C1QBP CRISPR Activation Plasmid (m): sc-419387-ACT

C1qbp encodes C1QBP, a multifunctional mitochondrial and cell-surface–associated protein implicated in mitochondrial ribosome function, oxidative phosphorylation homeostasis, and regulation of cellular stress responses. In mouse cells, C1QBP has been linked to control of apoptosis, metabolic adaptation, and innate immune signaling through interactions that influence complement-related processes and inflammatory cues. Perturbation of C1QBP expression can reshape energy metabolism and reactive oxygen species handling, affecting pathways relevant to proliferative capacity and tissue homeostasis. These functions make C1qbp a useful target for studying mitochondrial dysfunction mechanisms and inflammation-associated phenotypes in disease-relevant models.

C1QBP CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous C1qbp expression without altering the underlying DNA sequence.

C1QBP CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the C1qbp 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 C1qbp transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous C1QBP expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native C1qbp locus and enabling the study of C1QBP-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of C1QBP pathway restoration in tumor cells with silenced or reduced C1qbp expression.

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