TP53INP1 CRISPR Activation Plasmid (h): sc-402835-ACT

TP53INP1 (tumor protein p53 inducible nuclear protein 1) is a stress-responsive nuclear protein induced by p53 and related transcriptional programs during DNA damage and oxidative stress. It modulates cell cycle control, apoptosis, and autophagy through interactions that influence p53-dependent transcriptional outputs and broader stress-adaptation networks. Altered TP53INP1 expression has been linked to dysregulated stress signaling, proliferation, and survival pathways that are frequently perturbed in cancer biology and inflammatory contexts. As a nodal regulator of cellular stress responses, TP53INP1 is commonly studied for its impact on checkpoint regulation, mitochondrial integrity, and transcriptional reprogramming under genotoxic conditions.

TP53INP1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TP53INP1 expression without altering the underlying DNA sequence.

TP53INP1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TP53INP1 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 TP53INP1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TP53INP1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TP53INP1 locus and enabling the study of TP53INP1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TP53INP1 pathway restoration in tumor cells with silenced or reduced TP53INP1 expression.

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