FDX1L CRISPR/Cas9 KO Plasmid (m): sc-426948
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FDX1L 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 FDX1L 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 | |
FDX1L CRISPR/Cas9 KO Plasmid (m) | sc-426948 | 20 µg | $397.00 |
Overview
Fdx1l encodes ferredoxin 1-like (FDX1L), a mitochondrial ferredoxin family protein implicated in electron transfer reactions that support mitochondrial redox balance and oxidative metabolism. By shuttling electrons to mitochondrial enzymes, FDX1L is positioned to influence pathways linked to iron–sulfur cluster maintenance, steroidogenic or heme-associated reactions, and broader mitochondrial homeostasis. Perturbation of mitochondrial ferredoxin-dependent processes can alter reactive oxygen species handling, metabolic flexibility, and stress responses, making Fdx1l relevant to studies of mitochondrial dysfunction. In mouse systems, Fdx1l provides a tractable node for investigating how mitochondrial electron transfer interfaces with cellular metabolism and disease-relevant phenotypes driven by impaired mitochondrial activity.
FDX1L CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Fdx1l gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Fdx1l 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 Fdx1l 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 FDX1L protein expression.
This CRISPR knockout system enables efficient generation of Fdx1l-deficient cell models for investigation of FDX1L signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Fdx1l exon(s) critical for FDX1L 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 Fdx1l genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FDX1L CRISPR/Cas9 KO Plasmid (m) and FDX1L CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Fdx1l locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FDX1L HDR Plasmid (m) and FDX1L HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Fdx1l homology arms to support homology-directed repair at defined Fdx1l 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.