LTK Double Nickase Plasmid (h): sc-405150-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LTK 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
- LTK Double Nickase Plasmid (h) and LTK Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LTK. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LTK Antibody (B-6): sc-393465
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LTK Double Nickase Plasmid (h) | sc-405150-NIC | 20 µg | $410.00 | |||
LTK Double Nickase Plasmid (h2) | sc-405150-NIC-2 | 20 µg | $410.00 |
Leukocyte receptor tyrosine kinase (LTK) is a receptor tyrosine kinase that regulates signal transduction programs controlling cell growth, survival, and differentiation through phosphorylation-dependent recruitment of downstream effectors. LTK activity interfaces with canonical kinase pathways such as MAPK/ERK, PI3K–AKT, and JAK/STAT signaling, shaping transcriptional outputs and cytoskeletal dynamics in a context-dependent manner. Dysregulated receptor tyrosine kinase signaling, including aberrant LTK expression or activation, is relevant to oncogenic signaling networks and altered cellular state transitions. As a result, LTK is frequently studied for its contribution to pathway wiring, phosphoproteome remodeling, and genotype-to-phenotype relationships in disease-relevant models.
LTK Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LTK locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LTK. 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 LTK 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 LTK-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.