haptoglobin Double Nickase Plasmid (m): sc-420935-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- haptoglobin 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
- haptoglobin Double Nickase Plasmid (m) and haptoglobin Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Hp. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Haptoglobin α Antibody (C-8): sc-376893
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
haptoglobin Double Nickase Plasmid (m) | sc-420935-NIC | 20 µg | $410.00 |
Mouse Hp encodes haptoglobin, a secreted acute-phase glycoprotein that binds extracellular hemoglobin to limit heme-driven oxidative damage and conserve iron. The haptoglobin–hemoglobin complex is cleared primarily via CD163-mediated uptake in macrophages, linking Hp to innate immune regulation, redox homeostasis, and inflammatory signaling. Hp expression is strongly induced by cytokines such as IL-6 through acute-phase and JAK/STAT-associated transcriptional programs, making it a useful marker of systemic inflammation. Altered Hp biology is relevant to studies of hemolysis, anemia-associated tissue stress, liver acute-phase responses, and inflammatory remodeling in metabolic and cardiovascular phenotypes.
haptoglobin Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Hp locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Hp. 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 Hp 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 Hp-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.