ZFP106 Double Nickase Plasmid (h): sc-405869-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ZFP106 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
- ZFP106 Double Nickase Plasmid (h) and ZFP106 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ZNF106. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZFP106 Double Nickase Plasmid (h) | sc-405869-NIC | 20 µg | $410.00 | |||
ZFP106 Double Nickase Plasmid (h2) | sc-405869-NIC-2 | 20 µg | $410.00 |
ZNF106 encodes ZFP106, a zinc finger protein implicated in nuclear RNA metabolism and regulation of gene expression programs that support neuronal and muscle cell homeostasis. ZFP106 has been associated with RNA processing and transcript stability, linking it to pathways that coordinate differentiation, stress responses, and maintenance of long-lived cell types. Genetic studies connect ZNF106 dysfunction with neuromuscular and neurodegenerative phenotypes, consistent with roles in motor neuron integrity and muscle maintenance. These features make ZNF106 a useful target for investigating how RNA-handling factors shape cellular vulnerability and degeneration-associated transcriptional changes.
ZFP106 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ZNF106 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ZNF106. 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 ZNF106 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 ZNF106-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.