FUT7

Last update 08 May 2025

Basic Info

Synonyms

Alpha-(1,3)-fucosyltransferase 7, Fuc-TVII, fucosyltransferase 7

+ [5]

Introduction

Catalyzes the transfer of L-fucose, from a guanosine diphosphate-beta-L-fucose, to the N-acetyl glucosamine (GlcNAc) of a distal alpha2,3 sialylated lactosamine unit of a glycoprotein or a glycolipid-linked sialopolylactosamines chain through an alpha-1,3 glycosidic linkage and participates in the final fucosylation step in the biosynthesis of the sialyl Lewis X (sLe(x)), a carbohydrate involved in cell and matrix adhesion during leukocyte trafficking and fertilization (PubMed:11404359, PubMed:15632313, PubMed:15926890, PubMed:18402946, PubMed:18553500, PubMed:29593094, PubMed:8207002, PubMed:8666674, PubMed:8752218, PubMed:9299472, PubMed:9405391, PubMed:9461592, PubMed:9473504, PubMed:9499379). In vitro, also synthesizes sialyl-dimeric-Lex structures, from VIM-2 structures and both di-fucosylated and trifucosylated structures from mono-fucosylated precursors (PubMed:9499379). However does not catalyze alpha 1-3 fucosylation when an internal alpha 1-3 fucosylation is present in polylactosamine chain and the fucosylation rate of the internal GlcNAc residues is reduced once fucose has been added to the distal GlcNAc (PubMed:9473504, PubMed:9499379). Also catalyzes the transfer of a fucose from GDP-beta-fucose to the 6-sulfated a(2,3)sialylated substrate to produce 6-sulfo sLex mediating significant L-selectin-dependent cell adhesion (PubMed:10200296, PubMed:8752218). Through sialyl-Lewis(x) biosynthesis, can control SELE- and SELP-mediated cell adhesion with leukocytes and allows leukocytes tethering and rolling along the endothelial tissue thereby enabling the leukocytes to accumulate at a site of inflammation (PubMed:10386892, PubMed:29138114, PubMed:8666674, PubMed:9473504, PubMed:9834120). May enhance embryo implantation through sialyl Lewis X (sLeX)-mediated adhesion of embryo cells to endometrium (PubMed:18402946, PubMed:18553500). May affect insulin signaling by up-regulating the phosphorylation and expression of some signaling molecules involved in the insulin-signaling pathway through SLe(x) which is present on the glycans of the INSRR alpha subunit (PubMed:17229154).

100 Clinical Results associated with FUT7

100 Translational Medicine associated with FUT7

0 Patents (Medical) associated with FUT7

221

Literatures (Medical) associated with FUT7

07 Apr 2025·Oncogene

Identification of novel germline mutations in FUT7 and EXT1 linked with hereditary multiple exostoses

Article

Author: Xie, Xian-Biao ; Lin, Guo-Wang ; Peng, Wan ; Zuo, Xiao-Yu ; Lin, Dao-Chao ; Li, De-Jun ; Li, Gao-Fei ; Luo, Chun-Ling ; Liu, Shu-Qiang ; Lin, Qiao-Hong ; Cheng, Xi-Xi ; Bei, Jin-Xin ; Yin, Jun-Qiang ; Zhang, Yi-Yue

Hereditary multiple exostoses (HME) is an autosomal dominant skeletal disorder primarily linked with mutations in Exostosin-1 (EXT1) and Exostosin-2 (EXT2) genes. However, not all HME cases can be explained by these mutations, and its pathogenic mechanisms are not fully understood. Herein, utilizing whole-exome sequencing and genetic screening with a family trio design, we identify two novel rare mutations co-segregating with HME in a Chinese family, including a nonsense mutation (c.204G>A, p.Trp68*) in EXT1 and a missense mutation (c.893T>G, p.Phe298Cys) in FUT7. Functional assays reveal that the FUT7 mutation affects the cellular localization of FUT7 protein and regulates cell proliferation. Notably, the simultaneous loss of fut7 and ext1 in a zebrafish model results in severe chondrodysplasia, indicating a functional link between FUT7 and EXT1 in chondrocyte regulation. Additionally, we unveil that FUT7 p.Phe298Cys reduces EXT1 expression through IL6/STAT3/SLUG axis at the transcription level and through ubiquitination-related proteasomal degradation at the protein level. Together, our findings not only identify novel germline mutations in FUT7 and EXT1 genes, but also highlight the critical interaction between these genes, suggesting a potential 'second-hit' mechanism over EXT1 mutations in HME pathogenesis. This insight enhances our understanding of the mechanisms underlying HME and opens new avenues for potential therapeutic interventions.

