casein kinase IIα′ CRISPR Activation Plasmid (h): sc-401148-ACT

CSNK2A2 encodes the casein kinase II alpha′ catalytic subunit, a constitutively active serine/threonine kinase that partners with regulatory beta subunits to form the CK2 holoenzyme. CK2 phosphorylates a broad spectrum of substrates involved in chromatin organization, transcription and RNA processing, cell-cycle progression, and DNA damage responses, integrating signals across pathways such as Wnt/β-catenin, NF-κB, PI3K/AKT, and MAPK. Through these network-level functions, CSNK2A2 contributes to regulation of proliferation, stress adaptation, and apoptosis, making it relevant to mechanistic studies of oncogenic signaling, neurodevelopmental processes, and inflammatory pathway modulation. Dysregulated CK2 activity and altered CSNK2A2 expression have been associated with tumor biology, aberrant phosphorylation programs, and perturbed cellular homeostasis in multiple disease contexts.

casein kinase IIα′ CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CSNK2A2 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 CSNK2A2 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 CSNK2A2 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 CSNK2A2 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 CSNK2A2 expression.

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