ALK Double Nickase Plasmid (h): sc-400460-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ALK 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
- ALK Double Nickase Plasmid (h) and ALK Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ALK. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ALK Antibody (F-12): sc-398791
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ALK Double Nickase Plasmid (h) | sc-400460-NIC | 20 µg | $410.00 | |||
ALK Double Nickase Plasmid (h2) | sc-400460-NIC-2 | 20 µg | $410.00 |
Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase that regulates cellular proliferation, survival, and differentiation through phosphorylation-dependent signaling. Upon ligand engagement or aberrant activation, ALK can couple to downstream pathways including RAS–MAPK, PI3K–AKT, and JAK–STAT, influencing transcriptional programs and cytoskeletal dynamics. In human biology, ALK activity is tightly controlled during development, particularly in neural lineages, and dysregulation can rewire growth-factor signaling networks. Altered ALK expression or activating genomic rearrangements are widely studied as oncogenic drivers that perturb kinase signaling and cell-state control.
ALK Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ALK locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ALK. 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 ALK 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 ALK-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.