
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PLSCR1 CRISPR Activation Plasmid (h) | sc-402203-ACT | 20 µg | $397.00 |
Human PLSCR1 (phospholipid scramblase 1) is an interferon-inducible membrane-associated protein implicated in bidirectional phospholipid translocation, plasma membrane remodeling, and regulation of cell-surface phosphatidylserine exposure during cellular stress responses. Beyond lipid dynamics, PLSCR1 has been linked to innate immune signaling and transcriptional programs downstream of interferon/JAK–STAT pathways, influencing antiviral responses and cell growth control. Altered PLSCR1 expression has been reported across multiple tumor contexts and inflammatory states, making it a useful node for studying mechanisms connecting membrane organization, cytokine signaling, and immune-mediated phenotypes. Its broad subcellular localization and pathway connectivity support applications in dissecting signal transduction, apoptosis-related membrane changes, and host–pathogen response networks.
PLSCR1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PLSCR1 expression without altering the underlying DNA sequence.
PLSCR1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PLSCR1 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 PLSCR1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PLSCR1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PLSCR1 locus and enabling the study of PLSCR1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PLSCR1 pathway restoration in tumor cells with silenced or reduced PLSCR1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.