Midasin Lentiviral Activation Particles (h): sc-411690-LAC

Human MDN1 encodes midasin, a large AAA+ ATPase essential for nuclear ribosome biogenesis. Midasin coordinates late-stage maturation and quality control of the 60S preribosomal subunit by driving ATP-dependent remodeling and release of assembly factors, linking nucleolar function to proteostasis and cell-cycle progression. Through its role in ribosome production and translational capacity, MDN1 activity influences growth-control pathways and cellular stress responses. Disruption or dysregulation of ribosome biogenesis machinery, including MDN1-associated processes, is relevant to studies of genome stability, proliferative phenotypes, and ribosomopathy-like mechanisms in disease models.

Midasin 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 MDN1 upregulation across a broader range of human cell types.

Midasin 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 MDN1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Midasin expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native MDN1 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.