Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
SPAK CRISPR Activation Plasmid (h): sc-404440-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SPAK CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- SPAK CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by SPAK CRISPR Activation Plasmid (h) and SPAK CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the STK39 transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SPAK Antibody (430CT4.4.1): sc-517361
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SPAK CRISPR Activation Plasmid (h) | sc-404440-ACT | 20 µg | $397.00 |
Human STK39 encodes the serine/threonine kinase SPAK (STE20/SPS1-related proline/alanine-rich kinase), a stress-responsive regulator of ion transport and cell volume homeostasis. SPAK functions within the WNK–SPAK/OSR1 signaling axis to phosphorylate and control electroneutral cation–chloride cotransporters, influencing epithelial salt handling, neuronal chloride balance, and osmotic stress adaptation. Through modulation of MAPK-linked stress signaling and transporter phosphorylation dynamics, STK39 activity connects intracellular kinase networks to membrane transport processes. Dysregulation of this pathway has been associated with altered electrolyte physiology and has been investigated in contexts such as hypertension risk, neurophysiological excitability, and epithelial transport phenotypes.
SPAK CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous STK39 expression without altering the underlying DNA sequence.
SPAK CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the STK39 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 STK39 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SPAK expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native STK39 locus and enabling the study of SPAK-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SPAK pathway restoration in tumor cells with silenced or reduced STK39 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.