FucT-l CRISPR/Cas9 KO Plasmid (m): sc-420423
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FucT-l CRISPR/Cas9 Knockout (KO) Plasmid (m) 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-l 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FucT-l CRISPR/Cas9 KO Plasmid (m) | sc-420423 | 20 µg | $397.00 |
Overview
Fut1 encodes α(1,2)fucosyltransferase 1 (FucT-1), a Golgi-resident glycosyltransferase that transfers fucose from GDP-fucose to terminal galactose residues, generating α1,2-fucosylated glycans such as H-type antigens on glycoproteins and glycolipids. This enzymatic step is a core component of glycosphingolipid and glycoprotein maturation and shapes cell-surface carbohydrate patterns that influence lectin binding, membrane organization, and intercellular recognition. Fut1-dependent fucosylation intersects with pathways controlling epithelial differentiation, mucosal barrier function, and host–microbe interactions through modulation of glycan-mediated adhesion and signaling. Altered α1,2-fucosylation has been associated with inflammation and immune dysregulation in multiple contexts, making Fut1 a useful node for mechanistic studies of glycan-dependent phenotypes.
FucT-l CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Fut1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Fut1 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 Fut1 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-l protein expression.
This CRISPR knockout system enables efficient generation of Fut1-deficient cell models for investigation of FucT-l signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Fut1 exon(s) critical for FucT-l 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 Fut1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FucT-l CRISPR/Cas9 KO Plasmid (m) and FucT-l CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Fut1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FucT-l HDR Plasmid (m) and FucT-l HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Fut1 homology arms to support homology-directed repair at defined Fut1 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.