CIITA Lentiviral Activation Particles (m2): sc-419390-LAC-2

Mouse Ciita encodes the class II major histocompatibility complex transactivator (CIITA), a non-DNA-binding master regulator that coordinates transcription of MHC class II genes and accessory antigen-presentation factors through interactions with the RFX, NF-Y, and CREB/ATF enhanceosome. CIITA activity governs inducible antigen presentation in professional antigen-presenting cells and can be stimulated by cytokine signaling such as IFN-γ, linking innate immune cues to adaptive CD4+ T cell responses. Dysregulated Ciita/CIITA function is associated with altered MHC class II expression and immune phenotypes relevant to infection, autoimmunity, and tumor immune surveillance in mouse models. Ciita gene editing and CIITA-focused perturbation studies support mechanistic research on antigen presentation pathways, epigenetic control of immune gene transcription, and functional genomics screens in immunology and inflammation.

CIITA 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 Ciita upregulation across a broader range of human cell types.

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