Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
RhoA CRISPR Activation Plasmid (h): sc-400052-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RhoA CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- RhoA CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by RhoA CRISPR Activation Plasmid (h) and RhoA CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the RHOA transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: RhoA Antibody (26C4): sc-418
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RhoA CRISPR Activation Plasmid (h) | sc-400052-ACT | 20 µg | $397.00 | |||
RhoA CRISPR Activation Plasmid (h2) | sc-400052-ACT-2 | 20 µg | $397.00 |
RHOA encodes the small GTPase RhoA, a central regulator of actin cytoskeleton dynamics that coordinates stress fiber formation, focal adhesion turnover, and acto-myosin contractility. Through cycling between GDP- and GTP-bound states and signaling to effectors such as ROCK and mDia, RhoA integrates inputs from GPCRs, receptor tyrosine kinases, and integrins to control cell shape, migration, cytokinesis, and junctional integrity. RhoA activity intersects with Rho/ROCK, SRF/MRTF transcriptional programs, and mechanotransduction pathways that influence proliferation and differentiation. Dysregulated RHOA signaling and recurrent mutations have been linked to altered cell motility and adhesion phenotypes in cancer biology and to immune and vascular dysfunction contexts, supporting its broad relevance in disease-associated signaling networks.
RhoA CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RHOA expression without altering the underlying DNA sequence.
RhoA CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RHOA 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 RHOA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous RhoA expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RHOA locus and enabling the study of RhoA-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of RhoA pathway restoration in tumor cells with silenced or reduced RHOA expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.