LMX1A Double Nickase Plasmid (h): sc-418369-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LMX1A 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
- LMX1A Double Nickase Plasmid (h) and LMX1A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LMX1A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LMX1A Double Nickase Plasmid (h) | sc-418369-NIC | 20 µg | $410.00 | |||
LMX1A Double Nickase Plasmid (h2) | sc-418369-NIC-2 | 20 µg | $410.00 |
LMX1A encodes a LIM homeobox transcription factor that functions as a lineage-determining regulator during embryonic development, with prominent roles in midbrain dopaminergic neuron specification and pancreatic cell differentiation. By binding DNA through its homeodomain and coordinating cofactor interactions via LIM domains, LMX1A shapes transcriptional programs linked to neurogenesis, cell fate commitment, and tissue patterning. It interfaces with developmental signaling networks such as Wnt and BMP pathways that coordinate morphogen gradients and downstream gene expression. Altered LMX1A expression or regulatory control has been associated with neurodevelopmental phenotypes and has been explored in the context of dopaminergic neuron vulnerability relevant to Parkinson’s disease biology.
LMX1A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LMX1A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LMX1A. 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 LMX1A 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 LMX1A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.