TRAF7 CRISPR/Cas9 KO Plasmid (h): sc-404992
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRAF7 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 TRAF7 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRAF7 CRISPR/Cas9 KO Plasmid (h) | sc-404992 | 20 µg | $397.00 |
Overview
TRAF7 encodes an E3 ubiquitin ligase and adaptor protein in the TNF receptor–associated factor family that integrates receptor-proximal signaling with ubiquitin-dependent control of protein stability. TRAF7 regulates multiple stress and inflammatory pathways, including MAPK and NF-κB signaling, and influences apoptosis, cytoskeletal organization, and cell polarity through ubiquitination of key signaling components. Dysregulated TRAF7 activity and recurrent TRAF7 mutations have been reported in several tumor contexts, supporting roles in oncogenic signaling, transcriptional control, and microenvironmental responses. As a pathway node, TRAF7 is frequently studied in proteostasis, signal transduction, and context-dependent growth control.
TRAF7 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TRAF7 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TRAF7 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 TRAF7 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 TRAF7 protein expression.
This CRISPR knockout system enables efficient generation of TRAF7-deficient cell models for investigation of TRAF7 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TRAF7 exon(s) critical for TRAF7 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 TRAF7 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TRAF7 CRISPR/Cas9 KO Plasmid (h) and TRAF7 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TRAF7 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TRAF7 HDR Plasmid (h) and TRAF7 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TRAF7 homology arms to support homology-directed repair at defined TRAF7 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.