BAF170 CRISPR Activation Plasmid (h): sc-402023-ACT

SMARCC2 encodes BAF170, a core scaffold subunit of the ATP-dependent SWI/SNF (BAF) chromatin remodeling complex that modulates nucleosome positioning to regulate transcriptional programs. BAF170 contributes to enhancer and promoter accessibility, influencing lineage specification, cell-cycle control, and DNA damage–responsive transcription through coordinated chromatin remodeling. As part of the broader BAF/PBAF network, SMARCC2 interfaces with pathways governing differentiation, chromatin organization, and epigenetic stability. Dysregulation of SWI/SNF subunits is recurrent in human disease, and SMARCC2 perturbation has been linked to altered developmental gene expression and vulnerabilities in chromatin-dependent oncogenic contexts.

BAF170 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SMARCC2 expression without altering the underlying DNA sequence.

BAF170 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SMARCC2 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 SMARCC2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BAF170 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SMARCC2 locus and enabling the study of BAF170-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BAF170 pathway restoration in tumor cells with silenced or reduced SMARCC2 expression.

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