
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FAT10 Lentiviral Activation Particles (m) | sc-423986-LAC | 200 µl | $455.00 | |||
FAT10 Lentiviral Activation Particles (m2) | sc-423986-LAC-2 | 200 µl | $455.00 |
Mouse Ubd encodes FAT10 (ubiquitin D), a ubiquitin-like modifier that covalently conjugates to target proteins to promote rapid turnover by the 26S proteasome. FAT10ylation functions largely independently of canonical ubiquitin chains and is linked to inflammatory signaling, interferon-responsive programs, and antigen processing via MHC class I pathways. Ubd/FAT10 expression is inducible by pro-inflammatory cytokines and can reshape proteostasis, cell-cycle regulation, and stress-adaptive responses through altered protein stability. Dysregulated FAT10 has been associated with inflammatory states and cancer-relevant phenotypes in experimental models, making it a useful node for studying immune-metabolic crosstalk and proteasome-dependent regulation.
FAT10 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 Ubd upregulation across a broader range of human cell types.
FAT10 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 Ubd transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous FAT10 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Ubd 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.