Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
PDK4 Double Nickase Plasmid (h): sc-401355-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PDK4 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
- PDK4 Double Nickase Plasmid (h) and PDK4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PDK4. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: PDK4 Antibody (A-7): sc-518103
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PDK4 Double Nickase Plasmid (h) | sc-401355-NIC | 20 µg | $410.00 | |||
PDK4 Double Nickase Plasmid (h2) | sc-401355-NIC-2 | 20 µg | $410.00 |
PDK4 encodes pyruvate dehydrogenase kinase 4, a mitochondrial enzyme that phosphorylates and inhibits the pyruvate dehydrogenase complex, thereby reducing conversion of pyruvate to acetyl‑CoA and shifting carbon flux from glucose oxidation toward fatty acid utilization. Its expression is regulated by nutrient status and hormones and integrates signals from pathways such as PPAR signaling, insulin/FOXO-mediated transcriptional control, and cellular energy sensing that modulate mitochondrial metabolism. Altered PDK4 activity is associated with metabolic remodeling and mitochondrial substrate switching observed in contexts including insulin resistance, obesity, type 2 diabetes, and cardiac metabolic stress. Because PDK4 influences oxidative phosphorylation input and acetyl‑CoA availability, it is frequently studied in models of metabolic adaptation, oxidative stress, and inflammation-linked rewiring of energy metabolism.
PDK4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PDK4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PDK4. 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 PDK4 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 PDK4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.