Xanthine Oxidase CRISPR/Cas9 KO Plasmid (h): sc-401185
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Xanthine Oxidase 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 Xanthine Oxidase 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: Xanthine Oxidase Antibody (A-3): sc-398548
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Xanthine Oxidase CRISPR/Cas9 KO Plasmid (h) | sc-401185 | 20 µg | $397.00 |
Overview
Human XDH encodes xanthine oxidase, a molybdenum-dependent enzyme that catalyzes the terminal steps of purine catabolism by converting hypoxanthine to xanthine and xanthine to uric acid. During these reactions it can generate reactive oxygen species, linking purine metabolism to redox homeostasis and oxidative stress signaling. Xanthine oxidase activity influences endothelial function, inflammatory responses, and metabolic adaptation, and dysregulation has been associated with hyperuricemia-related biology, ischemia–reperfusion injury mechanisms, and cardiometabolic disease-relevant oxidative pathways. XDH is also studied in the context of hepatic metabolism and systemic nitrogen balance, where altered purine turnover can reshape cellular stress responses.
Xanthine Oxidase CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the XDH gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the XDH 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 XDH 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 Xanthine Oxidase protein expression.
This CRISPR knockout system enables efficient generation of XDH-deficient cell models for investigation of Xanthine Oxidase signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting XDH exon(s) critical for Xanthine Oxidase 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 XDH genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Xanthine Oxidase CRISPR/Cas9 KO Plasmid (h) and Xanthine Oxidase CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the XDH locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Xanthine Oxidase HDR Plasmid (h) and Xanthine Oxidase HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by XDH homology arms to support homology-directed repair at defined XDH 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.