twist Double Nickase Plasmid (h): sc-400108-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- twist 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
- twist Double Nickase Plasmid (h) and twist Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TWIST1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: twist Antibody (Twist2C1a): sc-81417
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
twist Double Nickase Plasmid (h) | sc-400108-NIC | 20 µg | $410.00 | |||
twist Double Nickase Plasmid (h2) | sc-400108-NIC-2 | 20 µg | $410.00 |
TWIST1 encodes twist, a basic helix-loop-helix transcription factor that regulates embryonic morphogenesis, lineage commitment, and cell-state plasticity through context-dependent transcriptional control of EMT programs. It modulates pathways governing cell migration, adhesion, and extracellular matrix remodeling, including crosstalk with TGF-β, WNT/β-catenin, and MAPK signaling. Dysregulated TWIST1 activity is linked to altered differentiation and invasive phenotypes, and germline or somatic perturbations have been associated with craniofacial developmental disorders and cancer progression. As a master regulator of mesenchymal traits, twist is widely studied in models of development, fibrosis-like remodeling, and tumor cell plasticity.
twist Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TWIST1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TWIST1. 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 TWIST1 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 TWIST1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.