BAT2 CRISPR Activation Plasmid (h): sc-409707-ACT

PRRC2A encodes the human BAT2 protein, a large proline-rich RNA-binding factor implicated in post-transcriptional gene regulation, including mRNA stability and translation control. BAT2 has been linked to stress-responsive RNA metabolism and broader regulation of gene expression programs that influence cell growth and differentiation. Genetic variation and dysregulated expression in the PRRC2A/BAT2 locus have been reported in immune-related traits and cancer-associated genomic regions, supporting its relevance to pathways that shape inflammatory signaling and tumor biology. These features make PRRC2A a useful target for dissecting RNA regulatory networks and their downstream effects on cellular phenotype.

BAT2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PRRC2A expression without altering the underlying DNA sequence.

BAT2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PRRC2A 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 PRRC2A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BAT2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PRRC2A locus and enabling the study of BAT2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BAT2 pathway restoration in tumor cells with silenced or reduced PRRC2A expression.

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