LMO3 Double Nickase Plasmid (h): sc-417939-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LMO3 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
- LMO3 Double Nickase Plasmid (h) and LMO3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LMO3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LMO3 Antibody (1A8): sc-517019
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LMO3 Double Nickase Plasmid (h) | sc-417939-NIC | 20 µg | $410.00 |
LMO3 encodes a LIM-only transcriptional regulator composed largely of LIM zinc-binding domains that function as protein–protein interaction modules rather than direct DNA-binding motifs. By assembling multiprotein complexes with transcription factors and cofactors, LMO3 helps shape gene expression programs linked to neuronal differentiation, axon guidance, and context-dependent control of proliferation and survival. Dysregulated LMO3 expression has been reported in multiple tumor contexts, including neuroblastoma and other solid cancers, where it is frequently associated with altered differentiation states and invasive phenotypes. These properties make LMO3 a useful target for studying developmental transcriptional networks, oncogenic reprogramming, and mechanisms of lineage specification.
LMO3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LMO3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LMO3. 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 LMO3 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 LMO3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.