Date published: 2026-7-4

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FANCF CRISPR/Cas9 KO Plasmid (h): sc-406909

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • FANCF 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 FANCF 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: FANCF Antibody (D-2): sc-271952
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    FANCF CRISPR/Cas9 KO Plasmid (h)

    sc-406909
    20 µg
    $397.00

    Overview

    FANCF encodes a core component of the Fanconi anemia (FA) DNA repair pathway that helps assemble and stabilize the FA core complex responsible for monoubiquitination of FANCD2 and FANCI. This modification coordinates repair of DNA interstrand crosslinks and promotes replication fork protection through crosstalk with homologous recombination and checkpoint signaling. FANCF function supports genome stability during S phase, and loss or dysregulation of FA pathway activity is linked to chromosomal instability and altered responses to replication stress. Genetic defects in FA genes, including FANCF, are associated with Fanconi anemia biology and are widely studied in the context of DNA damage tolerance mechanisms.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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