casein kinase IIα CRISPR Activation Plasmid (h): sc-418515-ACT

CSNK2A1 encodes the catalytic alpha subunit of casein kinase II (CK2α), a constitutively active serine/threonine kinase that phosphorylates a broad spectrum of nuclear and cytoplasmic substrates. CK2α integrates signals across core pathways controlling cell cycle progression, DNA damage responses, chromatin dynamics, transcription, and translation, with documented roles in Wnt/β-catenin, NF-κB, PI3K–AKT, and MAPK signaling networks. Through regulation of apoptosis, proteostasis, and stress adaptation, CK2α contributes to cellular homeostasis in multiple tissue contexts. Altered CSNK2A1 activity or expression has been associated with dysregulated proliferation and developmental phenotypes, supporting its utility as a mechanistic node in disease-relevant signaling research.

casein kinase IIα CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CSNK2A1 expression without altering the underlying DNA sequence.

casein kinase IIα CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CSNK2A1 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 CSNK2A1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous casein kinase IIα expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CSNK2A1 locus and enabling the study of casein kinase IIα-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of casein kinase IIα pathway restoration in tumor cells with silenced or reduced CSNK2A1 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.