
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
WNK1 CRISPR Activation Plasmid (h) | sc-403420-ACT | 20 µg | $397.00 |
WNK1 (with-no-lysine [K] kinase 1) encodes a serine/threonine kinase that functions as an upstream regulator of ion transport and cell volume homeostasis by modulating cation-chloride cotransporters through the WNK–SPAK/OSR1 signaling axis. It integrates osmotic stress cues to coordinate NaCl handling, cytoskeletal dynamics, and vesicular trafficking, influencing epithelial transport and neuronal excitability. WNK1 also interfaces with MAPK- and PI3K-related signaling outputs that affect proliferation and migration in a context-dependent manner. Genetic or signaling dysregulation of WNK1 has been linked to blood pressure phenotypes and neuropathy-related processes, making it a relevant node for mechanistic studies of electrolyte balance and stress-response signaling.
WNK1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous WNK1 expression without altering the underlying DNA sequence.
WNK1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the WNK1 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the WNK1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous WNK1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native WNK1 locus and enabling the study of WNK1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of WNK1 pathway restoration in tumor cells with silenced or reduced WNK1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.