APPL1 Double Nickase Plasmid (m): sc-428481-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- APPL1 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
- APPL1 Double Nickase Plasmid (m) and APPL1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Appl1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: APPL1 Antibody (A-1): sc-271901
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
APPL1 Double Nickase Plasmid (m) | sc-428481-NIC | 20 µg | $410.00 | |||
APPL1 Double Nickase Plasmid (m2) | sc-428481-NIC-2 | 20 µg | $410.00 |
Appl1 encodes APPL1, an endosomal adaptor protein that binds Rab5 and integrates signaling from receptor tyrosine kinases with downstream PI3K–AKT and MAPK pathways. Through interactions with adiponectin receptors and insulin signaling components, APPL1 contributes to regulation of glucose uptake, lipid metabolism, and cellular growth responses. APPL1 also participates in endocytic trafficking and signal compartmentalization, influencing survival, migration, and neuronal signaling programs. Dysregulated APPL1-linked signaling has been associated in the literature with metabolic phenotypes and altered growth-factor responses, supporting its relevance in studies of insulin resistance, obesity-related pathways, and signaling-driven disease mechanisms.
APPL1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Appl1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Appl1. 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 Appl1 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 Appl1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.