TMEM191B Lentiviral Activation Particles (h2): sc-417493-LAC-2

Human TMEM191B encodes transmembrane protein 191B, a predicted multi-pass membrane protein likely residing in intracellular or plasma membrane compartments and contributing to membrane organization and protein trafficking. Although TMEM191B remains poorly characterized, emerging annotations and expression patterns suggest roles in regulating vesicular transport, endomembrane dynamics, and cell signaling processes that depend on membrane microdomain composition. Altered regulation of membrane-associated trafficking and signaling networks is frequently implicated in cancer and neurodevelopmental or neurodegenerative phenotypes, making TMEM191B a useful target for probing pathway sensitivity to perturbations in membrane protein dosage. Gene editing of TMEM191B supports loss-of-function or tagging studies to map subcellular localization, identify interaction partners, and define its contribution to cellular homeostasis in human cell models.

TMEM191B 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 TMEM191B upregulation across a broader range of human cell types.

TMEM191B 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 TMEM191B transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TMEM191B expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TMEM191B 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.