ZNF74 Double Nickase Plasmid (h): sc-411084-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ZNF74 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
- ZNF74 Double Nickase Plasmid (h) and ZNF74 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ZNF74. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ZNF74 Antibody (B-11): sc-390612
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZNF74 Double Nickase Plasmid (h) | sc-411084-NIC | 20 µg | $410.00 | |||
ZNF74 Double Nickase Plasmid (h2) | sc-411084-NIC-2 | 20 µg | $410.00 |
ZNF74 encodes a human KRAB zinc-finger protein implicated in sequence-specific DNA binding and transcriptional repression, supporting chromatin-dependent regulation of gene expression. It has been studied in the context of nuclear organization and transcriptional control programs that shape cell identity and stress responses. Genomic variation and altered expression of ZNF74 have been associated with neuropsychiatric and developmental phenotypes, consistent with roles in regulatory networks sensitive to dosage and epigenetic state. These features make ZNF74 a useful target for interrogating transcriptional repression mechanisms and downstream pathway remodeling in human cell models.
ZNF74 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ZNF74 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ZNF74. 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 ZNF74 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 ZNF74-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.