fractalkine CRISPR/Cas9 KO Plasmid (m): sc-422853
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- fractalkine 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 fractalkine 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 | |
fractalkine CRISPR/Cas9 KO Plasmid (m) | sc-422853 | 20 µg | $397.00 |
Overview
Cx3cl1 encodes fractalkine (CX3CL1), a unique membrane-tethered and soluble chemokine that signals through CX3CR1 to regulate leukocyte adhesion, chemotaxis, and survival. In mouse tissues, fractalkine contributes to neuroimmune communication by modulating microglia–neuron interactions and shaping inflammatory responses in the CNS and peripheral organs. This axis integrates with chemokine-driven trafficking programs and adhesion mechanisms that influence myeloid cell recruitment, vascular inflammation, and tissue remodeling. Dysregulated CX3CL1–CX3CR1 signaling is commonly studied in contexts of neuroinflammation, atherosclerosis-like vascular pathology, and chronic inflammatory disease models.
fractalkine CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cx3cl1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cx3cl1 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 Cx3cl1 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 fractalkine protein expression.
This CRISPR knockout system enables efficient generation of Cx3cl1-deficient cell models for investigation of fractalkine signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Cx3cl1 exon(s) critical for fractalkine 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 Cx3cl1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by fractalkine CRISPR/Cas9 KO Plasmid (m) and fractalkine CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cx3cl1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by fractalkine HDR Plasmid (m) and fractalkine HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cx3cl1 homology arms to support homology-directed repair at defined Cx3cl1 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.