cyclin G2 CRISPR Activation Plasmid (h): sc-403620-ACT

CCNG2 encodes cyclin G2, an atypical cyclin that functions predominantly as a negative regulator of cell-cycle progression and cellular proliferation. Cyclin G2 is induced by growth-inhibitory and stress cues and contributes to checkpoint control by modulating cyclin-dependent kinase activity and integrating signals from pathways such as p53-dependent responses and phosphatase-associated regulatory networks. Through effects on G1/S transition, differentiation, and apoptotic sensitivity, CCNG2 expression is frequently studied in the context of altered cell-cycle control observed in cancer and other proliferative disorders. Dysregulated CCNG2 has also been linked to changes in invasion, metastasis-associated phenotypes, and therapy response pathways in tumor models, making it relevant for mechanistic studies of growth restraint.

cyclin G2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CCNG2 expression without altering the underlying DNA sequence.

cyclin G2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CCNG2 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 CCNG2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous cyclin G2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CCNG2 locus and enabling the study of cyclin G2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of cyclin G2 pathway restoration in tumor cells with silenced or reduced CCNG2 expression.

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