ZNF322A Double Nickase Plasmid (h): sc-417187-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ZNF322A 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
- ZNF322A Double Nickase Plasmid (h) and ZNF322A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ZNF322. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZNF322A Double Nickase Plasmid (h) | sc-417187-NIC | 20 µg | $410.00 | |||
ZNF322A Double Nickase Plasmid (h2) | sc-417187-NIC-2 | 20 µg | $410.00 |
ZNF322 (ZNF322A) encodes a human KRAB domain–containing C2H2 zinc-finger transcription factor implicated in sequence-specific DNA binding and transcriptional repression programs that shape cell state and stress-responsive gene expression. Reported functions link ZNF322A to regulation of proliferation, survival, and motility-associated transcriptional networks, consistent with roles in chromatin-associated control of downstream signaling pathways. Dysregulated ZNF322A expression has been associated with oncogenic phenotypes in multiple contexts, including altered epithelial programs and invasion-related signatures. As a nuclear regulatory protein, it is a useful target for dissecting transcriptional circuitry, chromatin-dependent gene control, and pathway rewiring in disease-relevant models.
ZNF322A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ZNF322 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ZNF322. 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 ZNF322 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 ZNF322-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.