CKR-2 CRISPR/Cas9 KO Plasmid (m): sc-419705
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CKR-2 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-2 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 | |
CKR-2 CRISPR/Cas9 KO Plasmid (m) | sc-419705 | 20 µg | $397.00 |
Overview
Ccr2 encodes the chemokine receptor CKR-2 (CCR2), a seven-transmembrane GPCR that binds CCL2/MCP-1 and related ligands to direct chemotaxis of monocytes and other myeloid subsets. Upon ligand engagement, CKR-2 signals through Gαi-dependent pathways to regulate PI3K/AKT and MAPK cascades, calcium flux, integrin activation, and cytoskeletal remodeling, shaping leukocyte trafficking and inflammatory polarization. In mouse, Ccr2 activity is central to recruitment of inflammatory monocytes to sites of tissue injury and infection and influences macrophage accumulation within diverse inflammatory microenvironments. Dysregulated CCR2-axis signaling is frequently studied in chronic inflammation, neuroinflammation, and tumor-associated myeloid biology as a driver of immune cell infiltration and cytokine networks.
CKR-2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ccr2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ccr2 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 Ccr2 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-2 protein expression.
This CRISPR knockout system enables efficient generation of Ccr2-deficient cell models for investigation of CKR-2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ccr2 exon(s) critical for CKR-2 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 Ccr2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CKR-2 CRISPR/Cas9 KO Plasmid (m) and CKR-2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ccr2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CKR-2 HDR Plasmid (m) and CKR-2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ccr2 homology arms to support homology-directed repair at defined Ccr2 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.