CaMKII gamma CRISPR Activation Plasmid (h): sc-400681-ACT

Human CAMK2G encodes CaMKII gamma, a Ca2+/calmodulin-dependent serine/threonine kinase that translates intracellular calcium transients into phosphorylation programs regulating synaptic plasticity, excitation–transcription coupling, cytoskeletal dynamics, and vesicle trafficking. CaMKII gamma participates in CaMK signaling with downstream effects on ion channel function, CREB-linked transcriptional responses, and cross-talk with MAPK and PI3K/AKT pathways. In non-neuronal contexts, CAMK2G contributes to calcium-regulated proliferation, migration, and stress responses, supporting broad roles in cell-state control. Dysregulated CaMKII activity and calcium signaling have been associated with neurodevelopmental and neurodegenerative phenotypes as well as altered signaling networks in cancer biology, making CAMK2G a useful node for mechanistic studies.

CaMKII gamma CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CAMK2G expression without altering the underlying DNA sequence.

CaMKII gamma CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CAMK2G 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 CAMK2G transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CaMKII gamma expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CAMK2G locus and enabling the study of CaMKII gamma-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CaMKII gamma pathway restoration in tumor cells with silenced or reduced CAMK2G expression.

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