BMCP1 (UCP5) CRISPR Activation Plasmid (h): sc-405051-ACT

SLC25A14 encodes BMCP1 (also known as UCP5), an inner mitochondrial membrane carrier that contributes to regulated proton leak and modulation of oxidative phosphorylation efficiency. By influencing mitochondrial membrane potential, reactive oxygen species production, and coupling of electron transport to ATP synthesis, BMCP1 intersects with pathways controlling bioenergetic homeostasis, stress responses, and mitochondrial dynamics. UCP5 is enriched in the nervous system and has been linked to cellular resilience under oxidative and metabolic stress, making it relevant to studies of neurodegeneration and mitochondrial dysfunction. Altered expression or activity of uncoupling proteins is also used as a readout in research on metabolism, apoptosis susceptibility, and mitochondrial quality control.

BMCP1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLC25A14 expression without altering the underlying DNA sequence.

BMCP1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLC25A14 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 SLC25A14 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BMCP1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLC25A14 locus and enabling the study of BMCP1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BMCP1 pathway restoration in tumor cells with silenced or reduced SLC25A14 expression.

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