
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BAZ2B Lentiviral Activation Particles (h) | sc-407635-LAC | 200 µl | $455.00 |
BAZ2B encodes a bromodomain-containing chromatin regulator that recognizes acetylated histones and helps coordinate ATP-dependent nucleosome remodeling to shape transcriptional programs. Through its roles in chromatin accessibility and gene expression control, BAZ2B contributes to processes such as cell-cycle regulation, DNA damage responses, and lineage-specific differentiation. Altered regulation of bromodomain proteins and chromatin remodeling pathways is frequently linked to dysregulated transcriptional states relevant to cancer biology and neurodevelopmental phenotypes, making BAZ2B a useful node for mechanistic epigenetics studies. Human BAZ2B is therefore commonly investigated in the context of transcriptional control, chromatin state transitions, and pathway rewiring during cellular stress and disease-associated signaling.
BAZ2B 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 BAZ2B upregulation across a broader range of human cell types.
BAZ2B 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 BAZ2B transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous BAZ2B expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native BAZ2B 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.