
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Ape2 Lentiviral Activation Particles (h) | sc-407307-LAC | 200 µl | $455.00 |
Human APEX2 (Ape2) encodes a DNA repair nuclease implicated in maintaining genome stability during DNA replication and in response to oxidative and alkylation damage. Ape2 participates in base excision repair and processing of abasic sites, coordinating with replication and checkpoint pathways to limit replication stress and DNA strand break accumulation. Altered APEX2 activity has been associated with defects in damage signaling, increased mutational burden, and cellular hypersensitivity to genotoxic stressors, linking it to cancer biology and broader mechanisms of genome maintenance. As a research target, APEX2 enables mechanistic studies of DNA repair pathway choice, replication fork integrity, and stress-induced signaling networks.
Ape2 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 APEX2 upregulation across a broader range of human cell types.
Ape2 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 APEX2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Ape2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native APEX2 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.