Rap 2B CRISPR Activation Plasmid (h): sc-403292-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Rap 2B CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Rap 2B 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 Rap 2B CRISPR Activation Plasmid (h) and Rap 2B CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the RAP2B transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Rap 2B CRISPR Activation Plasmid (h) | sc-403292-ACT | 20 µg | $397.00 |
RAP2B encodes Rap2B, a Ras-related small GTPase that cycles between GDP- and GTP-bound states to regulate signal transduction, membrane trafficking, and cytoskeletal remodeling. Rap2B participates in pathways linked to integrin-mediated adhesion, vesicle dynamics, and MAPK-related signaling outputs that shape cell migration and cellular responsiveness to extracellular cues. In hematopoietic and vascular contexts, Rap2B is closely associated with platelet activation and secretion processes, supporting studies of thrombosis biology and inflammatory signaling. Dysregulated RAP2B expression or activity has been reported across multiple disease-relevant settings, including cancer-associated invasion and metastasis phenotypes, making it a useful node for mechanistic pathway interrogation.
Rap 2B CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RAP2B expression without altering the underlying DNA sequence.
Rap 2B CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RAP2B 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 RAP2B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Rap 2B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RAP2B locus and enabling the study of Rap 2B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Rap 2B pathway restoration in tumor cells with silenced or reduced RAP2B expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.