CKR-1 CRISPR/Cas9 KO Plasmid (m): sc-419701
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CKR-1 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-1 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-1 CRISPR/Cas9 KO Plasmid (m) | sc-419701 | 20 µg | $397.00 |
Overview
Ccr1 encodes the chemokine receptor CKR-1 (CCR1), a G protein–coupled receptor that binds inflammatory CC chemokines to control leukocyte chemotaxis, adhesion, and tissue infiltration. CKR-1 signaling engages heterotrimeric G proteins to activate calcium flux, MAPK/ERK cascades, and PI3K-dependent pathways that coordinate cytoskeletal remodeling and directional migration. In mouse immune compartments, Ccr1 contributes to monocyte/macrophage and neutrophil trafficking and shapes cytokine-driven inflammatory circuits. Dysregulated CCR1 activity has been associated with inflammatory and autoimmune-like pathology models and has been studied in contexts including infection, fibrosis, and tumor-associated myeloid recruitment.
CKR-1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ccr1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ccr1 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 Ccr1 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-1 protein expression.
This CRISPR knockout system enables efficient generation of Ccr1-deficient cell models for investigation of CKR-1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ccr1 exon(s) critical for CKR-1 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 Ccr1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CKR-1 CRISPR/Cas9 KO Plasmid (m) and CKR-1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ccr1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CKR-1 HDR Plasmid (m) and CKR-1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ccr1 homology arms to support homology-directed repair at defined Ccr1 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.