BCoR CRISPR Activation Plasmid (h): sc-409976-ACT

BCOR (BCL6 corepressor) encodes BCoR, a nuclear transcriptional coregulator that partners with sequence-specific transcription factors and epigenetic modifiers to coordinate gene repression during development and lineage commitment. BCoR functions within noncanonical Polycomb repressive complexes, linking DNA-binding factors to chromatin remodeling and histone modification programs that shape cell identity and differentiation. Disruption or dysregulation of BCOR has been associated with altered transcriptional control in hematopoietic and mesenchymal contexts and is recurrently implicated in multiple tumor types and developmental disorders. As a chromatin-associated corepressor, BCoR is frequently studied for its role in transcriptional networks, cell fate transitions, and epigenetic stability.

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

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

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