Psoriasin CRISPR Activation Plasmid (h): sc-418211-ACT

S100A7 encodes psoriasin, a calcium-binding S100 family protein enriched in stratified epithelia and induced during inflammatory stress. Psoriasin contributes to epithelial differentiation, barrier defense, and innate immune signaling, and can function as a damage-associated mediator that shapes leukocyte recruitment and local cytokine networks. It is linked to keratinocyte hyperproliferation and inflammatory programs characteristic of psoriasis and other epithelial inflammatory states, and its dysregulation has been reported across multiple carcinoma contexts where it is associated with altered cell migration and tumor–microenvironment interactions. These properties make S100A7 a useful node for studying epithelial–immune crosstalk, stress-responsive transcriptional programs, and calcium-dependent signaling processes.

Psoriasin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous S100A7 expression without altering the underlying DNA sequence.

Psoriasin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the S100A7 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 S100A7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Psoriasin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native S100A7 locus and enabling the study of Psoriasin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Psoriasin pathway restoration in tumor cells with silenced or reduced S100A7 expression.

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