Date published: 2026-8-30

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Smad2 CRISPR/Cas9 KO Plasmid (m): sc-421525

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Smad2 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 Smad2 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: Smad2 Antibody (YZ-13): sc-101153
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Smad2 CRISPR/Cas9 KO Plasmid (m)

    sc-421525
    20 µg
    $397.00

    Overview

    Smad2 encodes an intracellular signal transducer in the canonical TGF-β/Activin/Nodal pathway, functioning as an R-SMAD that becomes C-terminally phosphorylated by type I receptors and forms transcriptional complexes with SMAD4. In mouse cells, SMAD2 regulates gene programs controlling embryonic patterning, stem cell fate decisions, epithelial–mesenchymal transition, extracellular matrix remodeling, and immune modulation. Through context-dependent transcriptional regulation, SMAD2 influences proliferation, differentiation, and apoptosis, integrating cues from TGF-β superfamily ligands with other signaling networks. Dysregulated SMAD2 signaling has been implicated in fibrosis-related processes, inflammatory phenotypes, and tumor biology via altered pathway output and target gene expression.

    Smad2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Smad2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Smad2 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 Smad2 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 Smad2 protein expression.

    This CRISPR knockout system enables efficient generation of Smad2-deficient cell models for investigation of Smad2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Smad2 exon(s) critical for Smad2 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 Smad2 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Smad2 CRISPR/Cas9 KO Plasmid (m) and Smad2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Smad2 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Smad2 HDR Plasmid (m) and Smad2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Smad2 homology arms to support homology-directed repair at defined Smad2 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.