GPR92 CRISPR/Cas9 KO Plasmid (m): sc-436329
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPR92 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 GPR92 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 | |
GPR92 CRISPR/Cas9 KO Plasmid (m) | sc-436329 | 20 µg | $397.00 |
Overview
Lpar5 encodes the G protein-coupled receptor GPR92 (also known as LPA5), a lipid-sensing receptor that responds to lysophosphatidic acid to regulate intracellular signaling dynamics. In mouse cells, GPR92 couples to heterotrimeric G proteins to modulate pathways such as cAMP/PKA and Rho-family GTPase-driven cytoskeletal remodeling, shaping adhesion, migration, and receptor-proximal inflammatory signaling. Lpar5 activity has been linked to immune cell behavior and barrier-associated responses, connecting lipid mediator biology to tissue inflammation and microenvironmental cues. Dysregulated LPA–GPR92 signaling is therefore relevant to mechanistic studies in immunology, cancer biology, and fibrosis-associated remodeling without implying clinical outcomes.
GPR92 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Lpar5 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Lpar5 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 Lpar5 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 GPR92 protein expression.
This CRISPR knockout system enables efficient generation of Lpar5-deficient cell models for investigation of GPR92 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Lpar5 exon(s) critical for GPR92 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 Lpar5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by GPR92 CRISPR/Cas9 KO Plasmid (m) and GPR92 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Lpar5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by GPR92 HDR Plasmid (m) and GPR92 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Lpar5 homology arms to support homology-directed repair at defined Lpar5 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.