UQCRC1 CRISPR Activation Plasmid (h): sc-404435-ACT

Human UQCRC1 encodes ubiquinol-cytochrome c reductase core protein 1, an essential structural component of mitochondrial respiratory chain complex III (cytochrome bc1) in the inner mitochondrial membrane. By supporting electron transfer from ubiquinol to cytochrome c and stabilizing complex III assembly, UQCRC1 contributes to oxidative phosphorylation, mitochondrial membrane potential maintenance, and regulation of reactive oxygen species. Perturbation of complex III function can shift cellular energy metabolism, influence apoptotic susceptibility, and alter redox-dependent signaling pathways. Altered UQCRC1 expression or mitochondrial complex III dysfunction has been linked in the literature to mitochondrial disorders and broader disease contexts characterized by impaired bioenergetics and oxidative stress.

UQCRC1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous UQCRC1 expression without altering the underlying DNA sequence.

UQCRC1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the UQCRC1 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 UQCRC1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous UQCRC1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native UQCRC1 locus and enabling the study of UQCRC1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of UQCRC1 pathway restoration in tumor cells with silenced or reduced UQCRC1 expression.

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