Date published: 2026-10-8

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TRP2/DCT CRISPR/Cas9 KO Plasmid (h): sc-400334

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TRP2/DCT 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 TRP2/DCT 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: TRP2/DCT Antibody (C-9): sc-74439
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    TRP2/DCT CRISPR/Cas9 KO Plasmid (h)

    sc-400334
    20 µg
    $397.00

    Overview

    DCT encodes dopachrome tautomerase (TRP2/DCT), a melanosomal enzyme that catalyzes the conversion of dopachrome to DHICA during eumelanin biosynthesis. Acting downstream of tyrosinase and coordinated with TYRP1, TRP2/DCT supports melanogenesis, melanosome maturation, and redox balance in pigment-producing cells. Its expression is regulated by lineage transcriptional programs such as MITF and intersects with pathways controlling pigmentation and oxidative stress responses. Altered DCT activity or expression has been linked to pigmentation phenotypes and is frequently studied in melanoma biology and antigen presentation contexts.

    TRP2/DCT CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the DCT gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the DCT 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 DCT 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 TRP2/DCT protein expression.

    This CRISPR knockout system enables efficient generation of DCT-deficient cell models for investigation of TRP2/DCT signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting DCT exon(s) critical for TRP2/DCT 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 DCT genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by TRP2/DCT CRISPR/Cas9 KO Plasmid (h) and TRP2/DCT CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the DCT locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by TRP2/DCT HDR Plasmid (h) and TRP2/DCT HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by DCT homology arms to support homology-directed repair at defined DCT 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.