Date published: 2026-8-17

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ARMER Lentiviral Activation Particles (h): sc-409837-LAC

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Datasheets
  • Target species: human
  • 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
  • ARMER Lentiviral Activation Particles (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
  • ARMER Lentiviral Activation Particles (h) 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 ARMER Lentiviral Activation Plasmid (h) and ARMER Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the ARL6IP1 promoter. One or both designs may be available
  • Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: ARMER Antibody (B-5): sc-514476
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    ARMER Lentiviral Activation Particles (h)

    sc-409837-LAC
    200 µl
    $455.00

    ARL6IP1 encodes ARMER, an endoplasmic reticulum–resident membrane protein implicated in maintaining ER homeostasis and regulating apoptosis through modulation of ER stress signaling. ARMER has been linked to unfolded protein response pathways and ER-associated processes that influence cell survival, calcium handling, and proteostasis under stress conditions. Altered ARL6IP1 expression has been reported across contexts involving dysregulated apoptosis and stress adaptation, including cancer biology and neurobiology, supporting its relevance for mechanistic studies of survival signaling and stress tolerance. As a human target, ARMER provides a useful node for probing how ER stress interfaces with mitochondrial apoptotic pathways and broader cellular quality-control networks.

    ARMER Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient ARL6IP1 upregulation across a broader range of human cell types.

    ARMER Lentiviral Activation Particles (h) 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 ARL6IP1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ARMER expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native ARL6IP1 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.