CPOX CRISPR/Cas9 KO Plasmid (h): sc-405130
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CPOX 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 CPOX 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: CPOX Antibody (B-9): sc-393388
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CPOX CRISPR/Cas9 KO Plasmid (h) | sc-405130 | 20 µg | $397.00 |
Overview
Coproporphyrinogen oxidase (CPOX) is a mitochondrial enzyme that catalyzes oxidative decarboxylation of coproporphyrinogen III to protoporphyrinogen IX, a key late step in the heme biosynthesis pathway. By controlling flux through porphyrin metabolism, CPOX supports heme-dependent processes including mitochondrial respiration, cytochrome function, and cellular redox homeostasis. Disruption of CPOX activity is linked to accumulation of porphyrin intermediates and has been associated with hereditary coproporphyria and related metabolic phenotypes. CPOX therefore serves as a mechanistically informative node for studying mitochondrial metabolism, oxidative stress responses, and heme/porphyrin pathway regulation in human cells.
CPOX CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CPOX gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CPOX 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 CPOX 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 CPOX protein expression.
This CRISPR knockout system enables efficient generation of CPOX-deficient cell models for investigation of CPOX signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting CPOX exon(s) critical for CPOX 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 CPOX genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CPOX CRISPR/Cas9 KO Plasmid (h) and CPOX CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CPOX locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CPOX HDR Plasmid (h) and CPOX HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CPOX homology arms to support homology-directed repair at defined CPOX 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.