Histamine H2 Receptor Double Nickase Plasmid (h): sc-401935-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Histamine H2 Receptor 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
- Histamine H2 Receptor Double Nickase Plasmid (h) and Histamine H2 Receptor Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HRH2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Histamine H2 Receptor Double Nickase Plasmid (h) | sc-401935-NIC | 20 µg | $410.00 |
HRH2 encodes the histamine H2 receptor, a G protein–coupled receptor that primarily couples to Gs to stimulate adenylyl cyclase, elevate cAMP, and activate PKA-dependent signaling. In epithelial and immune contexts, HRH2 signaling modulates secretion, barrier physiology, and inflammatory tone, integrating with second-messenger networks that influence gene expression and cellular metabolism. As part of histamine-driven communication in gastrointestinal and respiratory tissues, HRH2 is frequently studied in relation to mucosal homeostasis and dysregulated inflammatory microenvironments. Altered receptor signaling dynamics are also relevant to research on neuroimmune crosstalk and tumor-associated signaling pathways where cyclic AMP–dependent programs can reshape cell behavior.
Histamine H2 Receptor Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HRH2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HRH2. 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 HRH2 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 HRH2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.