
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Keratin 24 CRISPR Activation Plasmid (h) | sc-414948-ACT | 20 µg | $397.00 | |||
Keratin 24 CRISPR Activation Plasmid (h2) | sc-414948-ACT-2 | 20 µg | $397.00 |
KRT24 encodes keratin 24, a type I intermediate filament protein that contributes to the structural integrity and mechanical resilience of epithelial cells. As part of the keratin cytoskeleton, KRT24 participates in cytoskeletal organization, cell–cell cohesion, and epithelial differentiation programs that influence tissue homeostasis and barrier function. Perturbations in keratin network composition can impact stress-response signaling and remodeling processes linked to epithelial dysregulation. Consequently, KRT24 expression is frequently examined in studies of epithelial development and in disease-relevant contexts where differentiation state and cytoskeletal architecture are altered.
Keratin 24 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KRT24 expression without altering the underlying DNA sequence.
Keratin 24 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KRT24 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 KRT24 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Keratin 24 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KRT24 locus and enabling the study of Keratin 24-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Keratin 24 pathway restoration in tumor cells with silenced or reduced KRT24 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.