
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
R1 CRISPR Activation Plasmid (h) | sc-401712-ACT | 20 µg | $397.00 |
Human RRM1 encodes the R1 catalytic subunit of ribonucleotide reductase, the rate-limiting enzyme for de novo deoxyribonucleotide synthesis required for DNA replication and repair. R1 pairs with RRM2 or RRM2B to maintain balanced dNTP pools, linking nucleotide metabolism to S-phase progression, replication stress responses, and genome stability pathways. Dysregulated RRM1 activity can alter DNA damage tolerance and mutational burden, making it relevant to studies of proliferative signaling, chemogenomic response signatures, and mechanisms of genome maintenance in cancer and other disorders characterized by replication stress.
R1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RRM1 expression without altering the underlying DNA sequence.
R1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RRM1 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 RRM1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous R1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RRM1 locus and enabling the study of R1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of R1 pathway restoration in tumor cells with silenced or reduced RRM1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.