DENND2A Double Nickase Plasmid (h): sc-411968-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DENND2A 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
- DENND2A Double Nickase Plasmid (h) and DENND2A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DENND2A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DENND2A Double Nickase Plasmid (h) | sc-411968-NIC | 20 µg | $410.00 | |||
DENND2A Double Nickase Plasmid (h2) | sc-411968-NIC-2 | 20 µg | $410.00 |
DENND2A (DENN domain containing 2A) encodes a cytosolic guanine nucleotide exchange factor (GEF) that activates Rab GTPases involved in membrane trafficking, with reported roles in regulating Rab9-dependent transport and endosome-to-Golgi dynamics. Through these vesicular transport pathways, DENND2A contributes to intracellular cargo sorting, membrane organization, and signaling compartmentalization that can influence cell polarity and motility. Altered expression or regulatory disruption of DENND2A has been investigated in the context of tumor biology, where changes in trafficking and migration programs may affect invasion-related phenotypes. As a trafficking regulator, DENND2A is a useful target for mechanistic studies linking Rab-mediated transport to receptor turnover, organelle homeostasis, and stress-responsive signaling.
DENND2A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DENND2A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DENND2A. 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 DENND2A 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 DENND2A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.