
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Ras-GRF2 Lentiviral Activation Particles (h) | sc-404141-LAC | 200 µl | $455.00 |
Human RASGRF2 encodes Ras-GRF2, a calcium- and calmodulin-regulated guanine nucleotide exchange factor that activates Ras and related small GTPases, coupling neuronal activity and growth factor inputs to MAPK/ERK signaling. Through modulation of synaptic plasticity, neurite outgrowth, and activity-dependent transcriptional programs, Ras-GRF2 contributes to cellular processes such as differentiation, migration, and cytoskeletal remodeling. Aberrant Ras pathway dynamics and altered RASGRF2 expression or regulation have been associated with dysregulated signaling states relevant to cancer biology and neurobiological phenotypes. RASGRF2 is therefore studied as an upstream signaling node that shapes stimulus-dependent ERK output and downstream gene expression networks.
Ras-GRF2 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 RASGRF2 upregulation across a broader range of human cell types.
Ras-GRF2 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 RASGRF2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Ras-GRF2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native RASGRF2 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.