FucT-IV CRISPR/Cas9 KO Plasmid (h): sc-401795
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FucT-IV CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the FucT-IV genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: FucT-IV Antibody (MY-1): sc-59531
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FucT-IV CRISPR/Cas9 KO Plasmid (h) | sc-401795 | 20 µg | $397.00 |
Overview
FUT4 encodes the Golgi-resident α1,3-fucosyltransferase FucT-IV, an enzyme that transfers fucose to N-acetyllactosamine acceptors to generate fucosylated glycan epitopes such as Lewis X–type structures on glycoproteins and glycolipids. By shaping cell-surface glycosylation, FucT-IV influences selectin-mediated adhesion, leukocyte trafficking, and broader glycan-dependent signaling and receptor dynamics. FUT4 activity intersects with fucose metabolism and glycosylation pathways that regulate immune cell interactions, inflammatory responses, and cell migration. Dysregulated FUT4 expression and altered fucosylation patterns have been associated in the literature with tumor cell invasiveness, metastasis-related adhesion phenotypes, and changes in immune microenvironment interactions, making it a useful node for mechanistic studies of glycan-mediated biology.
FucT-IV CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the FUT4 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the FUT4 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the FUT4 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish FucT-IV protein expression.
This CRISPR knockout system enables efficient generation of FUT4-deficient cell models for investigation of FucT-IV signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting FUT4 exon(s) critical for FucT-IV function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple FUT4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FucT-IV CRISPR/Cas9 KO Plasmid (h) and FucT-IV CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the FUT4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FucT-IV HDR Plasmid (h) and FucT-IV HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by FUT4 homology arms to support homology-directed repair at defined FUT4 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.