AP-2μ1 Double Nickase Plasmid (h): sc-403095-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AP-2μ1 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
- AP-2μ1 Double Nickase Plasmid (h) and AP-2μ1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AP2M1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: AP-2μ1 Antibody (D-7): sc-515920
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AP-2μ1 Double Nickase Plasmid (h) | sc-403095-NIC | 20 µg | $410.00 | |||
AP-2μ1 Double Nickase Plasmid (h2) | sc-403095-NIC-2 | 20 µg | $410.00 |
AP2M1 encodes the µ1 subunit of the adaptor protein 2 (AP-2) complex, a core component of clathrin-mediated endocytosis at the plasma membrane. AP-2µ1 recognizes cargo sorting motifs and coordinates clathrin coat assembly to regulate internalization and recycling of receptors, transporters, and other membrane proteins. Through control of vesicle trafficking, AP2M1 influences signaling attenuation, nutrient uptake, and synaptic vesicle dynamics, linking it to pathways such as receptor tyrosine kinase and GPCR trafficking. Dysregulation of endocytic adaptor function has been associated with altered neuronal and metabolic homeostasis and is frequently relevant to studies of cancer cell signaling, neurodevelopmental phenotypes, and membrane protein turnover.
AP-2μ1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the AP2M1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within AP2M1. 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 AP2M1 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 AP2M1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.