Date published: 2026-9-5

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FAIM CRISPR/Cas9 KO Plasmid (m): sc-423872

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • FAIM 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 FAIM 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
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    FAIM CRISPR/Cas9 KO Plasmid (m)

    sc-423872
    20 µg
    $397.00

    Overview

    Faim encodes Fas apoptotic inhibitory molecule (FAIM), a cytoprotective factor that attenuates death receptor–triggered apoptosis and modulates cellular survival signaling in response to Fas/TNFR family cues. In mouse cells, FAIM has been linked to regulation of caspase activation, stress responses, and survival pathways such as NF-κB and PI3K/AKT, shaping outcomes during immune activation and tissue homeostasis. Altered FAIM activity has been associated with dysregulated lymphocyte survival, neurodegenerative stress sensitivity, and inflammatory phenotypes, making it relevant for studying apoptosis control and cell fate decisions. Functional interrogation of Faim supports mechanistic work in immunology, neurobiology, and pathways governing resistance to extrinsic apoptotic stimuli.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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