Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
DEDD CRISPR/Cas9 KO Plasmid (m): sc-423450
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DEDD 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 DEDD 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: DEDD Antibody (H-4): sc-271192
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DEDD CRISPR/Cas9 KO Plasmid (m) | sc-423450 | 20 µg | $397.00 |
Overview
Dedd encodes the death effector domain-containing DNA-binding protein DEDD, a regulator of apoptosis and transcriptional programs linked to caspase signaling. DEDD has been reported to associate with the nucleolus and chromatin, connecting death receptor pathways to downstream execution mechanisms and cell cycle-associated control of gene expression. In mouse models, perturbation of Dedd can influence the balance between survival and programmed cell death, processes central to immune homeostasis and tissue remodeling. Dysregulated apoptosis and stress-response signaling involving DEDD is relevant to studies of inflammatory disorders, neurodegeneration, and cancer biology where altered cell fate decisions contribute to disease phenotypes.
DEDD CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Dedd gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Dedd 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 Dedd 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 DEDD protein expression.
This CRISPR knockout system enables efficient generation of Dedd-deficient cell models for investigation of DEDD signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Dedd exon(s) critical for DEDD 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 Dedd genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by DEDD CRISPR/Cas9 KO Plasmid (m) and DEDD CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Dedd locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by DEDD HDR Plasmid (m) and DEDD HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Dedd homology arms to support homology-directed repair at defined Dedd 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.