c-Kit Lentiviral Activation Particles (h): sc-400106-LAC

Human KIT encodes the receptor tyrosine kinase c-Kit (CD117), a cell-surface receptor activated by stem cell factor that regulates cell survival, proliferation, differentiation, and migration. Ligand-dependent c-Kit signaling propagates through PI3K–AKT, RAS–MAPK, JAK–STAT, and SRC family kinase pathways, shaping hematopoiesis, melanocyte biology, germ cell development, and mast cell function. Aberrant KIT activity is implicated in oncogenic growth programs and altered microenvironmental signaling, while dysregulated c-Kit expression can perturb lineage commitment and immune cell activation states. Accordingly, KIT is widely studied as a context-dependent regulator of stem/progenitor cell behavior, receptor trafficking, and signal transduction dynamics.

c-Kit 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 KIT upregulation across a broader range of human cell types.

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