Cytokeratin 13 CRISPR Activation Plasmid (h): sc-401320-ACT

KRT13 encodes cytokeratin 13, a type I intermediate filament protein that heteropolymerizes with type II keratins to maintain epithelial structural integrity and mechanical resilience. It is enriched in stratified, non-keratinizing epithelia and contributes to cytoskeletal organization, cell–cell cohesion, and epithelial differentiation programs that shape tissue barrier function. Altered KRT13 expression patterns are associated with epithelial remodeling and dysregulated differentiation observed in squamous pathologies, making it a useful marker for investigating epithelial state transitions. As part of the keratin–intermediate filament network, cytokeratin 13 interfaces with pathways governing cytoskeletal dynamics and stress responses that influence cell morphology and tissue architecture.

Cytokeratin 13 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KRT13 expression without altering the underlying DNA sequence.

Cytokeratin 13 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KRT13 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 KRT13 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Cytokeratin 13 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KRT13 locus and enabling the study of Cytokeratin 13-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Cytokeratin 13 pathway restoration in tumor cells with silenced or reduced KRT13 expression.

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