
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Fis1 Lentiviral Activation Particles (m) | sc-426020-LAC | 200 µl | $455.00 |
Mouse Fis1 (fission 1) encodes an outer mitochondrial membrane protein that helps coordinate mitochondrial fission by engaging the DRP1 machinery and organizing scission sites, thereby shaping mitochondrial morphology and distribution. Through its effects on mitochondrial dynamics, Fis1 influences mitophagy, oxidative phosphorylation efficiency, reactive oxygen species homeostasis, and apoptosis signaling. Perturbation of Fis1-regulated fission–fusion balance has been linked to mitochondrial stress phenotypes relevant to neurodegeneration, cardiometabolic dysfunction, and inflammatory signaling in diverse model systems. As a result, Fis1 is frequently used to study mitochondrial quality control pathways and organelle-dependent regulation of cellular metabolism and survival.
Fis1 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 Fis1 upregulation across a broader range of human cell types.
Fis1 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 Fis1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Fis1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Fis1 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.