Date published: 2026-8-24

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SUMF1 CRISPR/Cas9 KO Plasmid (h): sc-406543

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • SUMF1 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 SUMF1 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: SUMF1 Antibody (B-9): sc-376035
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    SUMF1 CRISPR/Cas9 KO Plasmid (h)

    sc-406543
    20 µg
    $397.00

    Overview

    SUMF1 encodes the formylglycine-generating enzyme (FGE), an endoplasmic reticulum luminal oxidase required for post-translational activation of all sulfatases through conversion of a conserved cysteine to Cα-formylglycine. This modification is essential for lysosomal and extracellular sulfate ester hydrolysis, linking SUMF1 to glycosaminoglycan turnover, sphingolipid metabolism, and broader lysosome-dependent catabolic pathways. Disruption of SUMF1 reduces global sulfatase activity and can lead to lysosomal storage phenotypes characterized by impaired substrate clearance and altered cellular homeostasis. SUMF1 is therefore widely studied in the context of sulfatase biology, lysosome function, and mechanisms underlying multiple sulfatase deficiency–associated pathogenesis.

    SUMF1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SUMF1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SUMF1 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 SUMF1 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 SUMF1 protein expression.

    This CRISPR knockout system enables efficient generation of SUMF1-deficient cell models for investigation of SUMF1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting SUMF1 exon(s) critical for SUMF1 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 SUMF1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by SUMF1 CRISPR/Cas9 KO Plasmid (h) and SUMF1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SUMF1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by SUMF1 HDR Plasmid (h) and SUMF1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SUMF1 homology arms to support homology-directed repair at defined SUMF1 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.