MICA Lentiviral Activation Particles (h): sc-418864-LAC

Human MICA encodes MHC class I polypeptide–related sequence A, a stress-inducible ligand displayed on the cell surface that engages the activating receptor NKG2D on NK cells and subsets of CD8⁺ T cells. Its expression is regulated by DNA damage and cellular stress pathways, and it interfaces with immune surveillance programs controlling cytotoxic recognition and cytokine signaling. MICA is also subject to proteolytic shedding and allelic variation, processes that can modulate NKG2D signaling strength and immune evasion. Dysregulated MICA expression and shedding have been associated with tumor immunobiology, viral infection responses, and inflammatory conditions, making it a useful node for studying innate–adaptive immune crosstalk.

MICA 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 MICA upregulation across a broader range of human cell types.

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