
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RASAL3 CRISPR Activation Plasmid (h) | sc-404999-ACT | 20 µg | $397.00 |
RASAL3 (RAS protein activator like 3) encodes a Ras GTPase-activating protein that promotes conversion of active Ras-GTP to inactive Ras-GDP, thereby constraining Ras-dependent signaling amplitude and duration. Through negative regulation of Ras/MAPK and related small GTPase pathways, RASAL3 contributes to control of cell activation states, proliferation cues, and downstream transcriptional programs. Its activity is especially relevant to immune cell signaling contexts where Ras pathway tuning influences receptor-driven responses and cellular differentiation. Dysregulated Ras pathway control is implicated across inflammatory and oncogenic processes, making RASAL3 a useful node for mechanistic studies of signaling homeostasis.
RASAL3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RASAL3 expression without altering the underlying DNA sequence.
RASAL3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RASAL3 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 RASAL3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous RASAL3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RASAL3 locus and enabling the study of RASAL3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of RASAL3 pathway restoration in tumor cells with silenced or reduced RASAL3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.