RANTES CRISPR/Cas9 KO Plasmid (m2): sc-422845-KO-2
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RANTES CRISPR/Cas9 Knockout (KO) Plasmid (m2) 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 RANTES 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: RANTES Antibody (A-4): sc-365826
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RANTES CRISPR/Cas9 KO Plasmid (m2) | sc-422845-KO-2 | 20 µg | $397.00 |
Overview
Mouse Ccl5 encodes RANTES (CCL5), a chemokine secreted by activated T cells, NK cells, macrophages, and platelets that directs leukocyte trafficking through CCR1, CCR3, and CCR5 signaling. RANTES-driven chemotaxis shapes inflammatory cell recruitment, promotes immune cell–endothelial interactions, and coordinates cytokine networks that influence tissue remodeling and antiviral responses. Ccl5/RANTES activity intersects with NF-κB- and interferon-associated programs and can modulate myeloid polarization and lymphocyte effector localization. Dysregulated Ccl5 signaling has been implicated in chronic inflammatory and autoimmune models, neuroinflammation, metabolic inflammation, and tumor-immune microenvironment dynamics in mice.
RANTES CRISPR/Cas9 KO Plasmid (m2) is a pool of plasmids designed for targeted disruption of the Ccl5 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ccl5 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 Ccl5 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 RANTES protein expression.
This CRISPR knockout system enables efficient generation of Ccl5-deficient cell models for investigation of RANTES signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ccl5 exon(s) critical for RANTES 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 Ccl5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by RANTES CRISPR/Cas9 KO Plasmid (m) and RANTES CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ccl5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by RANTES HDR Plasmid (m) and RANTES HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ccl5 homology arms to support homology-directed repair at defined Ccl5 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.