
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CCDC69 Lentiviral Activation Particles (m) | sc-424629-LAC | 200 µl | $455.00 |
Mouse Ccdc69 encodes CCDC69, a coiled-coil domain–containing protein implicated in cytoskeletal organization and mitotic progression, with reported links to centrosome- and spindle-associated processes that help maintain genome stability. Coiled-coil scaffolding proteins commonly coordinate assembly of multi-protein complexes that regulate microtubule dynamics, checkpoint signaling, and cell-cycle–dependent remodeling. Altered regulation of these pathways can influence proliferation, aneuploidy, and stress responses, making Ccdc69 of interest for studying mechanisms that connect division fidelity to broader cellular homeostasis. In mouse model systems, modulation of Ccdc69 expression supports investigation of pathway-level effects on cell-cycle control and related disease-relevant phenotypes without implying clinical outcomes.
CCDC69 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 Ccdc69 upregulation across a broader range of human cell types.
CCDC69 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 Ccdc69 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CCDC69 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Ccdc69 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.