Date published: 2026-7-6

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C6 CRISPR/Cas9 KO Plasmid (m): sc-419396

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • C6 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 C6 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: C6 Antibody (3G11): sc-66191
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    C6 CRISPR/Cas9 KO Plasmid (m)

    sc-419396
    20 µg
    $397.00

    Overview

    Mouse C6 encodes complement component C6, a terminal pathway protein required for assembly of the membrane attack complex (MAC, C5b-9) that forms lytic pores on target membranes. Following complement activation through the classical, lectin, or alternative pathways, C6 binds C5b and initiates recruitment of C7, C8, and C9, linking opsonization and inflammatory signaling to direct membrane damage. C6 activity influences innate immune surveillance, host–pathogen interactions, and regulation of inflammatory microenvironments. Dysregulated terminal complement activity has been associated with inflammatory and immune-mediated tissue injury, making C6 a useful target for mechanistic studies of complement-driven pathology.

    C6 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the C6 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the C6 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 C6 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 C6 protein expression.

    This CRISPR knockout system enables efficient generation of C6-deficient cell models for investigation of C6 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting C6 exon(s) critical for C6 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 C6 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by C6 CRISPR/Cas9 KO Plasmid (m) and C6 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the C6 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by C6 HDR Plasmid (m) and C6 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by C6 homology arms to support homology-directed repair at defined C6 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.