BRD9 CRISPR Activation Plasmid (h): sc-404933-ACT

BRD9 encodes bromodomain-containing protein 9, an epigenetic reader that recognizes acetyl-lysine marks on histones and helps coordinate chromatin accessibility and transcriptional output. BRD9 functions as a subunit of non-canonical SWI/SNF (ncBAF) chromatin remodeling complexes, linking histone acetylation to ATP-dependent nucleosome positioning and enhancer regulation. Through these activities, BRD9 contributes to control of cell state programs including proliferation, differentiation, and stress-responsive transcription. Dysregulated BRD9-associated chromatin remodeling has been implicated across multiple disease-relevant contexts, particularly in cancers where altered transcriptional circuitry and lineage dependency are common research themes.

BRD9 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BRD9 expression without altering the underlying DNA sequence.

BRD9 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BRD9 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 BRD9 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BRD9 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BRD9 locus and enabling the study of BRD9-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BRD9 pathway restoration in tumor cells with silenced or reduced BRD9 expression.

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