
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BRP44L CRISPR Activation Plasmid (h) | sc-404976-ACT | 20 µg | $397.00 |
Human MPC1 encodes the BRP44L subunit of the mitochondrial pyruvate carrier, a key inner-membrane complex that imports pyruvate into the mitochondrial matrix to fuel the TCA cycle and oxidative phosphorylation. By regulating the balance between mitochondrial respiration and cytosolic glycolysis, MPC1 influences anaplerosis, redox homeostasis, and carbon flux into biosynthetic pathways. Altered MPC1/BRP44L activity has been linked to metabolic rewiring observed in proliferative states and to mitochondrial dysfunction phenotypes in diverse model systems. As a result, MPC1 is commonly studied in contexts involving energy metabolism, mitochondrial signaling, and nutrient-sensing pathways.
BRP44L CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MPC1 expression without altering the underlying DNA sequence.
BRP44L CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MPC1 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 MPC1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BRP44L expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MPC1 locus and enabling the study of BRP44L-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BRP44L pathway restoration in tumor cells with silenced or reduced MPC1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.