
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Krs-2 CRISPR Activation Plasmid (h) | sc-403632-ACT | 20 µg | $397.00 |
STK4 encodes the serine/threonine kinase Krs-2 (also known as MST1), a core component of the Hippo signaling network that integrates stress cues to regulate proliferation, apoptosis, and tissue homeostasis. In human cells, STK4 activation influences kinase cascades and transcriptional programs, including modulation of YAP/TAZ activity and crosstalk with MAPK and immune-related signaling nodes. Krs-2 participates in control of oxidative stress responses, cytoskeletal dynamics, and lymphocyte function, linking it to cellular fitness and inflammatory regulation. Altered STK4 signaling has been associated with dysregulated growth control and immune dysfunction, making it relevant for mechanistic studies of cancer biology and immune-related phenotypes.
Krs-2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous STK4 expression without altering the underlying DNA sequence.
Krs-2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the STK4 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 STK4 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Krs-2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native STK4 locus and enabling the study of Krs-2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Krs-2 pathway restoration in tumor cells with silenced or reduced STK4 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.