DP CRISPR/Cas9 KO Plasmid (m): sc-422478
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DP 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 DP 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 | |
DP CRISPR/Cas9 KO Plasmid (m) | sc-422478 | 20 µg | $397.00 |
Overview
Ptgdr encodes the mouse prostaglandin D2 receptor DP, a G protein–coupled receptor that primarily signals through Gs to elevate cAMP and engage PKA-dependent transcriptional programs. DP is activated by PGD2 produced via arachidonic acid metabolism and contributes to regulation of smooth muscle tone, vascular permeability, mucosal inflammation, and immune cell trafficking. In leukocytes and barrier tissues, DP-linked signaling interfaces with cytokine production and chemotaxis, shaping type 2 inflammatory responses and neuroimmune communication. Dysregulated PGD2–DP activity has been implicated in experimental models of asthma-like airway inflammation, allergic disease, and inflammatory pain pathways, making Ptgdr a useful node for dissecting lipid mediator signaling.
DP CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ptgdr gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ptgdr 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 Ptgdr 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 DP protein expression.
This CRISPR knockout system enables efficient generation of Ptgdr-deficient cell models for investigation of DP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ptgdr exon(s) critical for DP 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 Ptgdr genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by DP CRISPR/Cas9 KO Plasmid (m) and DP CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ptgdr locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by DP HDR Plasmid (m) and DP HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ptgdr homology arms to support homology-directed repair at defined Ptgdr 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.