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.
PRCC CRISPR Activation Plasmid (h): sc-407693-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PRCC CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- PRCC 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 PRCC CRISPR Activation Plasmid (h) and PRCC CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the PRCC 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: PRCC Antibody (D-3): sc-390527
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PRCC CRISPR Activation Plasmid (h) | sc-407693-ACT | 20 µg | $397.00 | |||
PRCC CRISPR Activation Plasmid (h2) | sc-407693-ACT-2 | 20 µg | $397.00 |
PRCC (papillary renal cell carcinoma translocation-associated) encodes a nuclear protein implicated in pre-mRNA splicing and transcriptional control through interactions with RNA-processing and regulatory complexes. It contributes to cellular programs governing gene expression fidelity, cell-cycle progression, and maintenance of nuclear architecture. PRCC is best known for involvement in chromosomal rearrangements observed in papillary renal cell carcinoma, where altered PRCC-associated regulation can perturb downstream transcriptional networks. As a research target, PRCC supports studies of spliceosome-linked mechanisms, oncogenic transcriptional dysregulation, and context-dependent effects on proliferation and stress-response pathways.
PRCC CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PRCC expression without altering the underlying DNA sequence.
PRCC CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PRCC 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 PRCC transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PRCC expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PRCC locus and enabling the study of PRCC-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PRCC pathway restoration in tumor cells with silenced or reduced PRCC expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.