PLAC1 CRISPR Activation Plasmid (h): sc-403605-ACT

PLAC1 (placenta-specific protein 1) is a trophoblast-enriched, membrane-associated protein implicated in placental development and maternal–fetal interface biology. In human tissues it is typically restricted to placental compartments, while ectopic expression has been reported in multiple tumor contexts, supporting its use as a marker of altered differentiation programs. PLAC1 has been linked to processes that influence cell adhesion, proliferation, and immune-related signaling at the cell surface, although its precise mechanistic partners can vary by model system. Dysregulated PLAC1 expression is studied in reproductive biology and cancer research to interrogate transcriptional control, lineage identity, and microenvironmental interactions.

PLAC1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PLAC1 expression without altering the underlying DNA sequence.

PLAC1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PLAC1 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 PLAC1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PLAC1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PLAC1 locus and enabling the study of PLAC1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PLAC1 pathway restoration in tumor cells with silenced or reduced PLAC1 expression.

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