
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RNF4 Lentiviral Activation Particles (m) | sc-422689-LAC | 200 µl | $455.00 |
Mouse Rnf4 encodes RNF4, a SUMO-targeted ubiquitin E3 ligase that recognizes poly-SUMOylated substrates via SUMO-interacting motifs and promotes their ubiquitination and proteasomal turnover. RNF4 integrates SUMO and ubiquitin signaling to regulate DNA damage responses, replication stress, transcriptional control, and maintenance of genome stability. By modulating the fate of SUMOylated repair and chromatin-associated factors, RNF4 influences cell-cycle progression and cellular adaptation to genotoxic stress. Dysregulated RNF4 activity has been linked to aberrant proteostasis and genome instability phenotypes relevant to cancer biology and related stress-response pathways.
RNF4 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 Rnf4 upregulation across a broader range of human cell types.
RNF4 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 Rnf4 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous RNF4 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Rnf4 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.