
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BMCP1 CRISPR Activation Plasmid (m) | sc-422996-ACT | 20 µg | $397.00 | |||
BMCP1 CRISPR Activation Plasmid (m2) | sc-422996-ACT-2 | 20 µg | $397.00 |
Slc25a14 encodes the mitochondrial carrier protein BMCP1, an inner membrane transporter implicated in regulating mitochondrial bioenergetics through modulation of proton leak and coupling efficiency. By influencing membrane potential, reactive oxygen species balance, and oxidative phosphorylation output, BMCP1 links mitochondrial metabolism to cellular stress responses and energy-sensing pathways. Altered BMCP1 activity has been associated with shifts in metabolic homeostasis, susceptibility to oxidative stress, and tissue-specific mitochondrial dysfunction, making Slc25a14 a relevant target for studying metabolic and neurodegeneration-associated mechanisms in mouse models.
BMCP1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Slc25a14 expression without altering the underlying DNA sequence.
BMCP1 CRISPR Activation Plasmid (m) 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.