BCoR Lentiviral Activation Particles (h): sc-409976-LAC

BCOR encodes BCL6 corepressor (BCoR), a nuclear transcriptional coregulator that associates with BCL6 and other DNA-binding factors to modulate gene expression programs controlling differentiation, cell-cycle progression, and lineage specification. BCoR participates in epigenetic repression through multiprotein complexes linked to chromatin remodeling and histone modification, including Polycomb-associated pathways, thereby shaping developmental and hematopoietic transcriptional states. Dysregulated BCOR function has been connected to altered transcriptional repression networks in cancer biology and congenital developmental disorders, making it a useful node for studying context-dependent gene regulation. In human cells, BCOR activity is commonly investigated in the setting of transcription factor–driven programs, chromatin occupancy, and epigenome-to-phenotype relationships.

BCoR Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient BCOR upregulation across a broader range of human cell types.

BCoR Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the BCOR transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous BCoR expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native BCOR genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

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