C3 Lentiviral Activation Particles (m2): sc-419391-LAC-2

Mouse C3 encodes complement component 3, a central hub of the complement cascade that is proteolytically processed into C3a and C3b to drive opsonization, immune cell recruitment, and amplification of innate immune responses through the classical, lectin, and alternative pathways. C3 activation supports clearance of pathogens and immune complexes, regulates crosstalk with coagulation and inflammatory signaling, and shapes tissue homeostasis by influencing phagocytosis and cytokine production. Dysregulated C3 activity is linked to complement-mediated inflammation and immune-complex pathology, with relevance to models of autoimmunity, infection, and neuroinflammatory processes. Gene editing of C3 in mouse systems enables mechanistic studies of complement activation, receptor-ligand interactions, and functional outcomes in vivo and in primary immune cell assays.

C3 Lentiviral Activation Particles (m2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient C3 upregulation across a broader range of human cell types.

C3 Lentiviral Activation Particles (m2) 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 C3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous C3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native C3 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.