Date published: 2026-7-13

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IL-15Rα Lentiviral Activation Particles (m2): sc-421090-LAC-2

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Datasheets
  • Target species: mouse
  • 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
  • IL-15Rα Lentiviral Activation Particles (m2) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
  • IL-15Rα Lentiviral Activation Particles (m2) contain the following SAM Activation elements: a deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, an MS2-p65-HSF1 fusion protein and a target-specific 20 nt guide RNA. They also contain the blasticidin, hygromycin and puromycin resistance genes
  • Upon transduction, the SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
  • gRNAs encoded by IL-15Rα Lentiviral Activation Plasmid (m2) and IL-15Rα Lentiviral Activation Plasmid (m22) target distinct regulatory regions of the Il15ra promoter. One or both designs may be available
  • Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: IL-15Rα Antibody (G-3): sc-374023
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    IL-15Rα Lentiviral Activation Particles (m2)

    sc-421090-LAC-2
    200 µl
    $455.00

    Mouse Il15ra encodes the interleukin-15 receptor alpha (IL-15Rα), a high-affinity binding subunit that captures IL-15 and enables trans-presentation to IL-2/15Rβ–γc complexes on responding lymphocytes, thereby amplifying JAK1/JAK3–STAT5 signaling. Through this mechanism, IL-15Rα regulates development, survival, and activation of NK cells and memory CD8+ T cells, and shapes cytokine-driven immune homeostasis during inflammation. Dysregulated IL-15/IL-15Rα axis activity is implicated in autoimmune and inflammatory pathology and in tumor-immune interactions via altered cytotoxic lymphocyte function. Il15ra-edited mouse models and derived immune cells are used to dissect cytokine receptor trafficking and trans-presentation, map downstream transcriptional programs, and evaluate immune regulation in infection, autoimmunity, and cancer-relevant microenvironments.

    IL-15Rα 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 Il15ra upregulation across a broader range of human cell types.

    IL-15Rα 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 Il15ra transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous IL-15Rα expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Il15ra 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.