BAZ2B CRISPR Activation Plasmid (h): sc-407635-ACT

BAZ2B (bromodomain adjacent to zinc finger domain protein 2B) is a chromatin-associated regulator that binds acetylated histones through its bromodomain and contributes to nucleosome remodeling and transcriptional control. By coordinating chromatin accessibility, BAZ2B influences RNA polymerase II–dependent gene expression programs involved in cell identity, proliferation, and differentiation. Altered chromatin reader activity and dysregulated transcriptional networks are recurrent features of cancer and neurodevelopmental phenotypes, making BAZ2B a useful node for studying epigenetic pathway perturbations. Investigating BAZ2B function supports mechanistic research into histone acetylation signaling, chromatin remodeling dynamics, and context-specific gene regulation.

BAZ2B CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BAZ2B expression without altering the underlying DNA sequence.

BAZ2B CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BAZ2B 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 BAZ2B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BAZ2B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BAZ2B locus and enabling the study of BAZ2B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BAZ2B pathway restoration in tumor cells with silenced or reduced BAZ2B expression.

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