MIP-1γ CRISPR/Cas9 KO Plasmid (m): sc-422849
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MIP-1γ 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-1γ 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-1γ Antibody (X-18): sc-74228
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MIP-1γ CRISPR/Cas9 KO Plasmid (m) | sc-422849 | 20 µg | $397.00 |
Overview
Ccl9 encodes the CC chemokine MIP-1γ, a secreted mediator that shapes innate immune cell trafficking by promoting chemotaxis and activation of myeloid populations such as monocytes and macrophages. MIP-1γ signaling contributes to inflammatory cytokine networks and leukocyte recruitment programs that intersect with NF-κB–driven responses and broader chemokine receptor signaling cascades. In mouse tissues, Ccl9 expression is commonly associated with immune activation states and microenvironmental remodeling, supporting studies of inflammation, host defense, and immune cell crosstalk. Dysregulated chemokine gradients involving MIP-1γ are relevant to models of chronic inflammatory disease, infection, and tumor-associated inflammation where myeloid infiltration influences pathology.
MIP-1γ CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ccl9 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ccl9 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 Ccl9 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-1γ protein expression.
This CRISPR knockout system enables efficient generation of Ccl9-deficient cell models for investigation of MIP-1γ signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ccl9 exon(s) critical for MIP-1γ 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 Ccl9 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by MIP-1γ CRISPR/Cas9 KO Plasmid (m) and MIP-1γ CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ccl9 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by MIP-1γ HDR Plasmid (m) and MIP-1γ HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ccl9 homology arms to support homology-directed repair at defined Ccl9 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.