TRAIL CRISPR/Cas9 KO Plasmid (h): sc-418124
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRAIL 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 TRAIL 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: TRAIL Antibody (D-3): sc-8440
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRAIL CRISPR/Cas9 KO Plasmid (h) | sc-418124 | 20 µg | $397.00 |
Overview
TNFSF10 encodes TNF-related apoptosis-inducing ligand (TRAIL), a type II transmembrane cytokine that can be proteolytically released as a soluble ligand. TRAIL engages death receptors and initiates extrinsic apoptosis via FADD-dependent activation of caspase-8/10, with downstream crosstalk to mitochondrial amplification and modulation by NF-κB and MAPK signaling. Through these pathways, TRAIL contributes to immune surveillance, inflammatory regulation, and cell fate decisions that influence tissue homeostasis. Dysregulation of TNFSF10/TRAIL signaling has been associated with altered apoptosis sensitivity and immune evasion phenotypes observed across diverse cancer and inflammatory disease research contexts.
TRAIL CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TNFSF10 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TNFSF10 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 TNFSF10 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 TRAIL protein expression.
This CRISPR knockout system enables efficient generation of TNFSF10-deficient cell models for investigation of TRAIL signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TNFSF10 exon(s) critical for TRAIL 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 TNFSF10 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TRAIL CRISPR/Cas9 KO Plasmid (h) and TRAIL CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TNFSF10 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TRAIL HDR Plasmid (h) and TRAIL HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TNFSF10 homology arms to support homology-directed repair at defined TNFSF10 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.