
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CUL-3 Lentiviral Activation Particles (m) | sc-424091-LAC | 200 µl | $455.00 |
Mouse Cul3 encodes CUL-3, a cullin scaffold that assembles BTB–CUL3–RBX1 E3 ubiquitin ligase complexes to control proteostasis through selective ubiquitination and proteasomal degradation of diverse substrates. By partnering with BTB adaptor proteins, CUL-3 regulates oxidative stress signaling (including KEAP1–NRF2), cell-cycle progression, cytoskeletal organization, and endosomal trafficking, integrating ubiquitin-dependent control with broader signaling networks. Dysregulated CUL-3–dependent ubiquitination has been linked to altered redox homeostasis and aberrant signaling programs relevant to cancer biology, neurodevelopmental phenotypes, and cardiovascular-related pathways in model systems.
CUL-3 Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Cul3 upregulation across a broader range of human cell types.
CUL-3 Lentiviral Activation Particles (m) 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 Cul3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CUL-3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Cul3 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.