C4BP CRISPR/Cas9 KO Plasmid (m): sc-419394
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C4BP 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 C4BP 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 | |
C4BP CRISPR/Cas9 KO Plasmid (m) | sc-419394 | 20 µg | $397.00 |
Overview
Mouse C4bp encodes C4b-binding protein (C4BP), a soluble regulator of the classical and lectin complement pathways that binds activated C4b to promote factor I–mediated inactivation and limit C3 convertase formation. By restraining complement amplification, C4BP helps maintain immune homeostasis, supports clearance of immune complexes and apoptotic material, and modulates inflammatory signaling in the extracellular milieu. Dysregulated complement control involving C4BP has been implicated in contexts such as autoimmunity, infection-associated inflammation, and tissue injury where excessive complement activation contributes to pathology. As a complement regulatory node, C4bp is relevant for studying innate immunity, inflammatory networks, and host–pathogen interactions in mouse models.
C4BP CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the C4bp gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the C4bp 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 C4bp 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 C4BP protein expression.
This CRISPR knockout system enables efficient generation of C4bp-deficient cell models for investigation of C4BP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting C4bp exon(s) critical for C4BP 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 C4bp genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by C4BP CRISPR/Cas9 KO Plasmid (m) and C4BP CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the C4bp locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by C4BP HDR Plasmid (m) and C4BP HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by C4bp homology arms to support homology-directed repair at defined C4bp 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.