Date published: 2026-8-14

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IFITM5 CRISPR/Cas9 KO Plasmid (h): sc-407248

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • IFITM5 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 IFITM5 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

    IFITM5 CRISPR/Cas9 KO Plasmid (h)

    sc-407248
    20 µg
    $397.00

    Overview

    IFITM5 (interferon induced transmembrane protein 5, also known as BRIL) is a bone-restricted membrane protein enriched in osteoblasts and osteocytes that contributes to skeletal development and mineralization. It participates in osteoblast differentiation programs and influences extracellular matrix deposition and hydroxyapatite formation, linking membrane-associated signaling to bone matrix maturation. Genetic alterations in IFITM5 are associated with osteogenesis imperfecta type V and abnormal bone remodeling phenotypes, making it relevant for studying genotype–phenotype relationships in heritable skeletal disorders. IFITM5 is therefore a useful molecular entry point for interrogating pathways controlling osteoblast function, matrix organization, and bone tissue homeostasis.

    IFITM5 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the IFITM5 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the IFITM5 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 IFITM5 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 IFITM5 protein expression.

    This CRISPR knockout system enables efficient generation of IFITM5-deficient cell models for investigation of IFITM5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting IFITM5 exon(s) critical for IFITM5 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 IFITM5 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by IFITM5 CRISPR/Cas9 KO Plasmid (h) and IFITM5 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the IFITM5 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by IFITM5 HDR Plasmid (h) and IFITM5 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by IFITM5 homology arms to support homology-directed repair at defined IFITM5 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.