
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BRCA2 Lentiviral Activation Particles (h) | sc-400700-LAC | 200 µl | $455.00 | |||
BRCA2 Lentiviral Activation Particles (h2) | sc-400700-LAC-2 | 200 µl | $455.00 |
BRCA2 encodes a central tumor suppressor that safeguards genome integrity by coordinating high-fidelity repair of DNA double-strand breaks through homologous recombination. BRCA2 promotes RAD51 filament formation and regulates replication fork protection, linking it to DNA damage response signaling, S-phase checkpoint control, and maintenance of chromosomal stability. Disruption or dysregulation of BRCA2 function is strongly associated with hereditary and sporadic cancer susceptibility, reflecting its role in preventing mutational accumulation and aberrant recombination. BRCA2 is therefore widely studied in pathways governing replication stress, recombination-mediated repair, and genome maintenance phenotypes relevant to oncogenic transformation.
BRCA2 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 BRCA2 upregulation across a broader range of human cell types.
BRCA2 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 BRCA2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous BRCA2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native BRCA2 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.