MK Lentiviral Activation Particles (h): sc-402064-LAC

Human MDK encodes midkine (MK), a secreted heparin-binding growth factor that modulates cell proliferation, survival, migration, and neurite outgrowth during development and tissue repair. MK engages cell-surface proteoglycans and receptor complexes to activate signaling programs including MAPK/ERK, PI3K–AKT, and JAK/STAT, influencing inflammatory responses, angiogenic processes, and extracellular matrix remodeling. Dysregulated MDK expression has been reported across multiple pathological contexts, where it is associated with altered tumor–stromal interactions, immune cell recruitment, and neuroinflammatory or injury-associated responses. These properties make MDK a useful molecular node for studying cell-state transitions and microenvironmental signaling in cancer biology, neurobiology, and inflammation-focused research.

MK 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 MDK upregulation across a broader range of human cell types.

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