HDC Double Nickase Plasmid (h): sc-403606-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HDC 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
- HDC Double Nickase Plasmid (h) and HDC Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HDC. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HDC Double Nickase Plasmid (h) | sc-403606-NIC | 20 µg | $410.00 | |||
HDC Double Nickase Plasmid (h2) | sc-403606-NIC-2 | 20 µg | $410.00 |
Histidine decarboxylase (HDC) catalyzes the pyridoxal phosphate–dependent conversion of L-histidine to histamine, a bioactive amine that regulates inflammation, gastric acid secretion, neurotransmission, and vascular permeability. In immune and barrier tissues, HDC-driven histamine production shapes mast cell and basophil effector responses through histamine receptor signaling and downstream GPCR pathways that modulate cytokine release and leukocyte trafficking. HDC activity is also linked to metabolic and redox programs via biogenic amine turnover and can influence cell–cell communication within tissue microenvironments. Dysregulated HDC expression or histamine biosynthesis has been associated with allergic inflammation, gastrointestinal disorders, and neuroinflammatory processes, making HDC a useful target for mechanistic studies of histaminergic signaling.
HDC Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HDC locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HDC. 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 HDC 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 HDC-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.