DMXL2 Double Nickase Plasmid (h): sc-417505-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DMXL2 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
- DMXL2 Double Nickase Plasmid (h) and DMXL2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DMXL2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DMXL2 Double Nickase Plasmid (h) | sc-417505-NIC | 20 µg | $410.00 |
DMXL2 (Dmx-like protein 2, also known as rabconnectin-3α) is a large WD-repeat–containing scaffold implicated in organization of endomembrane trafficking and regulation of vesicle acidification through interactions with V-ATPase–associated complexes. It has been linked to modulation of Notch signaling and neuroendocrine secretory processes, consistent with roles in synaptic and dense-core vesicle function and broader control of cellular communication. Genetic variation or altered expression of DMXL2 has been associated with neurodevelopmental phenotypes and reproductive axis dysfunction, supporting its relevance to studies of neuronal circuitry, endocrine regulation, and membrane trafficking–dependent signaling pathways. As a human gene, DMXL2 is frequently investigated in models of neuronal differentiation, secretory cell biology, and pathway crosstalk involving endosomal maturation.
DMXL2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DMXL2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DMXL2. 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 DMXL2 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 DMXL2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.