cyclin G1 CRISPR Activation Plasmid (h): sc-402045-ACT

CCNG1 encodes cyclin G1, an atypical cyclin that integrates stress signaling with cell-cycle control and transcriptional regulation. Cyclin G1 is strongly linked to p53-dependent DNA damage responses, modulating checkpoint behavior and influencing proliferation, apoptosis, and cellular homeostasis through interactions with phosphatase complexes and ubiquitin-associated regulatory circuits. Altered CCNG1 expression has been reported across multiple tumor contexts and is frequently studied as a node connecting genotoxic stress, growth control, and oncogenic pathway remodeling. As a human cell-cycle regulator responsive to environmental and intracellular cues, cyclin G1 provides a tractable target for dissecting pathway crosstalk between DNA repair, checkpoint signaling, and adaptive transcriptional programs.

cyclin G1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CCNG1 expression without altering the underlying DNA sequence.

cyclin G1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CCNG1 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 CCNG1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous cyclin G1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CCNG1 locus and enabling the study of cyclin G1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of cyclin G1 pathway restoration in tumor cells with silenced or reduced CCNG1 expression.

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