Date published: 2026-7-9

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Factor IX CRISPR/Cas9 KO Plasmid (h): sc-402469

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Factor IX 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 Factor IX 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: Factor IX Antibody (B-3): sc-377187
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Factor IX CRISPR/Cas9 KO Plasmid (h)

    sc-402469
    20 µg
    $397.00

    Overview

    Human F9 encodes coagulation factor IX, a vitamin K–dependent serine protease zymogen that is activated to factor IXa and functions within the intrinsic pathway of blood coagulation. In complex with factor VIIIa on phospholipid surfaces, factor IXa catalyzes activation of factor X, promoting thrombin generation and fibrin clot formation. F9 activity is modulated by post-translational γ-carboxylation and calcium-dependent membrane binding, linking it to hepatic protein processing and extracellular proteolytic cascades. Disruption or functional deficiency of F9 is associated with inherited bleeding phenotypes and is routinely studied to understand coagulation network regulation and protease cofactor interactions.

    Factor IX CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the F9 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the F9 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 F9 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 Factor IX protein expression.

    This CRISPR knockout system enables efficient generation of F9-deficient cell models for investigation of Factor IX signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting F9 exon(s) critical for Factor IX 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 F9 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Factor IX CRISPR/Cas9 KO Plasmid (h) and Factor IX CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the F9 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Factor IX HDR Plasmid (h) and Factor IX HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by F9 homology arms to support homology-directed repair at defined F9 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.