
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR55 CRISPR Activation Plasmid (m) | sc-432690-ACT | 20 µg | $397.00 |
Mouse Gpr55 encodes GPR55, an atypical G protein–coupled receptor implicated in lipid-sensing and signal transduction downstream of endogenous ligands such as lysophosphatidylinositol. GPR55 activity can engage Gα12/13- and RhoA-dependent pathways, modulate intracellular calcium dynamics, and influence MAPK/ERK signaling, linking receptor activation to changes in cytoskeletal organization and transcriptional programs. In immune and nervous system contexts, GPR55 has been associated with regulation of inflammatory signaling, cell migration, and neuronal excitability. Dysregulated GPR55-linked signaling has been investigated in models of inflammation, pain processing, and metabolic homeostasis, supporting its relevance for mechanistic studies of GPCR-driven phenotypes.
GPR55 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Gpr55 expression without altering the underlying DNA sequence.
GPR55 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Gpr55 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 Gpr55 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous GPR55 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Gpr55 locus and enabling the study of GPR55-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of GPR55 pathway restoration in tumor cells with silenced or reduced Gpr55 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.