
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
St3Gal-I CRISPR Activation Plasmid (h) | sc-411005-ACT | 20 µg | $397.00 |
ST3GAL1 encodes the human Golgi-localized sialyltransferase St3Gal-I, which catalyzes transfer of sialic acid in an α2,3 linkage onto Galβ1-3GalNAc structures to form sialyl-T antigen on O-glycans. This activity shapes mucin-type O-glycosylation, influencing glycoprotein maturation, cell–cell interactions, and lectin-mediated signaling at the cell surface. Altered ST3GAL1-dependent sialylation has been associated with changes in adhesion, migration, and immune recognition through modulation of glycan epitopes. Dysregulation of St3Gal-I activity is reported in multiple disease-relevant contexts, including tumor-associated glycosylation patterns and inflammatory microenvironments, making it a useful node for studying glyco-regulatory pathways.
St3Gal-I CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ST3GAL1 expression without altering the underlying DNA sequence.
St3Gal-I CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ST3GAL1 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 ST3GAL1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous St3Gal-I expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ST3GAL1 locus and enabling the study of St3Gal-I-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of St3Gal-I pathway restoration in tumor cells with silenced or reduced ST3GAL1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.