Date published: 2026-8-13

1-800-457-3801

SCBT Portrait Logo
Seach Input

dsg1 CRISPR/Cas9 KO Plasmid (h): sc-401442

0.0(0)
Write a reviewAsk a question

Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • dsg1 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 dsg1 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: dsg1 Antibody (B-11): sc-137164
    Gene Editing Promo Banner

    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    dsg1 CRISPR/Cas9 KO Plasmid (h)

    sc-401442
    20 µg
    $397.00

    Overview

    DSG1 encodes desmoglein-1 (dsg1), a cadherin-family desmosomal adhesion protein that strengthens cell–cell junctions in stratified epithelia and supports epidermal barrier integrity. By coupling to plakoglobin, plakophilins, and desmoplakin, DSG1 links intercellular adhesion to intermediate filament networks and coordinates differentiation, mechanical resilience, and tissue morphogenesis. Perturbation of DSG1-dependent desmosome assembly can alter keratinocyte signaling, junctional remodeling, and stress responses. Genetic and acquired DSG1 dysfunction is associated with skin fragility and inflammatory phenotypes, making it a relevant target for studying epithelial homeostasis and disease mechanisms.

    dsg1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the DSG1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the DSG1 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 DSG1 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 dsg1 protein expression.

    This CRISPR knockout system enables efficient generation of DSG1-deficient cell models for investigation of dsg1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting DSG1 exon(s) critical for dsg1 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 DSG1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by dsg1 CRISPR/Cas9 KO Plasmid (h) and dsg1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the DSG1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by dsg1 HDR Plasmid (h) and dsg1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by DSG1 homology arms to support homology-directed repair at defined DSG1 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.