C/EBP δ Lentiviral Activation Particles (m): sc-419624-LAC

Cebpd encodes the transcription factor C/EBPδ, a basic leucine zipper protein that regulates inducible gene expression programs in response to inflammatory and stress cues. It integrates signaling downstream of cytokines and innate immune pathways, including NF-κB and JAK/STAT, to coordinate transcriptional control of acute-phase responses, macrophage activation, and metabolic adaptation. In mouse tissues, C/EBPδ contributes to cell-cycle control, differentiation, and senescence-associated transcriptional remodeling, with context-dependent roles in epithelial, stromal, and immune compartments. Dysregulated C/EBPδ activity has been linked to chronic inflammation and tumor-associated microenvironmental programs, making it relevant for mechanistic studies of immune regulation and cancer biology.

C/EBP δ 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 Cebpd upregulation across a broader range of human cell types.

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