Date published: 2026-7-3

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c-Jun CRISPR/Cas9 KO Plasmid (h2): sc-400077-KO-2

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • c-Jun CRISPR/Cas9 Knockout (KO) Plasmid (h2) 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 c-Jun 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: p-c-Jun Antibody (KM-1): sc-822
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    c-Jun CRISPR/Cas9 KO Plasmid (h2)

    sc-400077-KO-2
    20 µg
    $397.00

    Overview

    JUN encodes c-Jun, a core component of the AP-1 transcription factor complex that integrates extracellular cues into context-dependent gene expression programs. c-Jun is rapidly induced by stress and mitogenic signals and is regulated by phosphorylation downstream of MAPK/JNK cascades, shaping transcriptional responses that control proliferation, differentiation, apoptosis, and inflammatory signaling. Through AP-1–dependent regulation of cytokines, matrix-remodeling enzymes, and cell-cycle regulators, c-Jun links signal transduction to changes in chromatin accessibility and transcriptional output. Dysregulated JUN/AP-1 activity has been implicated in oncogenic transformation, tumor invasion, and immune and neuroinflammatory processes, making it a key node for mechanistic studies in human disease models.

    c-Jun CRISPR/Cas9 KO Plasmid (h2) is a pool of plasmids designed for targeted disruption of the JUN gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the JUN 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 JUN 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 c-Jun protein expression.

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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