EDG-3 CRISPR/Cas9 KO Plasmid (h): sc-401366
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- EDG-3 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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-3 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 | |
EDG-3 CRISPR/Cas9 KO Plasmid (h) | sc-401366 | 20 µg | $397.00 |
Overview
S1PR3 (EDG-3) encodes a G protein-coupled receptor for sphingosine-1-phosphate that couples to Gαi, Gαq, and Gα12/13 to regulate calcium mobilization, MAPK/ERK signaling, Rho family GTPase activation, and cytoskeletal remodeling. Through these pathways, EDG-3 influences endothelial barrier function, vascular tone, leukocyte trafficking, and cell migration, integrating extracellular lipid cues with adhesion and inflammatory signaling programs. Altered S1PR3 activity has been associated with dysregulated inflammation and vascular remodeling and is frequently studied in contexts including atherosclerosis, fibrosis, and tumor–microenvironment interactions. These features make S1PR3 a useful target for dissecting sphingolipid signaling networks in immune and vascular biology.
EDG-3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the S1PR3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the S1PR3 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 S1PR3 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-3 protein expression.
This CRISPR knockout system enables efficient generation of S1PR3-deficient cell models for investigation of EDG-3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting S1PR3 exon(s) critical for EDG-3 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 S1PR3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by EDG-3 CRISPR/Cas9 KO Plasmid (h) and EDG-3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the S1PR3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by EDG-3 HDR Plasmid (h) and EDG-3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by S1PR3 homology arms to support homology-directed repair at defined S1PR3 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.