
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARHGAP21 CRISPR Activation Plasmid (h) | sc-403424-ACT | 20 µg | $397.00 |
ARHGAP21 encodes a Rho GTPase-activating protein that accelerates GTP hydrolysis on Rho-family GTPases, helping coordinate actin cytoskeleton remodeling, cell polarity, and membrane trafficking. Through modulation of RhoA/Cdc42/Rac signaling, ARHGAP21 influences processes such as cell migration, adhesion dynamics, and Golgi-associated transport, linking cytoskeletal organization to intracellular trafficking pathways. Altered Rho GTPase signaling is broadly implicated in cancer cell invasion, metastatic behavior, and vascular and inflammatory phenotypes, making ARHGAP21 a useful node for studying pathway rewiring in disease-relevant contexts. Researchers commonly interrogate ARHGAP21 function in models of cytoskeletal dysregulation, epithelial-to-mesenchymal transition programs, and signaling crosstalk that impacts proliferation and motility.
ARHGAP21 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ARHGAP21 expression without altering the underlying DNA sequence.
ARHGAP21 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ARHGAP21 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 ARHGAP21 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ARHGAP21 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ARHGAP21 locus and enabling the study of ARHGAP21-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ARHGAP21 pathway restoration in tumor cells with silenced or reduced ARHGAP21 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.