
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MRE11 CRISPR Activation Plasmid (h) | sc-401510-ACT | 20 µg | $397.00 |
MRE11 encodes a conserved nuclease that forms the MRE11–RAD50–NBN (MRN) complex, a central sensor and effector of DNA double-strand break repair. Through roles in DNA end processing, ATM/ATR checkpoint signaling, homologous recombination, and telomere maintenance, MRE11 helps preserve genome stability during replication stress and genotoxic challenge. Altered MRN function is linked to defective DNA damage responses, chromosomal instability, and cancer-associated phenotypes, and MRE11 activity is frequently interrogated in studies of replication fork dynamics and chromatin-associated repair. As a result, MRE11 serves as a key node for dissecting DDR pathway crosstalk and cellular sensitivity mechanisms to DNA-damaging perturbations.
MRE11 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MRE11 expression without altering the underlying DNA sequence.
MRE11 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MRE11 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 MRE11 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MRE11 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MRE11 locus and enabling the study of MRE11-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MRE11 pathway restoration in tumor cells with silenced or reduced MRE11 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.