ASCL1 Double Nickase Plasmid (m): sc-421562-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ASCL1 Double Nickase Plasmid (m) 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
- ASCL1 Double Nickase Plasmid (m) and ASCL1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ascl1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ASCL1 Antibody (G-7): sc-390794
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ASCL1 Double Nickase Plasmid (m) | sc-421562-NIC | 20 µg | $410.00 | |||
ASCL1 Double Nickase Plasmid (m2) | sc-421562-NIC-2 | 20 µg | $410.00 |
Achaete-scute family bHLH transcription factor 1 (ASCL1; Ascl1) is a proneural regulator that drives neuronal lineage commitment and differentiation in the developing mouse nervous system. By binding E-box motifs, ASCL1 coordinates transcriptional programs that couple cell-cycle exit with neurogenesis, interacting with Notch signaling, chromatin remodeling, and bHLH regulatory networks that shape neural progenitor fate decisions. Altered ASCL1 activity is used to model dysregulated differentiation states relevant to developmental neurobiology and to context-dependent neuroendocrine-like transcriptional programs observed in disease-associated cell state transitions.
ASCL1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ascl1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ascl1. 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 Ascl1 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 Ascl1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.