Rac 1 Lentiviral Activation Particles (m2): sc-422573-LAC-2

Mouse Rac1 encodes the small GTPase Rac1, a central regulator of actin cytoskeleton dynamics that controls lamellipodia formation, cell migration, adhesion, and polarity through cycling between GDP- and GTP-bound states. Rac1 signaling integrates cues from receptor tyrosine kinases and GPCRs to coordinate pathways including PI3K–AKT, PAK–MAPK, and NADPH oxidase–dependent reactive oxygen species production, shaping proliferation, survival, and innate immune functions. Dysregulated Rac1 activity is linked to aberrant tissue morphogenesis, inflammatory responses, and oncogenic signaling programs, making it a key node in studies of tumor cell invasion, vascular biology, and neurodevelopment. Gene editing of mouse Rac1 enables mechanistic dissection of Rho GTPase networks in vivo and in cultured cells, supporting assays of cytoskeletal remodeling, signal transduction, and cell-state transitions.

Rac 1 Lentiviral Activation Particles (m2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Rac1 upregulation across a broader range of human cell types.

Rac 1 Lentiviral Activation Particles (m2) 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 Rac1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Rac 1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Rac1 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.