γ2-COP CRISPR Activation Plasmid (h): sc-403467-ACT

COPG2 encodes the human γ2-COP subunit of the COPI coatomer complex, a core mediator of vesicle budding and retrograde transport from the Golgi to the endoplasmic reticulum and within Golgi cisternae. γ2-COP contributes to cargo selection and coat assembly that maintain Golgi architecture, secretory pathway fidelity, and membrane homeostasis, linking COPI function to protein maturation and intracellular trafficking networks. Disruption of coatomer-dependent trafficking can perturb ER stress responses, lipid handling, and proteostasis, processes frequently altered in proliferative and neurodegenerative disease contexts. COPG2 is therefore relevant for mechanistic studies of vesicular transport, Golgi–ER dynamics, and pathway-level consequences of altered intracellular trafficking.

γ2-COP CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous COPG2 expression without altering the underlying DNA sequence.

γ2-COP CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the COPG2 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 COPG2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous γ2-COP expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native COPG2 locus and enabling the study of γ2-COP-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of γ2-COP pathway restoration in tumor cells with silenced or reduced COPG2 expression.

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