
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Cytokeratin 16 CRISPR Activation Plasmid (h) | sc-403138-ACT | 20 µg | $397.00 | |||
Cytokeratin 16 CRISPR Activation Plasmid (h2) | sc-403138-ACT-2 | 20 µg | $397.00 |
KRT16 encodes cytokeratin 16, a type I intermediate filament protein that heterodimerizes with keratin 6 family members to reinforce the cytoskeletal network in stratified epithelia. It is rapidly induced during wound repair, mechanical stress, and inflammatory signaling, supporting keratinocyte proliferation, migration, and barrier remodeling. Cytokeratin 16 participates in keratin filament organization and epithelial differentiation programs that interface with stress-response pathways and cytoskeletal dynamics. Dysregulated KRT16 expression is associated with hyperproliferative skin states and keratinization disorders, making it a useful marker and functional node for studying epidermal homeostasis and epithelial stress responses.
Cytokeratin 16 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KRT16 expression without altering the underlying DNA sequence.
Cytokeratin 16 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KRT16 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 KRT16 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Cytokeratin 16 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KRT16 locus and enabling the study of Cytokeratin 16-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Cytokeratin 16 pathway restoration in tumor cells with silenced or reduced KRT16 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.