ΔN p73 CRISPR Activation Plasmid (h): sc-437274-ACT

Human ΔN p73 is an N-terminally truncated TP73 isoform that modulates transcriptional programs controlling cell-cycle progression, apoptosis resistance, differentiation, and cellular stress responses. By lacking the canonical transactivation domain, ΔN p73 can act in a dominant-negative manner toward p53 family members, reshaping downstream signaling networks that govern DNA damage responses and mitochondrial apoptosis. Altered ΔN p73 expression has been linked to dysregulated proliferation and survival phenotypes in multiple disease-relevant contexts, including tumor biology and neurodevelopmental processes. Its activity intersects with checkpoint control, chromatin regulation, and lineage-specific gene expression, making it a useful node for studying p53-family pathway rewiring.

ΔN p73 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous expression without altering the underlying DNA sequence.

ΔN p73 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the 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 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ΔN p73 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native locus and enabling the study of ΔN p73-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ΔN p73 pathway restoration in tumor cells with silenced or reduced expression.

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