Date published: 2026-7-9

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Gγ 10 Lentiviral Activation Particles (m2): sc-420613-LAC-2

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Datasheets
  • Target species: mouse
  • 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
  • Gγ 10 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
  • Gγ 10 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 Gγ 10 Lentiviral Activation Plasmid (m2) and Gγ 10 Lentiviral Activation Plasmid (m22) target distinct regulatory regions of the Gng10 promoter. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Gγ 10 Lentiviral Activation Particles (m2)

    sc-420613-LAC-2
    200 µl
    $455.00

    Mouse Gng10 encodes the heterotrimeric G protein γ10 subunit, a membrane-anchored component of GPCR signaling that assembles with Gβ subunits to form Gβγ complexes controlling receptor-dependent signal propagation. Gβγ derived from GNG10-containing heterotrimers modulates effectors such as ion channels, adenylyl cyclases, and phospholipase Cβ, shaping second-messenger pathways that regulate neuronal excitability, secretion, and cytoskeletal dynamics. Altered G protein subunit composition and Gβγ signaling has been implicated in disorders involving neurodevelopmental and sensory processing, as well as dysregulated cell migration and proliferation, making Gng10 a relevant target for mechanistic studies. Gene editing of Gng10 in mouse models supports pathway dissection of GPCR networks, protein–protein interaction mapping within G protein complexes, and functional genomics screens linking receptor inputs to downstream transcriptional and electrophysiological phenotypes.

    Gγ 10 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 Gng10 upregulation across a broader range of human cell types.

    Gγ 10 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 Gng10 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Gγ 10 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Gng10 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.