TNFα-IP 8 CRISPR/Cas9 KO Plasmid (h): sc-411806
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TNFα-IP 8 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 TNFα-IP 8 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 | |
TNFα-IP 8 CRISPR/Cas9 KO Plasmid (h) | sc-411806 | 20 µg | $397.00 |
Overview
TNFAIP8 encodes TNFα-induced protein 8 (TNFα-IP 8), a cytoplasmic regulator of cell survival and inflammatory signaling that is induced by TNFα and other immune stimuli. TNFα-IP 8 has been linked to modulation of apoptosis, NF-κB–associated responses, and stress-adaptive programs that influence cell proliferation, migration, and immune homeostasis. Altered TNFAIP8 expression has been reported in multiple disease contexts, particularly in cancer- and inflammation-associated transcriptional signatures. As a result, TNFAIP8 is frequently studied as a node connecting cytokine-driven signaling to phenotypes such as resistance to cell death and changes in motility.
TNFα-IP 8 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TNFAIP8 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TNFAIP8 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 TNFAIP8 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 TNFα-IP 8 protein expression.
This CRISPR knockout system enables efficient generation of TNFAIP8-deficient cell models for investigation of TNFα-IP 8 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TNFAIP8 exon(s) critical for TNFα-IP 8 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 TNFAIP8 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TNFα-IP 8 CRISPR/Cas9 KO Plasmid (h) and TNFα-IP 8 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TNFAIP8 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TNFα-IP 8 HDR Plasmid (h) and TNFα-IP 8 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TNFAIP8 homology arms to support homology-directed repair at defined TNFAIP8 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.