
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
G2A CRISPR Activation Plasmid (h) | sc-401866-ACT | 20 µg | $397.00 |
GPR132 encodes G2A, a G protein-coupled receptor implicated in sensing extracellular lipid mediators and microenvironmental cues that shape immune and stress responses. G2A signaling has been linked to regulation of leukocyte chemotaxis, macrophage activation, and inflammatory tone through GPCR-dependent second messenger pathways, influencing cell survival and differentiation programs. In human tissues, altered GPR132 activity is associated with dysregulated inflammation and remodeling processes that intersect with tumor–immune interactions and metabolic stress biology. As a membrane receptor with context-dependent signaling outputs, G2A is frequently studied for how lipid sensing integrates with immune cell trafficking and tissue homeostasis.
G2A CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GPR132 expression without altering the underlying DNA sequence.
G2A CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GPR132 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 GPR132 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous G2A expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GPR132 locus and enabling the study of G2A-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of G2A pathway restoration in tumor cells with silenced or reduced GPR132 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.