casein kinase Iγ1 CRISPR Activation Plasmid (h): sc-404681-ACT

CSNK1G1 encodes casein kinase Iγ1, a membrane-associated serine/threonine kinase in the CK1 family that modulates phosphorylation-dependent signaling and protein turnover. CK1 isoforms regulate multiple processes including receptor trafficking, circadian timing, and stress-responsive signaling, and they intersect with pathways such as Wnt/β-catenin, Hedgehog, and DNA damage responses through phosphorylation of key pathway components. By shaping phospho-signaling dynamics at membranes and within cytosolic complexes, CSNK1G1 influences cell-cycle control, polarity, and homeostatic feedback loops. Dysregulated CK1 activity has been linked to altered proliferative signaling and other disease-relevant phenotypes, making CSNK1G1 useful for mechanistic studies of kinase-driven pathway rewiring.

casein kinase Iγ1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CSNK1G1 expression without altering the underlying DNA sequence.

casein kinase Iγ1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CSNK1G1 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 CSNK1G1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous casein kinase Iγ1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CSNK1G1 locus and enabling the study of casein kinase Iγ1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of casein kinase Iγ1 pathway restoration in tumor cells with silenced or reduced CSNK1G1 expression.

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