Axl Lentiviral Activation Particles (h): sc-400393-LAC

Human AXL encodes Axl, a receptor tyrosine kinase of the TAM family that is activated primarily by GAS6 and signals through PI3K–AKT, MAPK/ERK, NF-κB, and STAT pathways to regulate cell survival, proliferation, migration, and epithelial-to-mesenchymal transition. Axl also modulates innate immune signaling by promoting efferocytosis and shaping inflammatory tone, linking tumor–immune interactions with tissue homeostasis. Dysregulated AXL expression or activity is frequently associated with invasive phenotypes, metastatic competence, and drug-tolerant states across multiple cancer models, and it has been implicated in fibrotic remodeling and chronic inflammatory contexts. As a result, AXL is widely studied as a node connecting receptor tyrosine kinase crosstalk, adhesion dynamics, and cytokine-driven signaling programs.

Axl 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 AXL upregulation across a broader range of human cell types.

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