Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
IP-10 CRISPR/Cas9 KO Plasmid (m): sc-421031
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IP-10 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 IP-10 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: IP-10 Antibody (E-2): sc-374092
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IP-10 CRISPR/Cas9 KO Plasmid (m) | sc-421031 | 20 µg | $397.00 |
Overview
Cxcl10 encodes the chemokine IP-10 (CXCL10), a secreted interferon-inducible ligand that binds CXCR3 to direct chemotaxis of activated T cells, NK cells, and other immune populations. IP-10 is commonly induced downstream of IFN-γ/STAT1 and pathogen-sensing pathways, shaping leukocyte trafficking, endothelial activation, and inflammatory cytokine networks. In mouse models, Cxcl10 contributes to immune cell recruitment within infected or damaged tissues and influences the balance between protective immunity and immunopathology. Dysregulated CXCL10 signaling is frequently used as a marker and mechanistic node in studies of chronic inflammation, autoimmune-like responses, and tumor immune microenvironment remodeling.
IP-10 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cxcl10 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cxcl10 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 Cxcl10 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 IP-10 protein expression.
This CRISPR knockout system enables efficient generation of Cxcl10-deficient cell models for investigation of IP-10 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Cxcl10 exon(s) critical for IP-10 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 Cxcl10 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by IP-10 CRISPR/Cas9 KO Plasmid (m) and IP-10 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cxcl10 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by IP-10 HDR Plasmid (m) and IP-10 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cxcl10 homology arms to support homology-directed repair at defined Cxcl10 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.