TIM-3 Lentiviral Activation Particles (h): sc-416365-LAC

HAVCR2 encodes T cell immunoglobulin and mucin domain–containing protein 3 (TIM-3), an immunoregulatory receptor expressed on activated T cells and other immune subsets that helps calibrate effector function, exhaustion, and peripheral tolerance. TIM-3 signaling interfaces with checkpoint control and inflammatory circuits, influencing cytokine production, antigen-specific responses, and the balance between immune activation and suppression. Dysregulated HAVCR2/TIM-3 activity has been associated with chronic infection and tumor-associated immune dysfunction, and it is also implicated in autoimmune and inflammatory disease contexts through its effects on T cell differentiation and myeloid cell crosstalk. These properties make HAVCR2 a relevant target for dissecting mechanisms of immune evasion, tolerance breakdown, and immune cell state transitions.

TIM-3 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 HAVCR2 upregulation across a broader range of human cell types.

TIM-3 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 HAVCR2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TIM-3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native HAVCR2 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.