PDF Double Nickase Plasmid (h): sc-409495-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PDF Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- PDF Double Nickase Plasmid (h) and PDF Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PDF. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PDF Double Nickase Plasmid (h) | sc-409495-NIC | 20 µg | $410.00 |
Human PDF (peptide deformylase, mitochondrial) encodes a metalloprotease that removes N-formyl groups from mitochondrially encoded nascent polypeptides, a key step in mitochondrial translation quality control and maturation of oxidative phosphorylation components. By coupling formyl group removal to downstream processing and stability of mitochondrial proteins, PDF supports respiratory chain assembly, mitochondrial proteostasis, and cellular energy metabolism. Perturbation of mitochondrial translation and proteostasis is widely linked to bioenergetic stress responses, altered reactive oxygen species handling, and apoptosis-related signaling. Accordingly, PDF is frequently studied in the context of mitochondrial dysfunction mechanisms relevant to neurodegeneration, cardiometabolic phenotypes, and cancer cell metabolic adaptation.
PDF Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PDF locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PDF. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt PDF function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of PDF-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.