Date published: 2026-9-9

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Mindin CRISPR/Cas9 KO Plasmid (h): sc-417294

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Mindin 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 Mindin 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: Mindin Antibody (A-10): sc-166868
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Mindin CRISPR/Cas9 KO Plasmid (h)

    sc-417294
    20 µg
    $397.00

    Overview

    SPON2 encodes mindin, a secreted extracellular matrix glycoprotein that functions as a pattern-recognition and adhesion molecule linking innate immune sensing to cell–matrix interactions. Mindin binds microbial components and integrin receptors, supporting leukocyte recruitment, macrophage activation, and modulation of inflammatory signaling pathways such as NF-κB and downstream cytokine networks. In stromal and vascular microenvironments, SPON2 contributes to extracellular matrix organization, chemotactic gradients, and tissue remodeling processes that influence tumor–immune interactions. Dysregulated SPON2 expression has been reported across multiple inflammatory and oncogenic contexts, making it relevant for mechanistic studies of immune surveillance, fibrosis-associated remodeling, and microenvironmental signaling.

    Mindin CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SPON2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SPON2 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 SPON2 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 Mindin protein expression.

    This CRISPR knockout system enables efficient generation of SPON2-deficient cell models for investigation of Mindin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting SPON2 exon(s) critical for Mindin 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 SPON2 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Mindin CRISPR/Cas9 KO Plasmid (h) and Mindin CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SPON2 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Mindin HDR Plasmid (h) and Mindin HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SPON2 homology arms to support homology-directed repair at defined SPON2 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.