galectin-1 CRISPR Activation Plasmid (h): sc-400941-ACT

LGALS1 encodes human galectin-1, a β-galactoside–binding lectin that regulates cell–cell and cell–matrix interactions by engaging glycosylated receptors at the cell surface and in the extracellular matrix. Galectin-1 influences integrin-mediated adhesion, immune cell signaling, and stress responses, and can modulate apoptosis, migration, and angiogenic programs in a context-dependent manner. Through its effects on glycan-dependent receptor clustering and signaling, galectin-1 impacts pathways linked to inflammation, tumor–stroma crosstalk, and tissue remodeling. Dysregulated LGALS1 expression has been associated with immune evasion phenotypes, fibrotic processes, and progression in multiple cancer types, supporting its use as a mechanistic node in microenvironment-focused research.

galectin-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LGALS1 expression without altering the underlying DNA sequence.

galectin-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LGALS1 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 LGALS1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous galectin-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LGALS1 locus and enabling the study of galectin-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of galectin-1 pathway restoration in tumor cells with silenced or reduced LGALS1 expression.

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