β2-Adaptin Double Nickase Plasmid (h): sc-402404-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- β2-Adaptin 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
- β2-Adaptin Double Nickase Plasmid (h) and β2-Adaptin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AP2B1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
β2-Adaptin Double Nickase Plasmid (h) | sc-402404-NIC | 20 µg | $410.00 | |||
β2-Adaptin Double Nickase Plasmid (h2) | sc-402404-NIC-2 | 20 µg | $410.00 |
AP2B1 encodes β2-Adaptin, a core subunit of the adaptor protein complex 2 (AP-2) that links cargo receptors to clathrin during clathrin-mediated endocytosis at the plasma membrane. Through recognition of sorting motifs and coordination with accessory factors, β2-Adaptin helps regulate internalization and recycling of receptors, transporters, and signaling complexes, influencing pathways such as receptor tyrosine kinase signaling and synaptic vesicle cycling. AP-2–dependent trafficking contributes to control of membrane composition and signal attenuation, with perturbations impacting cellular homeostasis and stress responses. Altered endocytic adaptor function has been associated with neurodevelopmental phenotypes and dysregulated receptor trafficking observed in cancer-relevant signaling contexts.
β2-Adaptin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the AP2B1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within AP2B1. 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 AP2B1 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 AP2B1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.