galectin-9 CRISPR Activation Plasmid (h): sc-402321-ACT

Human LGALS9 encodes galectin-9, a β-galactoside–binding lectin that modulates cell–cell and cell–matrix interactions through recognition of glycosylated receptors and extracellular matrix components. Galectin-9 influences immune signaling and inflammatory tone by shaping cytokine responses, leukocyte trafficking, and apoptosis programs, and it can remodel tumor–immune crosstalk via checkpoint-associated pathways such as TIM-3. Reported functions connect LGALS9 to regulation of T cell exhaustion, myeloid cell polarization, and epithelial–stromal communication, with relevance to cancer immunobiology, autoimmunity, and chronic inflammatory disorders. Its activity is also linked to stress-response and vesicular/secretory processes that impact the availability of soluble galectin-9 in tissue microenvironments.

galectin-9 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LGALS9 expression without altering the underlying DNA sequence.

galectin-9 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LGALS9 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 LGALS9 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous galectin-9 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LGALS9 locus and enabling the study of galectin-9-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of galectin-9 pathway restoration in tumor cells with silenced or reduced LGALS9 expression.

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