B7RP-1 Lentiviral Activation Particles (m): sc-424469-LAC

Mouse Icosl encodes B7RP-1 (also known as ICOS ligand/CD275), a B7 family co-stimulatory molecule expressed on antigen-presenting cells that engages ICOS on activated T cells. This interaction amplifies PI3K–Akt signaling and downstream transcriptional programs that support T cell expansion, survival, and effector differentiation, and it contributes to germinal center formation through regulation of T follicular helper cell function and B cell help. B7RP-1–ICOS signaling helps shape adaptive immune responses at mucosal and peripheral sites and is frequently studied in the context of immune tolerance, inflammation, and autoimmunity. Dysregulated ICOSL pathways have been implicated in altered humoral immunity and chronic inflammatory phenotypes, making Icosl a relevant target for mechanistic immunology research.

B7RP-1 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 Icosl upregulation across a broader range of human cell types.

B7RP-1 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 Icosl transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous B7RP-1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Icosl 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.