
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
tsg 101 Lentiviral Activation Particles (h) | sc-400290-LAC | 200 µl | $455.00 |
TSG101 (tumor susceptibility gene 101) encodes tsg 101, an ESCRT-I core component that recognizes ubiquitinated cargo and coordinates endosomal sorting, multivesicular body biogenesis, and lysosomal degradation. Through ESCRT-dependent membrane remodeling, TSG101 also supports cytokinetic abscission and contributes to plasma membrane repair and autophagy-related trafficking. These activities intersect with receptor downregulation, signal termination, and proteostasis pathways that influence cell growth and stress responses. Dysregulated TSG101 expression or ESCRT function is frequently studied in cancer biology and in host–pathogen interactions where membrane budding and vesicle trafficking are perturbed.
tsg 101 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 TSG101 upregulation across a broader range of human cell types.
tsg 101 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 TSG101 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous tsg 101 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TSG101 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.