Date published: 2026-7-4

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SULT1C1 CRISPR/Cas9 KO Plasmid (m): sc-423200

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • SULT1C1 CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 SULT1C1 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

    SULT1C1 CRISPR/Cas9 KO Plasmid (m)

    sc-423200
    20 µg
    $397.00

    Overview

    Sult1c1 encodes the cytosolic sulfotransferase SULT1C1, a phase II xenobiotic-metabolizing enzyme that transfers sulfate from PAPS to hydroxyl- and amine-containing substrates. This sulfation reaction typically increases aqueous solubility and modulates the bioactivity, transport, and clearance of small molecules, thereby shaping cellular chemical homeostasis. In mouse tissues, SULT1C1 contributes to coordinated detoxification and metabolic signaling alongside other conjugation pathways such as glucuronidation and glutathione conjugation. Altered sulfotransferase activity has been associated with differences in susceptibility to chemical stress, endocrine-disrupting compound handling, and inflammation-linked tissue responses, making Sult1c1 a useful target for mechanistic toxicology and metabolism studies.

    SULT1C1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sult1c1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sult1c1 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 Sult1c1 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 SULT1C1 protein expression.

    This CRISPR knockout system enables efficient generation of Sult1c1-deficient cell models for investigation of SULT1C1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Sult1c1 exon(s) critical for SULT1C1 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 Sult1c1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by SULT1C1 CRISPR/Cas9 KO Plasmid (m) and SULT1C1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sult1c1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by SULT1C1 HDR Plasmid (m) and SULT1C1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sult1c1 homology arms to support homology-directed repair at defined Sult1c1 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.