GPR55 CRISPR/Cas9 KO Plasmid (m): sc-432690
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPR55 CRISPR/Cas9 Knockout (KO) Plasmid (m) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the GPR55 genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR55 CRISPR/Cas9 KO Plasmid (m) | sc-432690 | 20 µg | $397.00 |
Overview
Mouse Gpr55 encodes GPR55, an orphan G protein-coupled receptor widely studied in the endocannabinoid-related signaling network and responsive to lipid mediators such as lysophosphatidylinositol. GPR55 couples to Gα12/13, Gαq, and downstream RhoA–ROCK and PLCβ–Ca2+ pathways, influencing cytoskeletal remodeling, migration, and transcriptional programs including MAPK/ERK signaling. In immune and stromal contexts, GPR55 activity has been linked to modulation of inflammatory signaling, osteoclast/osteoblast balance, and neuronal excitability. Dysregulated GPR55-associated signaling has been investigated in models of pain, metabolic phenotypes, bone disorders, and inflammation-associated tissue remodeling, supporting its use as a mechanistic node in GPCR pathway research.
GPR55 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Gpr55 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Gpr55 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the Gpr55 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish GPR55 protein expression.
This CRISPR knockout system enables efficient generation of Gpr55-deficient cell models for investigation of GPR55 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Gpr55 exon(s) critical for GPR55 function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple Gpr55 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by GPR55 CRISPR/Cas9 KO Plasmid (m) and GPR55 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Gpr55 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by GPR55 HDR Plasmid (m) and GPR55 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Gpr55 homology arms to support homology-directed repair at defined Gpr55 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.