Bcl-6 Lentiviral Activation Particles (h2): sc-400265-LAC-2

Human BCL6 encodes the Bcl-6 transcriptional repressor, a BTB/POZ zinc-finger protein that regulates germinal center B-cell fate by silencing target genes involved in DNA damage responses, cell-cycle checkpoints, apoptosis, and differentiation. Bcl-6 coordinates transcriptional programs downstream of antigen receptor and cytokine signaling, shaping germinal center reactions, somatic hypermutation, and class-switch recombination through epigenetic corepressor complexes. Dysregulated BCL6 expression or activity perturbs lymphocyte homeostasis and is implicated in lymphoid malignancies and aberrant immune regulation. Gene editing of BCL6 enables mechanistic studies of transcriptional repression networks, enhancer–promoter control, and immune cell differentiation in relevant human cell models.

Bcl-6 Lentiviral Activation Particles (h2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient BCL6 upregulation across a broader range of human cell types.

Bcl-6 Lentiviral Activation Particles (h2) 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 BCL6 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Bcl-6 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native BCL6 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.