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.
SNRK CRISPR Activation Plasmid (h): sc-407320-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SNRK CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- SNRK 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 SNRK CRISPR Activation Plasmid (h) and SNRK CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the SNRK 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: SNRK Antibody (A-3): sc-398557
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SNRK CRISPR Activation Plasmid (h) | sc-407320-ACT | 20 µg | $397.00 | |||
SNRK CRISPR Activation Plasmid (h2) | sc-407320-ACT-2 | 20 µg | $397.00 |
Sucrose non-fermenting related kinase (SNRK) is a serine/threonine kinase in the AMPK-related kinase family that integrates cellular energy status with metabolic and stress-adaptive programs. SNRK has been linked to regulation of mitochondrial function, lipid and glucose metabolism, and inflammatory signaling, with reported roles in endothelial and cardiac biology as well as adipose tissue homeostasis. Through phosphorylation-dependent control of downstream effectors, SNRK intersects with pathways governing nutrient sensing, oxidative stress responses, and cellular remodeling. Altered SNRK activity or expression has been associated with cardiometabolic phenotypes and inflammation-related disease mechanisms, making it a useful target for dissecting energy-regulated signaling networks in human cells.
SNRK CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SNRK expression without altering the underlying DNA sequence.
SNRK CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SNRK 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 SNRK transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SNRK expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SNRK locus and enabling the study of SNRK-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SNRK pathway restoration in tumor cells with silenced or reduced SNRK expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.