PTPMT1 CRISPR Activation Plasmid (h): sc-403905-ACT

PTPMT1 encodes a mitochondria-localized protein tyrosine phosphatase that resides on the inner mitochondrial membrane and regulates phospholipid metabolism, particularly dephosphorylation of phosphatidylglycerophosphate during cardiolipin biosynthesis. By shaping cardiolipin composition, PTPMT1 influences electron transport chain function, mitochondrial membrane architecture, and energy homeostasis, with downstream effects on redox balance and apoptotic susceptibility. Altered PTPMT1 activity has been linked to defects in mitochondrial respiration and metabolic reprogramming, processes frequently implicated in cancer biology and cardiometabolic disease mechanisms. As a result, PTPMT1 is studied in pathways connecting mitochondrial lipid signaling to oxidative phosphorylation, mitophagy, and stress responses.

PTPMT1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PTPMT1 expression without altering the underlying DNA sequence.

PTPMT1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PTPMT1 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 PTPMT1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PTPMT1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PTPMT1 locus and enabling the study of PTPMT1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PTPMT1 pathway restoration in tumor cells with silenced or reduced PTPMT1 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.