
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD30 CRISPR/Cas9 KO Plasmid (m) | sc-423446 | 20 µg | $397.00 |
Mouse Tnfrsf8 encodes CD30, a TNF receptor superfamily member expressed on activated lymphocytes that transduces signals through adaptor proteins such as TRAFs to modulate NF-κB and MAPK pathway activity. CD30-dependent signaling influences T cell and B cell activation programs, cytokine production, and survival decisions that shape immune homeostasis. In murine models, altered CD30 function has been used to interrogate mechanisms of lymphocyte differentiation, immune regulation, and inflammation within lymphoid tissues. Dysregulated CD30-associated pathways are relevant to studies of aberrant immune activation and lymphoproliferative phenotypes, supporting its utility as a genetic node for immunology research.
CD30 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tnfrsf8 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tnfrsf8 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 Tnfrsf8 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 CD30 protein expression.
This CRISPR knockout system enables efficient generation of Tnfrsf8-deficient cell models for investigation of CD30 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
CRISPRs +/- HDRs
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.