GCP-2 CRISPR/Cas9 KO Plasmid (m): sc-422852
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GCP-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 GCP-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 | |
GCP-2 CRISPR/Cas9 KO Plasmid (m) | sc-422852 | 20 µg | $397.00 |
Overview
Cxcl5 encodes granulocyte chemotactic protein-2 (GCP-2), a secreted CXC chemokine that signals primarily through CXCR2 to promote neutrophil chemotaxis, activation, and trafficking during acute inflammation. In mouse tissues, CXCL5 is induced by pro-inflammatory cues and participates in cytokine and chemokine networks downstream of NF-κB and MAPK signaling, shaping leukocyte recruitment and local immune microenvironments. This axis contributes to regulation of endothelial interactions, tissue remodeling, and host defense responses. Dysregulated CXCL5/GCP-2 signaling has been linked to inflammatory pathologies and tumor-associated inflammation, making it relevant for studies of myeloid biology, barrier tissues, and immune-mediated disease mechanisms.
GCP-2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cxcl5 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cxcl5 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 Cxcl5 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 GCP-2 protein expression.
This CRISPR knockout system enables efficient generation of Cxcl5-deficient cell models for investigation of GCP-2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Cxcl5 exon(s) critical for GCP-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 Cxcl5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by GCP-2 CRISPR/Cas9 KO Plasmid (m) and GCP-2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cxcl5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by GCP-2 HDR Plasmid (m) and GCP-2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cxcl5 homology arms to support homology-directed repair at defined Cxcl5 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.