DDC Double Nickase Plasmid (h): sc-403811-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DDC 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
- DDC Double Nickase Plasmid (h) and DDC Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DDC. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DDC Double Nickase Plasmid (h) | sc-403811-NIC | 20 µg | $410.00 | |||
DDC Double Nickase Plasmid (h2) | sc-403811-NIC-2 | 20 µg | $410.00 |
DDC encodes aromatic L-amino acid decarboxylase (AADC), a pyridoxal phosphate–dependent enzyme that catalyzes the decarboxylation of L-DOPA to dopamine and 5-hydroxytryptophan to serotonin. Through these reactions, DDC functions at a key branch point of monoamine neurotransmitter biosynthesis and influences downstream signaling networks that regulate neuronal excitability, motor control, mood-related pathways, and neuroendocrine communication. DDC activity intersects with tyrosine and tryptophan metabolism, presynaptic neurotransmitter homeostasis, and vesicular monoamine handling, linking metabolic flux to synaptic function. Dysregulation of DDC expression or enzymatic activity is relevant to studies of dopaminergic and serotonergic pathway perturbation, neurodevelopmental and movement-related phenotypes, and broader metabolic-neurotransmitter coupling mechanisms.
DDC Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DDC locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DDC. 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 DDC 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 DDC-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.