
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ABCA3 CRISPR Activation Plasmid (h) | sc-402388-ACT | 20 µg | $397.00 |
ABCA3 (ATP binding cassette subfamily A member 3) is a lipid transporter predominantly expressed in alveolar type II epithelial cells, where it localizes to lamellar bodies and supports surfactant phospholipid trafficking and packaging. As an ATP-dependent ABC transporter, ABCA3 contributes to intracellular membrane lipid homeostasis and vesicular transport processes that are essential for lung physiology. Disruption or reduced activity of ABCA3 is associated with impaired surfactant metabolism and has been linked to neonatal respiratory distress and interstitial lung disease phenotypes. ABCA3 biology is therefore widely studied in pathways involving lamellar body biogenesis, surfactant processing, and epithelial cell differentiation and stress responses.
ABCA3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ABCA3 expression without altering the underlying DNA sequence.
ABCA3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ABCA3 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 ABCA3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ABCA3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ABCA3 locus and enabling the study of ABCA3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ABCA3 pathway restoration in tumor cells with silenced or reduced ABCA3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.