
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PAK5 CRISPR Activation Plasmid (h) | sc-404073-ACT | 20 µg | $397.00 |
PAK5 (p21-activated kinase 5; PAK7) is a serine/threonine kinase and downstream effector of Rho-family GTPases such as CDC42 and RAC1 that regulates cytoskeletal remodeling, cell polarity, and survival signaling. In human cells, PAK5 influences actin dynamics and microtubule stability, shaping processes including neurite outgrowth, migration, and vesicular trafficking. It interfaces with MAPK/ERK and PI3K/AKT-associated networks and can modulate phosphorylation of substrates that coordinate adhesion and motility. Dysregulated PAK5 expression or signaling has been reported in multiple tumor contexts and is also relevant to neurobiology due to its roles in neuronal development and synaptic function.
PAK5 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PAK5 expression without altering the underlying DNA sequence.
PAK5 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PAK5 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 PAK5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PAK5 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PAK5 locus and enabling the study of PAK5-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PAK5 pathway restoration in tumor cells with silenced or reduced PAK5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.