C2 CRISPR/Cas9 KO Plasmid (m): sc-419389
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C2 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 C2 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 | |
C2 CRISPR/Cas9 KO Plasmid (m) | sc-419389 | 20 µg | $397.00 |
Overview
Complement component 2 (C2) is a central serine protease zymogen of the classical and lectin complement pathways in mouse, cleaved by C1s or MASP2 to generate C2a and form the C3 convertase (C4b2a). This step drives amplification of complement activation, opsonization, inflammatory signaling, and downstream membrane attack complex formation, linking innate immune recognition to clearance of immune complexes and pathogens. C2 activity interfaces with cytokine networks and Fc receptor–dependent responses, shaping leukocyte recruitment and antigen presentation in immune tissues. Altered C2 function is broadly relevant to studies of complement dysregulation associated with autoimmunity, infection susceptibility, and inflammatory tissue injury mechanisms.
C2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the C2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the C2 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 C2 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 C2 protein expression.
This CRISPR knockout system enables efficient generation of C2-deficient cell models for investigation of C2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting C2 exon(s) critical for C2 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 C2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by C2 CRISPR/Cas9 KO Plasmid (m) and C2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the C2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by C2 HDR Plasmid (m) and C2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by C2 homology arms to support homology-directed repair at defined C2 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.