CKR-9 CRISPR/Cas9 KO Plasmid (m): sc-419702
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CKR-9 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 CKR-9 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: CKR-9 Antibody (CW-2.2.1): sc-47722
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CKR-9 CRISPR/Cas9 KO Plasmid (m) | sc-419702 | 20 µg | $397.00 |
Overview
Ccr9 encodes CKR-9 (CCR9), a G protein–coupled chemokine receptor best known for binding CCL25 and directing chemotactic trafficking of lymphocytes. In mouse, CCR9 contributes to thymocyte development and gut-homing programs by shaping migratory cues, integrin-dependent adhesion, and positioning within tissue microenvironments. CKR-9 signaling interfaces with canonical GPCR pathways including calcium flux and MAPK/PI3K cascades that influence activation state, survival, and motility of immune cells. Dysregulated CCR9–CCL25 axis activity has been implicated in inflammatory processes at mucosal sites and in mechanisms that support aberrant leukocyte localization relevant to immune-mediated pathology.
CKR-9 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ccr9 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ccr9 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 Ccr9 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 CKR-9 protein expression.
This CRISPR knockout system enables efficient generation of Ccr9-deficient cell models for investigation of CKR-9 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ccr9 exon(s) critical for CKR-9 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 Ccr9 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CKR-9 CRISPR/Cas9 KO Plasmid (m) and CKR-9 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ccr9 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CKR-9 HDR Plasmid (m) and CKR-9 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ccr9 homology arms to support homology-directed repair at defined Ccr9 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.