MTFmt CRISPR/Cas9 KO Plasmid (h): sc-407106
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MTFmt 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 MTFmt 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 | |
MTFmt CRISPR/Cas9 KO Plasmid (h) | sc-407106 | 20 µg | $397.00 |
Overview
MTFMT encodes mitochondrial methionyl-tRNA formyltransferase (MTFmt), an enzyme that formylates the initiator Met-tRNAMet to generate fMet-tRNA, a key substrate for mitochondrial translation initiation. This activity supports efficient synthesis of oxidative phosphorylation (OXPHOS) components encoded by mitochondrial DNA and helps maintain respiratory chain integrity and ATP production. Disruption of MTFmt perturbs mitochondrial proteostasis and can trigger bioenergetic stress responses, linking the gene to pathways governing mitochondrial gene expression, electron transport, and metabolic homeostasis. Pathogenic variation or reduced function is associated with mitochondrial translation defects and phenotypes consistent with combined OXPHOS deficiency, making MTFMT a relevant target in studies of mitochondrial disease mechanisms.
MTFmt CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the MTFMT gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MTFMT 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 MTFMT 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 MTFmt protein expression.
This CRISPR knockout system enables efficient generation of MTFMT-deficient cell models for investigation of MTFmt signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting MTFMT exon(s) critical for MTFmt 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 MTFMT genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by MTFmt CRISPR/Cas9 KO Plasmid (h) and MTFmt CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the MTFMT locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by MTFmt HDR Plasmid (h) and MTFmt HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by MTFMT homology arms to support homology-directed repair at defined MTFMT 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.