galectin-3 CRISPR Activation Plasmid (h): sc-417680-ACT

Human LGALS3 encodes galectin-3, a β-galactoside–binding lectin that regulates cell–cell and cell–matrix interactions, endocytosis, and intracellular signaling across epithelial and immune compartments. Galectin-3 modulates pathways linked to inflammation and innate immunity, including macrophage activation, NF-κB-associated transcriptional programs, and cytokine-driven remodeling, and it can influence apoptosis resistance, autophagy, and oxidative stress responses in a context-dependent manner. Through its roles in adhesion, migration, and extracellular matrix turnover, LGALS3 is frequently studied in fibrosis biology and tumor microenvironment crosstalk, as well as in cardiometabolic and neuroinflammatory processes. Dysregulated galectin-3 expression has been associated with chronic inflammatory states and progression phenotypes in multiple cancers, making it a widely used molecular node for mechanistic pathway interrogation.

galectin-3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LGALS3 expression without altering the underlying DNA sequence.

galectin-3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LGALS3 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 LGALS3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous galectin-3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LGALS3 locus and enabling the study of galectin-3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of galectin-3 pathway restoration in tumor cells with silenced or reduced LGALS3 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.