Date published: 2026-7-10

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Mts1 CRISPR/Cas9 KO Plasmid (m): sc-422782

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Mts1 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 Mts1 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: Mts1 Antibody (X9-7): sc-100784
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Mts1 CRISPR/Cas9 KO Plasmid (m)

    sc-422782
    20 µg
    $397.00

    Overview

    Mouse S100a4 encodes Mts1, a calcium-binding S100 family protein that modulates cytoskeletal dynamics, cell motility, and cell–matrix interactions through calcium-dependent regulation of actin remodeling and associated signaling networks. Mts1 is linked to processes such as epithelial–mesenchymal transition, fibroblast activation, and immune cell trafficking, with reported connections to pathways involving Rho GTPase signaling and extracellular matrix remodeling. Altered S100a4/Mts1 expression is frequently used as a molecular readout of invasive and pro-migratory cell states and is studied in inflammation-associated tissue remodeling and tumor biology models. In mouse systems, S100a4 is also employed to interrogate stromal–immune crosstalk and lineage-specific contributions to pathological remodeling.

    Mts1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the S100a4 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the S100a4 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 S100a4 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 Mts1 protein expression.

    This CRISPR knockout system enables efficient generation of S100a4-deficient cell models for investigation of Mts1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting S100a4 exon(s) critical for Mts1 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 S100a4 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Mts1 CRISPR/Cas9 KO Plasmid (m) and Mts1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the S100a4 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Mts1 HDR Plasmid (m) and Mts1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by S100a4 homology arms to support homology-directed repair at defined S100a4 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.