Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
ARID3B Lentiviral Activation Particles (h): sc-411492-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- ARID3B Lentiviral Activation Particles (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
- ARID3B Lentiviral Activation Particles (h) contain the following SAM Activation elements: a deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, an MS2-p65-HSF1 fusion protein and a target-specific 20 nt guide RNA. They also contain the blasticidin, hygromycin and puromycin resistance genes
- Upon transduction, the SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by ARID3B Lentiviral Activation Plasmid (h) and ARID3B Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the ARID3B promoter. One or both designs may be available
- Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: ARID3B Antibody (C-6): sc-514741
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARID3B Lentiviral Activation Particles (h) | sc-411492-LAC | 200 µl | $455.00 |
ARID3B encodes an AT-rich interactive domain (ARID) DNA-binding protein that functions as a transcriptional regulator influencing cell fate decisions, lineage specification, and chromatin-dependent gene expression programs. As part of broader transcriptional and epigenetic control networks, ARID3B can modulate promoter and enhancer activity to shape proliferation, differentiation, and survival pathways. Dysregulated ARID3B expression has been reported in multiple cancer contexts and is studied for its impact on oncogenic transcriptional states, invasive phenotypes, and tumor cell plasticity. In addition, ARID3B is used as a molecular entry point to interrogate transcription factor circuitry and chromatin remodeling dynamics in human cells.
ARID3B 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 ARID3B upregulation across a broader range of human cell types.
ARID3B 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 ARID3B transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ARID3B expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native ARID3B 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.