
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SMG5 Lentiviral Activation Particles (h) | sc-406989-LAC | 200 µl | $455.00 |
SMG5 encodes a core component of the nonsense-mediated mRNA decay (NMD) machinery that promotes surveillance and turnover of transcripts containing premature termination codons. SMG5 cooperates with SMG6 and SMG7 downstream of UPF1 phosphorylation to recruit protein phosphatase complexes and facilitate UPF1 dephosphorylation, coupling translational termination to mRNA decay. Through this role, SMG5 helps maintain RNA quality control, shapes transcriptome homeostasis, and influences responses to cellular stress and differentiation programs. Dysregulated NMD and altered SMG5 function have been linked to aberrant gene expression networks implicated in cancer biology and neurodevelopmental and neurodegenerative disease mechanisms, making SMG5 a useful node for pathway interrogation.
SMG5 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 SMG5 upregulation across a broader range of human cell types.
SMG5 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 SMG5 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous SMG5 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SMG5 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.