CX3CR1 CRISPR/Cas9 KO Plasmid (m): sc-419886
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CX3CR1 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 CX3CR1 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 | |
CX3CR1 CRISPR/Cas9 KO Plasmid (m) | sc-419886 | 20 µg | $397.00 |
Overview
Cx3cr1 encodes CX3CR1, a seven-transmembrane chemokine receptor for CX3CL1 (fractalkine) that regulates leukocyte adhesion, chemotaxis, and tissue surveillance. In mouse, CX3CR1 is prominently expressed by monocytes/macrophages, dendritic cells, and microglia, linking chemokine GPCR signaling to cytoskeletal remodeling, integrin activation, and inflammatory transcriptional programs. CX3CR1-dependent pathways shape microglial homeostasis and neuroimmune communication, and are also implicated in vascular inflammation and myeloid cell trafficking in peripheral tissues. Accordingly, Cx3cr1 is widely used as a marker and functional node in models of neuroinflammation, atherosclerosis, and chronic inflammatory disorders.
CX3CR1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cx3cr1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cx3cr1 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 Cx3cr1 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 CX3CR1 protein expression.
This CRISPR knockout system enables efficient generation of Cx3cr1-deficient cell models for investigation of CX3CR1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Cx3cr1 exon(s) critical for CX3CR1 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 Cx3cr1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CX3CR1 CRISPR/Cas9 KO Plasmid (m) and CX3CR1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cx3cr1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CX3CR1 HDR Plasmid (m) and CX3CR1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cx3cr1 homology arms to support homology-directed repair at defined Cx3cr1 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.