
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
XRCC3 CRISPR Activation Plasmid (h) | sc-405570-ACT | 20 µg | $397.00 |
XRCC3 encodes a RAD51 paralog that functions in homologous recombination-mediated DNA double-strand break repair and the maintenance of replication fork stability. XRCC3 contributes to the formation and regulation of RAD51 nucleoprotein filaments, supporting accurate repair during S/G2 and limiting chromosomal aberrations. Through its role in genome surveillance, XRCC3 influences cellular responses to replication stress and DNA-damaging agents, linking it to pathways that preserve chromosomal integrity. Altered XRCC3 activity or expression has been associated with increased genomic instability and has been investigated in the context of cancer susceptibility and tumor biology.
XRCC3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous XRCC3 expression without altering the underlying DNA sequence.
XRCC3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the XRCC3 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 XRCC3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous XRCC3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native XRCC3 locus and enabling the study of XRCC3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of XRCC3 pathway restoration in tumor cells with silenced or reduced XRCC3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.