
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Vav Lentiviral Activation Particles (h) | sc-400606-LAC | 200 µl | $455.00 |
Human VAV1 encodes Vav, a hematopoietic guanine nucleotide exchange factor that links immunoreceptor and cytokine signaling to Rho family GTPases, including RAC1 and CDC42. Upon phosphorylation downstream of TCR/BCR and Fc receptor pathways, Vav coordinates actin cytoskeleton remodeling, integrin activation, calcium flux, and transcriptional programs that shape lymphocyte development, activation, and effector function. VAV1 activity intersects with PI3K–AKT, PLCγ, and MAPK signaling to regulate cell adhesion, migration, and immune synapse formation. Dysregulated VAV1 signaling and mutations have been associated with immune dysfunction and oncogenic signaling in hematologic malignancies, supporting its use in studies of immune signaling networks and transformation mechanisms.
Vav 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 VAV1 upregulation across a broader range of human cell types.
Vav 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 VAV1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Vav expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native VAV1 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.