HAH1 Double Nickase Plasmid (h): sc-404870-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HAH1 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
- HAH1 Double Nickase Plasmid (h) and HAH1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ATOX1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: HAH1 Antibody (D-9): sc-398742
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HAH1 Double Nickase Plasmid (h) | sc-404870-NIC | 20 µg | $410.00 | |||
HAH1 Double Nickase Plasmid (h2) | sc-404870-NIC-2 | 20 µg | $410.00 |
ATOX1 (HAH1) encodes a cytosolic copper chaperone that binds Cu(I) and delivers it to P-type ATPases ATP7A and ATP7B, supporting copper loading into the secretory pathway and maintenance of cellular copper homeostasis. Through this trafficking role, HAH1 influences the maturation of copper-dependent enzymes and helps coordinate redox balance and metal-responsive signaling processes. Dysregulated ATOX1-mediated copper handling has been linked to altered oxidative stress responses and pathways relevant to disorders of copper metabolism, providing a mechanistic entry point for studying metal-dependent proteostasis. In human cells, ATOX1 also serves as a model node for examining how copper distribution interfaces with intracellular trafficking and stress adaptation.
HAH1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ATOX1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ATOX1. 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 ATOX1 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 ATOX1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.