TMEM97 Lentiviral Activation Particles (h): sc-411997-LAC

TMEM97 encodes transmembrane protein 97, an endoplasmic reticulum–resident component of the sigma-2 receptor complex that modulates cellular cholesterol homeostasis and lipid trafficking. TMEM97 has been linked to regulation of low-density lipoprotein uptake through interactions with lipoprotein receptors and to broader membrane organization processes that influence signaling and metabolic adaptation. By shaping sterol distribution and proteostasis in the secretory pathway, TMEM97 can impact stress-response networks and organelle function. Altered TMEM97 expression and sigma-2 receptor–associated biology have been investigated in contexts including neurodegeneration, metabolic dysregulation, and cancer-related cell state changes, supporting its utility as a mechanistic target in pathway studies.

TMEM97 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 TMEM97 upregulation across a broader range of human cell types.

TMEM97 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 TMEM97 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TMEM97 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TMEM97 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.