
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TMEM173 Lentiviral Activation Particles (m) | sc-428364-LAC | 200 µl | $455.00 |
Mouse Tmem173 encodes TMEM173 (also known as STING), an endoplasmic reticulum adaptor that couples cytosolic DNA sensing to innate immune signaling. Upon binding cyclic dinucleotides generated by cGAS or bacterial enzymes, TMEM173 promotes TBK1 and IRF3 activation and can engage NF-κB programs, driving type I interferon and inflammatory transcriptional responses. This pathway interfaces with autophagy, cell death, and metabolic stress signaling, and is widely used to model host defense mechanisms. Dysregulated TMEM173 signaling is implicated in interferon-driven inflammatory phenotypes and contributes to tumor–immune crosstalk and responses to cytosolic nucleic acids in diverse mouse disease models.
TMEM173 Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Tmem173 upregulation across a broader range of human cell types.
TMEM173 Lentiviral Activation Particles (m) 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 Tmem173 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TMEM173 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Tmem173 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.