Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Heme Oxygenase 2 Double Nickase Plasmid (h): sc-402580-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Heme Oxygenase 2 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
- Heme Oxygenase 2 Double Nickase Plasmid (h) and Heme Oxygenase 2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HMOX2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Heme Oxygenase 2 Antibody (B-3): sc-17786
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Heme Oxygenase 2 Double Nickase Plasmid (h) | sc-402580-NIC | 20 µg | $410.00 | |||
Heme Oxygenase 2 Double Nickase Plasmid (h2) | sc-402580-NIC-2 | 20 µg | $410.00 |
HMOX2 encodes heme oxygenase 2 (HO-2), a constitutively expressed, ER-associated enzyme that catalyzes heme degradation to biliverdin, free iron, and carbon monoxide. Through regulation of intracellular heme and redox balance, HO-2 contributes to cytoprotection, mitochondrial function, and iron homeostasis, intersecting with oxidative stress responses and inflammatory signaling. HO-2 activity influences vascular tone and neuronal signaling via endogenous CO production, linking HMOX2 to pathways relevant to neurobiology and cardio-metabolic stress. Dysregulated heme handling and oxidative injury mechanisms implicate HMOX2 in studies of neurodegeneration, ischemia-reperfusion injury models, and inflammatory tissue damage without implying clinical outcomes.
Heme Oxygenase 2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HMOX2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HMOX2. 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 HMOX2 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 HMOX2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.