BMCP1 Lentiviral Activation Particles (m2): sc-422996-LAC-2

Mouse Slc25a14 encodes brain mitochondrial carrier protein 1 (BMCP1), an inner mitochondrial membrane carrier of the SLC25 family implicated in regulating proton leak and mitochondrial coupling efficiency. BMCP1 activity influences oxidative phosphorylation, membrane potential, ATP production, and reactive oxygen species homeostasis, thereby shaping neuronal and metabolically active tissue responses to energetic demand and stress. Altered Slc25a14 function has been studied in the context of mitochondrial dysfunction and redox imbalance relevant to neurodegeneration and metabolic phenotypes. Gene editing of Slc25a14 in mouse models supports mechanistic research on mitochondrial bioenergetics, stress-adaptive signaling, and genotype–phenotype relationships in mitochondrial carrier pathways.

BMCP1 Lentiviral Activation Particles (m2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Slc25a14 upregulation across a broader range of human cell types.

BMCP1 Lentiviral Activation Particles (m2) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the Slc25a14 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous BMCP1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Slc25a14 genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

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