01 Apr 2025·Biogerontology

Immune genes involved in synaptic plasticity during early postnatal brain development contribute to post-stroke damage in the aging male rat brain

Article

Author: Hermann, Dirk M ; Pirscoveanu, Denisa F V ; Olaru, Denissa Greta ; Ghinea, Flavia Semida ; Doeppner, Thorsten R ; Popa-Wagner, Aurel

Stroke remains a leading cause of mortality and long-term disability worldwide, underscoring the urgent need to identify novel therapeutic targets to enhance brain circuitry repair and functional recovery. This study explores the concept of longevity assurance genes, which primarily function within genetic pathways responsible for repair and maintenance. These pathways encompass molecular and metabolic processes as well as organ- and system-level functions. To investigate this, we employed comparative transcriptomics to analyze gene expression patterns across three age groups with progressively decreasing brain plasticity: native postnatal day seven brains, and young and old naïve and lesioned rat male brains. Analysis revealed a highly symmetrical distribution of upregulated and downregulated genes in postnatal day 7 brains. In contrast, the gene expression profiles of post-stroke brains exhibited significant asymmetry, with a disproportionate increase in upregulated genes compared to downregulated ones in both young and old post-ischemic brains. Gene variance in juvenile brains predominantly reflected processes associated with brain plasticity (e.g., Dcx, Tubb2b, Dok4, Dpysl5) and cell proliferation (e.g., Bex4). Conversely, gene expression variance in young and aged post-stroke brains was largely linked to inflammatory pathways, driven by cytokine and chemokine signaling. Notably, several genes specifically upregulated in aged brains were identified, including Ehd4, Fut7, Lilrb4, Plek, Slfn13, Slc14a1, and Smpdl3a. Immune genes that facilitate synaptic plasticity during early postnatal brain development-through processes such as pruning and sprouting to establish new connections in response to external stimuli-also contribute to post-stroke damage, confirming the concept of antagonistic pleiotropy. Our results suggest that targeting age-related immune responses could be an effective therapeutic strategy for stroke recovery.

01 Apr 2025·Gastroenterology

α1,3 Fucosyltransferase VII Improves Intestinal Immune Homeostasis in Inflammatory Bowel Disease by Enhancing Regulatory T-Cell Intestinal Homing and Immunosuppression

Article

Author: Ren, Yuexin ; Liu, Ke ; Ben, Teng ; Zhang, Xinyue ; Chen, Bingxia ; Chen, Yeling ; Li, Sheng ; Zhang, Yin ; Lin, Xinlong ; Xu, Jiahui ; Zhu, Fangqing ; Zhou, Qian ; Tan, Gao ; Zhi, Fachao

BACKGROUND & AIMSRegulatory T cells (Tregs) play a critical role in maintaining tissue immune homeostasis, but they are relatively insufficient at inflammatory intestinal sites in patients with inflammatory bowel disease (IBD). However, what controls Treg homing to the intestine in IBD is unknown.METHODSα1,3 Fucosyltransferase VII (FUT7) expression in Tregs from patients with active IBD was detected by RNA sequencing. To determine whether FUT7 controls Treg intestinal homing in IBD, Treg-specific Fut7 conditional knockout (CKO) mice were constructed and used in an IBD model induced by dextran sulfate sodium. To investigate whether up-regulating FUT7 expression in Tregs plays a therapeutic role in IBD, the nanocarrier CD4-LDP-Fut7, which specifically targets Tregs to express Fut7, was constructed and used in the IBD model. In addition, whether Fut7 regulates other Treg functions was explored by mass cytometry.RESULTSCompared with healthy controls, patients with active IBD had significantly decreased FUT7 expression in Tregs. In the IBD model, CKO mice had a lower frequency of colonic Tregs among CD4⁺ T cells and a lower ratio of colonic to splenic Tregs from the same mouse than their littermate controls did, indicating that Fut7 deficiency impaired the ability of Tregs to home to the intestine. Consistently, CKO mice had severe colitis, and CD4-LDP-Fut7 alleviated it in the IBD model. Mass cytometry analysis revealed that Fut7 down-regulated PD1 expression in Tregs via competition with Fut8 for the substrate GDP-fucose, thereby increasing the immunosuppressive capacity of Tregs.CONCLUSIONSFUT7 enhances Treg intestinal homing and immunosuppression. Thus, up-regulating FUT7 expression in Tregs could be a novel therapeutic strategy for IBD.

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