
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PMS2 CRISPR Activation Plasmid (h) | sc-401600-ACT | 20 µg | $397.00 |
PMS2 encodes a core component of the DNA mismatch repair (MMR) machinery that forms the MutLα heterodimer with MLH1 to detect and resolve base–base mismatches and insertion/deletion loops arising during DNA replication. Through ATP-dependent coordination of endonuclease activity, excision, and resynthesis, PMS2 helps preserve genome stability and limits mutational burden across proliferating cell populations. Disruption or reduced activity of PMS2 is linked to microsatellite instability phenotypes and is frequently studied in the context of hereditary cancer predisposition syndromes and tumor evolution driven by defective DNA repair. As a result, PMS2 is widely used to interrogate replication fidelity, DNA damage response crosstalk, and mechanisms shaping mutation spectra.
PMS2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PMS2 expression without altering the underlying DNA sequence.
PMS2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PMS2 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 PMS2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PMS2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PMS2 locus and enabling the study of PMS2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PMS2 pathway restoration in tumor cells with silenced or reduced PMS2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.