CLK2 Double Nickase Plasmid (h): sc-403326-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CLK2 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
- CLK2 Double Nickase Plasmid (h) and CLK2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CLK2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CLK2 Antibody (F-4): sc-393909
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CLK2 Double Nickase Plasmid (h) | sc-403326-NIC | 20 µg | $410.00 | |||
CLK2 Double Nickase Plasmid (h2) | sc-403326-NIC-2 | 20 µg | $410.00 |
CDC-like kinase 2 (CLK2) is a dual-specificity serine/threonine kinase that phosphorylates SR splicing factors, coupling transcription to pre-mRNA processing and regulating alternative splicing decisions. CLK2 activity helps control spliceosome dynamics and influences cell-cycle progression and stress-responsive transcriptional programs. Through these roles, CLK2 modulates gene-expression outputs linked to proliferation, differentiation, and metabolic adaptation. Dysregulated CLK2 expression or signaling has been associated with aberrant splicing patterns observed in multiple disease contexts, including cancer and other disorders characterized by perturbed RNA processing.
CLK2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CLK2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CLK2. 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 CLK2 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 CLK2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.