Dematin Double Nickase Plasmid (h): sc-405148-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Dematin 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
- Dematin Double Nickase Plasmid (h) and Dematin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DMTN. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Dematin Double Nickase Plasmid (h) | sc-405148-NIC | 20 µg | $410.00 | |||
Dematin Double Nickase Plasmid (h2) | sc-405148-NIC-2 | 20 µg | $410.00 |
DMTN encodes dematin, an actin-binding cytoskeletal regulator enriched at the cell cortex and membrane–cytoskeleton interfaces, where it contributes to filament organization, cell shape, and mechanical stability. Dematin associates with actin remodeling machinery and supports processes such as membrane ruffling, adhesion dynamics, and cytoskeletal coupling to signaling complexes. Through these roles, DMTN has been studied in contexts of altered cell architecture and motility that are frequently implicated in cancer cell behavior and other disorders involving cytoskeletal dysregulation. Its expression and functional perturbation provide a tractable readout for pathways governing cortical actin structure, cell integrity, and stress responses.
Dematin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DMTN locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DMTN. 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 DMTN 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 DMTN-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.