Date published: 2026-7-4

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C1r CRISPR/Cas9 KO Plasmid (h): sc-405842

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • C1r CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 C1r 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: C1r Antibody (F-7): sc-514105
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    C1r CRISPR/Cas9 KO Plasmid (h)

    sc-405842
    20 µg
    $397.00

    Overview

    C1R encodes complement C1r, a serine protease that forms the C1 complex with C1q and C1s to initiate the classical complement pathway. Upon activation, C1r undergoes autoactivation and cleaves C1s, propagating complement cascade signaling that drives opsonization, immune complex clearance, and inflammatory mediator generation. C1r activity is linked to regulation of innate immune surveillance and crosstalk with coagulation and inflammatory pathways in the extracellular milieu. Dysregulation of C1R has been associated with altered complement activation states and immune-mediated pathology, making it relevant for studies of complement biology and inflammation-related disease mechanisms.

    C1r CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the C1R gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the C1R 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 C1R 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 C1r protein expression.

    This CRISPR knockout system enables efficient generation of C1R-deficient cell models for investigation of C1r signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting C1R exon(s) critical for C1r 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 C1R genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by C1r CRISPR/Cas9 KO Plasmid (h) and C1r CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the C1R locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by C1r HDR Plasmid (h) and C1r HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by C1R homology arms to support homology-directed repair at defined C1R 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.