Date published: 2026-8-25

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MAGE-L2 Lentiviral Activation Particles (m): sc-424255-LAC

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Datasheets
  • Target species: mouse
  • 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
  • MAGE-L2 Lentiviral Activation Particles (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
  • MAGE-L2 Lentiviral Activation Particles (m) 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 MAGE-L2 Lentiviral Activation Plasmid (m) and MAGE-L2 Lentiviral Activation Plasmid (m2) target distinct regulatory regions of the Magel2 promoter. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    MAGE-L2 Lentiviral Activation Particles (m)

    sc-424255-LAC
    200 µl
    $455.00

    Magel2 encodes MAGE-L2, a member of the melanoma antigen gene (MAGE) family with prominent roles in hypothalamic and neuronal biology in mouse. MAGE-L2 participates in ubiquitin-dependent regulation of protein trafficking and stability, including modulation of endosomal sorting and receptor turnover through interactions with E3 ubiquitin ligase complexes. These processes influence neuroendocrine signaling, circadian and feeding-related circuits, and intracellular transport pathways that are critical for neuronal function. Altered MAGEL2 activity is linked to neurodevelopmental and metabolic phenotypes and is widely studied in the context of syndromic disorders affecting hypothalamic function.

    MAGE-L2 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 Magel2 upregulation across a broader range of human cell types.

    MAGE-L2 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 Magel2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MAGE-L2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Magel2 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.