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.
DRAK1 CRISPR Activation Plasmid (h): sc-411260-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DRAK1 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- DRAK1 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 DRAK1 CRISPR Activation Plasmid (h) and DRAK1 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the STK17A 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: DRAK1 Antibody (3064C6a): sc-81573
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DRAK1 CRISPR Activation Plasmid (h) | sc-411260-ACT | 20 µg | $397.00 |
STK17A encodes DRAK1, a serine/threonine kinase of the death-associated protein kinase family that modulates stress-responsive signaling and cell fate decisions. DRAK1 has been linked to regulation of apoptotic and survival pathways, with reported roles in phosphorylation-dependent control of transcriptional programs and cytoskeletal dynamics. Through its kinase activity, DRAK1 can influence processes such as mitochondrial integrity, cell cycle progression, and cellular responses to genotoxic or inflammatory cues. Altered STK17A/DRAK1 expression has been observed across multiple disease contexts, supporting its use as a mechanistic node for studying dysregulated apoptosis and signaling in human cell models.
DRAK1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous STK17A expression without altering the underlying DNA sequence.
DRAK1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the STK17A 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 STK17A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DRAK1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native STK17A locus and enabling the study of DRAK1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DRAK1 pathway restoration in tumor cells with silenced or reduced STK17A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.