Sos 1 Lentiviral Activation Particles (h): sc-401135-LAC

SOS1 encodes Son of sevenless homolog 1 (Sos 1), a Ras guanine nucleotide exchange factor that catalyzes GDP-to-GTP exchange on RAS downstream of activated receptor tyrosine kinases and adaptor complexes such as GRB2. By coupling growth factor signaling to RAS–RAF–MEK–ERK and intersecting with PI3K–AKT pathway activity, Sos 1 contributes to regulation of proliferation, differentiation, migration, and cytoskeletal dynamics. Altered SOS1 function or dysregulated upstream signaling can shift MAPK output and is relevant to studies of oncogenic signaling dependencies and developmental Rasopathy-associated mechanisms. SOS1 is therefore a useful node for dissecting stimulus-specific MAPK amplitude and duration, feedback control, and pathway crosstalk in human cells.

Sos 1 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 SOS1 upregulation across a broader range of human cell types.

Sos 1 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 SOS1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Sos 1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SOS1 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.