
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FucT-IV CRISPR Activation Plasmid (h) | sc-401795-ACT | 20 µg | $397.00 |
FUT4 encodes α(1,3)-fucosyltransferase IV (FucT-IV), a Golgi-localized glycosyltransferase that catalyzes terminal fucosylation of glycans to generate Lewis X–type epitopes on glycoproteins and glycolipids. By shaping cell-surface glycan architecture, FucT-IV influences selectin-mediated adhesion, leukocyte trafficking, and broader glycosylation-dependent signaling and receptor function. FUT4 activity contributes to regulation of immune cell interactions and inflammatory processes through modulation of fucosylated ligands. Dysregulated FUT4 expression and altered fucosylation patterns have been associated with aberrant cell adhesion and migration phenotypes and are frequently examined in the context of cancer biology and immunopathology.
FucT-IV CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FUT4 expression without altering the underlying DNA sequence.
FucT-IV CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FUT4 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the FUT4 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FucT-IV expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FUT4 locus and enabling the study of FucT-IV-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FucT-IV pathway restoration in tumor cells with silenced or reduced FUT4 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.