DTX3L Double Nickase Plasmid (m): sc-431621-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DTX3L 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
- DTX3L Double Nickase Plasmid (m) and DTX3L Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Dtx3l. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DTX3L Double Nickase Plasmid (m) | sc-431621-NIC | 20 µg | $410.00 | |||
DTX3L Double Nickase Plasmid (m2) | sc-431621-NIC-2 | 20 µg | $410.00 |
DTX3L (deltex E3 ubiquitin ligase 3L) is a RING-type E3 ubiquitin ligase that partners with PARP9 to regulate ubiquitin signaling linked to DNA damage responses and interferon-stimulated pathways. Through modulation of protein ubiquitination, DTX3L influences chromatin-associated processes, transcriptional programs, and cellular stress signaling that shape innate immune outputs. Mouse Dtx3l has been studied in contexts of inflammatory signaling and host–pathogen interactions, where ubiquitin-mediated regulation can affect immune cell function and cytokine-driven networks. Dysregulated ubiquitination and PARP-dependent pathways connected to DTX3L are also relevant to mechanisms of genome stability and oncogenic stress biology.
DTX3L Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Dtx3l locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Dtx3l. 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 Dtx3l 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 Dtx3l-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.