c-Rel Lentiviral Activation Particles (m): sc-422641-LAC

Mouse Rel encodes c-Rel, a member of the NF-κB family of transcription factors that regulates stimulus-dependent gene programs controlling lymphocyte activation, cytokine production, cell survival, and differentiation. c-Rel is activated downstream of antigen receptors, Toll-like receptors, and TNF receptor signaling via IKK-mediated phosphorylation and proteasomal degradation of IκB inhibitors, enabling nuclear translocation and promoter/enhancer binding. Its activity shapes inflammatory and immune regulatory pathways, including feedback control of NF-κB signaling and coordination with AP-1 and IRF networks. Dysregulated c-Rel signaling has been linked to aberrant immune activation and inflammatory pathology, making it a useful node for mechanistic studies in immunology and disease-relevant signaling models.

c-Rel 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 Rel upregulation across a broader range of human cell types.

c-Rel 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 Rel transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous c-Rel expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Rel 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.