Date published: 2026-8-14

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FGFR-4 CRISPR/Cas9 KO Plasmid (m): sc-420344

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • FGFR-4 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 FGFR-4 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: FGFR-4 Antibody (A-10): sc-136988
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    FGFR-4 CRISPR/Cas9 KO Plasmid (m)

    sc-420344
    20 µg
    $397.00

    Overview

    Fgfr4 encodes fibroblast growth factor receptor 4 (FGFR-4), a receptor tyrosine kinase that binds FGF ligands and heparan sulfate to initiate signaling through MAPK/ERK, PI3K–AKT, PLCγ/PKC, and STAT pathways. In mouse cells, FGFR-4 regulates proliferation, differentiation, and survival, with additional roles in tissue development and metabolic homeostasis. Altered FGFR-4 signaling has been linked to dysregulated growth-factor responses, changes in cell migration and invasion programs, and remodeling of the tumor microenvironment in multiple cancer model contexts. Because FGFR-4 integrates extracellular cues with transcriptional and cytoskeletal outputs, it is frequently studied in receptor signaling networks, feedback regulation, and pathway crosstalk with other RTKs.

    FGFR-4 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Fgfr4 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Fgfr4 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 Fgfr4 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 FGFR-4 protein expression.

    This CRISPR knockout system enables efficient generation of Fgfr4-deficient cell models for investigation of FGFR-4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Fgfr4 exon(s) critical for FGFR-4 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 Fgfr4 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by FGFR-4 CRISPR/Cas9 KO Plasmid (m) and FGFR-4 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Fgfr4 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by FGFR-4 HDR Plasmid (m) and FGFR-4 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Fgfr4 homology arms to support homology-directed repair at defined Fgfr4 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.