Date published: 2026-7-4

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pS2 CRISPR/Cas9 KO Plasmid (h): sc-402867

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • pS2 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 pS2 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: pS2 Antibody (A-10): sc-271464
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    pS2 CRISPR/Cas9 KO Plasmid (h)

    sc-402867
    20 µg
    $397.00

    Overview

    TFF1, also known as pS2, encodes a secreted trefoil factor that contributes to epithelial barrier integrity and mucosal repair by promoting cell migration and regulating restitution after injury. In human tissues it is prominently expressed in gastric and breast epithelium and is commonly regulated by hormone-responsive transcriptional programs, linking it to differentiation and luminal epithelial phenotypes. pS2 participates in stress and inflammation-adjacent signaling that influences epithelial homeostasis, including interactions with mucins and modulation of growth factor–associated responses. Dysregulated TFF1 expression is frequently used as a molecular readout in studies of gastrointestinal metaplasia and estrogen receptor–positive breast cancer biology, where it can reflect changes in epithelial state and microenvironmental signaling.

    pS2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TFF1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TFF1 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 TFF1 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 pS2 protein expression.

    This CRISPR knockout system enables efficient generation of TFF1-deficient cell models for investigation of pS2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting TFF1 exon(s) critical for pS2 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 TFF1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by pS2 CRISPR/Cas9 KO Plasmid (h) and pS2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TFF1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by pS2 HDR Plasmid (h) and pS2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TFF1 homology arms to support homology-directed repair at defined TFF1 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.