
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MDA5 Lentiviral Activation Particles (m) | sc-427977-LAC | 200 µl | $455.00 | |||
MDA5 Lentiviral Activation Particles (m2) | sc-427977-LAC-2 | 200 µl | $455.00 |
Mouse Ifih1 encodes melanoma differentiation–associated protein 5 (MDA5), a cytosolic DExD/H-box RNA helicase that detects long double-stranded RNA generated during viral replication. Upon RNA binding, MDA5 signals through MAVS to activate TBK1/IKKε and downstream IRF3/IRF7 and NF-κB programs, inducing type I interferons and interferon-stimulated genes. This pathway shapes innate antiviral immunity, crosstalks with autophagy and inflammasome-associated responses, and influences antigen presentation and inflammatory tone. Dysregulated MDA5 signaling has been implicated in aberrant interferon signatures and immune-mediated pathology, making Ifih1 a useful node for dissecting innate immune activation and inflammation-relevant phenotypes in mouse models.
MDA5 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 Ifih1 upregulation across a broader range of human cell types.
MDA5 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 Ifih1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MDA5 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Ifih1 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.