakaste LiisaTuomi TiinamaijaAhlqvist EmmaSmith Christopher AAllen MarieReimann FrankGribble Fiona MOhlsson ClaesHveem KristianMelander OlleNilsson Peter MEngström GunnarSmith J GustavMichaëlsson KarlÄrnlöv JohanOrho-Melander MarjuFall Tove - Pertussis (whooping cough) is caused by the bacterium . Among the virulence factors produced by pertussis toxin (PT) is responsible for key disease symptoms, including impacts on the immune system. PT is an AB toxin, consisting of a single catalytic A subunit and five B subunits. The B pentamer recognizes cell surface glycans and facilitates intracellular delivery of the catalytic A subunit. PT also impacts host cell signaling via mechanisms that do not depend on the catalytic activity of the A subunit. In particular, PT promotes signaling through the T-cell receptor (TCR), leading to activation of extracellular signal-regulated kinase (ERK) cascades. PT prefers to bind sialylated and N-linked glycans, but other aspects of PT's glycan binding specificity remain underexplored. Here we report that the absence of fucose on mammalian cell surfaces leads to increased binding by PT. Using pharmacological inhibitors in a human bronchial epithelial cell line, we observe that sialylation and N-linked glycosylation promote PT binding while fucosylation interferes with PT binding. Similarly, CHO and Colo205 cells deficient in fucosylation exhibited enhanced PT binding as compared to the corresponding wild-type cell lines. Genetic knockout of FUT3/FUT5/FUT6 or of FUT8 led to increased PT binding, suggesting that specific fucosylated epitopes mediate protection from PT. The functional impact of altered PT binding was examined in Jurkat T cells, where removal of cell surface non-core fucose led to increased PT-dependent ERK phosphorylation. In sum, our study identifies a role for fucosylation in protecting mammalian cells from PT. - Source: PubMed
Publication date: 2025/12/04
Konada Rohit Sai ReddyNischan NicoleSilva AuroraKohler Jennifer J - Association studies have linked many genetic variants to a variety of phenotypes but understanding the biological mechanisms underlying these signals remains a major challenge. Since genes operate within complex networks, statistical interactions between genetic mutations that reflect biological pathways are expected to exist. However, their discovery has been hampered by the vast search space of variant combinations and the multiplicatively small expected effect sizes of interactions. To increase power, we created a test for interaction between single-nucleotide polymorphisms (SNPs) and of other variants with a direct effect on a phenotype aggregated in a polygenic score (PGS) which can be performed for any quantitative trait. In realistic simulations, this method avoids false positives and is well powered to find interaction networks. We apply it to 97 quantitative phenotypes in European samples in the UK Biobank and identify 144 independent interactions affecting 52 different traits, including important disease risk variants at genes such as , or . We develop approaches to refine identified signals and detect 38 pairwise interactions between SNPs. These include known interactions between , and affecting alkaline phosphatase levels, which are shown to be part of a larger network including and , as well as an interaction for eosinophil levels between and , two genes whose functional interaction has recently been implicated in asthma. Finally, we propose a method to partition PGSs according to the binding sites of more than 1100 transcription factors using the HOCOMOCO motif database and test for interactions involving functionally partitioned scores. We identify 12 interactions affecting eight traits, two of which directly reflect known regulatory relationships such as that between (a key regulator of glucose metabolism) and the transcription factor , which are known to interact functionally within the Wnt signalling pathway, affecting glycated haemoglobin levels. This work substantially extends the set of known epistatic effects for human phenotypes and shows how statistical interactions can reflect biological interdependencies between genes. - Source: PubMed
Publication date: 2025/12/29
Ferreira Lino A FHu SileDavies Robert WMyers Simon R - DNA methylation (DNAm) provides a plausible mechanism by which adverse exposures become embodied and contribute to health inequities, due to its role in genome regulation and responsiveness to social and biophysical exposures tied to societal context. However, scant epigenome-wide association studies (EWAS) have included structural and lifecourse measures of exposure, especially in relation to structural discrimination. Our study tested the hypothesis that DNAm is a mechanism by which racial discrimination, economic adversity, and air pollution become biologically embodied, via a series of cross-sectional EWAS, conducted in two population-based samples of US-born Black non-Hispanic (Black NH), white non-Hispanic (white NH), and Hispanic individuals (My Body My Story:: n = 224 Black NH and 69 white NH;; and the Multi-Ethnic Study of Atherosclerosis:: n = 229 Black NH, n = 555 white NH and n = 191 Hispanic). Genome-wide changes in DNAm were measured using the Illumina EPIC BeadChip (MBMS; using frozen blood spots) and Illumina 450 k BeadChip (MESA; using purified monocytes). - Source: PubMed
Publication date: 2025/11/27
Watkins Sarah HolmesTesta ChristianSimpkin Andrew JSmith George DaveyCoull BrentDe Vivo ImmaculataTilling KateWaterman Pamela DChen Jarvis TDiez-Roux Ana VKrieger NancySuderman MatthewRelton Caroline