Date published: 2026-7-11

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SET7/9 CRISPR/Cas9 KO Plasmid (r): sc-437354

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Datasheets
  • Target species: rat
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • SET7/9 CRISPR/Cas9 Knockout (KO) Plasmid (r) 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 SET7/9 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: SET7/9 Antibody (C-11): sc-390823
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    SET7/9 CRISPR/Cas9 KO Plasmid (r)

    sc-437354
    20 µg
    $397.00

    Overview

    SET7/9 (also known as SETD7) is a lysine methyltransferase that predominantly catalyzes monomethylation of histone H3 at Lys4 (H3K4me1) and can also modify non-histone substrates, shaping transcriptional outputs and protein stability. In rat cells, SET7/9 activity integrates with chromatin remodeling to regulate cell-cycle control, differentiation programs, and stress-responsive gene expression. Through methylation-dependent crosstalk with pathways linked to p53 signaling and NF-κB–associated inflammatory transcription, SET7/9 influences genome maintenance and stimulus-induced transcriptional dynamics. Dysregulated SET7/9 function has been associated with epigenetic alterations relevant to cancer biology, metabolic and cardiovascular phenotypes, and inflammatory disease models, supporting its use as a mechanistic node in epigenetics research.

    SET7/9 CRISPR/Cas9 KO Plasmid (r) is a pool of plasmids designed for targeted disruption of the gene in rat cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the 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 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 SET7/9 protein expression.

    This CRISPR knockout system enables efficient generation of -deficient cell models for investigation of SET7/9 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting exon(s) critical for SET7/9 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 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by SET7/9 CRISPR/Cas9 KO Plasmid (r) and SET7/9 CRISPR/Cas9 KO Plasmid (r2) target distinct sites within the locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by SET7/9 HDR Plasmid (r) and SET7/9 HDR Plasmid (r2) contain a puromycin resistance cassette and an RFP reporter flanked by homology arms to support homology-directed repair at defined 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.