SETX CRISPR/Cas9 KO Plasmid (h): sc-402354
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SETX 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 SETX 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: SETX Antibody (QQ-7): sc-100319
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SETX CRISPR/Cas9 KO Plasmid (h) | sc-402354 | 20 µg | $397.00 |
Overview
SETX (senataxin) encodes a DNA/RNA helicase that resolves R-loops and other nucleic acid secondary structures arising during transcription, thereby coordinating transcription elongation with genome maintenance. It functions at the interface of transcription-coupled DNA damage response, replication stress control, and RNA processing, helping limit double-strand breaks and aberrant recombination at actively transcribed loci. SETX activity is linked to pathways involving RNA polymerase II, DNA repair factors, and surveillance of stalled transcription complexes. Dysregulation or mutation of SETX is associated with neurodegenerative phenotypes and genome instability syndromes, making it a relevant target for mechanistic studies of transcription-associated DNA damage and neuronal vulnerability.
SETX CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SETX gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SETX 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 SETX 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 SETX protein expression.
This CRISPR knockout system enables efficient generation of SETX-deficient cell models for investigation of SETX signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SETX exon(s) critical for SETX 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 SETX genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SETX CRISPR/Cas9 KO Plasmid (h) and SETX CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SETX locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SETX HDR Plasmid (h) and SETX HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SETX homology arms to support homology-directed repair at defined SETX 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.