EP3 CRISPR/Cas9 KO Plasmid (h): sc-402485
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- EP3 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 EP3 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: EP3 Antibody (5F5): sc-57105
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
EP3 CRISPR/Cas9 KO Plasmid (h) | sc-402485 | 20 µg | $397.00 |
Overview
PTGER3 encodes the prostaglandin E2 receptor EP3, a rhodopsin-like GPCR that couples to Gi/o (and in some contexts Gq) to regulate adenylate cyclase activity, cAMP signaling, and downstream kinase pathways. EP3 activation modulates processes including inflammation, vascular and smooth muscle tone, platelet function, and epithelial barrier regulation through context-dependent control of second messengers and transcriptional responses. PTGER3 participates in eicosanoid and arachidonic acid signaling networks that integrate COX-derived prostaglandin cues with immune and metabolic programs. Dysregulated EP3 signaling has been associated with inflammatory and cardiometabolic phenotypes and is frequently investigated in cancer and microenvironment studies where prostaglandin pathways shape proliferation, migration, and immune evasion.
EP3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PTGER3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PTGER3 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 PTGER3 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 EP3 protein expression.
This CRISPR knockout system enables efficient generation of PTGER3-deficient cell models for investigation of EP3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting PTGER3 exon(s) critical for EP3 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 PTGER3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by EP3 CRISPR/Cas9 KO Plasmid (h) and EP3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the PTGER3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by EP3 HDR Plasmid (h) and EP3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by PTGER3 homology arms to support homology-directed repair at defined PTGER3 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.