CPEB2 CRISPR Activation Plasmid (h2): sc-409367-ACT-2

Human CPEB2 (cytoplasmic polyadenylation element binding protein 2) is an RNA-binding protein that recognizes cytoplasmic polyadenylation elements in 3′ UTRs to regulate poly(A) tail length, mRNA stability, and translation in a context-dependent manner. By coordinating post-transcriptional control of gene expression, CPEB2 contributes to processes such as cell-cycle progression, stress-responsive translational reprogramming, and hypoxia-associated signaling through selective modulation of target transcripts. Altered CPEB2 expression or activity has been linked to dysregulated RNA metabolism and is studied in the context of cancer biology, neuronal function, and other diseases where translational control is perturbed. Gene editing of CPEB2 enables mechanistic dissection of RNA regulatory networks, mapping of transcript-specific translational effects, and functional interrogation of 3′ UTR–mediated control in human cell models.

CPEB2 CRISPR Activation Plasmid (h2) provides a targeted, non-destructive approach to upregulating endogenous CPEB2 expression without altering the underlying DNA sequence.

CPEB2 CRISPR Activation Plasmid (h2) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CPEB2 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 CPEB2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CPEB2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CPEB2 locus and enabling the study of CPEB2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CPEB2 pathway restoration in tumor cells with silenced or reduced CPEB2 expression.

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