LKB1 Double Nickase Plasmid (h): sc-400313-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LKB1 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
- LKB1 Double Nickase Plasmid (h) and LKB1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting STK11. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LKB1 Antibody (Ley 37D/G6): sc-32245
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LKB1 Double Nickase Plasmid (h) | sc-400313-NIC | 20 µg | $410.00 | |||
LKB1 Double Nickase Plasmid (h2) | sc-400313-NIC-2 | 20 µg | $410.00 |
STK11 encodes the serine/threonine kinase LKB1, a master regulator of cellular energy homeostasis that activates AMPK and a family of AMPK-related kinases to coordinate metabolism, autophagy, and stress responses. Through these pathways, LKB1 modulates mTOR signaling, cell polarity, and epithelial organization, linking nutrient sensing to growth control. LKB1 also influences cell-cycle progression and maintains genomic and tissue architecture by integrating signals that affect proliferation and differentiation. Loss-of-function alterations in STK11 are recurrent in human cancers and are associated with metabolic rewiring and disrupted polarity programs, making this axis central to studies of tumor biology and cell-state regulation.
LKB1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the STK11 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within STK11. 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 STK11 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 STK11-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.