DMRT2 Double Nickase Plasmid (m): sc-432587-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DMRT2 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
- DMRT2 Double Nickase Plasmid (m) and DMRT2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Dmrt2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DMRT2 Double Nickase Plasmid (m) | sc-432587-NIC | 20 µg | $410.00 | |||
DMRT2 Double Nickase Plasmid (m2) | sc-432587-NIC-2 | 20 µg | $410.00 |
Dmrt2 encodes DMRT2, a DM domain transcription factor that regulates embryonic patterning programs, including somitogenesis and axial skeletal development, by coordinating lineage-specific transcriptional networks. In mouse, DMRT2 contributes to somite polarity and left–right asymmetry cues that shape musculoskeletal organization during early development. Its activity intersects with developmental signaling pathways that govern mesoderm differentiation and morphogenetic timing, making it a useful node for studying transcriptional control of tissue specification. Dysregulated Dmrt2 function has been linked to congenital developmental abnormalities in model systems, supporting its relevance for mechanistic studies of gene regulatory circuits underlying morphogenesis.
DMRT2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Dmrt2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Dmrt2. 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 Dmrt2 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 Dmrt2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.