MTDH Lentiviral Activation Particles (h): sc-413927-LAC

Human MTDH (metadherin/AEG-1) encodes a multifunctional scaffold protein that coordinates transcriptional and post-transcriptional programs linked to cell survival, inflammation, and stress adaptation. MTDH has been implicated in modulation of NF-κB and PI3K/AKT signaling, regulation of epithelial–mesenchymal transition, and control of RNA metabolism through interactions with ribonucleoprotein complexes. Altered MTDH expression is associated with aggressive tumor phenotypes, including enhanced invasion, metastasis, and therapy resistance, and it is also studied in the context of neuroinflammation and metabolic dysregulation. These properties make MTDH a relevant node for dissecting oncogenic signaling networks, gene regulatory circuits, and microenvironmental response pathways in human cell models.

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

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