Date published: 2026-7-9

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SUMO-3 CRISPR/Cas9 KO Plasmid (h): sc-400788

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • SUMO-3 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 SUMO-3 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: SUMO-3 Antibody (76AT630.91.31): sc-130884
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    SUMO-3 CRISPR/Cas9 KO Plasmid (h)

    sc-400788
    20 µg
    $397.00

    Overview

    SUMO3 encodes SUMO-3, a small ubiquitin-like modifier that is covalently conjugated to target proteins to regulate their localization, stability, and interaction networks. SUMO-3–dependent SUMOylation supports dynamic control of transcription, DNA damage signaling and repair, chromatin organization, and cell-cycle progression, and it intersects with ubiquitin pathways to shape stress-adaptive proteostasis. SUMO3 activity is frequently studied in contexts of cellular stress responses, genome integrity maintenance, and innate immune regulation, where altered SUMOylation patterns have been linked to dysregulated signaling in cancer biology, neurodegeneration-associated proteotoxic stress, and inflammatory pathophysiology.

    SUMO-3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SUMO3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SUMO3 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 SUMO3 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 SUMO-3 protein expression.

    This CRISPR knockout system enables efficient generation of SUMO3-deficient cell models for investigation of SUMO-3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting SUMO3 exon(s) critical for SUMO-3 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 SUMO3 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by SUMO-3 CRISPR/Cas9 KO Plasmid (h) and SUMO-3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SUMO3 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by SUMO-3 HDR Plasmid (h) and SUMO-3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SUMO3 homology arms to support homology-directed repair at defined SUMO3 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.