SNAI 1 CRISPR Activation Plasmid (m): sc-423047-ACT

Snai1 encodes the zinc-finger transcription factor SNAI1, a master regulator of epithelial–mesenchymal transition (EMT) that represses epithelial junction genes such as Cdh1 and remodels cytoskeletal and adhesion programs. In mouse cells, SNAI1 integrates cues from TGF-β, WNT/β-catenin, Notch, and hypoxia-associated signaling to control lineage plasticity, motility, and extracellular matrix interactions. This transcriptional network is central to embryonic morphogenesis and tissue remodeling, and dysregulated SNAI1 activity is frequently studied in contexts of fibrosis and invasive tumor biology. SNAI1-dependent programs also intersect with inflammatory signaling and stem-like cell state maintenance, supporting its broad relevance in mechanistic pathway research.

SNAI 1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Snai1 expression without altering the underlying DNA sequence.

SNAI 1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Snai1 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 Snai1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SNAI 1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Snai1 locus and enabling the study of SNAI 1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SNAI 1 pathway restoration in tumor cells with silenced or reduced Snai1 expression.

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