ZNF532 Double Nickase Plasmid (h): sc-409998-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ZNF532 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
- ZNF532 Double Nickase Plasmid (h) and ZNF532 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ZNF532. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZNF532 Double Nickase Plasmid (h) | sc-409998-NIC | 20 µg | $410.00 |
ZNF532 encodes a zinc finger transcription factor implicated in sequence-specific DNA binding and regulation of gene expression programs that shape cell identity and differentiation. As a putative nuclear regulator, ZNF532 is linked to chromatin-associated processes and transcriptional networks that intersect with developmental pathways and lineage-specific transcriptional control. Altered regulation of zinc finger transcription factors can perturb epigenetic and transcriptional homeostasis, making ZNF532 a relevant node for studies of gene regulatory circuitry. In cancer biology and systems-level genomics, ZNF532 has been examined in the context of transcriptional dysregulation and genomic alterations that influence cell state and tumor-associated phenotypes.
ZNF532 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ZNF532 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ZNF532. 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 ZNF532 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 ZNF532-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.