c-Kit Lentiviral Activation Particles (m): sc-421289-LAC

Mouse Kit encodes c-Kit (CD117), a class III receptor tyrosine kinase that binds stem cell factor (SCF) to regulate hematopoietic stem and progenitor maintenance, mast cell development, melanocyte biology, and germ cell survival. Ligand-dependent receptor dimerization triggers autophosphorylation and engages PI3K–AKT, RAS–MAPK/ERK, JAK/STAT, and SRC-family signaling to coordinate proliferation, migration, and survival. Dysregulated KIT signaling and altered receptor expression are widely used as mechanistic entry points for studying lineage commitment, tissue homeostasis, and oncogenic receptor tyrosine kinase networks in model systems. In mice, Kit is also a key marker and functional node for dissecting stromal–immune crosstalk and niche-dependent regulation of stem cell behavior.

c-Kit Lentiviral Activation Particles (m) 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 (m) 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.