Histamine H4 Receptor Double Nickase Plasmid (m): sc-432522-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Histamine H4 Receptor 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
- Histamine H4 Receptor Double Nickase Plasmid (m) and Histamine H4 Receptor Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Hrh4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Histamine H4 Receptor Double Nickase Plasmid (m) | sc-432522-NIC | 20 µg | $410.00 |
Mouse Hrh4 encodes the histamine H4 receptor (HRH4), a G protein–coupled receptor predominantly linked to Gi/o signaling that modulates cAMP levels and downstream MAPK/ERK and PI3K-associated pathways. HRH4 is expressed in multiple immune cell populations where it influences chemotaxis, cytokine release, and leukocyte trafficking, integrating histaminergic cues with inflammatory microenvironments. Through these processes, HRH4 has been studied in models of allergic inflammation, pruritus, asthma-like airway responses, and broader immune dysregulation. Dissecting Hrh4 function helps clarify how histamine receptor signaling shapes innate and adaptive immune behaviors in vivo.
Histamine H4 Receptor Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Hrh4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Hrh4. 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 Hrh4 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 Hrh4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.