Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
EDG-5 CRISPR/Cas9 KO Plasmid (m): sc-420642
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- EDG-5 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 EDG-5 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: EDG-5 Antibody (E-12): sc-365963
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
EDG-5 CRISPR/Cas9 KO Plasmid (m) | sc-420642 | 20 µg | $397.00 |
Overview
S1pr2 encodes EDG-5 (sphingosine-1-phosphate receptor 2), a GPCR that binds the bioactive lipid sphingosine-1-phosphate to regulate cell migration, cytoskeletal remodeling, and vascular barrier properties. EDG-5 signals through heterotrimeric G proteins to engage RhoA/ROCK, MAPK/ERK, and PI3K-AKT pathway nodes, shaping adhesion dynamics, proliferation cues, and inflammatory responses. In mouse systems, S1pr2 activity has been linked to endothelial and immune cell trafficking, fibrosis-associated remodeling, and context-dependent control of tumor cell invasion and metastatic behavior. Dysregulated S1P–S1PR2 signaling is therefore relevant to studies of inflammation, vascular dysfunction, and tissue injury responses.
EDG-5 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the S1pr2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the S1pr2 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 S1pr2 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 EDG-5 protein expression.
This CRISPR knockout system enables efficient generation of S1pr2-deficient cell models for investigation of EDG-5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting S1pr2 exon(s) critical for EDG-5 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 S1pr2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by EDG-5 CRISPR/Cas9 KO Plasmid (m) and EDG-5 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the S1pr2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by EDG-5 HDR Plasmid (m) and EDG-5 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by S1pr2 homology arms to support homology-directed repair at defined S1pr2 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.