CKR-7 CRISPR/Cas9 KO Plasmid (m): sc-419708
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CKR-7 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-7 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-7 Antibody (ELC-Fc): sc-23936
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CKR-7 CRISPR/Cas9 KO Plasmid (m) | sc-419708 | 20 µg | $397.00 |
Overview
Ccr7 encodes the chemokine receptor CKR-7 (CCR7), a GPCR that binds CCL19 and CCL21 to direct chemotaxis and positional cues for T cells, B cells, and dendritic cells. CCR7 signaling engages Gαi-dependent pathways that influence actin remodeling, integrin activation, and MAPK/PI3K signaling, supporting leukocyte trafficking through lymphatic endothelium and secondary lymphoid organs. In mice, Ccr7 is central to immune surveillance, lymphoid tissue organization, and regulated immune cell migration during inflammation. Dysregulated CCR7-dependent trafficking is frequently studied in models of autoimmunity, chronic inflammation, and tumor immune microenvironments where altered cell homing can shape disease progression.
CKR-7 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ccr7 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ccr7 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 Ccr7 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-7 protein expression.
This CRISPR knockout system enables efficient generation of Ccr7-deficient cell models for investigation of CKR-7 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ccr7 exon(s) critical for CKR-7 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 Ccr7 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CKR-7 CRISPR/Cas9 KO Plasmid (m) and CKR-7 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ccr7 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CKR-7 HDR Plasmid (m) and CKR-7 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ccr7 homology arms to support homology-directed repair at defined Ccr7 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.