



Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CLK4 Double Nickase Plasmid (h) | sc-404084-NIC | 20 µg | $410.00 | |||
CLK4 Double Nickase Plasmid (h2) | sc-404084-NIC-2 | 20 µg | $410.00 |
CDC-like kinase 4 (CLK4) is a dual-specificity protein kinase that phosphorylates serine/arginine-rich (SR) splicing factors, linking signaling inputs to spliceosome assembly and alternative pre-mRNA splicing decisions. By modulating SR protein phosphorylation dynamics, CLK4 contributes to mRNA processing, transcription–splicing coupling, and broader RNA metabolism programs that shape cell cycle progression and stress-adaptive gene expression. Dysregulated CLK family activity can alter splicing patterns that influence oncogenic signaling networks, DNA damage responses, and differentiation states, making CLK4 a relevant node for mechanistic studies of splicing-associated phenotypes. Human CLK4 is therefore frequently investigated in contexts where transcript isoform switching and kinase-regulated splicing control are central to disease-relevant cellular behavior.
CLK4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CLK4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CLK4. 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 CLK4 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 CLK4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.