EXOSC10 CRISPR Activation Plasmid (h): sc-404272-ACT

Human EXOSC10 encodes a catalytic 3′–5′ exoribonuclease that functions as a core component of the RNA exosome, supporting RNA surveillance and processing across the nucleus and cytoplasm. EXOSC10 contributes to maturation and turnover of diverse RNA classes, including rRNA, sn/snoRNA, and unstable or aberrant transcripts, thereby influencing ribosome biogenesis, RNA quality control, and gene expression homeostasis. Through these activities, EXOSC10 intersects with pathways linked to nucleolar function, RNA metabolism, and cellular stress responses. Dysregulation of exosome-associated RNA processing has been associated with genome-wide transcriptome imbalance and disease-relevant phenotypes, making EXOSC10 a useful node for mechanistic studies of RNA decay and proteostasis-adjacent regulation.

EXOSC10 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous EXOSC10 expression without altering the underlying DNA sequence.

EXOSC10 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the EXOSC10 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 EXOSC10 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous EXOSC10 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native EXOSC10 locus and enabling the study of EXOSC10-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of EXOSC10 pathway restoration in tumor cells with silenced or reduced EXOSC10 expression.

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