CD151 CRISPR Activation Plasmid (h): sc-401969-ACT

CD151 (tetraspanin-24) is a human cell-surface tetraspanin that organizes tetraspanin-enriched microdomains and modulates the trafficking and signaling of partner receptors, most notably laminin-binding integrins such as ITGA3/ITGB1 and ITGA6/ITGB4. Through these complexes, CD151 influences cell–cell and cell–matrix adhesion, cytoskeletal remodeling, and directional migration, impacting processes including epithelial integrity, angiogenic responses, and immune cell motility. CD151-associated signaling intersects with focal adhesion dynamics and downstream pathways linked to actin regulation and receptor crosstalk, shaping invasive behavior in multiple cellular contexts. Dysregulated CD151 expression or altered tetraspanin–integrin coupling has been associated with phenotypes relevant to tumor cell dissemination, metastatic competence, and vascular remodeling in experimental systems.

CD151 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CD151 expression without altering the underlying DNA sequence.

CD151 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CD151 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 CD151 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD151 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CD151 locus and enabling the study of CD151-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD151 pathway restoration in tumor cells with silenced or reduced CD151 expression.

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