Date published: 2026-9-6

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NARF CRISPR/Cas9 KO Plasmid (h): sc-407124

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • NARF 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 NARF 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: NARF Antibody (32-7): sc-100654
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    NARF CRISPR/Cas9 KO Plasmid (h)

    sc-407124
    20 µg
    $397.00

    Overview

    NARF (nuclear prelamin A recognition factor) encodes a nuclear protein implicated in the processing and quality control of lamin A precursors, supporting proper nuclear envelope organization and genome stability. By interacting with prelamin A and related nuclear lamina components, NARF contributes to pathways that couple proteostasis with nuclear architecture, influencing chromatin organization, DNA damage responses, and cell-cycle progression. Perturbation of lamin A maturation and nuclear lamina homeostasis is linked to a spectrum of laminopathies and progeroid phenotypes, making NARF a useful node for studying mechanisms of nuclear stress. Human NARF function is also relevant to models examining how altered nuclear structure impacts transcriptional programs and cellular aging-associated processes.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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