
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Rho 8 CRISPR Activation Plasmid (h) | sc-403363-ACT | 20 µg | $397.00 |
RND3 (Rho 8) is an atypical Rho family GTPase that functions primarily as a regulator of actin cytoskeletal dynamics, cell shape, and motility. It modulates RhoA/ROCK signaling and downstream myosin light chain phosphorylation, influencing stress fiber assembly, adhesion, and contractility. RND3 also interfaces with pathways controlling cell-cycle progression and apoptosis, including PTEN–PI3K/AKT and p53-associated responses. Dysregulated RND3 expression has been reported across multiple cancer and cardiovascular-related research contexts, where altered cytoskeletal remodeling and survival signaling contribute to disease-associated phenotypes.
Rho 8 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RND3 expression without altering the underlying DNA sequence.
Rho 8 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RND3 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 RND3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Rho 8 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RND3 locus and enabling the study of Rho 8-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Rho 8 pathway restoration in tumor cells with silenced or reduced RND3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.