Diversin Double Nickase Plasmid (h): sc-405360-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Diversin 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
- Diversin Double Nickase Plasmid (h) and Diversin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ANKRD6. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Diversin Antibody (G-9): sc-365390
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Diversin Double Nickase Plasmid (h) | sc-405360-NIC | 20 µg | $410.00 |
ANKRD6 encodes Diversin, an ankyrin repeat–containing scaffold protein that coordinates signal transduction and cytoskeletal organization during development and tissue homeostasis. Diversin modulates Wnt signaling through interactions with core pathway components, linking β-catenin–dependent transcriptional outputs with planar cell polarity signaling and downstream JNK activity. Through these pathways, ANKRD6 influences cell polarity, migration, and differentiation programs that shape morphogenesis. Dysregulated Wnt pathway control and polarity signaling are frequently implicated in oncogenic transformation and congenital patterning defects, making Diversin a relevant target for mechanistic studies of pathway rewiring.
Diversin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ANKRD6 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ANKRD6. 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 ANKRD6 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 ANKRD6-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.