TMEM192 Lentiviral Activation Particles (h): sc-415021-LAC

TMEM192 encodes a multi-pass transmembrane protein that localizes predominantly to late endosomes and lysosomes, where it is used as a marker for lysosomal membranes and is implicated in membrane organization and organelle homeostasis. By influencing lysosome-related processes such as vesicular trafficking, cargo turnover, and responses to cellular stress, TMEM192 can modulate pathways connected to autophagy–lysosome function and endolysosomal maturation. Dysregulation of lysosomal dynamics and proteostasis is relevant to mechanisms studied in neurodegeneration, metabolic stress, and cancer cell adaptation, making TMEM192 a useful entry point for interrogating organelle-centered phenotypes. Measuring TMEM192-linked changes in lysosomal abundance, acidification, and trafficking can support studies of proteome clearance and intracellular compartment remodeling.

TMEM192 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 TMEM192 upregulation across a broader range of human cell types.

TMEM192 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 TMEM192 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TMEM192 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TMEM192 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.