apoC-I CRISPR Activation Plasmid (m): sc-419163-ACT

Mouse Apoc1 encodes apolipoprotein C-I (apoC-I), a secreted exchangeable apolipoprotein that associates with triglyceride-rich lipoproteins and HDL to modulate lipid transport and lipoprotein remodeling. apoC-I influences receptor-mediated lipoprotein clearance and impacts triglyceride metabolism by altering interactions among apolipoproteins, lipases, and cell-surface uptake pathways. In macrophages and other myeloid cells, APOC1 expression is linked to lipid handling programs that shape foam cell biology and inflammatory signaling in atherosclerosis-relevant contexts. Dysregulated APOC1 has also been associated with metabolic phenotypes and neuroinflammatory states, supporting its use in studies of lipid homeostasis, innate immune activation, and tissue-specific gene regulation.

apoC-I CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Apoc1 expression without altering the underlying DNA sequence.

apoC-I CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Apoc1 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 Apoc1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous apoC-I expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Apoc1 locus and enabling the study of apoC-I-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of apoC-I pathway restoration in tumor cells with silenced or reduced Apoc1 expression.

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