
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TARDBP Lentiviral Activation Particles (m) | sc-433014-LAC | 200 µl | $455.00 |
Mouse Tardbp encodes TARDBP (TDP-43), a ubiquitously expressed RNA/DNA-binding protein that regulates pre-mRNA splicing, RNA transport, mRNA stability, and microRNA biogenesis. TARDBP functions in RNA metabolism pathways and stress granule dynamics, and it shuttles between the nucleus and cytoplasm to coordinate gene expression programs linked to neuronal maintenance and cellular homeostasis. Perturbation of TARDBP levels or localization is associated with altered RNA processing, proteostasis imbalance, and dysregulated responses to cellular stress. These features make Tardbp a central research target in studies of RNA-binding protein networks, neurodegeneration-relevant mechanisms, and transcriptome-wide regulation.
TARDBP 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 Tardbp upregulation across a broader range of human cell types.
TARDBP 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 Tardbp transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TARDBP expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Tardbp 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.