MIAT Lentiviral Activation Particles (h2): sc-437346-LAC-2

Human MIAT (myocardial infarction–associated transcript) is a long noncoding RNA that functions as a regulatory scaffold in the nucleus and cytoplasm, modulating gene expression through interactions with chromatin-associated complexes and by acting as a competing endogenous RNA that sequesters microRNAs. It influences key cellular programs including transcriptional control, RNA processing, cell-cycle progression, apoptosis, and stress responses, with downstream effects on signaling networks implicated in vascular biology, neural differentiation, and inflammatory regulation. Dysregulated MIAT expression has been reported across cardiovascular and neurodegenerative contexts as well as multiple cancer types, where it is linked to altered proliferation, angiogenesis, and cell fate decisions. Gene editing or perturbation of MIAT enables mechanistic dissection of lncRNA-mediated regulatory circuits, mapping of miRNA–lncRNA–mRNA axes, and functional studies using disease-relevant human cell models and transcriptomic/epigenomic readouts.

MIAT Lentiviral Activation Particles (h2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient upregulation across a broader range of human cell types.

MIAT Lentiviral Activation Particles (h2) 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 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MIAT expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native 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.