Date published: 2026-8-28

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MEK-7 CRISPR/Cas9 KO Plasmid (h): sc-402363

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • MEK-7 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 MEK-7 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: MEK-7 Antibody (E-7): sc-25288
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    MEK-7 CRISPR/Cas9 KO Plasmid (h)

    sc-402363
    20 µg
    $397.00

    Overview

    MAP2K7 encodes MEK-7 (MKK7), a dual-specificity MAP kinase kinase that selectively phosphorylates and activates JNK (MAPK8/9/10) in response to inflammatory cytokines, oxidative stress, and genotoxic signals. MEK-7 functions within the MAPK/JNK cascade to regulate transcriptional programs controlling apoptosis, differentiation, cytokine production, and cytoskeletal remodeling. Through crosstalk with upstream MAP3Ks (e.g., TAK1/MAP3K7, MEKKs) and downstream AP-1 family factors, MAP2K7 helps shape stress-adaptive and innate immune signaling outputs. Dysregulated MAP2K7–JNK signaling has been linked to altered inflammatory responses and has been investigated in contexts including cancer biology, neurodegeneration, and metabolic stress models.

    MEK-7 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the MAP2K7 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MAP2K7 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 MAP2K7 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 MEK-7 protein expression.

    This CRISPR knockout system enables efficient generation of MAP2K7-deficient cell models for investigation of MEK-7 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting MAP2K7 exon(s) critical for MEK-7 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 MAP2K7 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by MEK-7 CRISPR/Cas9 KO Plasmid (h) and MEK-7 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the MAP2K7 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by MEK-7 HDR Plasmid (h) and MEK-7 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by MAP2K7 homology arms to support homology-directed repair at defined MAP2K7 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.