TRAF4 CRISPR/Cas9 KO Plasmid (m): sc-423495
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRAF4 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 TRAF4 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: TRAF4 Antibody (B-9): sc-390232
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRAF4 CRISPR/Cas9 KO Plasmid (m) | sc-423495 | 20 µg | $397.00 |
Overview
Tumor necrosis factor receptor–associated factor 4 (TRAF4), encoded by the mouse Traf4 gene, is an adaptor and E3 ubiquitin ligase that couples receptor-proximal signaling to downstream kinase and transcriptional networks. TRAF4 participates in regulation of NF-κB and MAPK signaling and has been linked to cytoskeletal dynamics, cell polarity, and epithelial barrier-related processes through context-dependent interactions with membrane and junctional complexes. In immune and epithelial compartments, Traf4 activity can influence inflammatory signaling amplitude and cellular stress responses. Dysregulated TRAF4-associated pathways have been studied in relation to tumor biology, tissue remodeling, and inflammatory disease mechanisms, making Traf4 a useful target for pathway dissection in mouse models and cell systems.
TRAF4 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Traf4 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Traf4 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 Traf4 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 TRAF4 protein expression.
This CRISPR knockout system enables efficient generation of Traf4-deficient cell models for investigation of TRAF4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Traf4 exon(s) critical for TRAF4 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 Traf4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TRAF4 CRISPR/Cas9 KO Plasmid (m) and TRAF4 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Traf4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TRAF4 HDR Plasmid (m) and TRAF4 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Traf4 homology arms to support homology-directed repair at defined Traf4 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.