
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CCRK CRISPR Activation Plasmid (h) | sc-409545-ACT | 20 µg | $397.00 |
CDK20 encodes cell cycle-related kinase (CCRK), a serine/threonine kinase that regulates cell-cycle progression and proliferative signaling through phosphorylation-dependent control of CDK-associated pathways. CCRK has been linked to modulation of Wnt/β-catenin activity and broader transcriptional programs that influence growth, differentiation, and cellular homeostasis. Altered CDK20/CCRK expression has been reported across multiple disease-relevant contexts, including dysregulated proliferation and changes in signaling network balance in cancer biology. As a result, CDK20 is frequently studied for its role in kinase signaling, cell-cycle control, and pathway crosstalk in human cells.
CCRK CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CDK20 expression without altering the underlying DNA sequence.
CCRK CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CDK20 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 CDK20 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CCRK expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CDK20 locus and enabling the study of CCRK-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CCRK pathway restoration in tumor cells with silenced or reduced CDK20 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.