SDHD Double Nickase Plasmid (m): sc-426271-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SDHD Double Nickase Plasmid (m) 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
- SDHD Double Nickase Plasmid (m) and SDHD Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Sdhd. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SDHD Double Nickase Plasmid (m) | sc-426271-NIC | 20 µg | $410.00 |
Mouse Sdhd encodes the SDHD subunit of succinate dehydrogenase (mitochondrial complex II), an essential component of the tricarboxylic acid cycle and the electron transport chain that couples succinate oxidation to ubiquinone reduction. SDHD supports mitochondrial respiration, redox homeostasis, and cellular energy metabolism, linking carbon flux to oxidative phosphorylation. Disruption of SDH complex integrity can cause succinate accumulation and downstream signaling changes that affect hypoxia-responsive pathways and epigenetic regulation via α-ketoglutarate–dependent dioxygenases. Sdhd is therefore widely studied in models of mitochondrial dysfunction, metabolic rewiring, and stress responses relevant to tumor-associated biology and neuroendocrine system research.
SDHD Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Sdhd locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Sdhd. 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 Sdhd 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 Sdhd-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.