MIP-2 CRISPR/Cas9 KO Plasmid (m): sc-422851
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MIP-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 MIP-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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MIP-2 Antibody (JJ19): sc-80518
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MIP-2 CRISPR/Cas9 KO Plasmid (m) | sc-422851 | 20 µg | $397.00 |
Overview
Cxcl2 encodes macrophage inflammatory protein-2 (MIP-2), a CXC chemokine that signals primarily through CXCR2 to promote chemotaxis and activation of neutrophils and other myeloid cells. MIP-2 is rapidly induced by innate immune stimuli and pro-inflammatory cytokines, linking NF-κB and MAPK signaling to cytokine and chemokine networks that coordinate leukocyte recruitment. This axis contributes to acute inflammatory responses, vascular activation, and tissue remodeling in settings such as infection, sterile injury, and endotoxemia. Dysregulated CXCL2/MIP-2 signaling is frequently used as a readout of inflammatory burden in models of lung inflammation, arthritis, colitis, and tumor-associated inflammation.
MIP-2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cxcl2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cxcl2 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 Cxcl2 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 MIP-2 protein expression.
This CRISPR knockout system enables efficient generation of Cxcl2-deficient cell models for investigation of MIP-2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Cxcl2 exon(s) critical for MIP-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 Cxcl2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by MIP-2 CRISPR/Cas9 KO Plasmid (m) and MIP-2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cxcl2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by MIP-2 HDR Plasmid (m) and MIP-2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cxcl2 homology arms to support homology-directed repair at defined Cxcl2 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.