ABC1 CRISPR Activation Plasmid (m): sc-418929-ACT

Mouse Abca1 encodes the ATP-binding cassette transporter ABC1, a key regulator of cellular cholesterol and phospholipid efflux to apolipoproteins, supporting nascent HDL biogenesis and lipid homeostasis. ABC1 activity integrates with LXR/RXR-driven transcriptional programs and intersects with macrophage lipid handling, membrane remodeling, and inflammatory signaling. Dysregulated Abca1 expression or function perturbs cholesterol trafficking, promotes foam cell formation, and is widely studied in the context of atherosclerosis-relevant pathways and lipid storage phenotypes. In mouse models, Abca1 is also used to investigate lipid-dependent effects on immune cell function, hepatic lipid metabolism, and neuroinflammatory processes linked to cholesterol transport.

ABC1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Abca1 expression without altering the underlying DNA sequence.

ABC1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Abca1 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 Abca1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ABC1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Abca1 locus and enabling the study of ABC1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ABC1 pathway restoration in tumor cells with silenced or reduced Abca1 expression.

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