
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
R-Ras CRISPR Activation Plasmid (h) | sc-402126-ACT | 20 µg | $397.00 |
RRAS encodes the small GTPase R-Ras, a Ras family signaling node that cycles between GDP- and GTP-bound states to regulate integrin-dependent adhesion, cytoskeletal dynamics, and membrane trafficking. In human cells, R-Ras contributes to control of cell migration and survival signaling through pathways that intersect with PI3K/AKT and MAPK cascades, influencing endothelial and smooth muscle cell behavior. Altered RRAS activity has been associated with dysregulated vascular remodeling and aberrant cell motility programs observed in cancer and developmental disorders. These properties make RRAS a useful target for dissecting adhesion-mediated signaling, invasion phenotypes, and context-specific Ras network wiring.
R-Ras CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RRAS expression without altering the underlying DNA sequence.
R-Ras CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RRAS 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 RRAS transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous R-Ras expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RRAS locus and enabling the study of R-Ras-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of R-Ras pathway restoration in tumor cells with silenced or reduced RRAS expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.