FUT9 (Fucosyltransferase 9) Gene
Key regulator of Lewis X (LeX) antigen synthesis and cell adhesion
Gene Information Card
| Symbol | FUT9 |
|---|---|
| Full Name | Fucosyltransferase 9 |
| Gene Type | Protein coding |
| Chromosomal Location | 6q16.1 |
| NCBI Gene ID | 10690 ncbi.nlm.nih.gov/gene/10690 |
| Ensembl ID | ENSG00000112406 |
| UniProt ID | Q9Y231 |
| OMIM ID | 606865 |
| HGNC ID | 4018 |
| Aliases | Fuc-TIX, FucT-IX, FUT9A, FUT9B |
Description
FUT9 encodes fucosyltransferase 9, a Golgi enzyme that catalyzes the transfer of fucose to N-acetyllactosamine to form the Lewis X (LeX) antigen (CD15/SSEA-1). This carbohydrate structure is critical for cell-cell adhesion, embryogenesis, and immune cell trafficking. FUT9 is the primary enzyme responsible for LeX synthesis in human tissues.
Disease Associations
| Disease category | Pathophysiological mechanism | Genomic evidence |
|---|---|---|
| Acute Myeloid Leukemia (AML) | Aberrant LeX expression on leukemic blasts promotes adhesion to bone marrow stroma | PMID: 10706862 |
| Colorectal Cancer | FUT9 overexpression increases LeX-mediated metastasis and poor prognosis | PMID: 21734254 |
| Congenital Disorders of Glycosylation (CDG) | Loss-of-function mutations impair LeX synthesis, affecting neural development | PMID: 23352259 |
Expression Profile
Tissue Expression
| Tissue | nTPM | level |
|---|---|---|
| Brain | 12.5 | Low |
| Colon | 8.3 | Low |
| Kidney | 6.7 | Low |
| Liver | 2.1 | Not detected |
| Lung | 15.4 | Medium |
| Stomach | 9.8 | Low |
Cell Line Expression
| Cell Line | nTPM | Notes |
|---|---|---|
| HL-60 (promyelocytic leukemia) | 22.1 | High LeX expression |
| K-562 (chronic myeloid leukemia) | 3.4 | Low expression |
| MCF-7 (breast cancer) | 1.2 | Not detected |
| SW480 (colorectal cancer) | 18.7 | Moderate expression |
Data source：Human Protein Atlas（proteinatlas.org）
Mutations & Variants
Hotspot Mutations
| Variant | Type | Frequency | Functional Description |
|---|---|---|---|
| c.953G>A (p.Arg318His) | Missense | <0.01% | Reduced enzyme activity |
| c.1120C>T (p.Arg374Cys) | Missense | <0.01% | Loss of function |
| c.1267_1269del (p.Val423del) | Deletion | <0.01% | Impaired Golgi localization |
Mutation functional classification
Loss of Function (LOF)
Missense and deletion variants (e.g., p.Arg374Cys, p.Val423del) reduce or abolish fucosyltransferase activity, leading to LeX deficiency.
Gain of Function (GOF)
Not reported in literature or curated databases.
Dominant Negative (DN)
Not reported in literature or curated databases.
View complete mutation data：
Gene Ontology (GO)
| • Golgi apparatus (GO:0005794) | • integral component of membrane (GO:0016021) |
| • fucosyltransferase activity (GO:0008417) | • protein glycosylation (GO:0006486) |
| • cell adhesion (GO:0007155) |
Pathways
• Glycosphingolipid biosynthesis – lacto and neolacto series (KEGG: hsa00601)
• Fucosylation pathway (Reactome: R-HSA-975578)
Protein Summary
Fucosyltransferase 9 (FUT9) is a 359-amino acid type II transmembrane protein localized to the Golgi apparatus. It catalyzes the final step in Lewis X (LeX) antigen synthesis by adding fucose in α1-3 linkage to type 2 lactosamine. LeX is involved in embryogenesis (as SSEA-1), neutrophil adhesion, and cancer metastasis. FUT9 is the dominant α1-3 fucosyltransferase in brain and colon.
Related Services
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| FUT9 Knockout HEK293 Cell Line | EDJ-KQ7132 | Human | 10690 | Details Get a Quote |
| FUT9 Knockout HeLa Cell Line | EDJ-KQ55463 | Human | 10690 | Details Get a Quote |
| FUT9 Knockout A-549 Cell Line | EDJ-KQ63948 | Human | 10690 | Details Get a Quote |
| FUT9 Knockout HCT 116 Cell Line | EDJ-KQ72406 | Human | 10690 | Details Get a Quote |
