TWEAK CRISPR/Cas9 KO Plasmid (h): sc-401202
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TWEAK 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 TWEAK 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: TWEAK Antibody (CARL-1): sc-56248
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TWEAK CRISPR/Cas9 KO Plasmid (h) | sc-401202 | 20 µg | $397.00 |
Overview
TNFSF12 encodes the cytokine TWEAK (TNF-like weak inducer of apoptosis), a type II transmembrane protein that can be released as a soluble ligand and signals primarily through the FN14/TNFRSF12A receptor. TWEAK–FN14 engagement modulates NF-κB and MAPK pathway activity to influence cell survival, proliferation, migration, differentiation, and inflammatory gene expression, with context-dependent effects on apoptosis and tissue remodeling. This axis is implicated in regulation of angiogenic and fibrotic programs, as well as immune cell recruitment and cytokine networks within damaged or stressed tissues. Dysregulated TWEAK/FN14 signaling has been associated with inflammatory and autoimmune pathobiology, neuroinflammatory processes, and tumor microenvironment remodeling, supporting mechanistic studies in immunology and cancer biology.
TWEAK CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TNFSF12 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TNFSF12 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 TNFSF12 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 TWEAK protein expression.
This CRISPR knockout system enables efficient generation of TNFSF12-deficient cell models for investigation of TWEAK signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TNFSF12 exon(s) critical for TWEAK 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 TNFSF12 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TWEAK CRISPR/Cas9 KO Plasmid (h) and TWEAK CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TNFSF12 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TWEAK HDR Plasmid (h) and TWEAK HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TNFSF12 homology arms to support homology-directed repair at defined TNFSF12 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.