MIP-1α CRISPR/Cas9 KO Plasmid (m): sc-422843
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MIP-1α 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-1α 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-1α Antibody (C-5): sc-365691
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MIP-1α CRISPR/Cas9 KO Plasmid (m) | sc-422843 | 20 µg | $397.00 |
Overview
Ccl3 encodes macrophage inflammatory protein-1α (MIP-1α), a CC chemokine that orchestrates leukocyte recruitment and activation during innate and adaptive immune responses. MIP-1α signals primarily through CCR1 and CCR5 to promote chemotaxis of monocytes/macrophages, T cells, and NK cells, integrating with NF-κB-driven inflammatory programs and cytokine/chemokine networks. In mouse models, Ccl3 is widely used to interrogate inflammatory cell trafficking, myeloid activation states, and tissue remodeling. Dysregulated MIP-1α production is frequently associated with chronic inflammation and immune-mediated pathology, making it a key node for studying microenvironmental cues in infection, autoimmunity, and tumor immunology.
MIP-1α CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ccl3 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ccl3 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 Ccl3 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-1α protein expression.
This CRISPR knockout system enables efficient generation of Ccl3-deficient cell models for investigation of MIP-1α signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ccl3 exon(s) critical for MIP-1α 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 Ccl3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by MIP-1α CRISPR/Cas9 KO Plasmid (m) and MIP-1α CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ccl3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by MIP-1α HDR Plasmid (m) and MIP-1α HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ccl3 homology arms to support homology-directed repair at defined Ccl3 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.