ABCA7 CRISPR Activation Plasmid (h): sc-403762-ACT

ABCA7 (ATP-binding cassette subfamily A member 7) is a human lipid transporter implicated in phospholipid and cholesterol homeostasis through ATP-dependent transmembrane transport. It is enriched in immune and neural contexts where it supports membrane remodeling, endocytic trafficking, and phagocytic clearance, linking lipid handling to innate immune signaling and cellular stress responses. ABCA7 activity intersects with pathways governing vesicle dynamics and lipid raft composition, influencing receptor signaling and antigen processing. Genetic and functional studies associate ABCA7 with neurodegenerative disease susceptibility and altered amyloid-related processing, making it relevant for mechanistic work in microglia-like models and neuronal systems.

ABCA7 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ABCA7 expression without altering the underlying DNA sequence.

ABCA7 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ABCA7 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 ABCA7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ABCA7 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ABCA7 locus and enabling the study of ABCA7-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ABCA7 pathway restoration in tumor cells with silenced or reduced ABCA7 expression.

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