
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARHGAP18 CRISPR Activation Plasmid (h) | sc-413983-ACT | 20 µg | $397.00 |
ARHGAP18 encodes a Rho GTPase-activating protein that downregulates Rho family signaling by accelerating GTP hydrolysis, helping tune the balance between active and inactive Rho GTPases. Through modulation of cytoskeletal remodeling, cell shape, adhesion, and migration, ARHGAP18 contributes to processes such as endothelial barrier regulation and coordinated cellular motility. These functions connect ARHGAP18 to pathways governing actin dynamics and junctional organization, making it relevant for studying vascular biology and stress-responsive changes in cell behavior. Dysregulated Rho GTPase signaling and altered ARHGAP18 activity or expression have been associated with phenotypes relevant to inflammation, aberrant migration, and cancer-related cell invasion in experimental systems.
ARHGAP18 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ARHGAP18 expression without altering the underlying DNA sequence.
ARHGAP18 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ARHGAP18 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 ARHGAP18 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ARHGAP18 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ARHGAP18 locus and enabling the study of ARHGAP18-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ARHGAP18 pathway restoration in tumor cells with silenced or reduced ARHGAP18 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.