Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
p53 CRISPR Activation Plasmid (h): sc-416469-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- p53 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- p53 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by p53 CRISPR Activation Plasmid (h) and p53 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the TP53 transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: p53 Antibody (DO-1): sc-126
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
p53 CRISPR Activation Plasmid (h) | sc-416469-ACT | 20 µg | $397.00 | |||
p53 CRISPR Activation Plasmid (h2) | sc-416469-ACT-2 | 20 µg | $397.00 |
TP53 encodes the human tumor suppressor p53, a sequence-specific transcription factor that integrates DNA damage sensing, oncogenic stress, and cell cycle checkpoints to maintain genomic stability. p53 regulates programs controlling G1/S and G2/M arrest, apoptosis, senescence, and DNA repair through canonical pathways involving ATM/ATR signaling and transcriptional targets such as CDKN1A (p21), BAX, and MDM2. Disruption of TP53 function is frequent in cancer and is associated with altered stress responses, chromosomal instability, and broad transcriptional rewiring. As a central node in cellular stress biology, p53 is widely studied in mechanisms of transformation, resistance to genotoxic stress, and pathway crosstalk with PI3K–AKT and MAPK signaling.
p53 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TP53 expression without altering the underlying DNA sequence.
p53 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TP53 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 TP53 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous p53 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TP53 locus and enabling the study of p53-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of p53 pathway restoration in tumor cells with silenced or reduced TP53 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.