
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Rrn3 CRISPR Activation Plasmid (h) | sc-403709-ACT | 20 µg | $397.00 |
Human RRN3 encodes the RNA polymerase I transcription initiation factor Rrn3 (also known as TIF-IA), a central regulator of ribosomal RNA synthesis and nucleolar function. Rrn3 bridges Pol I to promoter-bound factors to enable pre-rRNA transcription and supports ribosome biogenesis, thereby coupling cellular growth demands to protein synthesis capacity. Its activity is tightly controlled by nutrient and growth signaling pathways, including mTOR and MAPK/ERK, through post-translational regulation that modulates Pol I initiation competence. Dysregulated Pol I transcription and nucleolar stress linked to altered RRN3 function are relevant to proliferative biology and cellular stress responses frequently studied in cancer and metabolic signaling contexts.
Rrn3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RRN3 expression without altering the underlying DNA sequence.
Rrn3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RRN3 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 RRN3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Rrn3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RRN3 locus and enabling the study of Rrn3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Rrn3 pathway restoration in tumor cells with silenced or reduced RRN3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.