
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PB1 CRISPR Activation Plasmid (h) | sc-403988-ACT | 20 µg | $397.00 |
PBRM1 encodes the PB1 subunit of the PBAF form of the SWI/SNF (BAF) ATP-dependent chromatin remodeling complex, where its bromodomains recognize acetylated histones to regulate promoter and enhancer accessibility. Through coordination of nucleosome positioning, PB1 helps control transcriptional programs linked to DNA damage responses, differentiation, and maintenance of genome stability. Altered PBRM1 function is recurrently associated with disrupted epigenetic regulation and transcriptional dysregulation in human disease contexts, including cancers where chromatin remodeling pathways are frequently perturbed. These properties make PB1 a useful node for studying chromatin-state control of gene expression and pathway rewiring under stress and developmental cues.
PB1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PBRM1 expression without altering the underlying DNA sequence.
PB1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PBRM1 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 PBRM1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PB1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PBRM1 locus and enabling the study of PB1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PB1 pathway restoration in tumor cells with silenced or reduced PBRM1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.