ZNF138 Double Nickase Plasmid (h): sc-417406-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ZNF138 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
- ZNF138 Double Nickase Plasmid (h) and ZNF138 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ZNF138. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZNF138 Double Nickase Plasmid (h) | sc-417406-NIC | 20 µg | $410.00 | |||
ZNF138 Double Nickase Plasmid (h2) | sc-417406-NIC-2 | 20 µg | $410.00 |
ZNF138 encodes a KRAB-domain zinc finger protein that is predicted to function as a sequence-specific transcriptional regulator, coupling DNA-binding by C2H2 zinc fingers to epigenetic silencing through KRAB-associated co-repressor complexes. By recruiting chromatin-modifying factors, ZNF138 is expected to influence heterochromatin organization, transcriptional repression, and maintenance of cell-type–specific gene expression programs. Dysregulation of KRAB-ZNF networks has been linked to altered genome stability, aberrant differentiation, and oncogenic transcriptional states, supporting investigation of ZNF138 in disease-relevant gene regulatory pathways. Human ZNF138 is therefore a useful target for studying chromatin-dependent control of transcription and its impact on cellular phenotype.
ZNF138 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ZNF138 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ZNF138. 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 ZNF138 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 ZNF138-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.