ATP11B Double Nickase Plasmid (m): sc-429296-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATP11B 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
- ATP11B Double Nickase Plasmid (m) and ATP11B Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Atp11b. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATP11B Double Nickase Plasmid (m) | sc-429296-NIC | 20 µg | $410.00 | |||
ATP11B Double Nickase Plasmid (m2) | sc-429296-NIC-2 | 20 µg | $410.00 |
Atp11b encodes ATP11B, a P4-ATPase phospholipid flippase that helps maintain membrane lipid asymmetry by translocating aminophospholipids across bilayers within the endomembrane system. By shaping vesicle budding, membrane curvature, and trafficking through the trans-Golgi network and endosomal compartments, ATP11B supports cargo sorting, receptor recycling, and organelle homeostasis. Disruption of lipid transport and vesicular pathways governed by P4-ATPases can alter cell polarity, stress responses, and signaling outputs linked to inflammation and neurodegeneration-associated membrane dysfunction. In mouse models, Atp11b perturbation provides a tractable entry point to study how phospholipid remodeling interfaces with intracellular transport and proteostasis.
ATP11B Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Atp11b locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Atp11b. 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 Atp11b 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 Atp11b-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.