casein kinase IIβ CRISPR Activation Plasmid (h): sc-401684-ACT

CSNK2B encodes the regulatory beta subunit of casein kinase II (CK2), a constitutively active serine/threonine kinase complex that modulates substrate selectivity, enzyme stability, and subcellular localization of the catalytic subunits. CK2 signaling influences fundamental processes including cell cycle progression, DNA damage response, apoptosis, and transcriptional control, with broad integration into pathways such as Wnt/β-catenin, NF-κB, and PI3K/AKT. Through phosphorylation of numerous nuclear and cytoplasmic targets, CSNK2B contributes to chromatin regulation, RNA processing, and proteostasis. Dysregulated CK2 activity and altered CSNK2B expression have been associated with aberrant proliferation and stress-response signaling in cancer biology and with neurodevelopmental phenotypes, supporting its relevance in mechanistic disease models.

casein kinase IIβ CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CSNK2B expression without altering the underlying DNA sequence.

casein kinase IIβ CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CSNK2B 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 CSNK2B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous casein kinase IIβ expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CSNK2B locus and enabling the study of casein kinase IIβ-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of casein kinase IIβ pathway restoration in tumor cells with silenced or reduced CSNK2B expression.

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