Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
LMO7 Double Nickase Plasmid (h): sc-404373-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LMO7 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
- LMO7 Double Nickase Plasmid (h) and LMO7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LMO7. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LMO7 Antibody (B-7): sc-376807
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LMO7 Double Nickase Plasmid (h) | sc-404373-NIC | 20 µg | $410.00 | |||
LMO7 Double Nickase Plasmid (h2) | sc-404373-NIC-2 | 20 µg | $410.00 |
LMO7 (LIM domain only protein 7) is a multifunctional scaffold protein that localizes to cell–cell junctions, the actin cytoskeleton, and the nucleus, where it helps coordinate cytoskeletal organization, mechanotransduction, and transcriptional programs linked to epithelial integrity. By interacting with junctional and actin-associated complexes, LMO7 contributes to regulation of cell shape, adhesion remodeling, and stress-responsive signaling that influences differentiation and tissue architecture. Altered LMO7 activity has been associated with defects in barrier function and cytoskeletal dynamics, and its dysregulation is implicated in contexts involving epithelial–mesenchymal transitions, invasive behavior, and tumor-associated remodeling. These features make LMO7 a useful target for studying adhesion-dependent signaling, cytoskeleton–nucleus communication, and junctional homeostasis in human cell models.
LMO7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LMO7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LMO7. 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 LMO7 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 LMO7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.