ACTG2 Double Nickase Plasmid (h): sc-400007-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACTG2 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
- ACTG2 Double Nickase Plasmid (h) and ACTG2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ACTG2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACTG2 Double Nickase Plasmid (h) | sc-400007-NIC | 20 µg | $410.00 | |||
ACTG2 Double Nickase Plasmid (h2) | sc-400007-NIC-2 | 20 µg | $410.00 |
ACTG2 encodes smooth muscle gamma-actin, a core component of the actin cytoskeleton that supports contractile force generation, cell shape, and mechanotransduction in visceral smooth muscle. ACTG2-containing filaments interact with myosin and actin-binding proteins to coordinate cytoskeletal remodeling, adhesion dynamics, and signaling downstream of RhoA/ROCK and calcium-dependent contractile pathways. Proper ACTG2 function is essential for gastrointestinal and genitourinary smooth muscle motility and maintenance of tissue architecture. Pathogenic variants or dysregulated expression of ACTG2 have been linked to visceral myopathy phenotypes, including disorders affecting intestinal peristalsis and urinary tract function, making it a relevant target for modeling smooth muscle cytoskeletal disease mechanisms.
ACTG2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ACTG2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ACTG2. 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 ACTG2 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 ACTG2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.