ARID3A Lentiviral Activation Particles (h2): sc-404552-LAC-2

Human ARID3A encodes a DNA-binding transcription factor of the AT-rich interaction domain family that regulates chromatin accessibility and cell type–specific gene expression programs. ARID3A is implicated in B cell development and activation, modulation of interferon-responsive transcription, and coordination of transcriptional networks linked to differentiation and proliferation. Dysregulated ARID3A expression and altered regulatory activity have been associated with immune dysfunction and malignancy-related transcriptional states, including contexts relevant to hematologic cancers and autoimmune phenotypes. Gene editing of ARID3A enables mechanistic studies of enhancer–promoter control, lineage commitment, and cytokine-driven signaling outputs, supporting functional genomics screens and pathway mapping in human cellular models.

ARID3A 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 ARID3A upregulation across a broader range of human cell types.

ARID3A 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 ARID3A transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ARID3A expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native ARID3A 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.