CD2 Lentiviral Activation Particles (m): sc-419537-LAC

Mouse Cd2 encodes CD2, a surface adhesion and costimulatory receptor expressed primarily on T cells and NK cells that strengthens immune synapse formation through interactions with CD58/CD48 and coordinates signaling with the T cell receptor complex. CD2 engagement contributes to proximal tyrosine kinase cascades involving LCK, FYN, and ZAP70, shaping downstream MAPK and NF-κB–dependent transcriptional programs that govern activation, cytokine production, and cytotoxic effector function. Altered CD2 expression or signaling has been linked to dysregulated lymphocyte activation and tolerance, making Cd2 a useful node for studying inflammatory and autoimmune mechanisms as well as immune evasion in cancer microenvironments. In mouse models, CD2 biology is frequently leveraged to interrogate T cell development, trafficking, and antigen-driven expansion.

CD2 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 Cd2 upregulation across a broader range of human cell types.

CD2 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 Cd2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Cd2 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.