
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARID1B Lentiviral Activation Particles (h) | sc-402365-LAC | 200 µl | $455.00 |
ARID1B encodes a core subunit of the SWI/SNF (BAF) ATP-dependent chromatin remodeling complex that regulates nucleosome positioning and chromatin accessibility to control transcriptional programs. Through remodeling of enhancer and promoter architecture, ARID1B influences lineage specification, cell-cycle progression, and DNA damage response networks, integrating signals across developmental and differentiation pathways. Altered ARID1B activity perturbs epigenetic regulation and transcription factor occupancy, impacting cellular identity and chromatin state maintenance. Genetic disruption or dysregulation of ARID1B has been linked to neurodevelopmental phenotypes and cancer-associated chromatin remodeling defects, making it a widely studied node in transcriptional and epigenome-focused research.
ARID1B 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 ARID1B upregulation across a broader range of human cell types.
ARID1B 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 ARID1B transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ARID1B expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native ARID1B 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.