
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
claudin-8 CRISPR Activation Plasmid (h) | sc-404251-ACT | 20 µg | $397.00 |
CLDN8 encodes claudin-8, a tetraspan tight junction protein that regulates paracellular permeability and epithelial barrier integrity. Claudin-8 contributes to apical junctional complex organization and ion-selective sealing in polarized epithelia, integrating with pathways controlling cell polarity, adhesion, and transepithelial transport. Altered CLDN8 expression or junctional localization is linked to epithelial dysfunction and remodeling processes observed in inflammatory disorders and cancer-associated changes in barrier properties. As a junctional component, claudin-8 is widely used as a marker and mechanistic entry point for studying epithelial differentiation and tissue-specific permeability regulation.
claudin-8 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CLDN8 expression without altering the underlying DNA sequence.
claudin-8 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CLDN8 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 CLDN8 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous claudin-8 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CLDN8 locus and enabling the study of claudin-8-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of claudin-8 pathway restoration in tumor cells with silenced or reduced CLDN8 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.