
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DOCK 7 Lentiviral Activation Particles (h) | sc-404461-LAC | 200 µl | $455.00 |
DOCK7 encodes a member of the DOCK family of atypical guanine nucleotide exchange factors that preferentially activates Rac1 and Cdc42 to regulate actin cytoskeleton remodeling. Through control of membrane ruffling, lamellipodia formation, and cell polarity, DOCK7 influences neurite outgrowth, neuronal migration, and other adhesion- and motility-linked processes. DOCK7 activity interfaces with Rho GTPase signaling networks and pathways governing vesicular trafficking and cytoskeletal dynamics. Genetic disruption of DOCK7 has been associated with neurodevelopmental phenotypes, supporting its relevance for studying mechanisms of neuronal differentiation and excitability in disease-relevant cell models.
DOCK 7 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 DOCK7 upregulation across a broader range of human cell types.
DOCK 7 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 DOCK7 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous DOCK 7 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native DOCK7 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.