Hemoglobin δ Double Nickase Plasmid (h): sc-401567-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Hemoglobin δ 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
- Hemoglobin δ Double Nickase Plasmid (h) and Hemoglobin δ Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HBD. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Hemoglobin δ Double Nickase Plasmid (h) | sc-401567-NIC | 20 µg | $410.00 | |||
Hemoglobin δ Double Nickase Plasmid (h2) | sc-401567-NIC-2 | 20 µg | $410.00 |
HBD encodes the delta subunit of hemoglobin (Hemoglobin δ), a heme-containing oxygen transport protein that assembles with alpha-globin to form hemoglobin A2 in erythroid cells. Its expression is tightly coupled to erythropoiesis and heme biosynthesis programs, integrating with globin gene regulation at the β-globin locus and red blood cell maturation pathways. Variation in HBD and its regulatory context can influence hemoglobin composition and is studied alongside β-like globin genes in disorders affecting hemoglobin balance and erythrocyte physiology. As a marker within the globin cluster, HBD is also useful for probing locus control, developmental switching, and transcriptional regulation in hematopoietic differentiation models.
Hemoglobin δ Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HBD locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HBD. 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 HBD 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 HBD-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.