LRRK2 Double Nickase Plasmid (h): sc-402602-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LRRK2 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
- LRRK2 Double Nickase Plasmid (h) and LRRK2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LRRK2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LRRK2 Antibody (133AT1218): sc-130159
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LRRK2 Double Nickase Plasmid (h) | sc-402602-NIC | 20 µg | $410.00 | |||
LRRK2 Double Nickase Plasmid (h2) | sc-402602-NIC-2 | 20 µg | $410.00 |
Human LRRK2 encodes leucine-rich repeat kinase 2, a multifunctional serine/threonine kinase and GTPase that integrates signaling on endolysosomal and vesicular trafficking membranes. LRRK2 modulates Rab GTPase phosphorylation, cytoskeletal dynamics, and autophagy–lysosome pathway function, thereby influencing organelle homeostasis and inflammatory signaling. Dysregulated LRRK2 activity and variants are strongly linked to Parkinson’s disease biology and are also studied in immune cell pathways and neuroinflammation. As a central regulator of membrane trafficking and proteostasis, LRRK2 is widely used to interrogate stress responses and neuronal vulnerability mechanisms in human cellular models.
LRRK2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LRRK2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LRRK2. 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 LRRK2 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 LRRK2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.