ABCG1 CRISPR Activation Plasmid (m): sc-418933-ACT

Mouse Abcg1 encodes the ATP-binding cassette transporter ABCG1, a key regulator of intracellular lipid homeostasis that promotes cholesterol and phospholipid efflux to HDL and helps maintain membrane composition. ABCG1 activity interfaces with LXR/RXR-driven transcriptional programs and shapes macrophage foam cell biology, inflammatory signaling, and lipid handling in immune and metabolic tissues. In addition to roles in macrophages, ABCG1 contributes to pulmonary surfactant balance and cellular responses to oxidative and metabolic stress. Dysregulated ABCG1 expression or function is therefore relevant to studies of atherosclerosis-related pathways, metabolic inflammation, and lung lipid dysregulation in mouse models.

ABCG1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Abcg1 expression without altering the underlying DNA sequence.

ABCG1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Abcg1 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 Abcg1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ABCG1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Abcg1 locus and enabling the study of ABCG1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ABCG1 pathway restoration in tumor cells with silenced or reduced Abcg1 expression.

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