
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Rad51C CRISPR Activation Plasmid (h) | sc-403060-ACT | 20 µg | $397.00 | |||
Rad51C CRISPR Activation Plasmid (h2) | sc-403060-ACT-2 | 20 µg | $397.00 |
Human RAD51C encodes Rad51C, a RAD51 paralog that functions in homologous recombination and the Fanconi anemia/BRCA DNA damage response network to maintain genome stability. Rad51C contributes to RAD51 nucleoprotein filament dynamics, Holliday junction processing, and repair of DNA double-strand breaks arising during replication stress. Through these activities, RAD51C supports S-phase checkpoint integrity and prevents accumulation of chromosomal aberrations. Altered RAD51C function or expression has been linked to defective DNA repair capacity and genomic instability phenotypes studied in cancer biology and inherited DNA repair disorders.
Rad51C CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RAD51C expression without altering the underlying DNA sequence.
Rad51C CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RAD51C 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 RAD51C transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Rad51C expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RAD51C locus and enabling the study of Rad51C-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Rad51C pathway restoration in tumor cells with silenced or reduced RAD51C expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.