Date published: 2026-7-11

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FTCD CRISPR/Cas9 KO Plasmid (m): sc-420419

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • FTCD 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 FTCD 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: FTCD Antibody (G-3): sc-271788
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    FTCD CRISPR/Cas9 KO Plasmid (m)

    sc-420419
    20 µg
    $397.00

    Overview

    Mouse Ftcd encodes formiminotransferase cyclodeaminase (FTCD), a bifunctional cytosolic enzyme that catalyzes sequential steps in histidine catabolism and couples one-carbon metabolism to folate-dependent pathways. FTCD activity contributes to cellular pools of tetrahydrofolate derivatives that support nucleotide biosynthesis and methylation reactions, linking amino acid utilization to metabolic homeostasis. Altered FTCD function is associated with inborn errors of metabolism affecting formiminoglutamate handling and broader perturbations in one-carbon flux, making it relevant for studies of metabolic stress responses. Ftcd is also used as a hepatocyte-associated marker in mouse systems, supporting research into liver metabolism and differentiation state.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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