Trx CRISPR/Cas9 KO Plasmid (m): sc-423563
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Trx 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 Trx 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: Trx Antibody (D-4): sc-271281
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Trx CRISPR/Cas9 KO Plasmid (m) | sc-423563 | 20 µg | $397.00 |
Overview
Mouse Txn1 encodes thioredoxin (Trx), a conserved oxidoreductase that maintains cellular redox homeostasis by catalyzing disulfide bond reduction in target proteins. Trx functions within the thioredoxin system alongside thioredoxin reductase and NADPH to regulate redox-sensitive signaling, including MAPK and NF-κB pathways, and to buffer reactive oxygen species generated during metabolism and inflammation. Through control of protein folding, DNA synthesis support via ribonucleotide reductase, and modulation of apoptosis and autophagy, Txn1 contributes broadly to cellular stress adaptation. Dysregulated thioredoxin activity is frequently associated with oxidative stress phenotypes relevant to neurodegeneration, metabolic dysfunction, and inflammatory pathology, making Txn1 a useful node for mechanistic studies of redox-driven disease processes.
Trx CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Txn1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Txn1 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 Txn1 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 Trx protein expression.
This CRISPR knockout system enables efficient generation of Txn1-deficient cell models for investigation of Trx signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Txn1 exon(s) critical for Trx 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 Txn1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Trx CRISPR/Cas9 KO Plasmid (m) and Trx CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Txn1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Trx HDR Plasmid (m) and Trx HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Txn1 homology arms to support homology-directed repair at defined Txn1 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.