ARHGAP29 Double Nickase Plasmid (h): sc-407394-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ARHGAP29 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
- ARHGAP29 Double Nickase Plasmid (h) and ARHGAP29 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ARHGAP29. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ARHGAP29 Antibody (D-3): sc-365554
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARHGAP29 Double Nickase Plasmid (h) | sc-407394-NIC | 20 µg | $410.00 |
ARHGAP29 encodes a Rho GTPase-activating protein that negatively regulates RhoA signaling by accelerating GTP hydrolysis, thereby modulating actin cytoskeleton remodeling, cell polarity, and junctional dynamics. Through control of RhoA/ROCK-dependent contractility, ARHGAP29 contributes to epithelial morphogenesis, cell migration, and tissue integrity. Genetic and functional studies link ARHGAP29 to craniofacial development, with variants associated with nonsyndromic cleft lip and/or palate, and broader relevance to pathways governing adhesion and cytoskeletal tension. Its activity makes it a useful target for dissecting Rho-family GTPase circuitry and mechanotransduction-related phenotypes in human cell models.
ARHGAP29 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ARHGAP29 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ARHGAP29. 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 ARHGAP29 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 ARHGAP29-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.