BRCA1 Lentiviral Activation Particles (h): sc-400093-LAC

BRCA1 encodes the human BRCA1 tumor suppressor, a multifunctional nuclear protein essential for maintaining genome integrity. BRCA1 coordinates DNA double-strand break repair through homologous recombination, contributes to checkpoint signaling, and interfaces with replication stress responses and chromatin remodeling via protein complexes such as BRCA1–BARD1. Through ubiquitin ligase activity and regulation of transcription and DNA damage foci dynamics, BRCA1 helps control cell-cycle progression and preserves chromosomal stability. Disruption or dysregulation of BRCA1 is strongly associated with impaired DNA repair capacity and elevated genomic instability, making it a key node in DNA damage response pathways relevant to cancer biology research.

BRCA1 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 BRCA1 upregulation across a broader range of human cell types.

BRCA1 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 BRCA1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous BRCA1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native BRCA1 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.