SFXN2 CRISPR/Cas9 KO Plasmid (h): sc-414132
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SFXN2 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 SFXN2 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 | |
SFXN2 CRISPR/Cas9 KO Plasmid (h) | sc-414132 | 20 µg | $397.00 |
Overview
SFXN2 (sideroflexin 2) is an inner mitochondrial membrane carrier implicated in maintaining mitochondrial metabolic homeostasis and supporting oxidative phosphorylation–linked processes. As a member of the sideroflexin family, it is associated with transport functions that influence one‑carbon metabolism, amino acid utilization, and redox balance, thereby affecting mitochondrial respiration and reactive oxygen species handling. Altered mitochondrial transport and bioenergetic state can modulate stress signaling, innate immune pathways, and cell fate decisions. Consequently, SFXN2 is of interest in research areas connecting mitochondrial dysfunction to cardiometabolic and neurodegeneration-related phenotypes, as well as cancer cell metabolic remodeling.
SFXN2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SFXN2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SFXN2 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 SFXN2 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 SFXN2 protein expression.
This CRISPR knockout system enables efficient generation of SFXN2-deficient cell models for investigation of SFXN2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SFXN2 exon(s) critical for SFXN2 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 SFXN2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SFXN2 CRISPR/Cas9 KO Plasmid (h) and SFXN2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SFXN2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SFXN2 HDR Plasmid (h) and SFXN2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SFXN2 homology arms to support homology-directed repair at defined SFXN2 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.