Angiomotin Double Nickase Plasmid (h): sc-400940-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Angiomotin 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
- Angiomotin Double Nickase Plasmid (h) and Angiomotin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AMOT. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Angiomotin Antibody (B-4): sc-166924
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Angiomotin Double Nickase Plasmid (h) | sc-400940-NIC | 20 µg | $410.00 | |||
Angiomotin Double Nickase Plasmid (h2) | sc-400940-NIC-2 | 20 µg | $410.00 |
AMOT encodes angiomotin, a scaffold protein that localizes to tight junctions and the actin cytoskeleton where it coordinates cell polarity, adhesion, and directional migration. Angiomotin is a key regulator of Hippo pathway signaling through interactions with YAP/TAZ and junctional complexes, thereby influencing proliferation and contact inhibition. It also contributes to angiogenic behavior and endothelial morphogenesis by modulating cytoskeletal dynamics and membrane-associated signaling hubs. Dysregulated AMOT expression or localization has been linked to altered tissue organization and migratory phenotypes relevant to cancer biology and vascular remodeling.
Angiomotin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the AMOT locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within AMOT. 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 AMOT 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 AMOT-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.