TNF-R2 CRISPR/Cas9 KO Plasmid (m): sc-423443
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TNF-R2 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 TNF-R2 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: TNF-R2 Antibody (D-2): sc-8041
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TNF-R2 CRISPR/Cas9 KO Plasmid (m) | sc-423443 | 20 µg | $397.00 |
Overview
Tnfrsf1b encodes TNF-R2 (TNFRSF1B), a TNF receptor predominantly expressed on immune, endothelial, and certain stromal cell populations that preferentially responds to membrane-bound TNF. TNF-R2 signaling engages adaptor proteins to regulate NF-κB and MAPK pathway activity, shaping cell survival programs, cytokine responses, and tissue remodeling. In lymphocyte biology, TNF-R2 is closely linked to regulatory T cell stability and activation-induced signaling that modulates inflammatory balance. Dysregulated TNF-R2 axis activity has been implicated in models of chronic inflammation, autoimmunity, and neuroinflammatory processes, making it a useful node for mechanistic studies of TNF pathway specificity.
TNF-R2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tnfrsf1b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tnfrsf1b 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 Tnfrsf1b 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 TNF-R2 protein expression.
This CRISPR knockout system enables efficient generation of Tnfrsf1b-deficient cell models for investigation of TNF-R2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Tnfrsf1b exon(s) critical for TNF-R2 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 Tnfrsf1b genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TNF-R2 CRISPR/Cas9 KO Plasmid (m) and TNF-R2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tnfrsf1b locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TNF-R2 HDR Plasmid (m) and TNF-R2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tnfrsf1b homology arms to support homology-directed repair at defined Tnfrsf1b 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.