Date published: 2026-8-15

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DDI2 CRISPR/Cas9 KO Plasmid (m): sc-427193

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • DDI2 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 DDI2 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: DDI2 Antibody (A-3): sc-514004
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    DDI2 CRISPR/Cas9 KO Plasmid (m)

    sc-427193
    20 µg
    $397.00

    Overview

    Mouse DDI2 (DNA damage-inducible 1 homolog 2) encodes an aspartyl protease implicated in protein quality control and stress-response signaling, with reported roles in processing and regulating transcriptional programs linked to proteasome function. DDI2 activity connects to ubiquitin–proteasome system dynamics and cellular adaptation to proteotoxic stress, influencing turnover of misfolded or damaged proteins. Through these processes, DDI2 can affect pathways governing cell-cycle progression, apoptosis, and genome stability under stress conditions. Dysregulation of proteostasis and stress signaling is relevant to mechanisms studied in neurodegeneration, inflammation, and cancer biology, making Ddi2 a useful locus for pathway dissection in mouse models.

    DDI2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ddi2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ddi2 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 Ddi2 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 DDI2 protein expression.

    This CRISPR knockout system enables efficient generation of Ddi2-deficient cell models for investigation of DDI2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Ddi2 exon(s) critical for DDI2 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 Ddi2 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by DDI2 CRISPR/Cas9 KO Plasmid (m) and DDI2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ddi2 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by DDI2 HDR Plasmid (m) and DDI2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ddi2 homology arms to support homology-directed repair at defined Ddi2 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.