mitochondrial ferritin CRISPR/Cas9 KO Plasmid (h): sc-401694
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- mitochondrial ferritin 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 mitochondrial ferritin 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: mitochondrial ferritin Antibody (6G3): sc-517048
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
mitochondrial ferritin CRISPR/Cas9 KO Plasmid (h) | sc-401694 | 20 µg | $397.00 |
Overview
FTMT encodes mitochondrial ferritin, an iron-storage protein localized to the mitochondrial matrix that sequesters excess iron and limits iron-driven reactive oxygen species generation. By buffering labile iron pools, FTMT influences mitochondrial redox homeostasis, oxidative phosphorylation integrity, and the cellular response to metabolic and oxidative stress. Its activity intersects with iron metabolism and heme/Fe–S cluster biology, linking mitochondrial function to broader iron-handling pathways. Dysregulated FTMT expression has been associated with altered iron accumulation and oxidative injury phenotypes relevant to neurodegeneration, anemia-related stress responses, and mitochondrial dysfunction models.
mitochondrial ferritin CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the FTMT gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the FTMT 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 FTMT 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 mitochondrial ferritin protein expression.
This CRISPR knockout system enables efficient generation of FTMT-deficient cell models for investigation of mitochondrial ferritin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting FTMT exon(s) critical for mitochondrial ferritin 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 FTMT genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by mitochondrial ferritin CRISPR/Cas9 KO Plasmid (h) and mitochondrial ferritin CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the FTMT locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by mitochondrial ferritin HDR Plasmid (h) and mitochondrial ferritin HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by FTMT homology arms to support homology-directed repair at defined FTMT 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.